Race 2019

BASIC SCIENCE LECTURES
1 Gas Laws and its Applications in Anesthesia
Professor and Head, Gurudatt C L

J S S Medical College and Hospital,
Mysore
Key points
Some of the practical applications of gas laws in anesthesia:

Ø Boyle’s law can be applied to know the volume of oxygen remaining in a cylinder
Ø Universal gas constant – to know the content of the oxygen cylinder using Bourdon’s pressure gauge.
Ø Charle’s law can be used to know the volume of nitrous oxide remaining in a type E cylinder
Ø Gay Lussac’s law – when surrounding temperature increases, pressure increases inside the cylinder and
it may even explode
Ø Adiabatic process - cylinder should be opened slowly as rapid opening of the valve will produce a
rapid flow causing rapid compression of oxygen in the narrow tube producing a very high temperature
leading to possible explosion
Ø Joule thomson’s effect - used in the manufacture of oxygen from air
Ø Bernoulli’s principle - used to reduce the pressure in the Drager machines from the pressure regulators
to flow meter assembly
Ø In flow meters, Hagen – Poiseuille law is applied for lower laminar flows and Graham’s law for higher
turbulent flows
Ø Venturi’s effect – for performing Pethick’s test in checking Bain’s circuit
Ø Graham’s law - use of mixture of oxygen and helium improves flow in a patient with tracheal narrowing,
instead of oxygen and N2O or air
Ø Coanda effect - unequal gas flow to the alveoli when there is slight narrowing of the bronchiole before
it divides. Also used in ventilators.
Anesthesiologist will be dealing with many of the gases Fluids

which are needed for anesthetizing patients every
Substances may exist in solid, liquid or gaseous form.
day. These gases are delivered to the patient using
These forms or phases differ from each other according
anesthesia work stations. Many of the gas laws are also to the random movement of their constituent atoms
applicable to these gases used by the anesthesiologist or molecules. In solids, molecules oscillate about a
using anesthesia delivery system. A sound knowledge fixed point, whereas in liquids the molecules possess
about the application of these gas laws is essential for higher velocities and therefore higher kinetic energy;
every anesthesia trainee for safe use of the anesthesia they move more freely and thus do not bear a constant
delivery system and conduct of anesthesia as well. relationship in space to other molecules. The molecules
RACE 2019 Ramachandra Anesthesia Continuing Education

Gas Laws and its Applications in Anesthesia 4 Gurudatt C L
of gases possess even higher kinetic energy and move 13. Coanda effect
freely to an even greater extent. 14. Critical temperature
Both gases and liquids are termed fluids. Liquids are 15. Poynting effect
incompressible and at constant temperature occupy a 16. Henry’s law
fixed volume, conforming to the shape of a container; 17. Raoult’s law
gases have no fixed volume but expand to occupy the
total space of a container. Nevertheless the techniques Definitions of the gas laws
for analysing the behaviour of liquids and gases 1) Boyle’s Law: States that at constant temperature
(or fluids in general) in terms of their hydraulic and (T), the volume (V) of a given mass of a gas is inversely
thermodynamic properties are very similar. proportional to the absolute pressure (P).
In the process of vaporization, random loss of liquid V α 1/p
molecules with higher kinetic (thermal) energies from
the liquid occurs while vapour molecules randomly The equation can also be written as - PV = constant (if
lose thermal (kinetic) energy and return to the liquid T is kept constant)
state. Heating a liquid increases the kinetic energy of
2) Charle’s Law: States that at constant pressure, volume
its molecules, permitting a higher proportion to escape
of a gas is directly proportional to the temperature.
from the surface into the vapour phase. The acquisition
by these molecules of higher kinetic energy requires an V α T or
energy source and this usually comes from the thermal
V / T = constant.
energy of the liquid itself, which leads to a reduction
in its thermal energy as vaporization occurs and hence 3) Gay Lussac’s law: States that at constant volume,
the liquid cools. pressure is directly proportional to the temperature
Collision of randomly moving molecules in the gaseous P α T or
phase with the walls of a container is responsible for
the pressure exerted by a gas. P/T = constant
Gas laws 4) Avagadro’s hypothesis: States that equal volume of

gases contain equal number of molecules at standard
The common gas laws that are applicable in anesthesia temperature and pressure (STP).
are.
Based on the above hypothesis,
1. Boyles’s Law
One mole of a gas contains - 6.023 x10 23 molecules
2. Charle’s Law
3. Gay Lussac’s Law This law can also be defined as -
4. Avagadro’s Law or Hypothesis One mole (molecular weight) of any gas at STP occupies
5. Dalton’s Law of partial pressures 22.4 litres of volume.
6. Universal gas law
When mole (molecular weight) is expressed in grams
7. Hagen–Poiseuille law for laminar flow it’s called as gram molecular weight.
8. Graham’s law for turbulent flow
So 1 gram molecular weight of any gas at STP, will
9. Reynolds’s number
contain 6.023x10 23 molecules and occupies 22.4 litres
10. Graham’s law of diffusion. of volume.
11. Bernoulli’s principle
Standard temperature is 273 K and standard pressure
12. Venturi’s effect
is 760 mm of Hg.
The molecules of the gas in the centre of the system encounter lesser frictional resistance and move at a greater
velocity than those at the sides of the system.
Turbulent flow- is a rough, tumbling and an uneven flow pattern (Fig. 2).
Fig 2: Turbulent flow

Turbulent flow moves with a blunt front. Due to tumbling effect, all the molecules in the system encounter the
wall of the tube.
9) Graham’s law for turbulent flow: states that the flow rate is directly proportional to square root of pressure
gradient on either side of the tube and inversely proportional to square root of density of the fluid.
Where P1-P2 is pressure gradient across the tube.

Since flow α 1/ resistance, above equation can also be rewritten
10) Bernoulli’s principle: when a gas flowing through a tube encounters a constriction, at that point the pressure
drops and the velocity increases i.e. kinetic energy increases and the potential energy decreases. This is called
as Bernoulli’s principle (Fig 3)
Venturi is a tube with a cross section gradually decreases and then increases.
Fig 3: Bernoulli’s principle

Entrainment of air from the surrounding due to fall in pressure at the point of constriction is called as Venturi’s
effect (Fig 4).
Fig 4: Venturi effect

11) Coanda effect: is the tendency of the fluid jet to be attached to a nearby surface. This phenomenon is also
called as wall attachment. When a narrow tube encounters a Y junction of the wide bore, because the flow tends
to cling to one side, the flow will not evenly divide between the two outlets, but flows through only one limb of
the Y piece. This behaviour is called Coanda Effect (fig 5).
Fig 4: Coanda effect

12) Critical Temperature: This is the temperature above Considering the pressure in cylinder as P1 (2000 psi)
which the gas cannot be compressed to its liquid state and volume of the cylinder as V1 (5L) and volume of
with any amount of pressure. So a gas can remain in a oxygen available (V2) at a pressure of P2 (15 psi),
liquid state below its critical temperature.
The equation will be
Critical pressure is the pressure of the gas at its critical
P1V1= constant, and
temperature.
P2V2= constant
13) Poynting effect: When two gases, one of high
and another of low critical temperature are mixed in Hence the equation will be P1V1= P2V2
a container, the critical temperature of the gas with a
2000 X 5= 15 X V2
high critical temperature will decrease to a lower level
(pseudo critical temperature) and the mixture will V2=2000 x 5/15=665 litres
remain as a gas above this pseudo critical temperature.
So if we use 3 litres of oxygen, the E type full cylinder will
This effect is called as Poynting effect.
last for about 220 mins (5 liters of oxygen will remain
14) Adiabatic Changes: The three gas laws describe the in the cylinder and cannot be used).
behaviour of the gas when one of the three variables,
2. How Bourdon’s pressure gauge will indicate the
pressure, temperature or volume is constant. For these
content of the oxygen cylinder?
conditions to be applied, heat energy is to be taken off
or added to the gas as the changes occurs. The state The gas law applicable is Universal Gas Constant and
of the gas can also be attended without allowing the the equation used is
gas to exchange heat with the surroundings, and this
PV= nRT.
is called Adiabatic change. When the energy is neither
gained from or lost to the atmosphere the process is Where P=pressure
called as Adiabatic Process. This is also called as Joule
Thomson Effect. n=number of molecules
15) Raoult’s law states that the reduction of vapour R=universal gas constant and
pressure of a solvent is proportional to the molar T= temperature
concentration of the solute. This law is useful during
calculation of concentrations of volatile anaesthetics Since in this cylinder volume is constant, temperature is
in azeotropic mixtures. constant and R is already a constant P = n, i.e. pressure
shown in the Bourdon’s gauge is proportional to the
Applications of gas laws in the anesthesia delivery number of molecules which is the amount of gas in the
system cylinder. Hence the pressure gauge acts as a content
gauge.
1. What is the gas law applied to know the volume
of oxygen in a full “E” type of cylinder available for If the gauge pressure in E type cylinder is showing 1000
use at 15 psig (pressure at common gas outlet)? PSI (half full), then the volume of gas one can use will
be 330 litres at 15 PSI.
To know the volume of oxygen available one has to
apply Boyle’s law. As we know the volume of an E 3. How do you know how much of nitrous oxide is
type of cylinder is approximately 5 Litres. The service present in an E type of cylinder for use?
pressure at which the cylinder is filled is 2000 psig
Nitrous oxide has a critical temperature of 36.5o C.
Boyle’s law states that pressure × volume is constant Hence at room of temperature of 20 o C it remains
at constant temperature or PV = constant. as liquid. Since it is in liquid form one cannot use

Boyle’s law to calculate the volume available and also a volume of 5 litres and 5 litres of water will weigh 5
the pressure gauge will not show the content of the kgs., since the density of water is 1, 1 litre of water
cylinder. To calculate the amount of nitrous oxide to weighs 1 kg, the filling ratio represents the mass of
be used, one has to weigh the cylinder and deduct the N2O in kilograms divided by the internal volume of the
tare weight (weight of the empty cylinder) to know cylinder in litres.
the actual weight of liquid nitrous oxide in kgs. If the
0.67= weight of N2O
weight of the liquid nitrous oxide is 3.3 kgs, then using
5 kgs
Avagadro’s Hypothesis 1 gram molecular weight of any
substance will occupy 22.4 litres; the molecular weight Wight of the liquid N2O in an E type cylinder = 0.67 x
of N2O is 14 × 2 + 16= 44 ( molecular weight of Nitrogen 5= 3.35 kgs.
is 14 and oxygen is 16.)
So weight of liquid N2O that can be filled in an E type
So 44g of N2O will give 22.4 litres cylinder is 3.35 kgs.
3300 g will give 3300 X 22.4= 1680 litres. 6. Why oxygen cylinder should not be kept under
44 the sun?
A full E type nitrous oxide cylinder will give 1680 liters If oxygen cylinder is kept under the sun its temperature
of gas at STP (273 K and 760 mm of Hg) increases and according to Gay Lussac’s Law pressure
is directly proportional to temperature, volume being
As per Charle’s law, volume is directly proportional to
constant, Pressure increases inside the cylinder so
temperature,
much that the cylinder may even explode. Hence the
Room temperature is 273+ 20= 293K. oxygen cylinders should be stored in a cooler place. In
order to prevent accidental explosion safety valves are
Hence at room temperature (293 K) a full E type nitrous
incorporated in the cylinder valves.
oxide cylinder will give 1680 X 293 = 1803 litres.
273 7. How is the safety valve of the cylinder works?
4. A full E type nitrous oxide cylinder will give 1803 There are 3 types of safety valves in the cylinder
litres of gas at room temperature.
a) Fusible plug.
Why the Bourdon’s pressure gauge of N2O does not b) Frangible disc.
show the contents of the cylinder? c) Safety relief valve.
N2O is a liquid at room temperature and hence it will Safety valves are present just below the conical
not follow the universal gas constant equation. The depression of the cylinder valve.
pressure in the N2O Bourdon pressure gauge always
a. FUSIBLE PLUGS are made up of Woods metal
shows 750 psig till all the liquid N2O becomes vapour.
(an alloy of cadmium, bismuth, tin and lead)
750psig is the saturated vapour pressure of N2O at
and the metal melts at a temperature of 212 o F.
20oC. When all the liquid nitrous oxide converts into
If the temperature inside the cylinder increases
the vapor state, the Bourdon’s pressure gauge will act
when the cylinder is accidentally kept under
as the content gauge and Boyle’s law will be applicable.
the sun, the Woods metal in the fusible plug
5. What is filling density and how it is used to fill N2O? melts and gives vent for oxygen and prevents
explosion.
Filling density = Weight of liquid N2O
Weight of water b. FRANGIBLE DISC has a diaphragm that breaks
at a particular pressure. As the temperature
The filling density or filling ratio of N2O in the tropical
inside the cylinder increases, the pressure also
climate is 0.67. So in an “E” type of cylinder which has

increases (Gay Lussac’s law), the diaphragm in the pressure decreases. This is the principle adopted
the frangible disc breaks and gives vent to the in the construction of pressure regulators where in
gas and prevents explosion. high pressured gases from the cylinders are exposed
to larger area of the diaphragm inside the regulator,
c. SAFETY RELIEF VALVE opens at a particular where the force is kept constant by the spring, and the
pressure and closes once the pressure inside output pressure from the pressure regulator decreases.
the cylinder decreases. Pressure inside the
cylinder can increase as a result of increase in 12. How pressure is reduced in the DRAGER machines
temperature (Gay Lussac’s law) if accidentally from the pressure regulators to flow meter
the cylinder is heated up. assembly?
8. Why should you open the cylinder slowly? In Ohmeda machines, there will be a second stage
pressure regulators which reduces the output pressures
Cylinder should be opened slowly as rapid opening of O2 to 14 PSI and N2O to 26 PSI. In Drager machines,
of the valve will produce a rapid flow of oxygen into there is no second stage regulator. As the gases from the
the space in the tubing of the yoke assembly and the pressure regulators at a pressure of 45 to 60 psig move
pressure regulator, producing to an Adiabatic process towards the flow meter assembly they have to flow
as rapid compression of oxygen in the narrow tube through the “Flow restrictors” which are nothing but
produces a very high temperature leading to possible sudden narrowing of the tubes. According to Bernoulli’s
explosion. Hence oxygen cylinder should be opened principle here the pressure is further reduced, but flow
slowly to prevent adiabatic process. is increased before reaching the flow meter assembly.
9. Why liquid oxygen should be stored below -118 o C? 13. What is the importance of viscosity and density
regarding the accuracy of flow in the flow meters
Critical temperature of oxygen is -118 oC and boiling
at different atmospheric pressures?
point is -183 oC. Hence in order to maintain liquid state,
oxygen should be stored between -118 oC to -183 oC. Density is defined as mass per unit volume i.e. D= m/v.
10. How Joule Thomson’s effect is used in the Density of the gas can be obtained from Avagadro’s
manufacture of oxygen from air? hypothesis, as we know that 1 gram molecular weight
of any gas occupies 22.4 litres of volume at STP, Gram
When air is compressed suddenly, it gets heated up as molecular weight divided by 22.4 litres will give the
a result of adiabatic process. When this air is cooled density of the gas. e.g. N2O- molecular weight is 44
by external cooling and is made to suddenly expand, it hence 44/22.4 = 1.96. Since the viscosity and density
loses further temperature as energy is spent in order of each gas is different, the flow meters are calibrated
to hold the molecules together i.e. the Vander Waal for that particular gas and hence should not be
forces. This sudden loss of temperature is due to Joule interchanged.
Thomson’s effect. When this is repeated many times
the temperature reduces to less than -183 o C and Flow meters are tapered glass tubes. The internal
through fractional distillation, liquid oxygen collected diameter is narrower in the lower part and wider in the
in the lower part is separated from nitrogen with a upper part. In the lower part, flow of the gas is laminar
boiling point of -197 o C which collects at the top of and in the upper part the flow is orificial or turbulent,
the container. as the diameter of the tube is more than the vertical
length of the float or the bobbin. So, for lower flows, it
11. What is pressure and what is the principle adopted is laminar flow and for higher flows it is turbulent. The
in the construction of pressure regulators? flow meters are always calibrated at 760 mm of Hg. If
the anesthesia machine is used in a high altitude area,
Pressure is defined as force per unit area i.e. P= F/ A.
where the atmospheric pressure is very low, the density
This can be rearranged to F=PxA. When we keep the
of the gas decreases, but viscosity will not change. As
force constant and increase the area, then automatically
higher flows depend on density and as per Graham’s Rs. 7500, 1 ml will cost Rs 30. Then 40 ml would cost
Law For Turbulent Flow, flow is inversely proportional 40x30=1200 Rs.
to square root of density i.e. Flow ά 1/√ density. Flow
So the cost of sevoflurane anesthesia if it is used at
will be higher than the actual flows that are set in the
2% per hour is Rs. 1200 per 1 hr.
flow meters. The opposite will occur under hyperbaric
conditions. 16. Why would you not use connectors with sharp
curves?
14. How Avagadro’s Hypothesis is used to calculate
the amount of volatile liquid needed to make a At the sharp bends the flow converts into a turbulent
known percentage of vapors? flow as the Reynold number will be more than 2000.
This will increase the resistance to the flow. Every
Let us take sevoflurane as example. Molecular weight
piece of anaesthetic equipment, because of diameters
of sevoflurane is 200. Density of sevoflurane is 1.5
& shape of connectors, number & arrangement will
According to Avagadro’s Hypothesis, 200g of sevoflurane affect FGF. Wide bore & curved rather than sharp angles
gives 22400ml of vapor. should be preferred.
So 1g of sevoflurane will give - 22400/200= 112 ml of 17. What happens if you administer Entonox in very
vapors. cold climate?
Since the density is 1.5, 1.5 g is equal to 1 ml. Entonox is a 50:50 mixture of O2 & N2O. The critical
temperature of oxygen is -118 o C and of N2O is 37 o C.
So 1ml of sevoflurane liquid =112 x 1.5 = 168 ml.
when these gases are mixed in a same cylinder, then
This 168 ml of sevoflurane vapour is at standard the critical temperature of the mixture will be -6o C due
temperature of 273 K, one has to calculate at room to Poynting effect and the mixture will remain as gas at
temperature i.e. 293 K room temperature. In cold climates if the temperature
is less than -6 o C, then N2O will separate into its liquid
Based on Charle’s law, the volume of a liquid form and will remain in the bottom of the cylinder
anaesthetic is directly proportional and the patient will get only O2 initially and hence will
not produce any analgesia. Later patient gets only N2O
to temperature i.e. V/T= constant
which can result in hypoxia. Hence in such situation
V1/T1= V2/T2 V1=168 ml T1=273 K V2=? T2= 293 K cylinder should be thoroughly shaken before use.
V2= V1 x T1
18. How Venturi’s Effect is used in checking the
T2
integrity of the inner tube of the Bain’s Circuit?
V2= 168 x 293 = 180 ml
The integrity of the inner tube is very essential as any
273
leak in that can result in large apparatus dead space.
Thus 1 ml of sevoflurane at room temperature gives One of the tests used for the same is Pethick’s Test.
180 ml of sevoflurane vapor. In this test after closing the expiratory valve and the
inner tube, keeping 3 litres of flow of O2 one should
15. How do you estimate the cost of volatile
see that the reservoir bag is full. Then simultaneously,
anaesthetics?
O2 flush is activated and also the thumb occluding the
If 2% of sevoflurane is used with a fresh gas flow of outer tube is released. If the inner tube does not have
6 litres, then every minute 120 ml of vapor will be any leak, then the reservoir bag will collapse. This is
used and per hour it will be 7200ml of vapour. Since due to Venturi’s effect, because at the opening of the
1ml of liquid sevoflurane will give 180 ml of vapour, inner tube into the outer tube due to the flow of 30-70
then 7200/180=40 ml of the liquid sevoflurane will be litres of O2 which produces a sudden fall in the pressure,
used per hour. Since cost of 250 ml of sevoflurane is sucking the O2 from the bag & collapsing it. If there is
any leak in the inner tube, then the reservoir bag will have a decreased density compared to O2 or air. And
not collapse. hence using Heliox will decrease the resistance and
increase the flow.
19. What is the importance of selecting a right sized
endotracheal tube? 22. Why can there be unequal gas flow to the alveoli
where there has been a slight narrowing of the
The size of the endotracheal tube (ETT) selected for a bronchiole before it divides?
particular patient should not increase resistance for
breathing. So for an adult male patient one can select This due to Coanda effect as there is narrowing before
8.5 or 9 mm internal diameter ETT & for female patient the branching, the pressure drops, the velocity of the
7 or 7.5 mm internal diameter ETT should be selected. air increases, but the flow tends to cling to one side &
As we know that for laminar flow, according to Hegan- doesn’t divide evenly between the branches. Mucus
Poiseuille’s law, the resistance increases by 4th power plug at the branching of tracheo-bronchial tree may
whenever radius of the tube is decreased. Any increase cause maldistribution of respiratory gases. It may also
in there resistance will increase the work of breathing explain some cases of Myocardial Infraction, where
and produces an early fatigue of the respiratory muscles there may be some narrowing, before the branching
of the patient. Normal resistance offered by the adult of the coronaries. Unequal flow may result because of
airway is < 2 cms of H2O/ litre/sec. With the right sized atherosclerotic plaques in the vascular tree.
ETT, the resistance increases to 5 cms of H2O/ litre/ 23. How Coanda effect is used in ventilators?
sec. Whenever secretion gets collected inside of the
tube and decreases the lumen, then the resistance can If a tube is made to narrow and branch, the flow of the
increase to 10 cms of H2O/ litre/sec gases can be made to flow preferentially through one
of the branch & then alternately through the other
20. Why one should monitor the ETT cuff pressure branch by connecting two tubes inserted at each side
during prolonged surgeries when N2O is used as a at the exit of the narrow tube.
carrier gas and air is used to inflate the cuff?
24. What is entrainment ratio and how it is calculated?
N2O is 37 times more diffusible than N2. Hence N2O will
enter the cuff of the ETT before N2 can diffuse out the Entrainment ratio is defined as the ratio of entrained
cuff, which increases the pressure as the volume cannot flow to the driving flow. The total entrained flow is due
increase (Boyle’s Law). This can produce damage to the to the Bernoulli effect and jet entrainment.
tracheal mucosa & can produce post-operative sore Entrainment ratio = entrained flow/driving flow.
throat. So cuff pressure is essential. The same problem
can occur in closed pneumothorax patient if N2O is Thus a 9 to 1 entrainment ratio indicates that there are 9
used as the pressure in the pleural cavity may increase litres/min being entrained by a driving gas of 1 litre/min.
producing tension pneumothorax. Hence whenever the
25. What is the application of Henry’s law in knowing
patient develops pneumothorax N2O should be cut off.
the amount of gas carried in solution?
And also for patients posted for middle ear surgeries
use of N2O should be restricted. If a patient develops Henry’s law states that the amount of a gas dissolved in
an air embolism per operatively, N2O should be cut off. a unit volume of a solvent is directly proportional to its
partial pressure at STP. The law also predicts how much
21. How the use of mixture of oxygen and helium
of a gas dissolves in a liquid. According to this law, the
improves flow in a patient with tracheal narrowing,
volume of gas that dissolves in a liquid is equal to its
instead of oxygen and N2O or air?
solubility coefficient times its partial pressure.
Whenever there is tracheal stenosis, the flow of gases
V = α x PGAS
will be turbulent and hence there will be increase in the
resistance and decreases flow across the stenosis. Flow where V = volume of the gas dissolved, α is the solubility
and resistance will depend on the density of the gas as coefficient of the gas in the liquid and Pgas is the partial
per Graham’s law. Mixture of oxygen and helium will pressure above the liquid.
The amount of gas carried in solution in blood is • Record the expired tidal volume and the peak
governed by Henry’s law. inspiratory pressure (PIP) during Y-occlusion.
The solubility coefficient of oxygen is 0.003 ml/dl. Thus • Divide the expired tidal volume by the peak
at 100 mmHg of oxygen tension, the amount of oxygen inspiratory pressure. This will be the circuit
in the dissolved form will be 0.3 ml. compression factor.
Deep sea diving – when divers breathe gases under • Multiply the circuit compression factor (ml/
pressure, nitrogen and other gases pass into solution cmH2O) by the PIP during mechanical ventilation
in the tissues. If they return to atmospheric pressure, or PIP-PEEP if PEEP is used, to get the circuit
the nitrogen comes out of solution as small bubbles in compressible volume. Example – if the expired tidal
the joints and elsewhere giving rise to decompression volume is 150ml and PIP is 50cmH20, then Circuit
sickness. compression factor is 150/50=3 ml/cmH2O
26. What is an Azeotrope and how Raoult’s law is • If during mechanical ventilation PIP-PEEP is 15
applied for azeotropes? cmH2O, then the circuit compressible volume will
Raoult’s law states that the reduction of vapour pressure be 15x3=45 ml. This has to be deducted from the
of a solvent is proportional to the molar concentration expired tidal volume to get the corrected tidal
of the solute. Raoult’s law applies to all solutions and volume or actual tidal volume delivered to the
the substance dissolved in solution need not be a solid patient.
or a gas but may be another liquid. Azeotrope is a
References
mixture which vaporizes in the same proportion as the
volume concentrations of the components in solution. 1. Basic Physics and Measurement in Anesthesia,
Ether and halothane form an azeotrope, provided that Davis, P.D., Parbrook, G.D. and Kenny G.N.C,
they are in the ratio of one part of ether to two parts 4th Edition, Butterworth Heinemann, pp 2-3,
of halothane. The molar concentration of ether is 3.19 1995.
mol/litre and halothane is 6.30 mol/litre. According
to Raoult’s law, the vapour pressure will also be in the 2. Dr.Fred Senese,General Chemistry OnLine :
same proportions. This means that the components of h tt p : / / a n t o i n e . f s u . u m d . e d u / c h e m /
azeotrope evaporate in the ratio of one part of ether senese/101/gases/
to two parts of halothane, so the relative volume
concentration of the liquid mixture does not change. 3. Jones, E.R. and Childers, R.L, “Gas Laws
and Kinetic Theory ” in Contemporary
27. What is circuit compressible volume and how it College Physics Addison-Wesley, Reading,
is calculated? Massachusetts, 1993, p 281.
Circuit compressible volume is “the expansion of the 4. Park, John L. “The Kinetic Molecular Theory
ventilator circuits during inspiration due to positive of Ideal Gases, http://dbhs.wvusd.k12.ca.us/
pressure, leading to a small lost volume of gas that GasLaw/Basics-of-KMT.html
does not reach the patient, but is recorded as part of
the expired tidal volume”. 5. Jones, E.R. and Childers, R.L, “Gas Laws
and Kinetic Theory ” in Contemporary
Calculation of circuit compressible volume College Physics Addison-Wesley, Reading,
• Set the respiratory rate to 10/min and tidal volume Massachusetts, 1993, p 325-346
to 150 ml, and maximum high pressure alarm limit. 6. Clinical application of mechanical ventilation,
• Completely occlude the patient Y-connection of the second edition, David Chang, Delmer –
ventilator circuit. Thomson Learning, p 188-189

MCQ
1. Reynolds number is directly proportional to 4. Which Gas law is used to improve flow in a
all except patient with tracheal narrowing, while using
Heliox?
a. Velocity
a. Graham’s law
b. Density
b. Charles Law
c. Viscosity
c. Boyle’s law
d. Diameter
d. Universal gas constant
2. Oxygen is manufactured from air is based on
one of the following principle 5. Which Principle is used to reduce the pressure
in the Drager Anesthesia machines from the
a) Hagen – Poiseuille Law
pressure regulators to flow meter assembly?
b) Universal Gas Constant
a. Bernoulli’s principle
c) Coanda Effect
b. Reynolds number
d) Joule Thomson Effect
c. Universal gas constant
3. Higher flows in flow metersin Anesthesia Ma-
d. Joule Thomson Effect
chine is based on –
a) Hagen – Poiseuille law
b) Graham’s law
c) Charles law
d) Coanda Effect
5. (a) 4. (a) 3. (b) 2. (d) 1. (c)

Answers

2 Respiratory mechanics in anaesthesia
Chief Medical Officer : Mission Smile Ramkumar Venkateswaran

Former Professor and Head of Anaesthesiology,
Kasturba Medical College, Manipal
Key points
Ø Understanding respiratory mechanics during anesthesia helps to prevent postoperative pulmonary

complications
Ø The distribution of ventilation and perfusion are dependent not only on gravity but also on regional
changes in compliance and airway resistance
Ø Reduced FRC is one of the causative factors for postoperative hypoxaemia, atelectasis and pneumonia
Ø The volume of air remaining in the lungs at the point when small airways start closing is called closing
capacity
Ø Ensuring good postoperative analgesia, complete return of neuromuscular function and adequate
recovery from the sedative effects of residual anaesthetics form a well-planned anesthesia
Introduction Review of normal physiology of breathing

Movement of air between the atmosphere and the Oxygen is required to sustain life and every cell in the
lungs is brought about by pressure gradients created body is constantly consuming oxygen and producing
during inspiration and expiration. These gradients carbon dioxide as one of the end products of internal
determine the movement of gases from a point of respiration. We breathe to take in oxygen and to remove
higher pressure to one of lower pressure. It is important carbon dioxide from the body. Gases move into and
for one to first understand how these gradients are out of the lungs (external respiration) across pressure
created during spontaneous breathing before going gradients that are created primarily by the action of
on to the slightly different mechanisms that come into the diaphragm along with the action of the intercostal
play during their creation with intermittent positive and abdominal muscles. Descent of the diaphragm,
pressure ventilation. Induction of anaesthesia brings as well as the upward and outward movement of the
about changes in respiratory mechanics. A proper ribs during inspiration, brings about an increase in all
understanding of these changes brought about by three dimensions of the thoracic cage; top-to-bottom,
the induction of anaesthesia could possibly lead to front-to-back and side-to-side. Increase in the overall
the initiation of steps to counteract some of these dimensions of the thoracic cage during inspiration
adverse effects. In this review, we shall first analyse results in a drop of intraalveolar pressure to a few
the various interactions that bring about air exchange centimetres of water (cm H2O) below atmospheric. The
during spontaneous breathing in the awake subject pressure gradient that develops from the atmosphere
before going on to understand the changes that are to the subatmospheric pressure in the alveoli results in
brought on not only by the switch to positive pressure movement of air into the lungs. Return of the thoracic
ventilation but in addition, by the initiation of the cage to its resting position, brought about by the elastic
anaesthetised state. recoil of the lungs and chest wall, now creates a reversal
of the pressure gradient. The intraalveolar pressure

Respiratory mechanics in anaesthesia 16 Ramkumar Venkateswaran
now becomes a few cm H2O above atmospheric (supra- Though very brief, this background should make the
atmospheric), causing air to leave the lungs during reader familiar with how breathing is brought about in
expiration. a conscious and awake state, and how distribution of
ventilation depends on an interplay between inspiratory
Two properties of the lungs and chest wall determine time and regional differences in compliance and airway
how much air is moved into and out of the lungs by resistance not only in health but also in disease
the pressure gradients brought about by the action of conditions. Against this physiological background, we
the respiratory musculature. These two properties are shall now try to understand the changes in respiratory
compliance and airway resistance. The distribution mechanics that are brought about by induction of
of ventilation and perfusion are dependent not only anaesthesia (very often along with intermittent positive
on gravity but also on regional changes in compliance pressure ventilation). To make this subject unfold slowly
and airway resistance. Ventilation-perfusion ratio is and in an understandable manner, we shall examine
determined by these variations and is well matched these changes in respiratory mechanics under the
only near the hilar regions (or mid-zones) of the lung following headings:
in the erect position. In the erect position, ventilation
exceeds perfusion above the level of the hilum while • Functional residual capacity
perfusion exceeds ventilation nearer the lung bases • Closing volume, closing capacity and its
as distribution of blood flow is primarily gravity- relationship with functional residual capacity
dependent. This description follows the classic 3-zone • Peak expiratory flow rate
model of John B West. For long, it was believed that
Functional residual capacity
blood flow increases (like the layers of a cake) from the
top to the bottom of the lungs in the erect position. Functional residual capacity (FRC) refers to the volume
Recent perfusion scan studies (Peter Slinger) have of air remaining in the lungs at the end of a normal
demonstrated that blood flow is actually distributed expiration. It is the sum of residual volume and
in concentric spheres like the layers of an onion. This expiratory reserve volume. It approximates around
recent concept supports a distribution of blood flow 2000 to 2500 mL in a healthy 70 kg adult male. The
which is denser towards the hilum and gets sparser heart beats around 72 to 80 times a minute and
as one moves towards the peripheries making the creates a near-continuous blood flow through the
distribution more central to peripheral. The impact of alveolocapillary membranes. On the other hand,
this new concept on the distribution of ventilation and breathing is intermittent and results in exchange of
perfusion is yet to be fully understood. the vitiated alveolar gas with fresh inspired gas once
every 4 to 5 seconds (assuming a respiratory rate of
While this is largely true of the healthy lungs, around 12 to 16 breaths per minute). The gas within
additional factors are introduced in the diseased the alveoli is continuously participating in the exchange
lung. Regional changes in lung compliance (due to of oxygen and carbon dioxide between the pulmonary
atelectasis and infection), thoracic wall compliance capillary blood and the alveoli. The functional residual
(as in obesity and scoliosis) and airway resistance (due capacity is a gas exchange reservoir that ensures the
to bronchoconstriction as seen in asthma and chronic availability of a constant supply of oxygen in the lungs
obstructive airway disease) can further influence the for exchange to take place continuously (in the face of
distribution of ventilation. The concept of time constant the intermittent nature of breathing).
(which is the product of compliance and airway
resistance and therefore expressed in ‘seconds’) helps Taking FRC to be around 2000 to 2500 mL in a 70-
in understanding why some alveoli reach maximum kg healthy adult (and also presuming air to contain
distension faster than others (fast alveoli versus slow approximately 21% oxygen), the actual amount of
alveoli). oxygen present in the FRC while an individual is
breathing room air is around 500 mL. This reservoir

is theoretically sufficient to provide the oxygen Closing volume and closing capacity (and its relationship
requirements for 2 minutes (thereby allowing a with functional residual capacity)
maximum duration of apnoea lasting 2 minutes before
Functional residual capacity has been defined earlier
hypoxaemia sets in). This reserve can be extended
as the amount of air remaining in the lungs at the end
further to cater for approximately 9 to 10 minutes of
of a normal expiration. When an individual breathes
apnoea if one can replace the entire FRC with 100%
out forcibly from the position of FRC towards residual
oxygen. This, in fact, is what we try to achieve with the
volume (RV), a point is reached when the smaller
technique of preoxygenation for a minimum period of 3 airways begin to close. The volume of air remaining in
minutes prior to paralysis before airway intervention in the lungs at the point when small airways start closing
the operating room, intensive care unit and emergency is called closing capacity. The volume of air above the
room. residual volume at which airways begin to close is called
FRC is reduced by posture, age, body habitus, pregnancy closing volume (CV) while the amount of air remaining
and respiratory disease. FRC is also reduced during in the lungs at this point (RV + CV) when the small
anaesthesia and surgery. FRC is reduced by around airways close is called closing capacity (CC). One needs
to understand the relationship between FRC and CC as
20% (0.5 to 0.7 L) during anaesthesia induced with
it helps to understand certain events that happen with
thiopentone and maintained by inhalational agents
a change in position, increasing age and induction of
and intravenous narcotics, irrespective of whether
anaesthesia. It is important for us to remember that in
breathing is spontaneous or controlled. An initial
young, healthy adults, CC occurs between FRC and RV.
reduction of around 0.2 L occurs during injection
of thiopentone which coincides with the loss of FRC increases with increasing age. Assumption of the
consciousness. Computerised tomographic studies of supine position causes a reduction in FRC by about
the lungs following induction of anaesthesia reveal 0.8 to 1.0 L. There is a further reduction of 0.4 to 0.5
small areas of increased density in the most caudal, L with the induction of anaesthesia. Closing capacity
dependent portions of the lung. These densities that increases with age. In the healthy adult in the erect
represent areas of atelectasis appear within 5 minutes position, CC exceeds FRC around 66 years of age. This
of the induction of anaesthesia. They persist in 90% of occurs around 44 years in a healthy adult in the supine
patients for 1 hour after anaesthesia and in 50% for 24 position. With induction of general anaesthesia (which
hours. These areas of atelectasis represent shunt units for practical purposes is almost always in the supine
that result in impaired oxygenation. position), CC exceeds FRC at a much younger age
(around 25 years). The physiologic implications of these
The reduction in FRC seen with anaesthesia can be facts are that some parts of the lungs are atelectatic
partially reversed by continuous positive airway in the erect position in elderly persons (at 66 years)
pressure or positive end-expiratory pressure (PEEP), while such an event can happen in younger individuals
and by a 30-degree head-up tilt. While application of in the supine position by 44 years of age. Induction of
PEEP decreases the extent of atelectasis, it has not been general anaesthesia results in CC exceeding FRC even
shown to improve oxygenation. On the other hand, in individuals as young as 25 years. Onset of atelectasis
use of a recruitment manoeuvre of up to 55 cm H2O implies that gas exchange suffers, usually resulting in
for 10 seconds after induction of anaesthesia followed arterial hypoxaemia.
by a PEEP of 10 cm H2O has been shown to not only Decrease in FRC that is seen with the induction of
eliminate atelectasis but to also improve oxygenation. anaesthesia persists into the postoperative period.
The ability to produce such a combination of respiratory Reduced FRC is one of the causative factors for
manoeuvres is incorporated into the design of modern postoperative hypoxaemia, atelectasis and pneumonia.
anaesthesia workstations, thus empowering the well- The ‘guarded’ pattern of breathing with rapid, shallow
informed anaesthesiologist in providing better quality breaths seen in the postoperative period (often due to
of anaesthesia. pain) promotes atelectasis and leads to inefficient gas

exchange. Another important cause of postoperative exchange. One such change is the reduction in functional
hypoxaemia is premature airway closure. Though residual capacity that happens within minutes of the
closing capacity reduces after surgery, the quantum of induction of anaesthesia. The relatively greater decrease
reduction in FRC is far more than the reduction in CC. in functional residual capacity (FRC) as compared to the
decrease seen in closing capacity (CC) causes some
Close monitoring and management of postoperative
parts of the lungs in an anaesthetised patient to remain
pain can allow postsurgical patients to breathe better,
thereby preventing areas of atelectasis. Use of a closed even during normal tidal volume breathing. This
propped-up position and incentive spirometry in the reduction in FRC could persist into the postoperative
early postoperative period opens up these areas of period. Use of positive end-expiratory pressure along
atelectasis, reduces shunts and improves oxygenation. with recruitment manoeuvres intraoperatively could
potentially reverse these adverse effects on respiratory
Peak expiratory flow rate (and implications of changes mechanics, thereby overcoming one of the reversible
in these parameters with induction of anaesthesia) causes of postoperative hypoxaemia.
Peak expiratory flow rate (PEFR) is the maximum rate at Inadequate attention to postoperative pain can result in
which gases can be breathed out during expiration. It these changes in respiratory mechanics persisting into
is usually in the range of 9.5 L/second. Peak expiratory the postoperative period and causing postoperative
flow rate in females is around 350 to 500 litres per pulmonary complications. Residual neuromuscular
minute (LPM) while it is 450 to 600 LPM in males. blockade and persistent effects of anaesthetic or
Peak expiratory flow rate is reduced in patients with analgesic agents can further reduce peak expiratory
obstructive airway disease. A low PEFR results in an
flow rate which can impair the ability to cough and
inability to cough and clear secretions effectively. The
clear secretions, further predisposing to an increased
process of cough constitutes four phases – irritation,
inspiration, compression and expulsion. Presence of the incidence of postoperative pulmonary complications.
irritant within the tracheobronchial tree causes irritation Ensuring good postoperative pain management, along
which in turn is followed by a deep inspiration. The third with close attention to return of good neuromuscular
phase consists of forced expiration against a closed function and adequate recovery from the sedative
glottis which results in building up of high pressure in effects of residual anaesthetics, are both facets
the airways below the vocal cords. The fourth phase of of a well-planned anaesthetic. These can help in
expulsion is brought about by the sudden opening of minimising adverse changes in respiratory mechanics
the glottis with the release of pressure built up in the brought about by the anaesthetised state. Modern
third phase causing the irritant body to be expelled. day anaesthesia is thus focused on minimising adverse
For cough to be effective, the patient needs to have changes in respiratory mechanics that bring about
sufficient muscle power to not only create a large deranged gas exchange not only intraoperatively but
enough inspiration but also to create enough expiratory also in the postoperative period.
power against a closed glottis to eventually create the
explosive nature of cough. In the post-anaesthetised Recommended reading
state, inadequate PEFR due to residual neuromuscular
1) Slinger P. Gas Exchange. In Flood P, Rathmell
blockade or an overdose of an anaesthetic/analgesic JP, Shafer S, eds. Stoelting’s Pharmacology and
can result in retention of secretions and pulmonary Physiology in Anesthetic Practice, 5th Ed (South
complications. An inability to close the glottis because Asian Edition). New Delhi:Wolters Kluwer Health
of nerve palsies is another reason for poor cough in 2015;549-88.
the postoperative period with resultant increase in
postoperative pulmonary complications. 2) Lumb AB. Anaesthesia. In Nunn’s Applied Re-
spiratory Physiology, 8th Ed. Edinburgh:Elsevier
Summary 2017;291-318.
Induction of anaesthesia brings about changes in
respiratory mechanics that can adversely affect gas
MCQ
1. Lung volumes change with advancing age. 4. Which statement is not true?
Which of the following is true
a. Poiseuille’s equation gives pressure –
a. VC ↑, RV ↓, Closing Volume ↑, RV/ flow characteristics for Laminar Flow
TLC ↑
b. Air Flow in the upper (larger) airways
b. VC ↓, RV ↑, Closing Volume ↑, RV/ is laminar
TLC ↑
c. The major site of resistance in the
c. VC ↑, RV ↑, Closing Volume ↓, RV/ airways are the medium-sized bronchi
TLC ↓
d. Airway resistance decreases as lung
d. VC ↓, RV ↓, Closing Volume ↑, RV/ volume rises
TLC ↓
5. Which of these is untrue regarding ventilation
2. Regarding FRC, not true is at RV?
a. Volume of air remaining after tidal a. The alveoli at the apex have a big
expiration resting volume & a large expanding
b. FRC decreases with the onset of GA pressure
by 20% and muscle relaxation has no b. Ventilation is greater in the base
further effect because the alveoli are larger and
c. Recruitment manoeuvers stent the more expanded initially
alveoli and keep them open c. The base is situated on a steep part of
d. Generally, FRC is more than CC in adult the P-V Curve
and this reverses with age d. Intrapleural pressure is less negative at
3. Not True the bottom than the top of the lung
a. Assuming supine position from

standing decreases FRC by 1litre
b. CC increases in supine position
c. Basal atelectasis with induction of GA
is due to FRC falling below CC
d. RV = FRC + ERV
5. (b) 4. (b) 3. (b) 2. (c) 1.(b)

Answers

3 Dead Space and Shunt
Professor Anitha Shenoy

Kasturba Medical College
Manipal
Key points
Ø Anatomical dead space is represented by the volume of air that fills the conducting zone of respiration
Ø In a healthy adult, alveolar dead space can be considered negligible
Ø Physiologic or total dead space is equal to anatomic plus alveolar dead space
Ø Hypoxemia from a relative shunt can usually be partially corrected by increasing the inspired O2
concentration; hypoxemia caused by an absolute shunt cannot
Ø The vertical change in V/Q ratios in the lung is because although both ventilation and perfusion increase
from top to bottom of the lung, perfusion increases much quicker than ventilation
Ø Hypoxic pulmonary vasoconstriction is impaired by high concentrations of volatile agents
Ø Breathing >60% oxygen for prolonged periods can cause toxicity, so it is prudent to reduce pathological
shunt so as to reduce the inspired oxygen requirements
Introduction
Absolute Shunt Unit Normal Unit Absolute Dead Space Unit
An ideal alveolus will have ventilation and perfusion
well–matched to ensure adequate gas exchange. Shunt Effect Dead Space Effect
The ventilation-perfusion ratio of such an alveolus
is described in figure 1. Although grossly, the total
alveolar ventilation and perfusion are well-matched,
the lungs consist of a variety of alveoli which are
V/Q=0 V/Q=1 V/Q=∞
at the two ends of the spectrum of distribution of
ventilation and perfusion. When there is ventilation
to alveoli but their perfusion is minimal or absent, Pulmonary Pulmonary
such ventilation is described as wasted ventilation. Vaso-hypoxic Silent Unit Bronchiolar-
The ventilation-perfusion ratio in these alveoli will be Response Constrictive
more than 1. Similarly, when alveoli are perfused but Response
not ventilated, the situation is described as shunt and
here the ventilation-perfusion ratio will be less than
1. Although these are extreme situations, there can
exist alveoli where ventilation and perfusion can be V/Q= Undefined
mismatched with a range of ventilation-perfusion ratios
and the effects would depend on the collective effect
of all of them (Figure 1). Fig 1: Range of ventilation perfusion ratios of the lung

Dead Space and Shunt 22 Anitha Shenoy
DEAD SPACE space (and consequent hypercarbia). A patient’s
ability to increase his minute ventilation and sus-
Dead space is also called ‘wasted ventilation’. That tain it at high levels may be limited and progres-
part of the tidal volume that does not take part in gas sively, he can develop respiratory failure. When
exchange because of lack of perfusion is called dead the VD/VT exceeds 0.6, the patient will require
space. This is of three types: a) Anatomical dead space mechanical ventilation.
b) Physiological dead space and 3) Apparatus dead
3) The converse is also true. When a patient is being
space.
weaned off mechanical ventilation, it is not just
Anatomical dead space (VDanat) the arterial carbon dioxide and pH that need to
be watched but also the minute ventilation. The
This dead space is the air that is present in the trachea minute ventilation represents the work the pa-
and bronchi up to the respiratory bronchiole. No gas tient needs to do to eliminate the carbon dioxide.
exchange takes place here. It usually amounts to one- Generally, this is 100 ml/kg/min. If it exceeds 200
third of the tidal volume (0.3). ml/kg/min, it is an indication that the patient is
working very hard to maintain gas exchange.
Alveolar dead space
4) Similarly, if dead space has been imposed on a
Those alveoli that are ventilated but not perfused in patient by addition of apparatus dead space, the
the lung parenchyma constitute alveolar dead space. minute ventilation will need to be increased pro-
Normally, alveolar dead space should not exist, but if portionally to ensure adequate gas exchange.
there is overdistension of alveoli or there is reduced Conversely, if a patient develops hypercarbia in
pulmonary perfusion (as in shock or pulmonary spite of apparently adequate minute ventilation
embolism), there will be some underperfused alveoli. set on the ventilator, one must actively look to
see whether there is apparatus dead space that
Alveolar dead space and anatomical dead space
can be reduced or eliminated.
together constitute physiological dead space (VDphys).
Measurement of dead space
Apparatus dead space
Dead space can be measured in the following ways:
This is the fraction of tidal volume that is rebreathed
and does not help eliminate carbon dioxide. This usually 1) Using Bohr’s equation
includes that part of the connection near the patient
All carbon dioxide is eliminated through alveolar
end where fresh gas enters, for e.g., the junction of
volume. It can be written in the following equation:
y-piece or a catheter mount. This may add about
50 to 100 ml and to an adult it may not be of much VT x FeCO2 = (VT - VD) x FACO2
consequence. However, in a small baby, this can be
very significant. VT x FeCO2 = (VT x FACO2) – (VD x FACO2)
Implications of increase in dead space Rearranging and dividing both sides by VT
1) Carbon dioxide elimination is inversely propor- VD/VT x FACO2 = FACO2 – FeCO2

tional to alveolar ventilation. Tidal volume is the VD/VT = FACO2 – FeCO2 = PACO2 – PECO2
sum of dead space and alveolar volume. When
dead space increases, alveolar volume decreases FACO2 PACO2
and the arterial carbon dioxide increases (hyper-
carbia). Where, FACO2 is the fraction of carbon dioxide in the
arterial blood, FeCO2 is the fraction of carbon dioxide
2) When dead space increases, to maintain normal in the expired gas. PACO2 = Partial pressure of carbon
carbon dioxide elimination, the minute ventila-
dioxide in the alveolar gas. PECO2 = Partial pressure of
tion increases. The amount of increase required
carbon dioxide in the expired air.
is directly proportional to the increase in dead

Enghoff’s modification of Bohr’s equation: Here the any nitrogen since the patient had breathed in 100%
partial pressure of carbon dioxide in the alveolar gas oxygen in the previous breath. As the patient continues
is assumed to be the same as arterial carbon dioxide. to exhale, a mixture of dead space and alveolar gases
So, the equation is written as: get exhaled and the nitrogen concentration gradually
increases (Phase 2). The nitrogen concentration then
VD/VT = PaCO2 – PECO2
reaches a plateau when only alveolar gases are exhaled
PaCO2 (Phase 3). As the patient continues to exhale, at some
point, the basal alveoli begin to close and the gases
2) Using Fowler’s technique – Nitrogen washout from the apical alveoli (which contain more nitrogen)
technique
begin to be exhaled. This is noted by a sharp upstroke
In this method, the patient is asked to take a deep of nitrogen concentration. The volume left in the lungs
breath of 100% oxygen and then exhale. The nitrogen beyond this point represents the closing volume.
concentration of the expired gas is measured
A line is drawn perpendicular to the x-axis so as to
continuously and a graph can be constructed by plotting
divide Phase 2 exactly in the middle such that the
the nitrogen concentration against volume (Figure 2).
shaded areas (shown in the figure 2) are equal. The
This will look like a capnogram.
volume measured from beginning of expiration to the
As the patient exhales, at first the gases from anatomical point of intersection of this vertical line on the x-axis
dead space will be exhaled. This would not contain will represent anatomical dead space.
Fig 2: Fowler’s method of calculating anatomical dead space

Fig 4: Isoshunt diagram
The shunt fraction can be quantitated by relating such as endotracheal suction, bronchoscopy and re-
arterial oxygen tension to the inspired oxygen fraction. expansion of a collapsed lung, drainage of pleural
One could use the PF ratio, from an isoshunt table. effusion or pneumothorax, application of positive end-
expiratory pressure (PEEP) and diuretics can be tried as
PF ratio: The PaO2/FIO2 ratio can be graded as follows:
applicable after a thorough clinical examination. Since
> 500 – Normal breathing >60% oxygen for prolonged periods can cause
250-500 – Adequate toxicity, it is prudent to reduce the shunt so as to reduce
the inspired oxygen requirements.
100 – 250 – Poor
< 100 – Critical To summarise, shunt and dead space are two extremes
P(A – a)O2 of ventilation perfusion mismatch. Many alveoli of
the lung will have V/Q ratios in between these. The
In this, the alveolar PO2 is calculated using the ideal sum total of these ratios will determine the overall
alveolar equation and the arterial PO 2 is directly effect on the patient’s oxygenation and ventilation.
obtained from an arterial blood gas analysis. The While shunt affects oxygenation predominantly, dead
difference can be followed up to quantitate the progress space ventilation affects carbon dioxide elimination.
of the patient. Understanding the physiology is vital so that the
management can be directed towards identifying and
An increased shunt fraction implicates the need for
eliminating the cause.
higher FIO2 and consequent effects of inhaling high
concentrations of oxygen when it exceeds 60%. All Recommended reading:
measures needed to reduce the shunt fraction must
1) West JB. Respiratory Physiology: The Essentials.
be adopted when a patient is found to have increased
9th Ed. Philadelphia: Lippincott Williams and
shunt fraction. While causes such as peanut in the
Wilkins. 2012.
bronchus or endobronchial intubation are easily
treatable, pneumonic consolidation or ARDS will be 2) Lumb A. Nunn’s respiratory physiology. 9th edi-
more difficult to treat and manage. Various measures tion. Italy: Elsevier. 2017

MCQ
1. Above -------% of shunt is associated with sig- 3. Normal V/Q ratio at base of lung is
nificant hypoxemia
a. 3.3
a. 3%
b. 1
b. 5%
c. 2
c. 15%
d. 0.6
d. 1%
4. Prone position are associated with better V/Q
2. Pao2/Fio2 in normal individual is -------- than supine position – True/False
a. 100 5. As we move from apex to base of lung both
b. 200 ventilation and perfusion increases – True /
False
c. 300
d. 50
4. true 5. true 3. (d) 2. (c) 1. (c)

Answers

4 END TIDAL GAS MONITORING
Sathish K Ravi Shankar M

Assistant Professor, Professor & Dean,
SRIHER, Chennai. Mahatma Gandhi Medical College, Puducherry.
Key points
Ø Respiratory gas analysis (oxygen, carbon dioxide, volatile anaesthetic agents) is a standard monitoring
technique during anaesthesia.
Ø Paramagnetic oxygen analysers are the most common form of oxygen analyser used in the operating
theatre.
Ø Carbon dioxide analysis can be performed using either mainstream or sidestream capnography.
Ø Infrared absorption spectroscopy analyses molecules having dissimilar atoms which absorbs infrared
radiation
Ø Mass spectrometry is a very accurate technique; however, at present, it is impractical for routine
intheatre use
Introduction have the option of integrating, analyzing, displaying and

recording the data obtained from monitoring sensors.
A well‑equipped anaesthesia workstation is a boon for
better anaesthesia practice. The technical advancement Oxygen Analysis
in anaesthesia workstations has made intra‑operative
Oxygen analysis can be performed in inhaled and
anaesthesia better and safer. Apart from other
exhaled gases and from blood samples. In theatre,
monitoring options, respiratory gas analysis has
gas analysis usually takes the form of a paramagnetic
become an integral part of the modern anaesthesia
cell. This works on the principle that oxygen, along
workstation. This has been incorporated not only for
with nitric oxide, is a strong paramagnetic gas and
operating room anaesthesia machines but also for
is attracted into a magnetic field by virtue of having
that used in intensive care units, transfer of ventilated
unpaired electrons in their outer electron ring. Most
patients and at other places outside the operating room
other gases in anaesthesia are only very weakly
where anaesthesia services are required. Monitoring
attracted into a magnetic field. In older cells, a dumb-
devices, such as an oxygen analyser with an audible
bell and torsion wire system was used; however,
alarm, carbon dioxide analyser, a vapour analyser,
modern systems use a switched electromagnetic field
(whenever a volatile anaesthetic is delivered) have also
and pressure transducer (Fig 1). The electromagnetic
been recommended by various anaesthesia societies.
field is generated at approximately 110 Hz. This
Nowadays, anaesthesia workstations are being
creates a pressure differential between the reference
configured by manufacturers in either a modular way or
sample (usually clean air) and the patient’s sample. A
as a preconfigured approach. In the modular approach,
sensitive transducer detects the pressure fluctuations
the machine is equipped with basic monitors while
of approximately 20 – 50 mbar and converts them
in the preconfigured approach, it is more integrated
to a DC voltage, which is directly proportional to the
with multiple monitoring units and includes gas flow
concentration of oxygen.
monitors and analysers as well (Fig 1). Some units also

28 Ravi Shankar M
End Tidal Gas Monitoring Sathish K
Blood gas analysis is usually performed using a gas O2 + 2H2O + 4e- = 4OH-
bench measuring the partial pressure of dissolved
At the silver anode (negative), the following oxidative
oxygen and CO2. This is usually by means of a Clarke
reaction occurs:
electrode for oxygen, a Severinghaus electrode for CO2,
and a glass electrode for pH. Attempts at continuous 4Ag+ + 4Cl- + 4e- = 4AgCl
intravascular oxygen and CO2 monitoring have been
made, for example Paratrend 7; however, their routine Therefore, current flows in the presence of oxygen
clinical use is still some way off. and the current strength is directly pro-portional to
the concentration of oxygen present, in the range
of voltages used. The Teflon membrane is utilized
as it allows dissolved oxygen through, but retards
other gases. Temperature is factored into the output
equation. A concentration gradient exists between the
dissolved oxygen in the measured substance (usually
blood) and the electrolyte solution because of the
consumption of oxygen. This is required to advance
the response speed of the system. The thickness of
the membrane should also be considered and must be
compensated for as it ages.
The polarographic sensor will over-read in the
presence of N2O, as silver contamination will allow
reduction of N2O at the cathode. Both the anode and
electrolyte solutions degrade, requiring recalibration
and replacement. The systems are temperature and
pressure sensitive.
Fig 1: Schematic drawing of a Paramagnetic sensor;

oxygen is drawn towards the magnet and will
create a pressure difference between the limbs if the
concentration is different. This can be sensed and
turned into an acoustic signal
Clarke (Polarographic) Sensor
This system uses a noble metal (platinum, gold, or
palladium) cathode and a silver/silver chloride anode, in
a potassium chloride or potassium bromide electrolyte
buffer (Fig 2). This buffer is kept within a cellophane
compartment around both electrodes. An external
current is required to drive the cathode reaction, hence
the name polarographic.
Fig 2: Polarographic cell. I, ammeter, amplifier and
At the platinum cathode (positive), the following processor; Pt, platinum; Ag, silver; KCl, potassium
reduction is generated in the presence of oxygen: chloride solution

29 Ravi Shankar M
Galvanic Sensor, Hersch, or Fuel Cell Gaseous Analysis: Carbon Dioxide, Nitrous Oxide and
Volatile Agents
This is similar to the polarographic sensor, but the
electrodes are chosen to provide their own current. The In their gaseous states, these can be measured by a
cathode is often gold or silver, and the anode is usually number of techniques including: infrared absorption
lead, with potassium hydroxide as the electrolyte spectroscopy; photoacoustic spectroscopy; silicone rubber
solution. The cathode reaction is as described earlier; and piezoelectric absorption; refractometry; Raman
however, the anode reaction is as follows: scattering; and mass spectrometry. Most in-theatre side-
sampling benches presently utilize infrared absorption.
2Pb + 6OH- = 2PbO2H- + 2H2O + e-
Infrared Absorption Spectroscopy
The flow of electrons is proportional to the concentration
of oxygen present. The anode is sacrificial, the system is Molecules containing dissimilar atoms will absorb
temperature and acid sensitive, and can take a while to infrared radiation and convert this energy into
recover after exposure to high concentrations of oxygen molecular vibration. The vibration frequency depends
(oxygen shock). They have a limited life span but can on molecular mass and atomic bonding within the
molecule. Most molecules will absorb infrared at
be made relatively cheaply.
specific wavelengths and hence the molecule can be
Carbon dioxide in Solution identified and its concentration measured. Absorption
is according to the Beer-Lambert law, which states
The Stow–Severinghaus-type sensor is used for dissolved that there is a logarithmic dependence between the
CO2; measurement of CO2 in its gaseous state is described transmission of light through a substance and the
later in this article. The Stow–Severinghaus electrode (Fig concentration of that substance.
3) utilizes a glass pH electrode to measure the partial
pressure of CO2; over the range of 1.3 – 12 kPa, this Usually, the generated infrared radiation is focused
relationship is linear. Blood is again separated from a buffer through a chopper wheel (Fig 4) that has a number
by a Teflon membrane; CO2 can freely diffuse into the of narrowband filters to select specific infrared
buffer (usually hydrogen carbonate) with NaCl and AgCl. wavelengths. A reference channel and sample channel
are aligned side by side, with a means of detecting the
This is in contact with H+ sensitive glass. The ion selective
transmitted infrared (photocells or thermopiles) and
glass is designed to be H+ selective by manipulating its
amplifying and processing the signal. Pressure and
contents; they can also be made to select for Na+, K+,
temperature are integrated with the data. Alternatively,
Ca2+, and Li+. Inside the glass electrode are KCl and a
if the initial radiation is pulsed, the subsequent vibration
calomel (Hg/HgCl2) reference electrode. A further Ag/ pulse can be detected using a microphone and then
AgCl electrode is in contact with the hydrogen carbonate amplified (photoacoustic spectroscopy).
solution to complete the circuit.
At the wavelengths used to measure volatile agents,
there are other molecules that will interfere with
the absorption peaks. Carbon dioxide, nitrous oxide,
alcohol, water vapour, and carbon monoxide will all
absorb infrared between 3 and 12 µm. Modern gas
benches look at a series of absorption peaks enabling
agent identification. Carbon dioxide and nitrous oxide
will broaden each other’s peaks and those of volatile
agents (collision broadening). This is where the energy
absorbed by one molecule is transferred to another,
allowing further radiation energy to be taken up by
the first molecule. This is usually compensated for
electronically, after looking at various predictable peaks.
Fig 3: Stow – Severinghaus electrode

30 Ravi Shankar M
Fig 4: An infrared rapidly identifying analyser (courtesy of Drager)
In-line or mainstream infrared spectrometers can be at the fringe of the object. The nature of these bands
made small enough to sit in the patient’s ventilator will depend on the light waves arriving in or out of
circuit. They shine infrared light of a specific wavelength phase of each other, which in turn will depend on the
through the plastic housing to a photo-detector. At gaseous medium’s refractive index and concentration.
present, they are used only for carbon dioxide. A In the Rayleigh refractometer, a series of prisms split
disadvantage is that they add bulk to the patient end of the light source through sampling and control tubes.
the circuit; however, they are portable, do not require The refractometer is calibrated for a particular gas
any gas to be taken from the circuit, and are relatively and, by means of aligning the fringe patterns created
cheap. Sidestream infrared spectrometers are most by each sample, a scale can be made to give the
commonly used in theatre and require a sampling concentration of that gas. For the anaesthetic vapours,
flow rate of up to 200 ml/min. However, this can be the refractometer can be calibrated for halothane and,
returned to the circuit. Water vapour entering the then by reference to conversion tables, be used with
analysis chamber has to be prevented. There is a lag other anaesthetic vapours. These systems are difficult
time for the sample to reach the analyser dependent to use for breath-by-breath analysis; however, they
on the length of tubing used, usually approximately 2.5s are used to calibrate vaporizer output and theatre and
for 3 m tubing. The position of sampling also matters, environmental gas exposure.
particularly in conditions where small tidal volumes are
Piezoelectric Absorption
likely, as fresh gas flow may enter the sampling tube.
In neonates, there are sampling sites on the 15 mm A piezoelectric compound such as quartz can be made
endotracheal tube connector rather than the HME filter. to resonate at a particular frequency. In the Engstrom
Emma analyser, two quartz crystals are mounted
Refractometry
between electrodes. One is coated in silicone-based
By shining beams of a monochromatic light source oil that will absorb anaesthetic vapours; the other is
through a gaseous medium and focusing them on a not and becomes the reference. The oil will absorb
screen, a pattern of light and dark bands will appear the halogenated vapours and change the resonant

31 Ravi Shankar M
frequency in proportion to the concentration of are narrowband-filtered and detected by photo-voltatic

vapour present. There is a need to compensate for receptors, and the signal amplified and processed.
nitrous oxide, as it is minimally absorbed also. The
response time is fast but individual vapours cannot be In the quadrapole spectrometer, the magnetic field
differentiated by the machine. is a mixture of a DC field and an AC radiofrequency
field. If the AC components frequency and the cathode
Raman Scattering acceleration are altered, only the ions of interest will
be detected, as the others remain ‘trapped’ in the
When light meets an object, the light will be scattered,
magnet. These systems are very accurate and require
usually elastically, with no change in energy state.
tiny amounts of sample. They are able to distinguish
This is Rayleigh scattering and is responsible for the
between different compounds by looking at both
blue colour of the sky and colourful sunsets. However,
some of the light’s energy will be absorbed and a parent compound and predictable subsidiary peaks.
transformational shift will occur, either by absorption These subsidiary peaks are formed by degradation of
of the energy or by release of the energy as a photon, the compound, for example, nitrous oxide becomes
with a different wavelength. This is inelastic Raman NO, O2, N2, N, and O. Mass spectrometers require
scattering. With the advent of powerful argon lasers powerful vacuum pumps and the sample cannot be
and smaller cooling systems, portable anaesthetic returned to the patient owing to the ionic degradation.
monitors utilizing this phenomenon can be made. A The response and delay times can be quite long and
laser beam is concentrated in the analysis chamber, they are not yet cost-effective for widespread theatre
the scattered light is passed through specialized optics use. However, they are very accurate and have a place
and a series of narrow-band filters, to a photo-detector in research.
and signal processing unit. The filters allow only the Practical Concerns with Anaesthesia Gas Analysers
shifted photons of interest through. The amount of
emitted photons is proportional to the concentration The conventional anaesthesia sidestream gas analyser
of vapour or gas. uses high sample flow rate (which can exceed 200 mL/
min). This may be of concern in paediatric anaesthesia.
These units are still more expensive than infrared
If the patient exhales at a flow rate less than the
systems, but have the advantages of fast response times,
sampling rate, then inspired gas will contaminate the
no degradation of the molecule under examination,
sample. This is also an issue with the use of low flow
ability for multi-gas analysis, and accuracy greater
anaesthesia where very low flows are used where the
than infrared spectroscopy (approaching mass
possibility exists for more gas to be removed from the
spectrometry).
patient circuit than is added to it by the anaesthesia
Mass Spectrometry delivery system. The sidestream analysers are also
affected with water vapour, liquid water and patient
The sample gas is drawn or injected into a low-
secretions. So the design of the sensor should be
pressure sample chamber that is attached to another
such that these are controlled and prevented from
chamber, at a pressure nearing that of a vacuum. The
reaching and damaging the analysers or influencing
pressures are maintained by virtue of vacuum pumps.
the accuracy of the measurements. The water trap
A molecular leak pathway is constructed between the
and Nafion® tubing is a simple solution being used
two chambers. In the second chamber, the molecules
to alleviate this concern. Nafion® removes gases
are ionized, usually losing an electron. The resulting
ions are then accelerated by a cathode plate, towards based on their chemical affinity for sulfuric acid.
the second part of the chamber. Here, either fixed Certain agents and degradation products in the circuit
magnets or electro-magnets influence the ions and may hinder the accurate anaesthetic gas analysis.
allow separation by the ion’s mass and charge. The ions Compounds like terafluoroethane which are replacing
choloroflurocarbons, as medical aerosol propellants,
32 Ravi Shankar M
interfere with infrared spectroscopy identification with anaesthetic agents. Typical infrared instruments
of anaesthetic gases because of sharing of 8‑12 m sample at a flow rate between 50 and 150 ml/min.
wavelength. The sampled gas may be returned to breathing circuit
and is of concern when low flows are used. Also, the
Site of sampling for Gas Analysis
point of sampling should always be as near as possible
The two ways for sampling gas for analysis may be by to the patient’s airway and the sampled gas mixture
either a sidestream or a mainstream analyser. must not be contaminated by inspired gas during the
expiratory phase.
Sidestream Sampling
Mainstream Sampling
The sampling tube is used for sampling gas for analysis
[Figure 5a-c]. It is usually of 1.2 mm internal diameter. In mainstream type of analysers, the sample chamber
The tube is connected to a lightweight adapter near is positioned within the gas stream near the patient’s
the patient’s end of the breathing system. It delivers end of the breathing system. It does not remove any
the gas to the sample chamber. It is made of Teflon, so gas and no issue of water condensation from humidity
it is impermeable to carbon dioxide and does not react or from expired air happens.
Fig 5: (a-c) Sidestream gas analysers with water trap – different manufacturers.
Measurement of Volume and Flow of Gases flow exists when Re is less than 2000 and Re over
2000 indicates flow is likely to be turbulent. Laminar
The measurement of flows and volumes are essential
flow is efficient, with layers passing smoothly over
for anaesthetists. For the understanding of the
each other producing a parabolic flow profile, with
working principles of flow and volume in anaesthesia
the greatest velocity centrally. It is determined by the
workstation, review of basic science is needed.
Hagen‑Poiseuille formula, Q = P πr4/8 ɳl (where P is
Types of Flow pressure drop, r is the radius of the tube and l is the
length of the tube). This implies that flow is directly
Many physical variables influence whether the flow proportional to the pressure drop, proportional to the
is laminar or turbulent and this may be depicted by fourth power of the radius and related to the viscosity
Reynolds’ number, Re = vρd/ɳ (where v is linear velocity, but not the density of the gas. Turbulent flow is less
ρ is density, d is diameter and ɳ is viscosity). Laminar efficient, with multiple eddy currents occurring in the

33 Ravi Shankar M
overall direction of flow. Because of the variable nature based on total or partial volumes. This means some
of turbulence, there is no precise and comprehensive devices measure the whole gas and give the reading.
equation to calculate flow, but turbulent flow is related However, some devices split a known quantity of gas
to the square root of the pressure drop and density of and measure the split volume. This is extrapolated to
the gas rather than its viscosity. depict the total flow or volume of the gas. The former
technique is more commonly used.
Measurement Principles
Pneumotachograph
The gases flow and volume could be measured directly
or indirectly. The technique of direct measurement of The technique of pneumotachograph measures flow
gases may be done using bulk filling of a container of by pressure drop across a resistance in the gas flow
known volume. Certain gadgets like vitalograph, gas pathway. The pressure transducer measures rapidly
meter and water displacement spirometer may be used and accurately the pressure drop which is extrapolated
for direct measurement of the gases. Such devices are to find the flow rate and volume of the gas. For better
in limited use in clinical practice. For clinical use, the accuracy, laminar flow is maintained by means of
measurement of gases is usually done indirectly, using series of small‑bore tubes arranged in parallel through
a property of the gas that changes in parallel to flow which the gas flow must pass. The water vapour and
or volume. its condensation may affect the accuracy of flow
measurements. These sensors are accompanied with
Pressure drop across a resistance technique utilises
heating element to prevent water condensation. It
the phenomenon of measuring drop in pressure when
can be used for both the inspired and expired flow by
a gas flows across. This effect can be used to calculate
incorporating the sensors in both the inspiratory and
flow either by keeping the resistance constant and
expiratory limbs. The values may also be extrapolated
measuring the pressure change as the flow varies (e.g.
to measure airway pressures and compliance can be
pneumotachograph) or keeping a constant pressure
calculated and displayed in real time.
drop and varying the resistance in measurable way
(e.g. bobbin rotameter). The mechanical movement Rotameters
technique utilises kinetic energy of the moving gas
This is one of the common methods of measurement
molecules for rotation of a vane or bending a flexible
of continuous flow volume of gases in an anaesthesia
obstruction. These are measurable events and may be
machine. The rotameters are specific for a particular
transduced into an electrical signal. In the heat transfer
gas. It comprises of special tube called ‘Thorpe tube’.
technique, the heated element is cooled by a flowing
Thorpe tube is a vertical tapered tube containing a
gas which is calibrated and programmed to depict
bobbin or a ball. This moves up and down by the flow
amount of gas flowing past a heated element e.g. hot-
of the gas. The bobbin weight, i.e. the pressure drop
wire anemometer. In ultrasound interference, when a
required to maintain it, is balanced by the gas flow.
gas flows across the ultrasound signal, the velocity of
The higher the bobbin rises in the Thorpe tube, more
the ultrasound signal either increases if gas is flowing
is the area around it for gas flow and thus more is the
alongside it in the same direction or decreases if the
flow. The resulting dimensions lead to laminar flow
gas is flowing against it. This change in velocity is
but at the top of the tube, turbulent flow is observed.
measurable and gives the flow measurement.
Hence, the viscosity determines the flow at bottom of
Devices for Flow and Volume Measurement the Thorpe tube and density at the top of the tube.
The readings are measured by a marker which is
The various devices available for measurement of flow
usually on the top of bobbin or centre of the ball. For
and volume may also give flow characteristics. The
accurate measurements over a large range, two tubes
methods of measuring the flow and volume may be
are added, one for low and one for high flow rates. The

34 Ravi Shankar M
measurement could be affected by static electricity Ultrasonic Flowmeters

on inner side of the tube that may lead to sticking of
These are based on change in velocity of an ultrasound
bobbin to the tube. The bobbin top is fluted for easy
signal with the change in gas flow. The flowmeters
viewing of its rotation. The inner tube is also painted
comprise of a design so as to have a pair of ultrasound
with antistatic spray. The other components of flow
beams directed in opposite direction. So when a gas
meter assembly are needle valve, indicator float, knobs,
flow occurs, the time difference happens for the two
valve stops assembly.
beams and then this is used to calculate the gas velocity
Mechanical Flow Transducers and flow rate.
Such equipments have a small metal disc attached to Electronic Flowmeters
a flexible pin. The gas flow is proportionately split and
These are most commonly used in modern day
passed into small chamber with the disc attached,
anaesthesia workstation. The gas flow is indicated
which is perpendicular to the direction of flow. The
on the screen in the form of bar. Such flowmeters
strain gauge is placed behind the pin which bends
comprise of a needle valve by which gas is conducted
with the flow of the gas. The resulting electrical signal
to a chamber of known volume having solenoid. The
is processed to calculate the flow rate. This has a high
gas is held here till the transduced pressure within the
accuracy.
chamber reaches a preset limit. This measures the gas
Hot Wire Anemometer flow.
Such equipments work on the principle of cooling of Summary
a heating wire usually of platinum by the flow of a gas
The advancement in technology has been a boon for
which is extrapolated to display the flow. Some devices
perioperative care. The respiratory gas analysis has
use heated screen or film instead of a wire. The wire
progressed from mechanical crude techniques to more
is incorporated into the balanced Wheatstone bridge
advanced, automated and programmed technique with
circuit and any change in its temperature unbalances
better accuracy and reliability. The increasing use of low
the bridge. The temperature of the wire is maintained
flow anaesthesia has made the need of gas analysers
constant by application of correcting current. These
including oxygen analysers mandatory for anaesthesia
anemometers are very accurate.
management.

35 Ravi Shankar M
MCQ
1. infrared absorption wavelengths of carbon 4. Phenomenon of ‘collision broadening’ seen
dioxide,carbonmonoxide,nitrous oxide is with this technique
between
a. a.piezo electric absorption
a. a.2 and 6mm
b. b.infrared absorption spectroscopy
b. b.3 and 8mm
c. c.refractrometry
c. c.3 and 12mm
d. d.photoacousticsoectroscopy
d. d.6 and 12mm
5. False about pneumotocograph
2. samplingflowrate of sidestream infrared spec-
trometers is upto a. a.resistance is kept constant and pres-
sure change is measured
a. a.50ml/min
b. b. sensors are accompanied with heat-
b. b.100ml/min ing element
c. c.200ml/min c. c. used only for inspired flow
d. d.300ml/min d. d.measuresflowrate and volume of gas
3. False about paramagnetic oxygen analyser
a. a. unpaired electron is attracted in a

magnetic field
b. b. Affected by water vapours and re-
quires water trap
c. c.comprise two chambers with no
pressure transducer in between.
d. d.uses electromagnetic field at 110 HZ
5. (c) 4. (b) 3. (c) 1. (b) 2. (c)

Answers

5 PHARMACOKINETICS – TERMINOLOGY EXPLAINED
Professor, Naheed Azhar

Stanley Medical College,
Chennai.
Key points
Ø Pharmacokinetics is the relationship between drug administration and drug concentration at the site of
action
Ø The degree of metabolic breakdown of an orally administered drug that occurs in the intestine or liver
before it reaches the systemic circulation is known as the first pass effect
Ø Highly protein-bound drugs generally have a low volume of distribution
Ø Front end Kinetics describe the intravenous drug behavior immediately following administration
Ø Systemic clearance permanently removes drug from the body, either by eliminating the parent molecule
or by transforming it into metabolites. Intercompartmental clearance moves drug between plasma and
peripheral tissue tanks.
Ø First order kinetics is an exponential process and a constant proportion of drug is eliminated in a given
time
Ø The value of half-life is always shorter than that of time constant, as the reaction is only 50% complete
after one half-life compared to 63% complete after one time constant
Ø The most important determinants of drug transport across the cell membrane is its electrical charge, or
polarity
Ø The pKa is the pH at which 50% of the drug is in its ionized (and unionized) form
Ø For drugs with an extraction ratio of nearly 1, a change in liver blood flow produces a nearly proportional
change in clearance. For drugs with a low extraction ratio, clearance is nearly independent of the rate
of liver blood flow
Ø Compartments are one or more components of a mathematical model that aim to replicate the drug-
handling characteristics of a proportion of the body
Ø Decrement time predicts the time required to reach a certain plasma concentration once an infusion is
terminated
Ø Biophase refers to the time delay between changes in plasma concentration and drug effect
Ø The delay between peak plasma concentration and peak concentration at the effect site is called
hysteresis

Pharmacokinetics – Terminology Explained 38 Naheed Azhar
Pharmacokinetics is the study of how the body handles Redistribution
a drug. Pharmacokinetics is the relationship between
It is the movement of a substance from an area of high
drug administration and drug concentration at the site
regional blood flow to an area of medium or low regional
of action. The core concepts of drug pharmacokinetics
blood flow. This phenomenon may determine the
include volumes of distribution, drug clearance, transfer
duration of action of a drug. For example, thiopentone
of drugs between plasma and tissues, and binding of
is rapidly redistributed from its site of action, the highly
drugs to circulating plasma proteins.
perfused brain, to other tissues, leading to a short
It is comprised of several different areas. Firstly, duration of action. Factors determining the distribution
there are processes such as absorption, distribution, of a substance will also affect its redistribution. For
metabolism and excretion, which are sometimes example, highly lipid soluble drugs move rapidly across
referred to as the ADME scheme. Secondly, there are membranes and so are more rapidly distributed and
various pharmacokinetic measurements which are redistributed.
described by equations. This area is called metrics.
First pass metabolism
Thirdly, there is the analysis of measured data from in
vivo pharmacokinetic studies. This analysis is done by The degree of metabolic breakdown of an orally
modelling which may be compartmental, physiological administered drug that occurs in the intestine or
or non-compartmental. liver before it reaches the systemic circulation. It is
also known as the first pass effect and results in a
Absorption
reduction in the concentration of the drug. Drugs
It is the uptake of substances into or across tissues. For which are subject to first pass metabolism include
drug administration, it usually refers to uptake into the morphine, buprenorphine, diazepam and midazolam.
blood stream via a particular route of administration The process of first pass metabolism can be exploited
such as oral, intramuscular or topical. pharmacologically.
Distribution Prodrug
It is the reversible transfer of a substance from one A drug that is converted from an inactive form to an
location to another within the body. The distribution of active form by first pass metabolism. Codeine is an
drug to a particular tissue will depend upon its ability example of a pro drug and undergoes demethylation
to move across the cell membrane. to morphine, which is its pharmacologically active
component.
Factors influencing the passage of drug across a
membrane Bioavailability
• Molecular size Bioavailability is a subcategory of absorption and is the
• Lipid solubility fraction of an administered dose of unchanged drug
that reaches the systemic circulation. By definition,
• Protein binding when a medication is administered intravenously, its
• Ionization bioavailability is 100%. However, when a medication
is administered via other routes (such as orally), its
• Regional blood flow. A substance will initially
bioavailability generally decreases (due to incomplete
be distributed to tissues with high regional
absorption and first-pass metabolism) or may vary
blood flow such as the brain and kidneys
from patient to patient. Bioavailability is one of the
• Vascular permeability essential tools in pharmacokinetics, as bioavailability
• Distribution of a drug may be quantified by must be considered when calculating dosages for non-
assessing the volume of distribution of a drug intravenous routes of administration.

Volume of Distribution = Amount of dose /
Concentration
It is the theoretical volume (ml) into which a drug
distributes following its administration.
VD = Dose / C0
where VD is the volume of distribution and C0 is the
concentration at time 0. It is not possible to measure
C0 since mixing is not instantaneous.
Using a simple one-compartment model, the loading
dose (LD) and the infusion rate required to maintain
a constant plasma concentration can be calculated as
follows:
Fig 1: Bioavailability of oral and IV drugs LD = VD x C
Extraction ratio where LD is the loading dose and C is the required

plasma concentration.
It is the fraction of total drug removed from the blood
by an organ in each pass through that organ. and
Volume of distribution Rinf = C x Cl
Volume of distribution, or Vd, is a theoretical where Rinf is the infusion rate required and Cl is the
pharmacological parameter which is unique for each clearance.
drug and each individual . The injected drug distributes
When a drug is administered intravenously, some drug
throughout plasma and tissues is similar to the
stays in the vascular volume, but most of the drug
dilution of a drug dose into a tank of water. Volume
distributes to peripheral tissues. This distribution is
of distribution (Vd) is the apparent size of the tank
often represented as additional volumes of distribution
required to explain a measured drug concentration
(tanks) connected to a central tank (blood or plasma
from the tank water once the drug has had enough
volume).
time to thoroughly mix within the tank.
Fig 2: Understanding Vd – One compartment model

Front End Kinetics
They describe the intravenous drug behavior
immediately following administration. How a drug
rapidly moves from the blood into peripheral tissues
directly influences the peak plasma drug concentration.
If drug is injected into an arm vein and that the initial
concentration is measured in a radial artery, drug
appears in the arterial circulation 30 to 40 seconds
after injection. The delay likely represents the time
required for drug to pass through the venous volume
of the upper part of the arm, heart, great vessels, and
peripheral arterial circulation. More sophisticated
models (e.g., a recirculatory model) account for this
delay and are useful when characterizing the behavior
of a drug immediately following bolus administration,
Fig 3: Understanding Vd– Two compartment model such as with induction agents where the speed of onset
and duration of action are of interest.
Peripheral distribution volumes increase the total
volume of distribution. Drug not only distributes to
the peripheral tank and thus increases the volume of
distribution, but it also binds to tissue in that tank. This
process further lowers the measureable concentration
in the central tank. Thus, the total volume of distribution
may even be larger than the two tanks added together.
Some anesthetics have huge distribution volumes (e.g.,
fentanyl has an apparent distribution volume of 4 L/kg)
that are substantially larger than an individual’s vascular
volume (0.07 L/kg) or extracellular volume (0.2 L/kg).
Drugs that mainly stay in the vascular compartment,
as is the case with highly protein bound drugs such
as ibuprofen, have a low Vd. The opposite is true for
very lipophilic drugs, which diffuse widely into the
Fig 4: Front end kinetics
fatty tissues, and therefore have a high Vd. Highly
protein-bound drugs generally have a low volume of Clearance
distribution, as they are more or less confined to the
The volume of plasma from which a drug is removed
intravascular compartment because of their bond
per unit time (ml.min−1). Clearance refers to the amount
with plasma proteins. Lower concentrations of plasma
of plasma concerned as opposed to the amount of a
protein, and thus lower levels of protein binding, may
drug. The units is ml.min−1
lead to apparently higher volumes of distribution.
Clearance gives a value for the amount of plasma
In general,
cleared of a drug. The mechanism of this clearance can
Highly protein-bound = small Vd involve elimination, excretion or both. Two processes
Highly lipid-soluble = large Vd contribute to drug clearance: systemic clearance (out
Also, Vd < 3 L – drug entirely within plasma of the tank) and intercompartmental (between the
Vd > 42 L – drug is distributed beyond total body water tanks) clearance
All metabolic organs to which the drug is delivered have
an extraction ratio. The total clearance is the sum of
each clearance by metabolic organs such as the liver,
kidney and other tissues.
First-order kinetics
A situation where the rate of drug processing at any time
depends upon the concentration of the drug present at
that time. This is an exponential process and a constant
proportion of drug is eliminated in a given time. First
order is where the rate is directly proportional to the
Fig 5: Systemic and intercompartmental clearance amount of drug undergoing the process.
Systemic clearance permanently removes drug from the
body, either by eliminating the parent molecule or by
transforming it into metabolites. Intercompartmental
clearance moves drug between plasma and peripheral
tissue tanks.
Cl = Dose / AUC
Fig 6: First order kinetics
where AUC is the area under concentration–time curve
Zero-order kinetics
or
A situation where the rate of drug processing is
Cl = Q.ER independent of the concentration of drug and is,
where Q is the flow rate and ER is the extraction ratio. therefore, constant.
Or This time a constant amount of drug is eliminated in

a given time rather than a constant proportion. First-
Cl = VD . K order elimination may become zero order when the
elimination system (often a metabolic pathway) is
where VD is the volume of distribution and K is the rate
saturated.
constant of elimination
Zero order is where the rate is independent of the
Elimination
amount of drug undergoing the process;
It is the removal of drug permanently from the plasma.
This may be via distribution, metabolism or excretion.
Rate of elimination Relim = Concentration × Clearance
With long infusions, drug concentrations reach a steady-
state condition where the rate of drug elimination (dA/
dt) is in equilibrium with the rate of drug administration.
Clearance in a steady-state condition can be obtained Fig 7: Zero order kinetics
as follows: Non-Linear Pharmacokinetics
Clearance = Infusion Rate / Css Some drugs behave differently at different
where Css is the plasma concentration at steady state. concentrations. An example is Phenytoin, where the

clearance of the drug is dose dependent (first order) but as τ is the reciprocal of K
until the enzymes involved are saturated, at which
t1/2 = 0.693τ
point the clearance of the drug becomes constant (zero
order) and so the concentration rises much faster as or
the dosage increases.
t1/2 = 0:693 VD / Cl
Excretion
The value of half life (t1/2) is always shorter than that of
The removal of drug from the body. time constant (τ ) as the reaction is only 50% complete
after 1 half life compared to 63% complete after one
Time constant time constant. The conventional pharmacokinetic term
half-life has limited meaning to anesthetic practice since
The time taken for the plasma concentration of a drug
the clinical behavior of drugs used in anesthesia is not
to fall to 1/e of its former value
well described by half-life. Instead, the pharmacokinetic
or principles such as volume of distribution, clearance,
elimination, front-end kinetics, back-end kinetics,
The time that would be taken for the initial concentration context-sensitive half-time and biophase, describe how
to fall to zero were the initial rate of decline to continue drugs used in anesthesia will behave.
or Drug lipophilicity, Ionization, and Polarity
τ= 1/K The most important determinants of drug transport
across the cell membrane is its electrical charge, or
or
polarity. All drugs have a natural polarity, which is
τ = VD / Cl inherent to the molecule. Under normal circumstances,
a drug in solution exhibits an equilibrium between its
where K is the rate constant of elimination of the ionized and non ionized subforms. The equilibrium
reaction and Cl is the clearance. constant of this equation is Ka, more commonly known
in its logarithmic form, pKa. The pKa is the pH at which
As the value of K rises, the time τ falls. The symbol e has
50% of the drug is in its ionized (and unionized) form,
a numerical value of 2.718 and so 1/e is 0.368.
and, depending on the environmental pH, defines the
Half life degree of ionization of the agent. Ionized forms of drug
cannot traverse cell membranes and non-ionized forms
The time taken for the plasma concentration of a drug cannot occupy receptor sites.
to fall by half. (t1/2) or, for a zero order reaction
t1/2 = C0 / 2K
where t1/2 is half life, C0 is the concentration at time

zero and K is the rate constant of elimination for the
reaction.
Zero order reactions are fairly uncommon in

pharmacological and physiological terms and so the
more appropriate equation for first order reactions is
as shown.
t1/2 = 0.693 / K Fig 8: Drug transfer across membranes and lipophilicity

A relative but not an excessively hydrophobic character concentration at the effect site. It may already occur
is most conducive to transport. Very polar molecules in the absorption phase, when, for example, gastric
will fail to enter the membrane, whereas extremely emptying is delayed by concomitantly used opioids,
hydrophobic molecules will enter readily but may have which may thus affect drug uptake from the gut. The
a hard time leaving it on the other side. addition of adrenaline to local anaesthetic solutions,
in order to slow local anaesthetic uptake in the plasma
Protein binding and ‘free fraction’
by inducing vasoconstriction, is another example of a
Drugs circulate through the body as free molecules, or pharmacokinetic interaction in the absorption phase.
reversibly bound to plasma proteins, such as albumin,
Pharmacokinetic interactions can also occur during
α1- acid glycoprotein, and lipoproteins. Albumin is the
distribution of drugs in the body, through changes
main transporter protein in the human body. Albumin
in protein binding or alterations in blood flow. Drugs
mainly binds acidic drugs such as diazepam, barbiturates,
can be displaced from their binding sites on plasma
propofol, and salicylates. Alpha1- acid glycoprotein, on
proteins by another drug, thus increasing the free
the other hand, is an acute-phase protein, also known
fraction of the previously bound drug and increasing
as orosomucoid. It carries basic and neutral drugs, such
its concentration at the effect site. The most important
as fentanyl, lidocaine, and propranolol. Only the free
of this interaction is the displacement of warfarin by
molecules of the drug, unbound to plasma proteins,
concomitant administration of phenylbutazone or
are able to penetrate biomembranes into peripheral
chloral hydrate.
tissues, exert their pharmacological effect, and undergo
hepatic metabolism. Most anaesthetic drugs are known to affect vasomotor
tone and systemic blood flow. The pharmacokinetic
The drug molecules bound to plasma proteins can be
properties of most anaesthetics are also dependent
seen as a reservoir for the free drug molecules. Protein
on systemic and hepatic blood flow, interactions
binding is reversible, plasma protein concentration,
between different anaesthetics occur because of their
however, may change during disease or physiological
influence on blood flow. In the presence of midazolam,
changes of the body, resulting, for example, from ageing
the distribution and clearance of propofol is markedly
or pregnancy. Many diseases may cause a decrease
decreased. Propofol plasma concentrations are highly
in serum albumin concentration including chronic
dependent on rapid redistribution (in addition to
liver and kidney disease, acute myocardial infarction,
elimination), addition of midazolam leads to higher
rheumatoid arthritis and other chronic inflammatory
propofol plasma concentrations. In addition to opioids,
states. Serum albumin is also decreased in malnutrition
epidural blockade with ropivacaine also affects the
and pregnancy. Alpha-acid glycoprotein concentrations
elimination clearance of propofol. Epidural blockade
are elevated, being an acute-phase protein, in cancer,
of 20 segments reduces the elimination clearance of
acute and chronic infection, burns, and trauma, surgery.
propofol from 2.6 litres/min to 1.9 litres/min. As a
Alpha1- acid glycoprotein concentration is reduced
result, in the presence of high epidural blockade, blood
in pregnancy. In the elderly population (>70 years of
propofol concentrations become elevated by about 30%
age), serum albumin concentrations are about 10– 20%
compared to when no epidural blockade is present.
lower than in a younger. Lower protein binding may also
This may be the result of an epidural blockade-induced
lead to a higher free fraction, and therefore to higher
reduction of hepatic and/ or renal perfusion resulting
diffusion speeds to the effect site, resulting in higher
in a reduced clearance of this high hepatic extraction-
effect site concentrations, thus decreasing the dose
ratio drug.
needed to exert a certain drug effect.
Hepatic extraction
Pharmacokinetic drug–drug interactions are those in
which the administration of one drug leads to changes The clearance of anaesthetic agents by the liver is the
in the disposition of another drug, hence altering its product of the amount of drug delivered to the liver

as governed by liver blood flow and cardiac output,
and the efficiency of drug removal from the blood
as represented by the hepatic extraction ratio. The
hepatic extraction ratio is defined as the fraction of
drug that is irreversibly removed during one passage of
blood through the liver. For agents with a low intrinsic
clearance, the metabolism is independent of liver blood
flow but is significantly affected by protein binding.
Changing the drug supply of such an agent to the liver
will not change the drug clearance. Such agents such Table 1: Sites of drug metabolism
as, for example, diazepam are referred to as exhibiting
a low extraction ratio (<0.3). Pharmacokinetic models
These are mathematical models that are used to
When intrinsic activity is high, almost all of the drug is
interpret pharmacokinetic data from experiments and
cleared from the blood once it passes through the liver.
may also be used to predict the plasma concentration
Protein binding then does not influence clearance; only
of a drug at a given time. There are several different
the blood flow to the liver will affect the drug clearance.
types of modelling which vary in the complexity of the
Propofol,for example, is a high extraction-ratio (>0.7)
mathematics involved:
agent and its clearance is known to be blood flow
dependent. Midazolam, exhibit an intermediate hepatic • Non-compartmental modelling
extraction ratio (between 0.3 and 0.7) and the clearance • Compartmental modelling which is subdivided
of these agents is thus dependent on intrinsic activity, into catenary and mamillary
protein binding, and liver blood flow. For drugs with an • Physiological modelling
extraction ratio of nearly 1 (e.g., propofol), a change in Non-compartmental modeling
liver blood flow produces a nearly proportional change
in clearance. For drugs with a low extraction ratio (e.g., This is the simplest form of pharmacokinetic modelling
alfentanil), clearance is nearly independent of the and it does not make any assumptions about the
rate of liver blood flow. If nearly 100% of the drug is number of compartments to which a drug distributes.
extracted by the liver, this implies that the liver has a Instead, it uses information from a concentration vs.
very large metabolic capacity for the drug. In this case, time curve to estimate pharmacokinetic variables
the rate-limiting step in metabolism is the flow of drug such as bioavailability, volume of distribution and
to the liver, and such drugs are said to be “flow limited.” clearance. However, there are some limitations to non-
compartmental analysis:
For many drugs (e.g., alfentanil), the extraction ratio
is considerably less than 1. For these drugs, clearance • It requires a drug to follow linear kinetics
• It cannot be used to make predictions about
is limited by the capacity of the liver to take up and
the concentration of a drug at any given time,
metabolize drug. These drugs are said to be “capacity
which is possible with more complex types of
limited.” Clearance will change in response to any
modelling
change in the capacity of the liver to metabolize such
drugs, as might be caused by liver disease or enzymatic Compartmental modeling
induction. However, changes in liver blood flow
The concept of compartmental modeling allows
caused by the anesthetic regimen or other changes in
predictions of drug behaviour to be made from
splanchnic circulation usually have little influence on
mathematical models of the body that are more
clearance because the liver handles only a fraction of
accurate than the assumption of the body being a simple
the drug that it sees.
container. Compartments are one or more components
Fig 9: Multicompartment model
of a mathematical model that aim to replicate the drug- The terminology for the so-called ‘central’ compartment
handling characteristics of a proportion of the body. is V1. There are various rate constants that should be
Models may contain any number of compartments but included in the diagram: I is the rate constant for a drug
single-compartment models are generally inaccurate moving from the outside of the body (compartment 0)
for studying pharmacokinetics. A three-compartment to the central compartment (compartment 1); K10 is
model allows fairly accurate modelling with only limited the rate constant of elimination from V1 to V0. Single-
complexity. compartment models do not occur physiologically.
Catenary • Two-compartment model
A form of multicompartmental modelling in which
all compartments are linked in a linear chain with
each compartment connecting only to its immediate
neighbour.
Mamillary
A form of multicompartmental modelling in which
there is a central compartment to which a stated
number of peripheral compartments are connected.
Compartmental pharmacokinetic models are strictly
empirical. The models have no anatomic correlates.
They are solely based on fitting equations to measured
plasma concentrations following a known dose.
Fig 11: Two compartment model
Although more intuitive, these models have no
physiologic correlates. A second (peripheral) compartment can now be
added, which may mathematically represent the less
• One-compartment model
vascular tissues of the body. All the rate constants
that were in the previous model still apply but in
addition, there are additional constants relating to
this new compartment. The terminology is the same;
K12 represents drug distribution from V1 to V2 and
K21 represents drug redistribution back into V1.
The intercompartmental micro rate constants (k12,
k21, etc.) describe movement of drug between the
central and peripheral compartments. Each peripheral
compartment has at least two micro rate constants,
one for drug entry and one for drug exit. Elimination
occurs only from V1 only, no matter how many other
Fig 10: One compartment model
compartments are present.
A semi-log plot of drug concentration versus time will
no longer be linear as the drug has two possible paths
to move along, each with their own associated rate
constants.
Fig 13: Three compartment model

The third compartment mathematically represents the
least vascular tissues of the body. All the rate constants
that were in the previous model still apply but in addition,
there are additional constants relating to this new
compartment. The terminology is the same. Elimination
occurs only from V1 no matter how many other
Fig 12: Semi-log drug concentration vs time plot in two compartments are present. Most anaesthetic drugs
compartment model are accurately modelled in this way. The compartments
are not representing precise physiological regions of
A two compartment model is not a linear graph but a the body. Instead they are designed to model areas
bi-exponential curve. Phase 1 equates to distribution of the body that share similar properties in terms of
of drug from V1 to V2 whereas phase 2 represents drug rates of equilibration with the central compartment.
elimination from V1. Formula for two-compartment One of the peripheral compartments models slowly
model equilibrating tissues while the other models tissues
Ct = A.e−αt + B.e−βt that are equilibrating more rapidly. The volume in the
center of the three-compartment model is the central
where Ct is the concentration at time t, A is the y volume. The other volumes are peripheral volumes.
intercept of line a, α is the slope of line a, B is the y The sum of all volumes is the volume of distribution at
intercept of line b and β is the slope of line b. The steady state, Vdss. Clearance in which the drug leaves
value of Ct can, therefore, be found simply by adding the central compartment to the outside is the central
the values of exponential declines a and b at any given or metabolic clearance. Clearances between the central
time. The terms α and β are the rate constants for these compartment and the peripheral compartments are the
processes. intercompartmental clearances.
• Three-compartment model Concentration versus time in 3 compartment model

from the central compartment will, therefore, affect
the length of time taken to eliminate a drug fully. The
prediction of the concentration of a drug at a given
time using a three compartmental model requires the
combination of data from multiple exponential curves.
To create this form of pharmacokinetic modeling,
therefore, requires specialist computer software.
This curve has the characteristics common to most
drugs when given by intravenous bolus. First, the
concentrations continuously decrease over time.
Second, the rate of decline is initially steep but
continuously becomes less steep, until we get to a
Fig 14: Semi-log drug concentration vs time plot in three portion that is log-linear. It consists of 3 distinct phases.
compartment model A rapid-distribution phase begins immediately after
injection of the bolus. Very rapid movement of the
Three compartment models have a tri-exponential
drug from plasma to the rapidly equilibrating tissues
decline. Line a represents distribution to rapidly
characterizes this phase. The second, slow-distribution,
equilibrating tissues and line c represents distribution
phase, which is characterized by movement of drug into
to slowly equilibrating tissues. Line b always represents
more slowly equilibrating tissues and return of drug
elimination from the body. Tangents drawn to these
to plasma from the most rapidly equilibrating tissues.
lines intercept the y axis at points A, B and C. The sum
The terminal phase is a straight line when plotted on
of A + B + C should equal C0.
a semilogarithmic graph. The terminal phase is often
Formula for three-compartment model: called the elimination phase because the primary
mechanism for decreasing drug concentration during
Ct = A.e−αt + B.e−βt + C.e−γt the terminal phase is elimination of drug from the
where C is the y intercept of line c and γ is the slope body. The distinguishing characteristic of the terminal
of line c. The equation is compiled in the same way as elimination phase is that the plasma concentration
that for a two-compartment model. is lower than tissue concentrations and the relative
proportion of drug in plasma and peripheral volumes
B.e−βt continues to represent the terminal elimination of distribution remains constant. During this terminal
phase and the term C.e−γt is added to represent slowly phase, drug returns from the rapid and slow-distribution
equilibrating compartments, where t is the time volumes to plasma and is permanently removed from
since the bolus, C(t) is the drug concentration after plasma by metabolism or excretion.
a bolus dose, and A, α, B, β, C, and γ are parameters
of a pharmacokinetic model. A, B, and C are called Physiological modeling
coefficients, whereas α, β, and γ are called exponents. This type of modelling uses realistic physiological
In a three-compartment models the drug first enters a parameters to construct the model. These include organ
central (first) compartment, is then distributed rapidly blood flow, the volume of different tissues and the
to a second and slowly to a third while being eliminated tissue:blood partition coefficient. This is also known as
only from the first. Distribution to, and redistribution physiologically based pharmacokinetic (PBPK) modeling
from, the peripheral compartments occurs continuously and is the most complex type of modeling.
according to prevailing concentration gradients. These In physiological models, the compartments are defined
peripheral compartments may act as reservoirs keeping according to different organs or tissues. More complex
the central compartment full even as elimination is models will have many different compartments,
occurring from it. The ratio of the rate constants to and
whereas simpler versions will group organs or Decrement time
tissues with similar perfusion rates and lipid contents
The time taken for the plasma concentration of a
together. Equations are written to describe the rate
drug to fall to the specified percentage of its former
of transfer into and out of each compartment, with
value after the cessation of an infusion designed to
each compartment having a different equation. The
maintain a steady plasma concentration (time). The
rate of distribution of drug to a tissue may either be
Context Sensitive half Time (CSHT) is, therefore, a form
limited by the perfusion of the tissue (for example for
of decrement time when the ‘specified percentage’ is
small lipophilic drugs which rapidly cross membranes)
50%. When using propofol infusions, the decrement
or the permeability of the tissue membrane to the
time is commonly quoted as the time taken to reach a
drug. Although this type of modelling is potentially
plasma level of 1.2 μg/ml, as this is the level at which
the most accurate as it more closely represents what
wake up is thought likely to occur in the absence of any
happens in the body, in reality it has some significant
other sedative agents.
limitations. Often, much of the data used is actually
based on extrapolation from animal models because
human data would require intensive tissue sampling
and is not practical. The diagram below is an example of
a simple structure for a PBPK model for an inhalational
anaesthetic agent.
Fig 16: Decrement time

Decrement times for a target-controlled infusion set
to maintain a target propofol concentration of 4 μg/
Fig 15: Physiologically based pharmacokinetic (PBPK) mL for 30, 60, and 120 minutes. Once terminated, the
modeling time required to reach 0.5 μg/mL was 30, 40, and 65
minutes for each infusion is found to be different. The
Back End Kinetics longer the infusion duration, the longer the time taken
for the drug to decrease to the desired concentration.
Back-end kinetics provides descriptors using estimates
Decrement times are determined as the time required
of distribution volume and clearance of how plasma
to reach a target percentage of the concentration just
drug concentrations decrease once a continuous
before the termination of a continuous infusion. A
infusion is terminated. Decrement time predicts the
popular decrement time is the 50% decrement time,
time required to reach a certain plasma concentration
also known as the context-sensitive half-time. The term
once an infusion is terminated. Decrement times are
context-sensitive refers to infusion duration. The term
a function of infusion duration.
half-time refers to the 50% decrement time.

Fig 17: 80% decrement time of some commonly used drugs
Context-sensitive half time Propofol

The time taken for the plasma concentration of a drug The line is a smooth curve rising steadily towards a
to fall by half after the cessation of an infusion designed CSHT of around 40 min after 8 h of infusion. Propofol
to maintain a steady plasma concentration (time). There is not context insensitive as its CSHT continues to
is no recognized definition for the term ‘context’, it is rise; however it remains short even after prolonged
used to identify the fact that the half time will usually infusions.
alter in the setting of varying durations of drug infusion.
Alfentanil
The curve rises from the origin until reaching a CSHT of
50 min at around 2 h of infusion. Thereafter, the curve
becomes horizontal. This demonstrates that alfentanil
is also context insensitive for infusion durations of 2 h
or longer.
Thiopental
The curve begins at the origin but rises more steeply
than the others so that the CSHT is 50 min after only 30
min infusion duration. The curve has a slightly slurred
build-up exponential reaching a CSHT of 150 min after
Fig 18: CSHT of some commonly used drugs
8h of infusion. As the CSHT continues to rise, thiopental
Remifentanil does not become context insensitive.
This is the exceptional drug in anaesthetic practice in Fentanyl

that it is context insensitive. The line starting from the
The most complex curve begins at the origin and is
origin and becoming near horizontal after the CSHT
sigmoid in shape. It should cross the alfentanil line at
reaches 5 min. This demonstrates that the half time is
2 h duration and rise to a CSHT of 250 min after 6 h of
not dependent on the length of infusion as clearance
infusion. Again, as the CSHT continues to rise, fentanyl
by plasma esterases is so rapid.
does not become context insensitive.
CSHT does not predict the time to patient awakening from the central compartment to the effect site, and
but simply the time until the plasma concentration of a ke0 describes the elimination of drug from the effect-
drug has fallen by half. The patient may need the plasma site compartment. The site of drug effect is connected
concentration to fall by 75% in order to awaken, and to plasma by a first-order process. The equation
the time taken for this or any other percentage fall to that relates effect-site concentration to plasma
occur is known as a decrement time. concentration is
Biophase dCe / dt = ke0 × (Cp − Ce)
Biophase refers to the time delay between changes where Ce is the effect-site concentration, Cp is the
in plasma concentration and drug effect. Biophase plasma drug concentration, and ke0 is the rate constant
accounts for the time required for drug to diffuse from for elimination of drug. The constant ke0 describes the
the plasma to the site of action plus the time required rate of rise and off set of drug effect.
(once drug is at the site of action) to illicit a drug
effect. During induction and emergence) when drug The concentration of drug in the biophase cannot be
concentrations are in flux, changes in drug effect will lag measured because it is usually inaccessible, at least
behind changes in drug concentration. This lag between in human subjects. The time course of drug effect can
the plasma concentration and effect usually result in the be calculated by using rapid measures of drug effect.
phenomenon called hysteresis, in which two different The effect-site concentration is not a real measurable
plasma concentrations – one corresponds to the drug concentration but rather a virtual concentration
effect and the other to plasma concentrations. The in a theoretic compartment without a volume. If a
reason is that additional time is required for the drug to constant plasma concentration is maintained, then
be transported to the target organ, penetrate the tissue, the time required for the biophase concentration
bind to a receptor, and induce intercellular processes to reach 50% of the plasma concentration (t1/2ke0)
that ultimately lead to the onset of drug effect. This can be calculated as 0.693/ke0. For drugs with a very
delay between peak plasma concentration and peak rapid decline in plasma concentration after a bolus
concentration at the effect site is called hysteresis. This (e.g., adenosine with a half-life of several seconds),
lag is often modeled with an effect-site compartment the effect-site concentration peaks within several
added to the central compartment. The relationship seconds of the bolus, regardless of ke0. For drugs with
between plasma and the site of drug effect is modeled a rapid ke0 and a slow decrease in concentration after
with an effect-site model. a bolus injection (e.g., pancuronium), the peak effect-
Kinetic micro rate constants used to describe biophase site concentration is determined more by ke0 than by
include k1e and ke0. The k1e describes drug movement plasma pharmacokinetics.
Fig 19: Biophase

Target controlled infusion calculates the initial bolus dose required to achieve this
concentration as quickly as possible. This calculation is
It is an infusion controlled by a microprocessor-driven
based on allowing the plasma concentration to rise to
pump that alters the infusion rate to maintain a user
an optimum level above the effect site concentration (to
defined target plasma concentration.
provide a concentration gradient between the plasma
The target controlled infusion (TCI) microprocessor is and effect-site) and also preventing an overshoot of
programmed with pharmacokinetic models for different the effect-site concentration. After administration
drugs. These are generally three compartment models of the bolus dose, the infusion pauses to allow the
based on pharmacokinetic studies in volunteers and plasma concentration to fall to that of the effect-site.
they are adjusted according to patient variables such A more rapid estimation for speed of removal of drug
as age, weight and height. When first introduced, the from the plasma will lead to a larger initial dose being
user selected a plasma concentration (Cp) to target. administered.
However, now it is more common to target an effect
Plasma-site targeting
site concentration (Ce). The effect site is an additional
compartment that has been introduced more recently This is when the user programs a plasma concentration
to reflect the hysteresis between plasma concentration for the microprocessor to target. This will lead to a
and the clinical effect observed. smaller initial dose being administered. This mode is
Infusion rates are calculated as an initial bolus to fill rarely used.
the central compartment to the concentration targeted
(B), followed by a continuous infusion at a rate equal
to the elimination rate from the plasma (E) plus the
redistribution rate to the peripheral compartments
(also known as the transfer rate, T). This BET regimen
was first proposed in 1968 although TCI pumps were
not introduced until 1997.
keo
It is the first order rate constant that describes the
rate of equilibration between the plasma and the
effect site (e). keo depends upon the pharmacological
characteristics of the drug as well as patient factors
affecting drug delivery. The effect site is considered to Fig 20: Plasma site targeting
have negligible volume and so separate constants for Infusion rate (solid line)
movement in and out of the compartment are felt to be
unnecessary. Therefore, it can be considered to be the The machine delivers an initial dose at a fast infusion
proportional change in concentration gradient between rate (1200 ml/h) to achieve the targeted effect site
the plasma and effect site per unit time. concentration (3.0 μg/ml). The infusion then pauses
to allow the plasma concentration to fall to that
A small (slow) keo value leads to a larger initial dose
of the effect site, which occurs by elimination and
being given to provide a greater concentration gradient
redistribution of the initial bolus. The infusion then re-
and a more rapid achievement of the effect-site
starts at a much lower rate to maintain the programmed
concentration programmed.
concentration. This maintenance rate will depend
Effect-site targeting upon the ongoing redistribution and clearance rates.
Increasing the target concentration to 6.0 μg/ml leads
This describes the process by which a user programs an to a repeat of this process, with a further rapid bolus
effect-site concentration as a target. The microprocessor
being administered before a pause in infusion rate and as the infusion recommences rapidly increases the Cp
a re-commencement at a higher maintenance rate. to match that of the effect site.
Decreasing the target concentration back to 3.0 μg/ml
The plasma and effect site concentrations are calculated
at 10 minutes leads to a pause in the infusion to allow
not measured (as compared with end tidal agent
the plasma concentration to fall. This time when the
monitoring). The target concentration must be adjusted
infusion restarts a small bolus is given to bring Cp back for the individual patients and clinical circumstances
up to the same concentration as Ce, before the infusion and used in conjunction with clinical observation. The
restarts at a lower rate. cardiovascular effects of the drug will depend upon
Ce (dashed line) the maximum plasma concentration achieved and
so in frail, elderly patients a large overshoot in the
The concentration increases exponentially to 3.0 plasma concentration when a bolus is given can lead
μg/ml after which it plateaus as the infusion maintains to significant haemodynamic compromise.
a constant concentration. When the user increases the
In morbidly obese patients with a BMI > 42, with
target concentration, a similar shaped curve occurs,
increasing body weight, the calculation of Lean Body
with this time the plateau being 6.0 μg/ml. When
Mass (LBM) used in the Schnider model paradoxically
the target concentration decreases an exponential
decreases. This decrease leads to a higher estimated
decreasing curve goes back to 3.0 μg/ml, where the
clearance and thus a larger initial bolus dose and higher
curve plateaus again.
infusion rate will be administered. The manufacturers
Cp (dotted line) of TCI systems thus prevent programming of their
pumps with weight and height combinations giving
During the initial bolus, the Cp increases above that of a BMI outside this range. V1 is fixed in the Schnider
the Ce. The magnitude of the overshoot will depend on model, whereas it is weight adjusted in the modified
the keo and thus differs according to the pharmacokinetic Marsh model. When using plasma site targeting in the
model (see above). The peak concentration will be just Schnider model, then the bolus dose, which is directly
after the infusion terminates and then the Cp will fall to proportional to V1, is not adjusted for weight. With
that of the Ce targeted. A similar pattern occurs when effect site targeting, this is not the case as the overshoot
the second bolus is given. When the target is decreased accounts for age, weight and height. Thus, in most
again, the Cp falls more rapidly than the Ce, which circumstances, the Schnider model should be used in
reflects the hysteresis between the two. The short bolus effect site mode only.

MCQ
1. The volume of distribution of a drug 4. In first order Kinetics for drugs
a. increases with advanced age a. The plasma decay is nonexponential
b. decreased in pregnancy b. Enzyme mediated process
c. unaffected by protein binding c. Rate of reaction is independent of the
d. lipid soluble drugs have very high Vd concentration of drug
2. One of the following drugs shows context d. Rate of reaction is dependent on
insensitivity concentration of the drug
5. False about about Propofol kinetics
a. Propofol
b. Fentanyl a. The distribution and clearance of
propofol is markedly decreased by
c. Remifentanil
midazolam.
d. Thiopentone sodium
b. Plasma concentrations are highly
3. In PBPK Models, The Compartments are dependent on rapid redistribution
based on
c. Epidural blockade reduces clearance
a. Central and Peripheral distributions of propofol
ratios d. Exhibits low hepatic extraction-ratio
b. Organ blood flow, tissue: Blood
Partitions Co efficient
c. Combinations of distributions and
eliminations
d. Prediction from Effect site
concentration
5.(d) 4.(d) 3.(b) 2.(c) 1.(d)

Answers

CLINICAL LECTURES
6 Anaesthetic management of a patient presenting with Eclampsia
Seema Partani Sunanda Gupta

Professor, Professor and Head,
Geetanjali Medical College, Geetanjali Medical College,
Udaipur Udaipur
Key points
Ø The role of anesthesiologist in the management of eclamptic patients is many. Control of seizures
and blood pressure and establishing airway in an emergency are key factors that determine patient
outcome.
Ø Monitoring during magnesium therapy should include hourly urine output, respiratory rate, oxygen
saturation and patellar reflexes.
Ø MgSO4 is the drug of choice for seizure prophylaxis in an eclamptic patient, not as an antihypertensive.
Ø Low dose epidural analgesia is advantageous for optimal blood pressure control during labour, if there
is no coagulopathy or thrombocytopenia.
Ø Coagulation tests may be normal in the presence of abnormal platelet function or low platelet counts.
Ø The severely preeclamptic parturient has a contracted, underfilled and a porous vasculature.
Ø Intravenous fluid should not be administered in eclampsia for the purpose of volume expansion or for
the treatment of oliguria when renal function and serum creatinine levels are within normal range.
Ø In patients who require general anaesthesia, BP and convulsions should be maximally controlled and
invasive monitoring inserted prior to induction of general anaesthesia.
Introduction gestation, molar pregnancy, triploidy, pre-existing

hypertension, renal disease, Type1/2 diabetes
Eclampsia is an unpredictable, life threatening
mellitus, previous severe preeclampsia or eclampsia,
complication of severe preeclampsia, characterized
non-immune hydrops fetalis and systemic lupus
by new onset of grand mal seizure activity and/or
erythematosus.
unexplained coma during pregnancy or postpartum
in a woman with signs or symptoms of preeclampsia. Pathophysiology
Eclampsia and preeclampsia account for approximately
63,000 maternal deaths annually worldwide. In Impaired trophoblastic cell invasion results in inhibition
developed countries, the maternal death rate is of uterovascular development which stimulates
reportedly 0-1.8%. The perinatal mortality rate from placenta to release inflammatory factors leading
eclampsia in the United States and Great Britain ranges to endothelial dysfunction. Endothelial damage
from 5.6% to 11.8%. The maternal mortality rate is as and subsequent increase in vascular reactivity and
high as 14% in developing countries. permeability and coagulation cascade activation
result in organ dysfunction. It may involve a loss of the
Risk factors for eclampsia include young maternal normal cerebral autoregulatory mechanism, resulting
age, nulliparity, pregnancy interval >10 years, multiple
Anaesthetic management of a patient 58 Sunanda Gupta
presenting with Eclampsia Seema Partani
in hyperperfusion, leading to interstitial or vasogenic Differential Diagnosis

cerebral edema, decreased cerebral blood flow and
causes seizures. The increased leptin molecules in the Conditions simulating eclampsia include:
circulation also results in platelet aggregation, most • Seizure disorder, stroke, hypertensive
likely contributing to the coagulopathy associated with encephalopathy, ischemia or hypoxia, cerebral
eclampsia. space-occupying lesion
Clinical Features
• Systemic diseases (e.g., systemic lupus
Eclampsia can occur suddenly at any time in the erythematosus, sickle cell anemia), infection
puerperium, however mostly they occur intrapartum (e.g., meningitis, encephalitis)
or within first 48 hours of delivery. Late Eclampsia is
• Electrolyte and endocrine disturbances
defined as onset of seizures from 48 hours after delivery
upto 4 weeks postpartum. About 80% of patients will • Posterior reversible encephalopathy syndrome
have premonitory neurologic symptoms which can (PRES)
occur before or after the onset of seizures, which
includes headache, visual disturbances, photophobia, • Vasculitis or angiopathy
epigastric or right upper quadrant pain, hyperreflexia
• Amniotic fluid embolism
and altered mental status.
• Medications (withdrawal, illicit drug use)
Course of Seizures
• Multiorgan failure
Seizures have an abrupt onset. Each seizure generally
lasts for 60-75 seconds and may be divided into 2 Role of anaesthesiologist in management of patients
phases : presenting with eclampsia (Fig 1)
Phase 1: is tonic phase which persists for 15 to 20 I. To help obstetrician in controlling
seconds and begins with facial twitching. The body seizures and to prevent recurrent
becomes rigid leading to generalized muscular seizures
contractions.
II. Control blood pressure
Phase 2: phase1 progresses to a generalized
clonic phase 2 characterized by apnea, which lasts III. Emergency measures (ABC) to
approximately 60 seconds. establish a clear airway and prevent
major complications (Ex: hypoxemia,
Breathing generally resumes with a long stertorous aspiration)
inspiration, and the patient enters a postictal state
with a variable period of coma. Cardio-respiratory IV. To provide labor analgesia
arrest and pulmonary aspiration of gastric contents
V. To provide anesthesia for cesarean
can complicate a seizure.
section

Fig 1: Management of Eclampsia
I. Control of Seizures
The elementary goals of seizure control are to prevent maternal injury, ensure oxygenation, provide
cardiorespiratory support and prevent aspiration. These patients should not be left alone and immediate help
should be called for, along with the emergency Eclampsia Box containing all emergency medicines and infusions.
(Table 1)

Table 1: Emergency Box for Eclampsia
Majority of the eclamptic seizures are self limiting and magnesium sulphate (MgSO4) is the anticonvulsant drug
of choice. MgSO4 acts by preventing calcium ion transport, cerebral vasodilatation, and prevention of platelet
aggregations, thus relieving cerebral ischaemia. Other beneficial effects include a mild antihypertensive effect,
tocolytic activity and lowering of plasma endothelin-1 levels. It impairs peripheral neuromuscular transmission
and the intensity of neuromuscular block correlates with elevated serum Mg and decreased serum calcium
levels. Protocol for MgSO4 therapy is given in Table 2.
Loading dose- magnesium sulphate (4g)
• Draw up 8ml of 50% magnesium sulphate (4g) and dilute with 12ml Normal Saline
(0.9%) to give a total volume of 20ml and administer 20ml (4g) slowly over 10-20 min
via syringe infusion pump at 60ml/hr
Maintenance
• Following loading dose start a continuous maintenance infusion at 1g/h by diluting

20ml of 50% MgSO4 (10 g) with 30ml Normal Saline (0.9%) to give a total volume of 50
ml and infusing at a rate of 5ml/hr
If seizure recurs
• Draw up 4ml of 50% MgSO4 (2 g) diluted with 6ml Normal saline (0.9%) to give 10ml
and give IV over 5 minutes.
If seizure continues
• Despite a further bolus dose of magnesium sulfate, treat with phenytoin (15 mg/kg) or
diazepam (10 mg) midazolam (0.2mg/kg) or thiopentone (50 mg IV).Resistant seizures
should be managed with non depolarizing muscle relaxant and IPPV.
Table 2: Magnesium Sulphate protocol

Side effects of MgSO4 therapy includes potentiation d. If Respiratory Arrest occurs: Stop MgSO4 infusion,
of neuromuscular blockade, respiratory depression, Give IV 10% 10 ml Calcium Gluconate over 10 min and
hypotension, cardiac arrest, atonic postpartum start IPPV after intubation.
hemorrhage and reduced beat to beat variability in
the fetal heart rate. e. If Cardiac Arrest occurs: Commence CPR, Stop MgSO4
infusion and give IV Calcium Gluconate. Immediate
Monitoring during magnesium therapy should delivery should be done, if cardiac arrest occurs in the
include hourly urine output, respiratory rate, oxygen antepartum period
saturation and patellar reflexes, every 10 minutes
for first two hours and then every 30 minutes. Check II. Control of hypertension
serum magnesium levels every day if infusion is
continued for >24 hours. Serum Mg levels should be Antihypertensive treatment is started when systolic
estimated if respiratory rate < 16 breaths/minute, blood pressure is > 160 mmHg or diastolic blood
urine output < 25 ml/hour for 4 hours, loss of patellar pressure >110 mmHg. Systolic BP > 180mm Hg is
reflexes and if recurrent seizures occur. Signs and defined as a hypertensive crisis and is considered a
symptoms of impending toxicity with MgSO4 is given medical emergency. The goal is to lower the systolic
in Table 3. BP between 140 and 160 mm Hg and diastolic BP
between 90 and 110 mm Hg, at a rate of 10-20 mm
Sign and symptoms Serum Magne- Hg every 10-20 min, to prevent maternal and fetal
sium levels complications as a result of precipitous falls in BP
Feeling of warmth, flushing, 3.8-5.0 mmol/l below the critical perfusion thresholds.
double vision Slurred speech
Drugs that can be safely used include Labetalol,
Loss of tendon reflexes >5.0 mmol/l Nifedipine and Hydralazine. Drugs that should be
Respiratory Depression >6.0 mmol/l avoided for the reduction of blood pressure are high
Respiratory Arrest >6.3-7.1 mmol/l dose diazoxide, ketanserin, sublingual nifedipine,
Cardiac Arrest. >12.0 mmol/l nimodipine and magnesium sulphate (MgSO4).
Normal therapeutic level of serum magnesium are
• Labetalol
2.0 to 4.0 mmol/l
Labetalol bolus – 20 mg IV bolus (4ml of 5mg/ml
Table 3: Impending toxicity with MgSO4 solution) over at least 1 minute and repeat at 15
minute intervals as 20mg, 40 mg, 80 mg, with a gap
Management of Magnesium toxicity
of 20 min, to a maximum dose of 220mg until blood
a. If Urine output is <100 ml in 4 hours and if there pressure is controlled.
are no clinical signs of magnesium toxicity, decrease
Maintenance infusion – dilute 200mg (40ml of 5mg/
rate to 0.5 g/hour. Review overall management with
ml Labetalol with 10 ml 0.9% sodium chloride: giving
attention to fluid balance and blood loss.
a final concentration of 4mg/ml) and commence
b. If patellar reflexes are absent: Stop MgSO4 infusion infusion at 5ml/hr (20mg/hr). Double the infusion
until reflexes return rate every 30 min to a maximum of 40ml/hr (160mg/
hr) and titrate to keep the diastolic blood pressure
c. If Respiratory Depression is present: Stop MgSO4 between 90 – 100 mmHg. If hypertension persists
infusion and give oxygen via facemask, placing the on maximum rate or Labetalol is contraindicated or
patient in recovery position as she may have impaired causing side effects, add / replace with a Hydralazine
level of consciousness infusion.

• Hydralazine of baseline investigations known, seizures and

BP should be under control. Low dose epidural
Hydralazine bolus - Dilute 40 mg Hydralazine in 40 ml analgesia (bupivacaine/ropivacaine 0.125%
Normal Saline to give a concentration of 1mg/ml and with 2 µg/ml fentanyl as bolus or 10-12 ml/
give 5ml (5mg) slowly. After 20 minutes, if diastolic hr infusion) is advantageous for optimal blood
blood pressure is >100 mm Hg, give further 5 ml pressure control during labour and may be
(5 mg) over 15 min. Once the diastolic BP is 90 – 100 administered safely provided that there is no
mmHg commence maintenance infusion. coagulopathy or thrombocytopenia. Coagulation
Hydralazine infusion: Using same concentration as tests may be normal in the presence of abnormal
above, set infusion pump rate to 5 ml/hr (5 mg/hr). platelet function or low platelet counts. In such
The usual maintenance dose is 2-3 ml/hr (2-3 mg/ situations, adequate pain relief for labour may
hr) with a maximum dose upto 18 ml/hr (18 mg/hr). be provided with systemic opioids.
If significant side effects appear (headache, tremor, V. Management of anaesthesia in caesarean
nausea and tachycardia) or if maternal tachycardia is section for eclamptic parturients
>130 bpm, then reduce the dosage.
Cesarean delivery may be necessary for obstetric
• Other antihypertensive agents indications or a deteriorating maternal condition.
o Oral nifedipine 10-20 mg every 30 min to The patient should be stabilized with respect to
a maximum dose of 90 mg, (Nifedipine seizures, oxygenation and hemodynamic status
should be given orally and not sublingually). before the initiation of cesarean delivery. BP should
be controlled and coagulopathies monitored or
o Glyceryl trinitrate, which is administered as corrected.
an infusion of 5 µg/min, increasing every
3-5 min to a maximum dose of 100 µg/min. Preanaesthetic evaluation
o Atenolol, angiotensin converting enzyme Assessment of seizure control and neurologic function
(ACE) inhibitors, angiotensin receptor- is important to rule out possibility of raised intracranial
blocking drugs (ARB) and diuretics should pressures because of an underlying intracranial
be avoided pathologic process. Maintenance of blood pressure
below 160 mm Hg systolic and 110 mm Hg diastolic
o Diuretics are used if pulmonary edema should be ensured.
occurs prior to delivery.
Assessment of target organs involved
o Labetalol should be avoided in preeclamptic
patients with known history of bronchial • Cardiovascular system: Hypertension control,
asthma LV function and intravascular volume depletion
(check osmolality)
III. Emergency measures (ABC) to establish a clear
airway and prevent major complications is • Respiratory system: For signs of pulmonary
given in Figure 1. edema
IV. Labour analgesia • Renal: Degree of oliguria and creatinine level

It is essential that a preeclamptic patient is
stabilized prior to delivery. The appropriate level • Central nervous system: persistent coma and
of monitoring should be instituted, the results localizing signs may indicate intra cranial pathology.

• Liver: Liver function tests, clinical features of Monitoring

stretching of liver capsule
HR, ECG, BP, SpO2, capnography, temperature, urine
• Coagulation profile: Platelet count, prothrombin output and neuromuscular monitoring should be
time, activated partial thromboplastin time mandatory. Improved hemodynamic monitoring in
patients with severe preeclampsia may help to reduce
• Airway examination: Degree of airway edema the risk of peripartum pulmonary edema, renal failure
and cerebral complications. The parturient with PE
• Eye: visual disturbances should at least have an 18-gauge indwelling intravenous
catheter and should be encouraged to remain on her
• ABG analysis: Acidemia left side to avoid aortocaval compression. Supplemental
oxygen should be administered during labour and
• Imaging studies may be indicated after initial delivery.
stabilization, especially if there is doubt about
Invasive Monitoring
the diagnosis or possible injuries secondary to
seizure activity. Computed tomography (CT) This should be a multidisciplinary decision and the
scanning of the head, with or without contrast, Consultant Anaesthetist and Obstetrician should
can exclude cerebral venous thrombosis, be involved.
intracranial hemorrhage and central nervous
system lesions, all of which can occur in • Continuous intra arterial blood pressure
pregnancy and present with seizures. Consider monitoring is recommended in patients
CT scanning or MRI in patients who have with
been involved in trauma, are refractory to
1. consistently uncontrolled, upward
magnesium sulfate therapy or have atypical
swings in BP > 160/110 mmHg
presentations (Ex: seizures >24 h after delivery,
absence of severe hypertension). 2. When vasodilator infusions are
deemed necessary
Routine investigations
3. Coagulopathy requiring repeated
No single laboratory test is useful in predicting maternal blood sampling
or neonatal outcome in women with eclampsia. Full
4. Obese patients or presence of
blood count with special emphasis on platelet count
marked edema with difficult
along with:
venipuncture
1. Coagulation profile: BT, CT, INR, PT,
5. If pulmonary edema develops, the
APTT
arterial line can be used to monitor
2. Serum urea, electrolytes, creatinine arterial blood gases.
3. Liver function tests
• Continuous non-invasive monitoring of cardiac
4. Blood glucose level output may herald a new era in which we
5. Urine tests: Urinary protein/Creatinine focus on blood flow instead of blood pressure
ratio (PCR) and 24-h urine collection as the key hemodynamic variable in obstetric
for Proteinuria (>300 mg/24h both anesthesia. It provides better understanding
confirm and quantify proteinuria ) of the hemodynamic changes in women with
severe preeclampsia.
• Central venous pressure monitoring (CVP) Use of oxytocic agents

is often indicated in severe preeclamptic or
eclamptic patients, particularly in those with The management of life-threatening postpartum
marked hypertension, pulmonary oedema, haemorrhage in the setting of severe pre-eclampsia
oliguria and if blood loss is excessive. is a complex and challenging situation. Reversible
causes of uterine atony need to be addressed and
• Pulmonary artery pressure monitoring is mechanical methods to facilitate uterine contraction
rarely indicated but may be helpful in patients should be utilized. Syntocinon is the drug of choice for
who have evidence of pulmonary edema or uterine contraction in severe hypertension and should
oliguria/anuria. be carefully titrated according to haemodynamic
responses (20 IU in 1 L of Ringer lactate at 10
• Recently, Transoesophageal Doppler guided drops/min). Ergometrine has been associated
fluid management has been advocated in these with hypertensive crises and death in women with
patients. preeclampsia; therefore, ergometrine should be
avoided in the third stage of labour. Misoprostol is
Fluid therapy
associated with elevations in blood pressure, although
to a lesser degree than ergometrine.
The roles of fluid infusion and invasive monitoring
in oliguria are the most controversial aspects of Technique of Anaesthesia management
fluid management. The severely preeclamptic
parturient has a vasculature that has been 1. Regional Anaesthesia
described as “contracted and porous due to
• Neuraxial anesthetic techniques are preferable
endothelial damage but not underfilled”. As to GA in conscious eclamptic women with no
preeclampsia predisposes to pulmonary edema, evidence of increased intracranial pressure
fluid administration has to be monitored carefully and whose seizures are well controlled as it
by assessing urine output, the clinical condition of avoids the risks of aspiration, difficult and
the patient and pulse oximetry. failed intubations and laryngoscopic response
Reduction in urine output is extremely common of intubation seen with general anesthetic
immediately before delivery and for 12-18 hours techniques
postpartum. Oliguria could be due to hypovolemia • The current guidelines recommend that low
or due to renal vasoconstriction. Evidence suggest dose aspirin therapy is not a contraindication
that intravenous fluid should not be administered to regional techniques, which in the absence
in eclampsia for the purpose of volume expansion of bleeding are considered safe when the
or for the treatment of oliguria when renal platelet count is >75,000/mm3
function and serum creatinine levels are within
normal range. Although there is poor correlation • Platelet counts of < 50,000/mm3 are generally
between CVP and PCWP, a low CVP at <4 mmHg considered a contraindication. Within the
is a reliable indicator of hypovolemia. If CVP is > 4 range 50,000-75,000/mm3 an individual
mmHg, then additional fluids are not required as it assessment considering patient risks,
can raise CVP and precipitate pulmonary oedema. coagulation tests and thromboelastography
or platelet function should be important for
It is important to reemphasize that mothers no
decision making. Risk reduction strategies like
longer die from renal failure due to hypovolemia,
an experienced operator, single-shot spinal
but rather from adult respiratory distress
anaesthesia or flexible tip epidural catheter
syndrome that may complicate over transfusion,
can further reduce chances of hematoma.
fluid overload and pulmonary edema.

• Platelet counts with <100,000/mm3 in Incremental doses of 0.5% bupivacaine (3

women with severe preeclampsia are usually ml) in a dose sufficient to obtain a T8/ T10
associated with hypocoagulation and should dermatomal sensory level of analgesia with
prompt further investigation of aPTT, fibrinogen monitoring of maternal vital signs and fetal
and PT values. Regional anaesthesia should heart rate tracing, is an established technique.
be attempted only on an individual basis, Once the epidural catheter has been proven
considering the benefits and risks involved. functional with stable maternal hemodynamics
and fetal heart rate tracing, surgical anesthesia
a. Spinal anesthesia
may then be achieved to the T4 sensory
• Spinal anesthesia is the most common and dermatome necessary for cesarean delivery.
preferred anesthetic technique in doses of CSE provides the reliability of spinal anesthesia
0.5% bupivacaine (8-10mg) along with 20ug and at the same time the flexibility of good
fentanyl. It has no effect on Apgar scores and postoperative pain relief through an epidural
umbilical artery pH in preeclampsia as long catheter infusion. The epidural component of
as the systolic blood pressure is maintained the CSE offers superior hemodynamic stability
greater than 80% or more of the baseline. The over spinal anesthesia. There is no difference
incidence of spinal induced hypotension and in neonatal outcome between spinal and
the vasopressor requirement are significantly epidural anesthetic techniques.
lowered in preeclampsia when compared with
2. General anesthesia
normal parturients undergoing CS delivery.
The increased production of circulating GA is only indicated in the presence of severe
factors with potent pressor effect and the fetal compromise; pulmonary oedema;
increased sensitivity to vasopressor drugs haemodynamic instability; intra spinal
in preeclampsia is an important factor for haematoma risk (e.g. placental abruption;
decrease in the spinal induced hypotension severe thrombocytopenia) or after eclampsia,
in preeclampsia. Cardiac output monitoring where altered consciousness or neurological
after spinal anesthesia has shown that neither deficit persists. Anaesthesia is achieved with
spinal anesthesia nor the use of phenylephrine thiopental/propofol, opioid, muscle relaxant
to treat hypotension reduce cardiac output and hyperventilation technique.
during CS delivery, further supporting its
safety in pre-eclampsia. Continuous spinal Anaesthetic concerns during general
anesthesia offers the flexibility of titration of anaesthesia in eclampsia
local anesthetic agents in small aliquots; thus,
graded sympathetic block could be achieved • Airway oedema and increased vascularity
with a lower degree of sympathectomy in makes the airway more difficult to intubate,
these parturients. However, the higher rate leading to difficulty in airway management
of infection, injury to nerve roots, postdural
puncture headache and technical difficulty • Although cholinesterase levels decrease, the
are potential pitfalls so this technique is not duration of action of succinylcholine and ester
frequently used. local anesthetics is seldom affected
b. Epidural anesthesia • Exaggerated hypertensive responses to

endotracheal intubation and extubation can
Epidural anesthesia may be instituted in a be life threatening. Pharmacological therapy
sequential manner for elective CS delivery. used to obtund the pressor response include

short acting opiates (Alfentanil 10 mg/kg,), retardation, extreme prematurity and fetal hypoxia
beta-blockers (Esmolol 0.5 mg/kg or labetalol also contribute to fetal demise.
10-20 mg) and Lidocaine (1.5 mg/kg 5min Continuing critical care management of the eclamptic
prior to intubation) parturient, should take place in a high dependency unit
adjacent to the obstetric unit with a multidisciplinary
• Drug interaction with magnesium may
team approach and should involve:
prolong effect of both depolarizing and
non depolarizing muscle relaxants. Non • Effective postoperative analgesia reduces the
depolarizing muscle relaxants should be given stress response and consequent hypertension
under guidance of a neuromuscular monitor caused by poorly controlled pain; however
NSAIDs should be avoided until proteinuria
• Extubation should be done in the left lateral has resolved and there is no evidence of
position when patient is fully conscious or impairment of renal or platelet function.
else patient should be transferred to ICU
for ventilatory support depending on the • Adequate steps to prevent development of
preoperative condition and intraoperative pulmonary oedema or convulsions within 24
behavior. hours of delivery. These events may occur as
an epidural block dissipates.
• Hypoxia, hyperthermia and hyperglycemia
should be avoided to prevent exacerbation of • MgSO4 therapy should be continued, usually
neurologic injury. for 48 hours postpartum, or other long-acting
Therefore in patients who require general anaesthesia, oral anticonvulsants may be substituted.
BP and convulsions should be maximally controlled and Likewise, antihypertensive therapy is
ideally, invasive monitoring inserted prior to induction continued with longer-acting preparations
replacing intravenous infusions.
of general anaesthesia. A senior anaesthetist should
be present to manage these challenging cases. • A strict intake output chart should be
maintained for atleast 24 hours or until diuresis
Major maternal complications develops. A total intake of 75-80 ml/hr should
not be exceeded until the patient begins to
• Cerebrovascular accidents
mobilize her extracellular water.
• Disseminated intravascular coagulopathy
• Acute Renal failure • Prophylaxis for thromboembolism should be
mandatory
• Pulmonary aspiration
• Pulmonary edema Post-preeclampsia outcomes
• Venous thromboembolism
• Hypertensive encephalopathy associated with
• Cardiopulmonary arrest specific neuro radiologic imaging has been
The most significant maternal complication of named “Posterior reversible encephalopathy
syndrome” (PRES). This syndrome is
eclampsia is permanent CNS damage secondary
characterized by headaches, seizures, altered
to recurrent seizures or intracranial bleeding.
mental status and visual disturbances and has
Fetal/neonatal mortality been found in patients with preeclampsia,
renal failure, hypercalcemia and those taking
The fetal mortality rate varies from 13-30% due to immunosuppressive and chemotherapeutic
premature delivery and its complications. Placental drugs. The purported mechanism of PRES
infarcts, abruptio placentae, intrauterine growth includes endothelial dysfunction, acute
increases in BP that may exceed the upper

limit of cerebral autoregulation and vasogenic 4) Gupta S. Pregnancy induced hypertension: Scien-
oedema. The prompt diagnosis and early tific riddles and rational solutions. In Year Book of
management of PRES, may help in preventing Anaesthesiology. Paras Publications. Ed Chandra
subsequent irreversible white matter lesions U, Basu AK.vol 2; 2012
of the brain.
5) Guidelines and Audit Implementation Network
• Post eclampsia cognitive dysfunction: It has (GAIN)of the department of Health, Social ser-
been found that women who had experienced vices and Public safety, Northern Ireland .2012
eclamptic seizures were shown to have
6) National Institute of Health and Clinical Excel-
deficient cognitive function including memory
lence. Hypertension in Pregnancy, The manage-
impairment and distractibility.
ment of hypertensive disorders during pregnan-
• In later life, preeclampsia has been found cy. Clinical guidelines CG107 Issued. 2012
to be associated with an increased risk 7) Parthasarathy S, Hemant Kumar VR, Sripriya R,
of hypertension, fatal and non-fatal Ravishankar M. Anesthetic management of a pa-
ischaemic heart disease, strokes and venous tient with eclampsia. Anesth Essays Res. 2013;7
thromboembolism. (3):307-12.
Conclusion 8) American College of Obstetricians and Gynecol-
ogists, Task Force on hypertension in Pregnancy.
Although the incidence of eclampsia has declined Hypertension in pregnancy. Report of the Amer-
in recent years, mainly due to the improvement of ican College of Obstetricians and Gynecologists’
healthcare, serious adverse outcomes still exist. Five task force on hypertension in pregnancy. Obstet
percent of patients with hypertension develop severe Gynecol 2013;122(5)
preeclampsia, and about 25% of women with eclampsia
have hypertension in subsequent pregnancies. About 9) Gupta S. Management of severe PIH for elective
2% of women with eclampsia develop eclampsia LSCS. RACE 2014
with future pregnancies. Multiparous women with
10) Fitzpatrick K, Hinshaw K, Kurinczuk J et al. Risk
eclampsia have a higher risk for the development of
factors, management, and outcomes of hemoly-
essential hypertension, and they also have a higher
sis, elevated liver enzymes, and low platelets syn-
mortality rate in subsequent pregnancies than do
drome and elevated liverenzymes, low platelets
primiparous women.
syndrome. ObstetGynecol2014; 123:618–27
Recommended Reading 11) D Leslie BSc (Hons) MBBCh (Hons) FRCA* and RE
1) Karumanchi SA, Lindheimer MD. Advances in the Collis MB BS FRCA MScHypertension in pregnan-
understanding of eclampsia. CurrHypertens Rep. cy BJA Education, 2016;16(1):33–37
2008; 10:305-12. 12) Dhariwal NK, Lynde GC. Update in the manage-
2) Polley LS. Hypertensive disorders. In: Chestnut ment of patients with preeclampsia. Anesthesiol-
DH, Polley LS, Tsen LC, Wong CA, editors. Chest- ogy Clin2017;35:95-106.
nut’s Obstetric anaesthesia: Principles and prac- 13) Ross MG, Ramus RM, at al. Eclampsia.Medscape
tice. 4th ed. Philadelphia: Mosby Elsevier; 2009:
2018: 1-20
975-1000.
14) Ismail S. Anesthetic management of pregnant pa-
3) Cunningham FG, Leveno KJ, Bloom SL, Hauth JC,
Rouse DJ, Spong CY. Williams Obstetrics. Pregnan- tients with hypertensive disorders. In: Obstetric
cy hypertension. 23rd ed. Chap. 34, New York: Anesthesia for co-morbid conditions. ED: Gunay-
McGraw-Hill; 2010:706-56. din B, Ismail S, 1st edition Switzerland: Springer;
2018:17-30

MCQ
1. Treatment for eclamptic seizure is 4. Loss of tendon reflexes occur when serum
magnesium level exceeds
a. Loading dose of 2g MgSo4 iv followed
by 1g/hr infusion a. 3 mmol/L
b. Loading dose of 4g MgSo4 im followed b. 4 mmol/L
by 1g/hr infusion
c. 5 mmol/L
c. Loading dose of 4g MgSo4 iv followed
by 0.5g/hr infusion d. 6 mmol/L
d. Loading dose of 4g MgSo4 iv followed 5. Drugs that should be avoided in preeclamptics

by 1g/hr infusion for control of blood pressure are all except
2. Seizures not responding to MgSO4 are treated a. Ketanserin

with b. Sublingual nifedipine
a. phenytoin (15 mg/kg) c. MgSo4
b. diazepam (10 mg) d. Oral nifedipine
c. midazolam (0.2mg/kg)
d. thiopentone (50 mg IV)
e. All of the above
3. Antihypertensive treatment is started when
a. SBP ≥ 150 mm Hg and DBP ≥ 100 mm

Hg
b. SBP ≥ 160 mm Hg and DBP ≥ 110 mm
Hg
c. SBP ≥ 160 mm Hg or DBP ≥ 110 mm Hg
d. SBP ≥ 150 mm Hg or DBP ≥ 100 mm Hg
5.d 4.c 3.c 2.e 1.d

Answers

7 Anesthesia for children with
congenital heart disease for non cardiac surgery
Dwarakesh Thalamati Ranjith Karthekeyan B

Assistant Professor, Professor,
SRIHER, SRIHER,
Chennai. Chennai.
Key points
Ø 30% of children with congenital heart disease have extracardiac malformations that may interfere with
anesthesia management
Ø Ventricular septal defect is the most common CHD in all populations
Ø Breathlessness due to increased pulmonary blood flow is a common respiratory symptom in children
with cardiac failure
Ø Most frequently observed hematologic abnormalities in a CHD child includes thrombocytopenia,
platelet dysfunction, hypofibrinogenemia, and deficiency in clotting factors
Ø Echocardiogram should be reconsidered if there is no information available or if the last cardiology visit
date was more than 6 to 9 months earlier
Ø Significant anemia in a CHD child may cause subendocardial ischemia in some defects
Ø Hypocarbia might decrease cardiac output, increase SVR, increase left-to-right shunts, shift the
hemoglobin-oxygen dissociation curve to the left and limit O2 transfer, decrease the serum potassium
level, resulting in arrhythmias
Ø Deranged coagulation profile and platelets in cyanotic children must be kept in mind before attempting
regional blocks
Introduction the underlying disease is essential in developing an

anesthetic plan for the child that does not interfere
The challenge for anesthesiologists in handling patients
with the hemodynamic or respiratory equilibrium.(1)
with congenital heart disease(CHD) coming for non
cardiac surgery relies on the patients age, complexity Incidence
of the heart lesion, child’s capacity to compensate,
The incidence of CHD is approximately 8:1000 live births
urgency of surgery and coexisting diseases. Improved
in the west. The frequency of different lesions varies
outcomes after surgical repair of congenital heart
between populations, with ventricular septal defect
defects has contributed to the steady increase in the
being the most common in all populations.
number of children requiring anesthesia for noncardiac
surgery. Anesthesiologists should be aware that 30% of Spectrum of Congenital heart disease
children with congenital heart disease have extracardiac
malformations that may interfere with the anesthesia Classification of CHD according to the pathophysiology
management. Preoperative evaluation as well as helps us in understanding the blood flow dynamics and
the recognition of the physiologic consequences of device appropriate management plan.

Anesthesia for children with congenital heart 70 Ranjith Karthekeyan B
disease for non cardiac surgery. Dwarakesh Thalamati
Pathophysiology Common examples Clinical notes
Left-to-right shunt Small ASD, VSD, PDA Large (‘non-restrictive’) lesions are
Restrictive’ lesions associated with severe CCF in infancy
If unrepaired, may lead to pulmonary
Non-restrictive’ lesions Large VSD, PDA, AVSD, common hypertension and reversal of shunt
arterial trunk (Eisenmenger’s
syndrome).
Obstructive lesions Aortic stenosis, coarctation of the Severity of lesion determines age at
aorta, pulmonary stenosis presentation – neonates with severe
obstruction may be critically ill with a duct
dependent circulation
Cyanotic lesions
Right-to-left shunt Tetralogy of Fallot: May present with severe cyanosis and
• VSD with aortic override hypercyanotic ‘spells’, or if unrepaired in
• Right ventricular outflow tract an older child, with cyanosis, fatigue and a
Obstruction history of ‘squatting’
• Right ventricular hypertrophy,
Transposition of the TGA may be associated with ASD, Long term survival requires intervention in
Great VSD, PDA early infancy (arterial switch operation)
Arteries (TGA)
Single ventricle Hypoplastic left heart syndrome Duct dependent circulation; survival
physiology (HLHS), Hypoplastic right heart requires intervention in the neonatal period
syndrome, Tricuspid atresia.
Mixing lesions Total anomalous pulmonary Present with heart failure and/or cyanosis –
venous drainage (TAPVD). survival requires intervention in the
neonatal period
Preoperative assessment The history and examination should focus on

Children coming for anesthetic management fall in any a. Complete understanding of the anatomical changes
one the following category. due to cardiac defect or palliative procedure
b. Direction and amount of shunting
1. Children with uncorrected cardiac defect
c. Presence and severity of pulmonary hypertension
2. Children who had previous palliative surgery d. Pulmonary flow - reduced or increased
e. Degree of hypoxemia, polycythemia
3. Children in whom total correction has been done f. Coagulation abnormalities
but they may have residual defects requiring certain g. Pathophysiological findings that will influence the
procedures management
h. Functional status of the child

Respiratory symptoms levels, especially in children receiving digoxin, diuretics

or angiotensin-converting enzyme inhibitors before
Breathlessness due to increased pulmonary blood
surgery.
flow is a common respiratory symptom in children
with cardiac failure. Frequent respiratory tract ECG
infections and poor weight gain are common in older
A systematic approach to the ECG must be followed to
children.
avoid abnormalities that may have clinical importance.
Chest pain A 12-lead ECG should always be considered especially
in the presence of an arrhythmia or pulmonary
Coronary artery abnormalities and chest pain due to
hypertension. Pulmonary hypertension on ECG include
angina, is rare. Chest pain in children is mostly due to
the presence of a P-wave amplitude greater than
musculoskeletal problems if other cardiac causes are
2.5 mm in leads II, III, and aVF, or greater than 1.5 mm
ruled out. Sudden collapse may be due to arrhythmias,
in V1 (reflecting right atrial enlargement), right axis
and collapse with exercise is seen in a child with
deviation greater than 1100, and a dominant R-wave
significant left ventricular outflow tract obstruction
in V1 (>7 mm).
such as aortic stenosis.
Chest X-Ray
Poor weight gain – common in conditions causing heart
failure or associated with increased pulmonary blood Chest x-ray is useful in evaluating heart shadow and the
flow such as VSD. Older children with acquired heart pulmonary vascularization. In the presence of pulmonary
disease such as endocarditis or cardiomyopathy may vascular disease, cardiomegaly and peripheral pruning
have anorexia and weight loss. Conditions associated of the vasculature with a hypertranslucent appearance
with cyanosis and reduced pulmonary blood flow such in association with dilatation of the hilar and proximal
as TOF are not usually associated with poor weight gain. vessels is seen. Whereas in case of hypoperfusion of the
lungs, a homogeneous translucent appearance is seen.
Medication history must also be elicited. Patients
with CHD may be on of aspirin, warfarin, diuretics, Echocardiogram
angiotensin converting enzyme inhibitors, and
Echocardiogram should be reconsidered if there is no
antiarrhythmics.
information available or if the last cardiology visit date
Preoperative Tests was more than 6 to 9 months earlier. Results should be
compared with previous reports and can be discussed
Laboratory Testing
with the cardiologist.
Routine blood investigations based on patient
Risk stratification
characteristics and organs systems involved is advised.
Hematocrit of 60% is more likely to be associated with The risk of perioperative complications is associated
coagulation abnormalities. These anomalies are related with individual patient characteristics of the underlying
to the degree of chronic hypoxemia as well as to the disease. Risk stratification of cardiac conditions is
degree of hyperviscosity. Most frequently observed difficult due to the varied range of presentation and
anomalies include thrombocytopenia, platelet procedures. However the commonly quoted risk
dysfunction, hypofibrinogenemia, and deficiency in stratification in literature is mentioned below in table
clotting factors. It is important to check electrolyte 1. (2)

High risk Intermediate risk Low risk

Physiologically poorly Physiologically normal or well Physiologically normal or
compensated and/or presence of compensated well compensated
major complications
(a) Cardiac failure
(b) Pulmonary hypertension
(c) Arrhythmias
(d) Cyanosis
Complex lesions (single-ventricle Simple lesions Simple lesions
or balanced circulation
physiology, cardiomyopathy, aortic
stenosis)
Major surgery (intraperitoneal, Major surgery (intraperitoneal, Minor (or body surface)
intrathoracic, anticipated major intrathoracic, anticipated major surgery
blood loss requiring transfusion) blood loss requiring transfusion)
Under 2 yr old Under 2 yr old Over 2 yr old
Emergency surgery Emergency surgery Elective surgery
Preoperative hospital stay more Preoperative hospital stay more Preoperative hospital stay
than 10 days than 10 days less than 10 days
ASA physical status IV or V ASA physical status IV or V ASA physical status I – III
Table 1: Risk stratification of a child with CHD
Preoperative preparation refuse inhalation induction, intramuscular ketamine

in pre-operative holding area with monitoring will
Fasting
facilitate induction intraoperatively and reduces the
Fasting guidelines for children allowing clear fluid up risk of a cyanotic spell by increasing SVR and decreasing
to 2 hours before anesthesia has a significant benefit right-to-left shunt.
for cyanotic children and those depending on an
Endocarditis prophylaxis
arterial shunt, because they are particularly sensitive
to prolonged fasting and dehydration. In cases in The American Heart Association has advised the use of
which oral intake is not possible or in the presence of antibiotics only in “high‑risk” patients- which include
dehydration, an intra venous infusion is recommended patients with prosthetic cardiac valves, Patients with
before anesthetic induction prior infective endocarditis, patients with unrepaired or
palliated cyanotic CHD including shunts and conduits,
Premedication
Patients with CHD repair with prosthetic material or
Premedication should provide anxiolysis and sedation device placed by surgery or catheter intervention
without hemodynamic or respiratory impairment that during first 6 months after placement, patients with
may cause hypoxia and hypercarbia with consequent CHD repair with residual defect at the site or adjacent
detrimental effects on pulmonary hypertension. In to the site of prosthetic patch or device that inhibits
children with severe cyanotic cardiac disease who endothelialisation.

ANESTHESIA MANAGEMENT • Fluid balance to maintain optimal cardiac filing

pressures
Monitoring
• Maintain hematocrit- Cyanotic children are
Routine ASA monitors should be applied before
particularly dependent on a greater hematocrit
induction of anaesthesia if the child is cooperative.
(Hct > 40–45 %). Significant anemia may cause
Invasive arterial and central lines are reserved for
subendocardial ischemia in some defects
children who fall under high risk group and undergo
prolonged procedures with significant volume shifts. • Optimize ventilation for each child
However, invasive monitoring may also be required
• M a i n t a i n n o r m o c a p n i a : a v o i d
in other scenarios based on the underlying cardiac
hyperventilation,unless indicated for
condition and disease state.
the management of increased PVR. The
Goals resulting hypocarbia might, decrease
cardiac output, increase SVR, increase
• Minimize effects on the cardiovascular system
left-to-right shunts, shift the hemoglobin-
by
oxygen dissociation curve to the left
• Avoiding agents that cause excessive andlimit O2 transfer, decrease the serum
myocardial depression potassium level, resulting in arrhythmias
• Ensuring adequate premedication - to • Maintain body temperature in procedures
reduce anxiety, agitation and smooth where duration of surgery is prolonged
induction of anesthesia
• Control of pulmonary hypertension • Prevent detrimental changes in cardiac shunts-
factors affecting PVR and SVR ratio must be
• Maintain myocardial function and cardiac
kept in mind. (Table 2)(3)
output
Increase pulmonary output Increase systemic output
Decrease PVR Increase PVR

• Hypocapnia • Extracardiac or • Hypoxia
• Pulmonary aorto-pulmonary • Hypercarbia
vasodilators (nitrous shunt • Hypothermia
oxide, Volatile • High Heamatocrit
anaesthetics, • IPPV
Vasopressin, PDE • Metabolic acidosis
inhibitors) • Atrial level Shunt • Alpha Adrenergic
• Metabolic Alkalosis Stimulation
Decrease SVR
Increases SVR • Vasodilators-Nitrites,
• Sympathetic • Ventricular level PDE inhibitors
stimulation shunt • Spinal and epidural
• Vasoconstrictors Anaesthesia
• hypothermia • Deep GA
• Hyperthermia
• Low haematocrit
• Beta Agonists
Table 2: Factors affecting PVR and SVR

Induction inhalation induction keeping in mind its depressant

effects and action on SVR and PVR. Airway management
Induction plan and precautions to be followed must
with endotracheal intubation or a supraglottic airway
be formulated preoperatively, an example is given in
device in shorter procedures is usually done. The airway
table 3(4). Intravenous or inhalation induction may be
should be controlled during procedures associated with
planned, depending on the availability of intravenous
high risk of peri‑procedure haemodynamic instability,
access, and the child’s physiological condition and
procedures with high risk of complications.
cooperation. Sevoflurane can be safely used for
CHD Subset Physiology Issues Choice of agents Precautions

Uncorrected • Uncorrected • Desaturation • SVR fall needs • Avoid excessive
cases for defects to be avoided: tachycardia and
• PHT
non cardiac etomidate for bradycardia
• Shunting
surgery. • Arrhythmias induction followed
• For TOF, maintain SVR
• Balance by vecuronium
or single or atracurium as • Avoid inotropes to
ventricular choice of relaxant. reduce chances of
physiology infundibular spasms.
• Fentanyl or
• May be remifentanil for • Central line- avoid as
associated pain relief or arrhythmias may occur
with other dexmedetomidine during insertion. May
congenital can be used. need inotropic support
defects in perioperative period.
Corrected • Normal • Minimal issues Regular induction For Fontan procedure,
cardiac physiology with normal agents if normal avoid fluid overload
condition if complete physiology. physiology. but preload must be
and correction. maintained.
• For single
anesthesia. If using IPPV, avoid high
• Single ventricle, need
Inspiratory pressures and
ventricular to maintain
prolonged inspiratory
physiology passive
time
for Fontan. pulmonary
Keep ventilation near
flow with
FRC and maintain
spontaneous
normocapnea.
ventilation
Table 3: Example of an anesthetic induction plan in a CHD child
Maintenance and peripheral nerve blocks should be used wherever

necessary, the deranged coagulation profile and
Oxygen and air with an inhalation agent is preferred platelets in cyanotic children must be kept in mind
for maintenance of anaesthesia in many centers. before attempting regional blocks. Intraoperatively,
Increased inspired oxygen concentrations are used small doses of fentanyl might be required to blunt
when attempting to reduce pulmonary vascular haemodynamic and stress response. Paracetamol and
resistance. Regional anesthesia in the form of caudal local anaesthetic infiltration are usually adequate for
post‑procedural analgesia. Fluid management - Isotonic with complex underlying pathology, a multidisciplinary
maintenance fluids will be required in majority of cases, approach involving the anesthesiologist, pediatrician,
with attention to blood sugar monitoring in neonates. It cardiologist should be planned before any intervention
is also important to account for the volume and flushes in order to understand the hemodynamic changes
used during sampling. Volume loading in a poorly induced by the CHD, to determine the anesthesia risk,
compliant heart can impair cardiac function. and to define the perioperative care will be required.
Postoperative References
Paediatric intensive care is reserved for ill or high risk 1) Pediatric anesthesia basic principles - Bruno bis-
cases, those with pulmonary hypertension and those sonnette.
where intraoperative and postoperative complications 2) Michelle C White, James M Peyton; Anaesthetic
are anticipated. Postoperative care should be given by management of children with congenital heart
experienced staff caring for this subset of paediatric disease for non-cardiac surgery, Continuing Educa-
patients. Adequate pain relief must be provided along tion in Anaesthesia Critical Care & Pain, Volume 12, Is-
with treatment of case specific issues - dysrhythmias, sue 1, 1 February 2012, Pages 17–22.
bleeding and thromboembolic events should be
3) Anesthesia for the patient with congenital heart
addressed. (5)
disease presenting for noncardiac surgeryCurrent
Conclusion Opinion in Anaesthesiology.June. 26(3):318–326.
Children with heart disease are at increased risk 4) Junghare SW, Desurkar V. Congenital heart
of perioperative complications. The cardiovascular diseases and anaesthesia. Indian J Anaesth
2017;61:744-52.
anatomy and physiology is complex and each child
requires individual evaluation of risk factors. In patients 5) Pediatric cardiac anesthesia- Carol L. Lake.

MCQ
1. A 1 year child with cyanotic heart disease 4. ABG of a VSD child showing pco2 levels of
coming for intraperitoneal emergency surgery 20 due to hyperventilation- which of the
– which of the options below best suites the following physiological response is more likely
above scenario
a. Increased cardiac output
a. High risk surgery
b. Decreased SVR
b. Intermediate risk surgery
c. Increase left-to-right shunt
c. Low risk surgery
d. ODC shift to right
d. All emergency surgeries are high risk
surgeries 5. In a child with right to left shunt all are true
except
2. Which of the following factors decrease PVR
a. Fast uptake of inhaled anesthetics into
a. Metabolic alkalosis the blood
b. Hypothermia b. Extreme danger of systemic emboli
c. High Heamatocrit from venous air embolism.
d. IPPV c. Potential for overdosing intravenous
drugs.
3. Pulmonary hypertension is diagnosed in ECG
by all except d. An increased arterial to PetCO2
gradient
a. P-wave amplitude greater than 2.5
mm in II, III, and aVF,
b. P wave greater than 1.5 mm in V1
(reflecting right atrial enlargement)
c. Rominant R-wave in V1 (>7 mm)
d. RSR pattern v1
5.(a) 4.(c) 3.(d) 2.(a) 1.(a)

Answers

8 CRANIOFACIAL SYNDROMES CHILDREN AND ANESTHETIC CONCERNS
Professor and HOD, Aruna Parameswari

SRIHER,
Chennai.
Key points
Ø Children with syndrome can be undiagnosed at the time of presentation to the anesthesiologist, so
vigilance is of prime importance
Ø Syndromes resulting in increased amount of soft tissue in relation to the volume of the oral cavity
typically produce airway obstruction on induction of anesthesia
Ø In cases of restricted mouth opening, it is important to determine if rigidity is fixed or may be overcome
once the patient is anaesthetized
Ø Patients with abnormalities of the ears can be expected to have upper airway abnormalities, due to the
common embryonic origin of these structures
Ø Involvement of the facial skeleton may result in upper airway obstruction, exophthalmos and raised
intracranial pressure
Ø Intubation may be more difficult after corrective surgery as a result of the altered relationships of the
maxilla and mandible and reduced temporomandibular joint movement in Apert syndrome
Ø The measurement most commonly used to determine cervical spine instability is the atlantodens
interval(ADI)
Ø Down’s syndrome children are prone to increased secretions, difficult airway and increased incidence
of bradycardia with sevoflurane, so preinduction antisialogogue may be useful in them
Ø Spontaneous ventilation should be maintained if any difficulty with intubation is anticipated
Ø Upper airway obstruction at induction is very common in syndromic children (especially with craniofacial
syndromes) and can be relieved with OPA, NPA or LMA
Ø In children with micrognathia, a paraglossal approach to direct laryngoscopy may be more effective
Introduction
Rare diseases and syndromes are of special interest the child undergoes general anesthesia, for example,
to pediatric anesthesiologists, as each of them has 38% of children who have Hurler’s disease undergo at
very specific anesthesia concerns1. Knowledge of the least one general anesthetic in infancy before diagnosis
pathophysiology, symptomatology, treatment options of their disease. Pediatric anesthesiologists therefore
of these diseases and tailored anesthesia management need to be vigilant and aware of this possibility and
forms the basis of provision of safe anesthesia care need to be able to pick up the subtle signs associated
to these group of children, avoiding mortality and with the syndromes. There are also specific books and
morbidity. The disease can be undiagnosed at the time websites for these syndromes which can be very useful.

Craniofacial Syndromes Children and 79
Anesthetic Concerns Aruna Parameswari
macroglossia. Syndromes like mucopolysaccharidoses of restricted opening, it is important to determine if

result in further narrowing of the box due to deposition rigidity is fixed or may be overcome once the patient
of mucopolysaccharides in the tongue, tonsils and is anaesthetized. In congenital syndromes, the rigidity
pharynx resulting in airway obstruction. Maxillary and is fixed and will not change with anaesthesia, unlike
mandibular abnormalities will change the volume of the in trismus secondary to pain or inflammation, where
box for the same tongue size and hence again result in it may be possible to open the TMJ to access the oral
airway obstruction. cavity once the patient is asleep.
Anterior mandibular space Vertebral column
The anterior mandibular space is the available space The movements of the vertebral column, particularly
within the mandible into which the soft tissue of the the lower cervical region and the atlanto-occipital
tongue can be displaced during laryngoscopy. If this region are crucial to visualization of larynx during
space is small relative to the size of the tongue, direct direct laryngoscopy, by providing a line of sight for
laryngoscopy and tracheal intubation will be more intubation. Cervical mobility could be restricted due to
difficult. Mandibular hypoplasia (micrognathia) and vertebral fusion, hemivertebrae and arthritic changes
retrognathia as occurs in Pierre Robin sequence and making tracheal intubation difficult or impossible by
Treacher Collins syndrome are good examples where conventional laryngoscopy. Other disease processes
the anterior mandibular space is less, making direct or congenital conditions may cause instability of the
laryngoscopy difficult. Another condition is an anterior vertebral column and put the spinal cord in danger of
larynx in which the larynx sits high, under the base of impingement. In these circumstances, motion of the
the tongue. Because an anterior larynx leaves no space neck must be avoided during intubation.
into which to displace the tongue, the larynx remains Soft tissues
anterior to the laryngoscope blade and cannot be seen
during intubation. Soft tissue conditions that cause airway management
problems usually fall into two categories: those that
Maxillary considerations limit movement of the airway and those that distort
Similar to macroglossia and micrognathia, maxillary the airway by mass effects.
hypoplasia can also change the mass-to-volume ratio Some syndromes like the Freeman-Sheldon syndrome
of the upper airway, making airway obstruction more is associated with fixed microstomia – limitation of
likely. Patients who have maxillary hypoplasia as in movement of oral tissues that does not respond to
Apert syndrome, often have some degree of nasal efforts at muscular relaxation.
obstruction and/or choanal stenosis. The result is that
these patients are primarily mouth breathers and suffer Macroglossia is one of the commonest soft tissue issues
obstruction if their mouths are closed. However, these in syndromic children. The tongue is enlarged and
patients have mandibles of normal size, so that tracheal fills the oral cavity, making visualization of the larynx
intubation is not difficult. difficult. Macroglossia occurs in Beckwith-Weidemann
syndrome, Down’s syndrome, Sturge-Weber syndrome
Temporomandibular joint and various syndromes associated with dwarfism.
Mucopolysaccharidoses is another condition where
The temporomandibular joint (TMJ) is the hinge that
soft tissue deposition of glycosaminoglycans can alter
opens the upper airway and also translocates the
the volume of the upper airway. Syndromes associated
lower jaw forward. Restricted opening of the TMJ is
with macroglossia are listed in Table 1.
more common than failure of translocation. In cases

Down’s syndrome feeding difficulties, failure to thrive, airway obstruction

and apneic spells. Obstructive sleep apnea can occur,
Beckwith-Weidemann syndrome
especially when there is glossoptosis as well.
Mucopolysaccharidoses
Pierre Robin sequence
Table 1: Syndromes associated with macroglossia
Treacher Collins syndrome
Patients with abnormalities of the ears can be expected Stickler’s syndrome
to have upper airway abnormalities, due to the common Goldenhar syndrome
embryonic origin of these structures (from first and
Beckwith-Weidemann syndrome
second branchial arches and first branchial cleft). For
Trisomy 18, 13
example, 2% of children with unilateral microtia and
42% of children with bilateral microtia have difficult Seckel syndrome
laryngeal view5. The advantage of understanding this
Table 2: Syndromes associated with micrognathia
association is that it is clinically easier to recognize
microtia than mandibular hypoplasia. Congential Facial abnormalities can also be functionally classified
micrognathia is commonly associated with several based on the site of abnormality7. This is summarized
syndromes6 (Table 2). Micrognathia is associated with in Table 3.
Supraglottic abnormalities Abnormalities also involving Subglottic abnormalities

the glottis
Maxillary hypoplasia Mucopolysaccharidoses Subglottic stenosis
Syndromic Hunter, Down,

Craniosynostosis - Hurler syndromes Larsen,
Apert, Crouzon, Fraser syndrome
Pfeiffer, Saethre
Chotzen, Carpenter
Mandibular hypoplasia
Pierre Robin sequence,

Treacher Collins,
Hemifacial
microsomia/
Goldenhar syndrome
Table 3: Functional classification of facial anomalies according to site involved
Spine
Many syndromes are associated with anomalies of concerns with providing regional anesthesia. Atlanto-
the spine. Conditions affecting the cervical spine can axial instability can have serious, life-threatening
lead to difficulties in laryngoscopy and intubation. implications. Some of the syndromes with cervical spine
Scoliosis leads to respiratory abnormalities and also abnormalities are listed in Table 4.
Down syndrome bleeding in affected children associated with trauma

or surgeries. Some of these syndromes associated with
Mucopolysaccharidoses (MPS I, IV, VI)
thrombocytopenia are given in the table below.
Goldenhar syndrome
Klippel Feil syndrome (vertebral fusion) Down syndrome (7–28%)
Noonan syndrome Turner syndrome (31%)
Ehlers Danlos syndrome DiGeorge syndrome (30%)
Crouzon syndrome (vertebral fusion) Trisomy 13 (54%) and Trisomy 18 (86%)
Noonan syndrome (6.2%)
Table 4: Syndromes associated with atlantoaxial Cornelia de Lange syndrome (35%)
instability and cervical spine abnormalities
Table 6: Syndromes with thrombocytopenia
Heart
Patient with conditions involving connective tissue can
Cardiac lesions in syndromic children can be congenital also manifest with clotting abnormalities.
or acquired. Approximately 30% of congenital heart
disease is thought to be related to genetic syndromes Metabolic and Endocrine derangements
accompanied by extra-cardiac anomalies (Table 5). Some syndromes are associated with metabolic
Genetic syndrome Cardiac anomalies and endocrine abnormalities. Hypoglycemia,
hypercholesterolemia and hypothyroidism can occur in
Down syndrome ASD, VSD, AVCD, TOF
Beckwith-Weidemann syndrome. Hypothyroidism is also
Turner syndrome CoA, BAV, AS, HLHS a well known risk in patients with Down syndrome and
Williams syndrome Supravalvular AS, PPS Williams syndrome. Hypercalcemia can occur in Williams
Noonan syndrome PS, HCMP, ASD syndrome while hypocalcemia due to hypoparathyroidism
Velocardiofacial VSD, TOF, TA, TGA, can occur as a feature of DiGeorge syndrome.
syndrome (DiGeorge Pulmonary atresia, right Neuromuscular Disorders
syndrome) sided aortic arch
Klippel Feil syndrome VSD, PDA, MVP, BAV, CoA Many syndromic children have myopathies that
can lead to concerns regarding the airway, bulbar
ASD : Atrial Septal Defect, VSD : Ventricular Septal Defect,
AVCD : Atrioventricular Canal Defect, TOF : Tetralogy of Fallot, muscle function, respiratory and cardiac function and
CoA : Coarctation of Aorta, BAV : Bicuspid Aortic Valve, AS : Aortic sensitivity to anesthetic agents. Children may be prone
Stenosis, HLHS : Hypoplastic Left Heart Syndrome, PPS : Peripheral
Pulmonary Stenosis, PS : Pulmonar Stenosis, HCMP : Hypertrophic
to malignant hyperthermia, hypermetabolic crisis and
cardiomyopathy, TA : Truncus arteriosus, TGA : Transposition of Great acute rhabdomyolysis. Children with King-Denborough
Arteries, PDA : Patent ductus arteriosus, MVP : Mitral valve prolapse. syndrome are susceptible to malignant hyperthermia.
Those with Duchenne muscular dystrophy and Becker
Table 5: Syndromes associated with congenital muscular dystrophy can develop acute rhabdomyolyis
cardiac anomalies in response to inhalational agents and succinylcholine.
Acquired cardiac anomalies can be secondary to the SPECIFIC SYNDROMES
primary condition as may occur in mucopolysaccharidoses.
Craniofacial Syndromes
Coagulation
These include Apert, Crouzon, Pfeiffer and Saethre-
There are some syndromes associated with Chotzen which are associated with craniosynostosis
thrombocytopenia, inherited platelet disorders, and others like Pierre Robin syndrome, Goldenhar and
factor deficiencies, connective tissue disorders, and Treacher Collins syndrome that affect only the facial
vascular abnormalities, which pose a real risk of skeleton and not the skull.

Syndromic craniosynostosis impacts on both the skull Even if upper airway obstruction does occur, difficult
vault and the facial skeleton. In addition to prematurely laryngoscopy is unusual in patients with midface
fused cranial sutures, involvement of the facial skeleton hypoplasia (unless coexistent cervical spine anomaly is
may result in upper airway obstruction (secondary present), with only three of 199 laryngoscopies being
to maxillary hypoplasia), exophthalmos and raised graded as Cormack and Lehane grade III in the above
intracranial pressure. The commonest are Apert, series. A muscle relaxant can, therefore, safely be
Crouzon, Pfeiffer and Saethre-Chotzen syndrome. administered once the ability to ventilate the child has
The upper airway obstruction ranges from mild nasal been confirmed. An important caveat to this is children
obstruction to obstructive sleep apnea, which occurs who have undergone corrective surgery in the form of
in almost 50%. mid-face advancement surgery. Intubation may be more
difficult after corrective surgery as a result of the altered
Apert syndrome
relationships of the maxilla and mandible and reduced
Apert syndrome (Acrocephalosyndactyly), with an temporomandibular joint movement. The presence
incidence of 1in 65,000 births, was described in 1906 by of bamboo trachea requires the use of a smaller than
the French physician, Eugene Apert. It is characterized anticipated tracheal tube.
by craniosynostosis, midface hypoplasia and symmetric
It has been reported that these children suffer a higher
syndactyly of the hands and feet. Premature fusion of
incidence of bronchospasm. Children with Apert
the coronal suture and cranial base sutures leads to
syndrome have profuse secretions that may lead to
hypertelorism and midface hypoplasia, high arched
increased airway irritability9. It is wise to postpone
palate which is often covered with excess soft tissue.
elective procedures until symptoms related to airway
Maxillary hypoplasia with impaired anteroposterior and
secretions and infections have been optimized.
downward growth of the maxilla results in narrowed
nasopharyngeal airway and this deformity increases Crouzon syndrome
with age. This leads to obstructive sleep apnea. 71%
Crouzon syndrome, named after the French neurologist
have fused cervical vertebrae and in 50% of these
Octave Crouzon has an incidence of 1 in 60,000 births. It
children, the trachea may be narrow with fused tracheal
is characterized by ocular hypertelorism, small beaked
rings (referred to as a “bamboo trachea”).
nose, proptosis, exophthalmos, hypoplastic maxillar
These children usually undergo surgery for and mandibular prognathism10. Hydrocephalus, descent
craniosynostosis, cleft palate repair or for syndactyly. of the cerebellar tonsils and anomalies in jugular venous
The risk of airway complications may increase further drainage can be present. Upper airway obstruction
during the perioperative period, particularly after can occur at induction of anesthesia as well as during
induction of anaesthesia. In a retrospective review of emergence, due to maxillary hypoplasia. Care should be
509 anaesthetics in 61 children with Apert syndrome taken to avoid eye injury during mask ventilation. Spine
over a 14 year period, 31 perioperative respiratory abnormalities may be present, decreasing cervical spine
complications occurred in 6.1% of patients8. Supraglottic movement, leading to difficult intubation. Crouzon
airway obstruction occurred in 4.5% of cases. The syndrome may be associated with PDA and coarctation
majority of these upper airway obstructions occurred of aorta.
at induction of anaesthesia in children under the age
Pierre Robin sequence
of 2 years, with only four incidences of postoperative
obstruction. Simple airway manoeuvres, adjuncts Pierre Robin sequence (PRS), described by the French
such as an oropharyngeal airway or nasopharyngeal stomatologist Pierre Robin in 1923, has an incidence
airway and CPAP are usually effective in relieving the that varies from 1:5000 to 1:85,000. The clinical triad of
obstruction. micrognathia (small mandible), glossoptosis (backward,

Treacher Collins syndrome patients with Goldenhar syndrome should undergo

cardiac evaluation. Partial or complete unilateral lung
Treacher Collins syndrome(TCS) is a disorder of hypoplasia can compromise pulmonary function and
craniofacial development that involves the first and increases the risk of respiratory infections, pulmonary
second branchial arches and was first described by hypertension and pneumothorax. Spine deformities can
the English surgeon and ophthalmologist, Dr Edward lead to a restrictive lung disease. Verterbral anomalies
Treacher Collins in 1900. It occurs in 1:10000 live of cervical vertebra such as occipitalization, cervical
births. These patients have maxillary, mandibular vertebral fusion and C1-C2 subluxation can lead to
and zygomatic hypoplasia, a high arched, cleft difficult intubation13. Difficult intubation can also be
palate, small oral aperture and abnormalities of the
due to mandibular hypoplasia and tracheal deviation
temporomandibular joint. Cervical spine anomalies can
to one side.
be seen in 17.5% of patients with TCS. Other findings
include antimongoloid obliquity of the palpebral Genitourinary malformations such as ectopic or
fissures and external ear abnormalities including fused kidneys, renal agenesis, ureteropelvic junction
anotia with atresia of the external auditory canal. obstruction or vesicoureteral reflux might be associated
Facial retrognathia or micrognathia is also commonly with Goldenhar syndrome. It might be helpful to be
associated. Cleft palate is present in up to 35% of aware of possible kidney malformations prior to major
patients. surgery with expected large fluid shifts, prolonged
urinary catheter placement and postoperative ICU
Airway management and intubation becomes
admission.
increasingly difficult with increasing age. In a
retrospective review of 240 anesthetics, the incidence Down Syndrome
of failed intubation was 5% and procedure cancellation
due to failed intubation was 0.8%12. 26% had grade 3 Down Syndrome or Trisomy 21 with an incidence
of 1 in 800 births is the most common autosomal
and 26% had Grade 4 views with direct laryngoscopy.
chromosomal disorder in humans and was first
Intubation techniques other than conventional direct
described by Dr. John Langdon Down in 1866. These
laryngoscopy was used in 41% of cases. Successful
children are easily recognized by their typical facial
intubations have been described in TCS using fiberoptic
features, which include brachycephaly, flat nasal bridge
intubation, FOB via LMA and videolaryngoscopy.
and upslanting palpebral fissures, simian crease (single
Goldenhar syndrome palmar crease), hypoplastic middle phalanx of fifth
finger, larger than normal gap between the great toe
Oculo-auriculo-vertebral syndrome or Goldenhar-Gorlin and second toe, decreased muscle tone, developmental
syndrome was first described by Maurice Goldenhar delays, short stature and obesity.
in 1952 and has an incidence varying from 1:3000 to
1:25000. It is a form of hemifacial macrosomia that Airway in Down syndrome
affects the first and second branchial arches resulting
Airway anomalies include macroglossia, high arched
in unilateral underdevelopment of the eye, ear, nose,
narrow palate, micrognathia, short broad neck, soft
soft palate, lip and mandible. Major manifestations
palate hyperplasia, larygomalacia, subglottic stenosis
of HFM are orbital distortion, mandibular hypoplasia,
and tracheal stenosis and can lead to upper airway
ear anomalies, nerve involvement and soft tissue
obstruction and difficult intubation14, 15. These features
deficiency (OMENS classification). In addition, patients
with Goldenhar syndrome can present with heart, are compounded by adenotonsillary hypertrophy,
kidney and lung malformations as well as limb pharyngeal muscle hypotonia, obesity, increased
deformities. Congenital heart defects occur in 5–58% secretions and frequent infections. The incidence
of patients, with septal defects and TOF being the of symptomatic subglottic stenosis is 6% in children
most commonly seen congenital cardiac defects. All with Down syndrome compared to only 0.63% in the
general pediatric population. If intubation is required,
Adults Children with Down syndrome

Basion-dental interval a
>12 mm >12 – 12.5 mm
Basion-posterior axial line >12 mm >12 mm
intervala
Atlanto-occipital joint sublux- >2 mm >7 mm
ationa
Atlantodens interval (ADI)b >3 mm >4 - 5 mm
Posterio atlantodens interval < 14 mm < 14 mm
(PADI)b
Powers ratiob >1 >1
Table 7: Common radiologic parameters used to identify atlanto-occipital(a) and atlanto-axial instability(b).
Fig 5: Normal (A) and pathological (B) plain radiographs of cervical spine. In picture “A”, ‘C1 – C4’ – first four
vertebrae; ‘a’ – basion-dental distance; ‘b’ – basion-posterio axial; ‘c’ – posterior axial line; ‘d’ – atlandodens
interval (ADI); ‘e’ – posterior atlantodens interval (PADI) or C1 space available for the cord (SAC); ‘f’ – C4 space
available for the cord (SAC). In picture “B”, atlantoaxial instability is seen (ADI = 9.8 mm)

Iatrogenic neurological injury due to craniocervical children, the incidence of age-defined bradycardia after
junction instability in Down syndrome patients has sevoflurane anesthesia was 28% in children with Down
been reported. Though the incidence is rare, the syndrome compared to 9% in controls23.
consequences can be severe. In one recently published
Mucopolysaccharidoses (MPS)
systematic review, 16 cases of iatrogenic neurological
injury in DS patients have been reported, including The mucopolysaccharidoses are a group of inherited,
during intubation, sedation and intraoperative head chronic progressive, metabolic diseases and include
and neck positioning20. Of these, no cases resolved seven eponymously named syndromes caused by
spontaneously, 2 progressing to brain death and deficiencies of 11 different lysosomal enzymes that
12 requiring surgical stabilization, underscoring the are required for the catabolism of glycosaminoglycans
importance of recognizing this concern and taking (heparan sulfate, dermatan sulfate, chondroitin
precautions to prevent this complication. sulfate)24. The incidence of MPS is 1:25,000. There is
accumulation of glycosaminoglycans (GAG) in several
To prevent neurological injury, careful preoperative
body tissues leading to involvement of multiple
assessment is necessary to identify patients at risk.
organ systems including airway, cardiac, respiratory
Videolaryngoscopy use should be encouraged as
and skeletal systems. Systemic involvement and
compared to direct laryngoscopy. Direct laryngoscopy
severity of disease progress with time. MPS I (Hurler
should be performed in neutral position with
syndrome) and MPS II (Hunter syndrome) manifest
MILS (manual in line stabilization) or neck collar.
tracheobronchial complications, cardiac disease (mitral
Adenotonsillectomy should be performed with neck
valve involvement, aortic valve anomaly, left ventricular
in neutral position and Neck rotation for surgeries like
hypertrophy) and hepatosplenomegaly. Restrictive
myringotomy should be limited to 60 degrees. Rolling
lung disease due to skeletal involvement is seen in
the operating table rather than rotating the head is
MPS IV (Morquio syndrome) and VI (Maroteaux-Lamy
preferred. Supports and straps should be considered
syndrome).
to limit head movements.
Airway obstruction occurs due to macroglossia,
Other anomalies in Down syndrome
adenotonsillary hypertrophy and deposition of GAG
Incidence of cardiac malformations in Down syndrome in the pharyngeal wall and larynx25. GAG infiltrate
is 44%, the commonest being atrioventricular septal the connective tissues of the oropharynx and airways
defects. Pulmonary hypertension can occur in children causing airway obstruction, obstructive sleep apnea,
with Down syndrome. This can be secondary to difficult mask ventilation and difficult intubation.
congenital heart disease, upper airway obstruction or Submucosal GAG deposits in the upper airway (tongue,
abnormalities in lung development. Gastrointestinal floor of mouth, epiglottis, ary-epiglottic folds) and
problems like duodenal atresia, Hirschsprung’s disease tracheal wall impart a rigid anatomy. They also can
and gastroesophageal reflux are frequent in these have a short, immobile neck with limited mobility of
patients. They have a relative immune deficiency the cervical spine and temporomandibular joint, further
and increased susceptibility to all infections. 80% contributing to difficult airway. Odontoid dysplasia and
of newborn with down syndrome has neutrophilia, radiographic subluxation of C1 on C2 is common in MPS
upto 66% have thrombocytopenia and upto 34% have I, IV and VI and may cause anterior dislocation of the
polycythemia21. Hypothyroidism is seen in 40% of DS atlas and spinal cord compression. They can also have
children. abnormal laryngeal and tracheal cartilage and copious
secretions, compounding the situation. Older age is
Children with Down syndrome are more likely to
associated with increased risk of difficult intubations,
develop bradycardia during inhalational induction
due the effect of the progressive anatomic alterations
with sevoflurane22. In a study of 11,201 anesthetics in
of MPS.
GAG accumulate in the cardiac tissues, causing valvular together with respiratory muscle weakness can lead to
abnormalities and cardiac insufficiency (myocardial difficulty in extubation.
deposits). They also accumulate in the bones, joints
Anesthesia Management in Syndromic Children
and ligaments leading to atlantoaxial instability.
Developmental delay and progressive neurologic Preanesthetic assessment
decline are also seen in these patients.
A detailed history and physical examination is necessary
The incidence of anesthesia related complications is to identify all the congenital anomalies present in
high in MPS patients. Incidence of difficult intubation this children and to make an appropriate anesthesia
is 25% – 80%, failed intubation is 2% - 10% and that of plan. Special attention should be paid to the airway,
perioperative cardiorespiratory complications range cardiovascular and respiratory systems. History and
between 5% and 25%. records should be obtained about previous anesthetic
management. Preoperative evaluation should be aimed
In a retrospective review of anesthesia records of 19
at identifying patients with OSA and those who do
children with MPS over a 9 year period, the incidence of
not tolerate supine positioning. These children will be
respiratory and cardiovascular complications was 24%
more difficult to mask ventilate and may require airway
and 4% respectively26. The respiratory complications
adjuncts like oro/nasopharyngeal airways or LMAs.
were airway obstruction at induction, difficult mask
Recent history of upper respiratory tract infections
ventilation, difficult intubation and failed intubation.
should be noted. A detailed airway assessment should
Airway obstruction during emergence occurred
be done to identify children who would have difficult
after 13 anesthetics. The cardiac complications were
intubation. The presence of cervical spine instability
hypotension, bradycardia and perioperative circulatory
should be specifically looked for in children with Down
arrest.
syndrome and MPS. Physical examination should
In a recently published retrospective analysis of 54 include room air oxygen saturation in addition to heart
patients with MPS in an Italian tertiary referral centre, rate, blood pressure and respiratory rate. Patients with
16 patients had atleast 1 anesthetic complication during moderate to severe airway obstruction present with
their clinical course27. Hypoxia, airway obstruction, stridor, intercostal and sternal retractions, nasal flaring
hypoventilation and laryngospasm was observed in and oxygen desaturation in the supine position.
11, 4, 4 and 2 procedures, respectively. 19 (29%) of
Investigations include complete blood count and other
intubation attempts were difficult and of these, 3
tests depending on comorbidities and include serum
were achieved with fiberoptic technique, 6 by video
electrolytes, renal function tests, thyroid function tests,
assisted laryngoscopy and the remaining by repeated
echocardiography, videolaryngoscopy, cervical spine X
direct laryngoscopies. During 3 (1.8%) of these cases,
rays, Chest X ray and CT.
face mask ventilation was inadequate to provide
oxygenation, emergency intubation failed and patients Premedication
were salvaged with the LMA. However, there is also a
case report of failure of the LMA to secure the airway Conditions which dictate the use or avoidance of
in a patient with MPS type II (Hunter syndrome), premedication and choice of drug include age,
where a subsequent rigid bronchoscopy revealed a neurologic status of the child, the presence of
pedunculated polyp just above the epiglottis, with obstructive sleep apnea, difficult airway and cardiac
diffuse infiltration of the pharyngeal and laryngeal comorbidities. The possible sensitivity of Down
mucosa and a smaller trachea 28. Postobstructive syndrome children to atropine has been the subject of
pulmonary edema during anesthesia in 5 patients with debate. It was reported that there was an increased
severe form of MPS has also been reported29. Chronic heart rate response to parenteral atropine in these
myelopathy can lead to central hypoventilation, which children, but subsequent studies have not confirmed

this. Considering these children are prone to increased If a fiberoptic intubation is planned, it can be placed orally
secretions, difficult airway and increased incidence of thorugh an LMA or nasally. A nasopharyngeal airway
bradycardia with sevoflurane, an antisialogogue may can be used to maintain anesthesia and oxygenation,
be useful in them. during the process of fiberoptic intubation. ENT surgeon
should be available for emergency tracheostomy or
Induction of anesthesia and Airway management
rigid bronchoscopy. Alternative plans for intubation
The choice of technique depends on the risk of and rescue plans should be in place before induction of
rhabdomyolysis, malignant hyperthermia(MH) and anesthesia. Some children present with a tracheostomy
the ability to maintain the airway and the anticipated that was already done to relieve airway obstruction.
difficulty with intubation. Inhalational agents and
Maintenance of anesthesia
succinylcholine should be avoided in those at risk
of rhabdomyolysis or MH. Spontaneous ventilation There are no specific anesthetic drugs recommended
should be maintained if any difficulty with intubation and the choice is determined by the organ systems
is anticipated. LMA can be placed under topical affected. The presence of hypotonia, as with Down
anesthesia, especially in neonates and children with syndrome should suggest caution with the dose
severe respiratory distress, and then general anesthesia of muscle relaxants and should prompt the use of
can be induced. A fiberoptic scope can be subsequently neuromuscular monitoring. A regional technique can
used to facilitate endotracheal tube placement. be used wherever indicated.
Fiberoptic intubation has been used as the firstline
of airway management in several of these syndromic Postoperative care
children30. If extubation is planned, an awake technique should
General anesthesia can also be induced before be preferred in children with difficult airways. Airway
securing the airway, however, maintaining spontaneous obstruction can also occur at emergence, after
ventilation is essential. Upper airway obstruction extubation and can be managed with nasopharyngeal
at induction is very common in syndromic children airways. Postoperatively, patients have to be monitored
(especially with craniofacial syndromes) and can be carefully.
relieved with OPA, NPA or LMA. Choanal stenosis
Conclusion
(as in Apert syndrome) could preclude placement
of a nasopharyngeal airway, nasotracheal tube and Children with congenital syndromes with multiple
nasogastric tube. anomalies need a multidisciplinary approach totheir
care. It is advisable to actively look for specific
Care should be taken to protect the cervical spine during
anomalies associated with the particular syndrome.
direct laryngoscopy, especially in children with Down
Systems that may be affected include cardiovascular,
syndrome and MPS. A straight laryngoscope blade
respiratory, airway, spine, coagulation, metabolic and
is useful in children with micrognathia and a curved
endocrine systems. Specific websites and books are
blade is more useful in children with macroglossia. In
also available as references. An individualized tailored
children with micrognathia, a paraglossal approach (far
lateral approach) to direct laryngoscopy may be more approach to anesthesia care is important to avoid
effective than standard direct laryngoscopy. Smaller anesthetic complications in these special group of
sized tracheal tubes should be used in children with children.
Down syndrome or MPS as they can have tracheal References
narrowing or subglottic stenosis.
1) Veyckemans F. Why rare diseases are of special
Videolaryngoscopes can be chosen as the first option interest to pediatric anesthesiologists. Pediatr
in case a difficult airway is anticipated. Anesth 2015; 25: 1074-5.

2) Smith DW. Classification, nomenclature, and 15) Hamilton J, Yaneza MC, Clement WA, Kubba H.
naming of morphologic defects. J Pediatr 1975; The prevalence of airway problems in children
87: 162-4. with Down’s syndrome. Int J Pediatr Otorhinolar-
yngol 2016; 81: 1-4.
3) Spranger J, Benirschke K, Hall JG, Lenz W, Lowry
RB, Opitz JM et al. Errors of morphogenesis: Con- 16) Borland LM, Colligan J, Brandom BW. Frequency
cepts and terms. J Pediatr 1982; 100: 160-5. of anesthesia-related complications in children
with Down syndrome under general anesthesia
4) Nargozian C. The airway in patients with cranio- for noncardiac procedures. Pediatr Anesth 2004;
facial abnormalities. Pediatr Anesth 2004; 14: 53- 14: 733-8.
59.
17) Bertolizio G, Saint-Martin C, Ingelmo P. Cervical
5) Uezono S, Holzman RS, Goto T, Nataka Y, Naga- instability in patients with Trisomy 21: the eternal
ta S, Morita S. Prediction of difficult airway in gamble. Pediatr Anesth 2018; 28: 830-3.
school-aged patients with microtia. Paediatr An-
aesth 2001; 11: 409-13. 18) Hata T, Todd M. Cervical spine considerations
when anesthetizing patients with Down syn-
6) Bester K. The syndromic child and anaesthesia. drome. Anesthesiology 2005; 102: 680-5.
South African J Anesth Analg 2014; 20: 197-201.
19) Steward DJ. Anesthesia considerations in children
7) deBeer D, Bingham R. The child with facial abnor- with Down syndrome. Seminars in Anesthesia,
malities. Curr Opin Anaesthesiol 2011; 24: 282-8. Perioperative Medicine and Pain 2006; 25: 136-
8) Barnett S, Moloney C, Bingham R. Perioperative 141.
complications in children with Apert syndrome: a 20) Husnudinov R, Ibrahim G, Propst E, Wolter N. Iat-
review of 509 anesthetics. Pediatr Anesth 2011; rogenic neurological injury in children with triso-
21: 72-77. my 21. Int J Pediatr Otorhinolaryngol 2018; 114:
9) Elwood T, Sarathy PV, Geiduschek JM, Ulma GA, 36-43.
Karl HW. Respiratory complications during anaes- 21) Lewanda A, Matisoff A, Revenis M, Harahsheh A,
thesia in Apert syndrome. Pediatr Anesth 2001; Futterman C, Nino G et al. Preoperative evalua-
11: 701-3. tion and comprehensive risk assessment for chil-
10) Kumar A, Goel N, Sinha C, Singh A. Anesthetic dren with Down syndrome. Pediatr Anesth 2016;
implications in a child with Crouzon syndrome. 26: 356-62.
Anesth Essays Res 2017; 11: 246-7. 22) Roodman S, Bothwell M, Tobias J. Bradycardia
11) Cladis F, Kumar A, Grunwaldt L, Otteson T, Ford with sevoflurane induction in patients with triso-
M, Losee JE. Pierre Robin sequence: A periopera- my 21. Pediatr Anesth 2003; 13: 538-40.
tive review. Anesth Analg 2014; 119: 400-12. 23) Bai W, Voepel-Lewis T, Malviya S. Hemodynamic
12) Hosking J, Zoanetti D, Carlyle A, Anderson P, Co- changes in children with Down syndrome during
sti D. Anesthesia for Treacher Collins syndrome: and following inhalation induction of anesthesia
a review of airway management in 240 peidatric with sevoflurane. J Clin Anesth 2010; 22: 592-7.
cases. Pediatr Anesth 2012; 22: 752-8. 24) Mahoney A, Soni N, Vellodi A. Anaesthesia and
13) Raj D, Luginbuehl I. Managing the difficult airway the mucopolysaccharidoses: a review of patients
in the syndromic child. Continuing Education in treated by bone marrow transplantation. Pediatr
Anesthesia, Critical Care and Pain 2015; 15: 7-13. Anesth 1992; 2: 317-24.
14) Mitchell V, Howard R, Facer E. Down’s syndrome 25) Frawley G, Fuenzalida D, Donath S, Yaplito-Lee J,
and anaesthesia. Pediatr Anesth 1995; 5: 379-84. Peters H. A retrospective audit of anesthetic tech-
niques and complications in children with muco-

polysaccharidoses. Pediatr Anesth 2012; 22: 737- 28) Busoni P, Fognani G. Failure of the laryngeal mask
44. to secure the airway in a patient with Hunter’s
syndrome (mucopolysaccharidosis type II). Pedi-
26) Megens J, de Wit M, van Hasselt P, Boelens J, atr Anesth 1999; 9: 153-5.
van der Werff D, de Graaff J. Perioperative com-
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saccharidosis and the impact of enzyme replace- Postobstructive pulmonary edema during anes-
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30) Fujii M, Tachibana K, Takeuchi M, Nishio J, Kinou-
27) Scaravilli V, Zanella A, Ciceri V, Bosatra M, Flandoli chi K. Perioperative management of 19 infants
C, La Bruna A et al. Safety of anesthesia for chil- undergoing glossopexy (tongue-lip adhesion)
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tive analysis of 54 patients. Pediatr Anesth 2018; 2015; 25: 829-33.
28: 436-42.

MCQ
1. The clinical triad of Pierre Robin sequence 4. Which of the following syndromes is not
includes usually associated with micrognathia?
a. Micrognathia, glossoptosis, airway a. Treacher Collins syndrome
obstruction
b. Pierre Robin syndrome
b. Micrognathia, glossoptosis, cleft
palate c. Goldenhar syndrome
c. Micrognathia, glossoptosis, cleft lip d. Apert syndrome
d. Micrognathia, cleft lip, cleft palate 5. Which of the following syndromes is not
usually associated with macroglossia?
2. The most common airway problem with
maxillary hypoplasia is a. Down syndrome
a. Increased incidence of larygospasm b. Hunter syndrome
b. Decreased oral space available for c. Beckwith-Weidemann syndrome

laryngoscopy d. None of the above
c. Upper airway obstruction with
induction of anesthesia
d. Difficult intubation due to micrognath-
ia
3. The upper limit of normal atlantodens interval

in children with Down syndrome above which
atlantoaxial instability is a concern is
a. 2 mm
b. 4 mm
c. 7 mm
d. 10 mm
5. (d) 4. (d) 3. (b) 2. (c) 1.(a)

Answers

9 Massive Transfusion Protocol - A Must for All
Associate Professor Gyorgy (George) Frendl

Harvard Medical School
Director of Surgical Critical Care Research
Brigham and Women’s Hospital
Key points
Ø Massive Transfusion Protocol(MTP) facilitates the timely delivery of sufficient blood products to the
care providers, in the setting of massive hemorrhage
Ø Hypothermia, acidosis and coagulopathy constitute the TRIAD OF DEATH in a patient with massive
hemorrhage
Ø Minimising transfusion of untyped blood and products can reduce harmful effects of MTPs.
Introduction • Design a massive transfusion protocol for

your institution and effectively manage such
The management of patients requiring massive efforts
transfusions (weather trauma or incidental blood loss
• Understand the benefits and risks that the
related) can be challenging and may lead to adverse
use of massive transfusion protocol poses to
outcomes if not accomplished in a timely fashion. patients and the community
A comprehensive systems-based solution called • Effectively manage patients suffering from
“Massive Transfusion Protocol” has been proposed massive blood loss
and implemented in many hospitals to facilitate the Goal
timely delivery of sufficient blood products to the
care providers. This requires a collaborative, unified Enable the best outcomes for your patients suffering
system between the blood bank and clinical care units from large blood loss
(operating theater, emergency department, ICUs etc) Approach
and a strategy agreed upon in advance by all providers
for the “ideal” mix of blood products of RBCs, plasma Design the best blood utilization system for managing
(FFP), and platelets. massive blood loss cases by using the principles of
Massive Transfusion Protocols (MTP)
The presentation will discuss the components of such a
comprehensive system, and the benefits and possible Thought process
adverse effects of such strategy. • Patients suffering from massive blood loss are
After this presentation you should be able to at high risk for loss of life
• Expeditious and effective blood delivery sys-
• Identify patients who suffer from massive tems can save lives
blood loss and are candidates for blood trans- • The use of massive transfusion protocols can
fusion with a massive transfusion protocol save lives and help the health care provides to
(MTP) in order to improve their outcomes be more effective in caring for patients
(survival) • MTPs are not without risks

Massive Transfusion Protocol - A Must for All 96 Gyorgy Frendl
The clinical problem

1. Your patient is suffering from massive blood 3. You are struggling to obtain sufficient amount
loss of blood products to stabilize your patient
2. This can be anticipated for major debulking 4. You review the literature on the most efficient
tumor surgeries or unanticipated for traumas blood delivery systems that can help and save
or incidental intraoperative bleeding lives
Hy
is
po
os
th
id
er
Ac
m
ia
Coagulopathy
The Triad of Death

Past Strategies
Defining massive (large volume) blood loss requiring

massive transfusions

How can MTPs Help?

The components of a Massive Transfusion Protocols
(MTP) and an example of a hospital-wide MTP
The benefits of MTPs

Possible Harm of MTP
The Vision of The Future

References 5. Acosta. J. Am. Coll. Surgery 1998. 186:528

1. Repine TB. Et al. J Trauma. 2006 Jun;60(6 6. Borgman. J of Trauma 2007 63:805
Suppl):S59-69 7. Eder AF, 2013 Transfusion 53:1442
2. MacLeod, J of Trauma 2003 55:39. 8. JAMA 2015. 313(5):471-482.
3. Como Transfusion 2004, 44:809. 9. CRASH Trial. Lancet 2010. 376:23.
4. Cothren World J of Surgery 2007. 31:1507. 10. Transfusion. 2012 May;52 Suppl 1:30S-7S
MCQ
1. Triad of death in MTP includes all except: 4. All are complications of massive blood trans-
fusion except:
a. Hypothermia
b. Hypotension a. Hypercalcemia
c. Coagulopathy b. Hypothermia
d. Acidosis c. Hyperkalemia
d. Citrate toxicity
2. Massive blood transfusion refers to:
5. All are delayed complcations of MBT except:
a. >50U in 24 hours
b. >4 U in 4 hours a. TRALI
c. >10 U in 24 hours b. SIRS
d. >20U in 48 hours c. Thrombotic complications
d. Acidosis
3. The RBC: FFP: Platelet prefixed ratio is:
a. 1:1:1
b. 1:2:3
c. 3:2:1
d. 2:2:2
5. (d) 4. (a) 3. (a) 1. (b) 2. (c)

Answers

10 CHEST X-RAY: INTERPRETATION
Professor & Consultant Radiologist, Anupama Chandrasekaran

SRIHER,
Chennai.
Key points
Ø While reading a X ray, it is important to develop a search pattern that can be applied to every radiograph
Ø The AP view results in magnification of the anterior structures and an increase in the width of the
mediastinum.
Ø Poor inspiratory film alter the apparent size of the heart and mediastinum, which may appear 10-40%
larger or wider
Ø The ideal position of the tracheostomy tube is with its tip located 1/2 to 2/3rd the distance from the
stoma to the carina.
Ø The presence of air-bronchogram is useful in making a diagnosis of consolidation, the cause depends
on the clinical presentation
Ø Meniscus sign is seen in the chest X ray of a patient with pleural effusion, on erect film
Ø Deep costophrenic sulcus sign is observed in pneumothorax, on chest X ray
Chest radiographs form a part of every anesthetist’s PA vs AP

daily practice. It is important to develop a search
PA view is the optimal view because it results in reduced
pattern that can be applied to every radiograph. This
magnification and increases the sharpness of structures
will help in ensuring that maximum information is
and pathologies. In this view, the scapulae are projected
obtained. A systematic and ordered approach to chest
away from the lung fields, the inverted ‘V’ of the lower
X ray interpretation will go a long way in this regard. It
cervical spinal laminae are clearly seen, the ribs are less
is not that experienced hands do not miss findings on
oblique and the entire length of the clavicle is seen.
chest X rays, just that they miss fewer ones.
Before coming to actually reading an x ray and looking
for pathologies, certain essentials have to be verified:
• Patient information – Name, Age, Sex, Date of
Radiograph and if multiple X rays are available,
arrange them in chronological order
• Identify radiographic technique - AP/PA film,
inspiratory/expiratory, exposure, rotation,
patient position (supine or erect)
CXR: PA view
Chest X-Ray: Interpretation 104 Anupama Chandrasekaran
AP view: This is usually obtained with a portable X ray 15% increase in the width of the mediastinum can be
unit on very sick patients and infants, and is most often expected. In addition, supine positioning widens the
a supine X ray. In this view, the scapulae are projected mediastinum and heart due to gravitational effects.
over the lung fields, the rectangular shape of the lower The supine position also diverts more pulmonary
cervical vertebral bodies are clearly seen, the ribs are blood flow to the upper lobes and redistributes pleural
more oblique and the clavicle is foreshortened. fluid. Similarly, pneumothorax may be more difficult
to detect.
The AP view results in magnification of the anterior
structures - the clavicle, sternum, and heart and a
CXR: AP view
Inspiratory vs Expiratory ill patients are usually unable to maintain inspiratory

hold positions. Poor inspiratory film alter the apparent
Ideally, radiographs should be taken at the peak of
size of the heart and mediastinum, which may appear
inspiration. On good inspiration, the diaphragm should
10-40% larger or wider. Crowding of lung markings may
be found at the level of the anterior ends of the 5th or 6th
lead to over-diagnosis of basal atelectasis, lung edema
rib, or the posterior ends of the 9th or 10th rib. Critically
etc.
Difference in CXR image at inspiration(left) vs expiration

Chest X-Rays: Interpretation 105 Anupama Chandrasekaran
Exposure VIII. Subdiaphragmatic regions
A good X ray also requires adequate penetration of the IX. Bones and soft tissues
patient by radiation. In a correctly penetrated film, the LINES, TUBES AND OTHER INVASIVE DEVICES
thoracic spine intervertebral disc spaces should be just
visible through the cardiac shadow. If the entire spine If present, are they correctly positioned ? If
is clearly visible, it implies that it is an overpenetrated malpositioned, are there any resultant complications?
film. In such an X ray, the lung fields appear excessively Many devices are used routinely for patient monitoring
dark and lucent. Lung lesions may be masked resulting and support. Malpositioning of these tubes may
in failure to accurately gauge their presence and precise occasionally be life threatening. Therefore while
extent. Another fallacy is that the lucent areas may viewing an x ray, it is essential to ensure that they are
raise the false possibility of a pneumothorax or cause correctly positioned .
a pneumothorax to be missed. On the other hand,
Endotracheal and Tracheostomy tubes
underpenetrated films can result in relatively increased
opacification of the lung fields. The endotracheal tube has a radioopaque line running
along its entire length. The ideal position is with its
Problems with penetration have been obviated to major
tip 5 – 7 cm above the carina ( D 4-5 level), with the
extent with the advent of Computed Radiography (CR)
head in the neutral position. The optimal width of the
and Digital Radiography (DR).
tube should be between one half and two thirds of
Centering/Rotation the tracheal lumen. With an abnormally low position,
a right endobronchial intubation may occur resulting
In a correctly centered chest X ray , the medial ends in overventilation of the right lung or right upper lobe
of both clavicles should be equidistant from the collapse, with hypoventilation of the left lung. With
adjoining spinous process of the dorsal vertebrae. Any an abnormally high placement, the tube may get
asymmetry implies the presence of rotation. The side extubated with resultant vocal cord damage. Esophageal
of the hemithorax which is closer to the film appears intubation is rare and can cause hypoventilated lungs
excessively opaque whereas the contralateral side with gross gastric distension.
appears more lucent.
The ideal position of the tracheostomy tube is with its
Once these technical parameters have been taken into tip located 1/2 to 2/3rd the distance from the stoma to
account, one can proceed with the actual interpretation the carina.
of the X rays. There is no fixed or prescribed protocol
for reading chest X rays. One can read a a X ray from the Nasogastric Tube
centre to the periphery or vice-versa, or from the top
The radioopaque tip of the tube should lie at least 8
to the bottom. However, in keeping with the intention
cm within the stomach to reduce the risk of aspiration.
to stick to a standard protocol, one useful format is as
follows: Central venous line
I. Position of lines, tubes and other invasive device Its ideal location is with its tip beyond the last venous
II. Cardiac size and contour valves and hence its preferable location is within the
superior vena cava.
III. Mediastinum including trachea
PA catheter
IV. Hila
It is also known as Swan Ganz catheter. The catheter is
V. Lung fields
commonly inserted via the internal jugular vein and it
VI. Costophrenic angles traverses the right atrium and ventricle before entering
VII. Diaphragm the pulmonary trunk and main pulmonary artery. The

tip of this catheter should lie within 1-2 cm of the Hila
hilum.
Bilateral hila should be of the same size and density.
Cardiac Size and Contour Also check their position. Usually, the left hilum lies at
a higher level than the right, though occasionally they
Is the heart enlarged and if so, is it possible to
may lie at the same level.
identify individual chamber enlargement? The normal
cardiothoracic ratio is less than 50% in adults. Lung Fields
Mediastinum including Trachea In a correctly centred X ray, bilateral lung fields should
The following questions should be answered while appear similar. Compare the right upper, mid and lower
evaluating the mediastinum: zones with the corresponding zones on the left side.
Any abnormal looking opacities or lucencies should be
Is the mediastinum widened ? There are two ways to carefully evaluated.
subjectively assess mediastinal widening. Firstly the width
of the mediastinum above the level of the carina should There are two important sign , the ‘Silhouette sign’ and
not exceed 8 cm. Alternatively, the mediastinum should the ‘Air Bronchogram’ sign which are important in the
not form more than 25 % of the width of the chest at evaluation of air space diseases.
this level. However these criteria are not absolute and
Silhouette sign
sometimes a subjective assessment may also be useful.
A r e t h e r e a ny a b n o r m a l l u c e n c i e s w i t h i n An intra-thoracic radio-opacity, if in anatomic contact
the mediastinum to suggest the presence of with a border of heart, aorta or diaphragm, will obscure
pneumomediastinum ? Also check for mediastinal that border. An intra-thoracic lesion not anatomically
shift and abnormalities in contour, or the presence contiguous with a border or a normal structure will
of any mass . The normal trachea either lies in the not obliterate that border. e.g. a right middle lobe
midline or a little to the right. This shift to the right is collapse or consolidation will obscure the right heart
exaggerated on expiratory radiographs. About 2/3rds margin while a lingular pathology will obscure the left
of the heart normally lies to the left of the spine. cardiac border and a lower lobe lesion will obscure the
diaphragm.
Loss of cardiac Silhouette (right) : Silhouette sign

Air Bronchogram sign Bones and Soft Tissues
This commonly signifies alveolar disease with a patent Look carefully at the bones especially in the setting of
bronchus (pneumonia, pulmonary edema, ARDS, etc.), trauma. In addition to the ribs, clavicles and scapula,
but may be seen in partial atelectasis. On a normal information about the spine, shoulder joints and
radiograph, the bronchi are not normally visible unless humerus may also be obtained if they are clearly seen
seen end on, or if there is bronchial wall thickening. or included on the film
When the alveoli no longer contain air and opacify,
SPECIFIC PATHOLOGIES
the air-filled bronchi passing through the same area
may be visible as branching linear lucencies, or air The following is a brief summary of the chest X ray
bronchograms findings in some of the commonly encountered chest
pathologies which are of significance to the anesthetist:
Some commonly encountered causes of opacities are :
Collapse
• Atelectasis / collapse
• Pneumonia The radiological appearances depend upon the
• Pulmonary edema mechanism of collapse, degree of collapse, presence
or absence of consolidation, and the pre-existing state
• ARDS
of the pleura.
• Hemorrhage
• Effusion Direct Signs of Collapse
Pathological lucencies may represent • Displacent of interlobar fissures - most reliable

sign
• Emphysema • Loss of aeration resulting in increased density
• Bulla, Cysts of a collapsed area
• Pneumothorax • Crowding of vessels and bronchi
• Pneumomediastinum
• Subcutaneous emphysema
Costophrenic Angles
Is it effaced (pleural effusion) or abnormally deep and
lucent (pneumothorax in the supine position)?
Diaphragm
Check out the contour and position. The difference in
heights between the apices of the two hemidiaphragms
should not exceed 3 cm. The diaphragm should not
be abnormally flattened (seen in hyperinflation/
pneumothorax) or inverted (considered a radiological
sign of tension pneumothorax)
Subdiaphragmatic regions
Do not forget to look at the subdiaphragmatic
regions. The presence of any abnormal lucencies in
this location should alert one to the possibility of Collapse right lung
pneumoperitoneum or subdiaphragmatic abscess.
From 5 – 7 days: i) Pulmonary embolism without infarction. The
findings may be
• Clearing is frequently secondary to the effects
of CPP ventilation rather than true healing • Normal chest x ray
• Focal oligemia – Westermark Sign (in X ray
• Pneumonia may superimpose – difficult to
below, indicated by a red circle)
impose but look for new focal infiltrates and
pleural effusion • Reduction in regional lung volume
• Plate like atelectasis
More than 1 week
• Coarse reticular interstitial disease which may

lead to fibrosis
Lung Abscess
The radiological findings include
• Cavitation within an area of consolidation
• Lung nodule with surrounding consolidation

(in the stage before the abscess communicates
with a bronchus)
• Cavity with an air-fluid level

Westermark Sign (circled area)
ii) Pulmonary Embolism with infarction
• Pleural based, hump shaped opacity when
seen in profile (see X ray below) and faint ill-
defined rounded opacity when seen en-face
• Associated pleural effusion
Lung Abscess
Pulmonary Embolism (PE)

Chest x rays show abnormalities in approximately half of
the patients with pulmonary embolism. Unfortunately,
these findings are most often non-specific and a high
index of clinical suspicion for the diagnosis is required.
The chest X ray findings reflect the pathophysiological
changes and can be divided into three broad categories: Hump shaped opacity (arrow mark)

iii) Pulmonary embolism associated with cardiac or Pneumothorax
pulmonary disease – The plain radiograph findings
• Detection of a white visceral pleural line
of the underlying condition predominate.
beyond which lung markings are not seen
Mitral Stenosis
• Supine pneumothorax – ‘Deep costophrenic
The plain radiographic findings include sulcus’ sign, and abnormal clarity and lucency
along the anterior cardiophrenic sulcus
• Straightening of left heart border
• Bulge along left heart border due to enlarged
left atrial appendage (in rheumatic heart
disease)
• Widened carinal angle
• ‘Double density’ of left atrial enlargement
• Valve calcification
• Findings of pulmonary edema and cardiac
failure
Pleural Effusion
The appearances depend upon the quantity of fluid as
well as the position of the patient at the time that the
X ray was taken. Right pneumothorax
Pericardial Effusion
• Erect X ray – Blunting of the costophrenic angle
followed by development of the ‘meniscus The appearances depend upon the amount of fluid and
sign”. Massive effusion can result in complete its distribution.
opacification of the hemithorax.
• Symmetrical cardiomegaly without specific
• Supine X ray – Veil like opacity in the affected chamber enlargement and clear lungs rather
hemithorax through which lung markings may than congested lungs – results in ‘flask’ or
be seen ‘water-bottle’ configuration in the erect
position and globular configuration in the
supine position.
Right pleural effusion with meniscus sign Pericardial Effusion

MCQ
1. one good inspiration the diaphragm should be 4. The tip of this catheter should lie within
found at the level of the anterior ends of
a. 1-2 cm of the hilum.
a. 5th or 6th rib
b. 3-4 cm of the hilum.
b. 7th or 8th rib
c. 5 cm of the hilum.
c. 3rd or 4th rib
d. at the hilum
d. 8th or 9th rib
5. In an adult patient, the width of the mediasti-
2. The AP view results in magnification of the num above the level of the carina should not
anterior structures like mediastinum by exceed
a. 30% a. 8cm
b. 2% b. 10cm
c. 15% c. 12cm
d. 50% d. 2 inches
3. The ideal position of the tip of endotracheal
tube should be
a. T4 vertebra body
b. T3 vertebra body
c. T5 vertebra body
d. T6 vertebra body
5. (a) 4. (a) 3. (a) 2. (c) 1. (a)

Answers

11 Acute Heart Failure: Understanding
Pathophysiology and Management
Assistant Professor, Associate Fellowship Director, Seema Deshpande

University of Maryland School of Medicine,
Baltimore.
Key points
Ø All episodes of AHF are accompanied by an increase in LV end-diastolic pressure, there are certain
patients for whom volume removal is appropriate and others where afterload reduction or inotropic
support is most needed
Ø Diastolic dysfunction (DD) is defined as an abnormality of left ventricular (LV) relaxation, filling or
compliance, irrespective of the ejection fraction
Ø In the perioperative setting, the types of acute heart failure seen typically are Systolic Heart Failure,
Diastolic Heart Failure and Right Heart Failure
Ø Increased wall stress is the precipitating event for development of LV systolic dysfunction
Ø As HF progresses, there is diminishing responsiveness to increasing levels of ANP and BNP, further
contributing to chronic fluid overload
Ø The majority of acute perioperative heart failure occurs in patients who have decreased cardiovascular
reserve prior to surgery
Ø If signs or symptoms of acute decompensated HF are present, elective surgery is contraindicated (ACC/
AHA)
Ø Intraoperative and postoperative TEE and postoperative TTE should be performed as early as possible
in patients suspected of perioperative heart failure
Ø IABP has been shown to be useful in the prevention of major adverse cardiac events (MACE) in patients
with severe cardiac dysfunction undergoing high-risk noncardiac surgery.
Ø Indicators of major clinical risk in the perioperative period are: unstable coronary syndromes,
decompensated HF, significant arrhythmias and severe valvular disease
Ø Titration of anesthetic drugs to the hemodynamic goal is more important than the anesthetic drugs
chosen
Ø Phosphodiesterase III inhibitors caused a less pronounced increase in heart rate and decreased the
likelihood of arrhythmias compared to dobutamine
Ø Mechanical Circulatory Support Devices includes IABP, ECMO and VAD
Ø The general rationale for using mechanical circulatory support (MCS) in patients with cardiogenic shock
is to restore adequate systemic perfusion pressure, to allow the ventricle time to recover

Acute Heart Failure: Understanding 114
Pathophysiology and Management Seema Deshpande
Objectives: Dr.Seth and his group at AIIMS, New Delhi, which

indicated a higher in-hospital and short-term mortality
• Incidence of acute heart failure in patients with ADHF in India. (3)
• Etiology of acute heart failure, particularly
perioperative heart failure
• Pathophysiology and clinical presentation
• Preoperative evaluation and monitoring
• Perioperative management
Heart failure (HF) is a leading and increasing cause of
morbidity and mortality worldwide. As a disease entity,
it has wide-reaching implications not just in terms of
mortality and morbidity for patients but also for the
infrastructure and resources required to provide care
for these patients. Fig 1: Graphical representation of multifactorial
etiology of HF in India (4)
Acute heart failure (AHF) is broadly defined as a rapid
onset of new or worsening signs and symptoms of Clinical Presentation
HF. It is often a potentially life-threatening condition,
requiring hospitalization. Emergency treatment is The clinical syndrome of acute decompensated HF
(ADHF) ranges from moderate volume overload
aimed predominantly at managing hemodynamic
to cardiogenic shock. Most of the patients have
compromise and fluid overload (1).
congestion, some present with low cardiac output and
Incidence hypoperfusion, with or without congestion, especially
those presenting to tertiary care centers.
The burden of HF in India appears high, and estimates
of prevalence range from 1.3 million to 4.6 million, with The majority (80%) of patients hospitalized with heart
an annual incidence of 4,91,600–1.8 million.(2) failure present as an acute decompensation of chronic
HF. These patients become refractory to oral therapies
The burden of cardiovascular disease is increasing in and decompensate following a relatively mild insult
India. Estimates based both on data of established risk or develop new cardiac disease (e.g., ischemia or
factors for heart failure, as well as small studies suggest atrial fibrillation) that may result in decompensation.
that the burden of HF in India is about 2–5 million Newly diagnosed heart failure accounts for 15% of
patients with an estimated prevalence of 2–3/1000 cases. Finally, end-stage patients refractory to therapy
population. Results from clinical trials show that in- comprise fewer than 5% of hospitalizations. (5)
hospital mortality associated with cardiovascular
disease is higher in India than in Western nations. (3) Often, AHF is considered a homogenous disorder
(ie, congestive heart failure) with volume overload
In-hospital published mortality rates of acute as the primary problem. Accordingly, patients are
decompensated heart failure (ADHF) in the US and usually treated based on this. However, an evolution
Europe range from 4% to 7%. Even with best medical in thinking has emerged, suggesting that a uniform
therapy based on the current guidelines, 6-month approach to intervention is not equally beneficial
adverse event rates approximate 35%. Similar data for all patients. Closer analysis shows that there
was not available for HF from India until 2015 when are several common AHF phenotypes with distinct
a prospective study of 90 patients was published by pathophysiological manifestations. Such phenotypes

can occur by themselves and in patients with pre- for whom volume removal is appropriate and others
existing chronic heart failure, whether EF is preserved where afterload reduction or inotropic support is most
(HFpEF) or reduced (HFrEF). Thus, while all episodes needed. (6) The following table reviews the etiology of
of AHF are accompanied by an increase in LV end- decompensation.(5)
diastolic pressure (LVEDP), there are certain patients
TYPES OF HF EXACERBATION PRECIPITATING FACTORS

Worsening chronic heart failure Dietary indiscretion
Uncontrolled HTN
Concurrent non-cardiac illness (e.g., infection
especially pneumonia, pulmonary embolus,
thyroid disease, renal failure)
Substance abuse (e.g., alcohol, other)
Medication related
Medication nonadherence
Use of medications with negative inotropic
properties (e.g. diltiazem, verapamil)
New or worsening cardiac processes Ischemia/Myocardial infarction
Arrhythmias (e.g., atrial fibrillation, ventricular
tachycardia, other)
Hypertensive urgency/emergency
De novo heart failure Large myocardial infarction
Sudden elevation in blood pressure
Stress-induced (takotsubo) cardiomyopathy
Myocarditis
Peripartum cardiomyopathy
Acute valvular insufficiency – stenosis,
regurgitation, endocarditis
Aortic dissection
End-stage HF with progressive worsening of
cardiac output
Table 1: Precipitating factors of heart failure exacerbation

Another clinical terminology commonly used is congestion, with low left ventricle filling pressures; It
Heart Failure with reduced ejection fraction (HFrEF) is important to make a clear differentiation between
–commonly systolic heart failure and Heart Failure patients with chronic HF who eventually develop signs
with preserved ejection fraction (HFpEF) or diastolic and symptoms of right HF (elevated jugular venous
heart failure. Diastolic dysfunction (DD) is defined as pressure, peripheral edema, hepatomegaly, gut
an abnormality of left ventricular (LV) relaxation, filling, congestion) versus patients with new-onset isolated
or compliance, irrespective of the ejection fraction. right heart failure, often secondary to either acute
HFpEF, also known as diastolic heart failure, is defined coronary syndrome (ACS) or pulmonary embolism.
as a syndrome of heart failure signs and symptoms,
echocardiographic signs of abnormal diastolic function, Cardiogenic Shock
with a normal to near-normal ejection fraction. The
Cardiogenic shock comprises of severe peripheral
presence of HFP\pEF or DD, even in the absence of overt
hypoperfusion with subsequent end-organ damage;
heart failure, is associated with increased morbidity and
typically it is associated with low blood pressure
mortality. (7) Multiple clinical presentations is a typical
(systolic BP < 90 mmHg) and low urine output (< 0.5
feature of Acute Heart Failure. (8)
mL/kg/min).
Clinical Classifications
Acute Coronary Syndrome(ACS) Complicated by Heart
According to the European Society of Cardiology Failure
guidelines (2012), a patient with AHF may present with
one of the following clinical categories. 40% of patients with AHF may have ACS as a precipitating
factor (9)
Decompensated Chronic Heart Failure
In the perioperative setting, the types of acute heart
Occurs when a patient with chronic HF develops failure seen are typically (10):
progressive deterioration and worsening in signs
and symptoms; peripheral edema and/or pulmonary • Systolic Heart Failure: commonly seen in
congestion is present; these patients may appear with cardiac surgery after CPB
low blood pressure which is often associated with
• Diastolic Heart Failure
impaired LVEF and predicts poor prognosis.
• Right Heart Failure
Pulmonary Edema
For many physicians, pulmonary edema is the real Pathophysiology
clinical presentation of AHF; typically, signs and Because of myocyte injury, pressure or volume
symptoms develop rapidly and patients demonstrate overload, or dilated cardiomyopathy, increased wall
severe respiratory distress with tachypnea, orthopnea, stress is the precipitating event for development of LV
and pulmonary congestion. systolic dysfunction.
Hypertensive Heart Failure This leads to changes in myocyte filaments producing
Hypertensive heart failure is associated with elevated hypertrophy and interstitial fibrosis, and necrosis. This
blood pressure with accompanying dyspnea and results in pathologic remodeling of the LV, producing
signs of pulmonary congestion, often in patients with dilation, impaired contractility and decreased cardiac
relatively preserved LVEF. output. The decrease in cardiac output first activates
the sympathetic nervous system. This is followed by
Isolated Right Heart Failure the activation of renin-angiotensin-aldosterone (RAAS)
Isolated right heart failure is characterized by low system, and in chronic HF, the arginine vasopressin
output syndrome in the absence of pulmonary and natriuretic peptide systems. This elevation in

catecholamine levels, including norepinephrine Increased levels of endotoxin activate the immune
and epinephrine; result in direct myocyte toxicity, system, leading to increased circulating levels of pro-
leading to apoptosis and myocardial remodeling, and inflammatory cytokines, including tumor necrosis factor
also the downregulation of adrenergic receptors. (TNF) and interleukins 1 and 6. Increased TNF levels
Systemic vasoconstriction and sodium and water in the plasma and the myocardium produce multiple
retention occurs. Ultimately, these responses become adverse effects including negative inotropy, inhibiting
maladaptive and result in pulmonary congestion, adrenergic receptor responsiveness, contributing to
impaired contractility and reduced tissue perfusion. LV remodeling, downregulating nitric oxide synthase,
Vasopressin is a vasoconstrictor also implicated in inducing myocyte apoptosis and skeletal muscle
ventricular remodeling. As with norepinephrine and wasting and influencing thermogenesis, to name a few.
angiotensin II, elevated levels of vasopressin are Interleukins further compromise myocardial function by
associated with a worse outcome. reducing contractility and inhibiting myocyte adrenergic
responsiveness. Elevated levels are associated with a
The neurohormonal induced increase in total body
poorer New York Heart Association (NYHA) class and a
water increases both atrial and ventricular wall
prolonged hospital length of stay.
tensions, resulting in a release of atrial (ANP) and brain
(BNP) natriuretic peptides. These peptides attempt to The net result of the increased wall stress and
restore cardiac output by decreasing peripheral vascular subsequent neurohormonal activation is an increase
resistance and by promoting renal sodium excretion. As in total body water and the development of a dilated,
HF progresses, there is diminishing responsiveness to spherical LV with impaired myocardial shortening.
increasing levels of ANP and BNP, further contributing Mitral regurgitation (MR) often develops because of
to chronic fluid overload. annular dilation and restrictive leaflet function, further
The catecholamine-induced myocyte apoptosis also decreasing cardiac output. All these mechanisms are
causes the release of endotoxin into the circulation. illustrated in the following figures 2, 3 and 4. (11)
Fig 2: Adaptive mechanisms to maintain cardiac output (11)

Diastolic Dysfunction The anesthetic management of patients with AHF

requires careful planning, preparation, and monitoring.
HFpEF is characterized by a stiff noncompliant LV, with
The first step is to obtain a thorough history and physical
a steep diastolic pressure volume relationship, which is
examination.
shifted upward and to the left compared to the normal
LV. This decreases LVEDV, leading to a compensatory rise In the perioperative setting, these patients present
in LV filling pressures to maintain cardiac output. This with orthopnea related to increased left-sided filling
results in increased diastolic wall stress, normal systolic pressures and abdominal discomfort, nausea and
wall stress, and preserved ejection fraction, initially vomiting caused by right-sided overload. The physical
presenting as impaired exercise tolerance. Because examination may demonstrate signs of heart failure
of the ventricular stiffness and decreased LV filling, severity: hypotension, tachycardia, dyspnea, hepatic
forward flow is reduced, resulting in pulmonary edema. congestion, oliguria, cyanosis, mottling and altered
consciousness.
Alterations in calcium handling also affect LV relaxation
and stiffness. The decreased rate of calcium elimination Low cardiac output and tissue hypoxia in the absence of
during diastole results in increased cytosolic calcium hypovolemia is the defining feature of cardiogenic shock.
during diastole with a corresponding reduction of It is supported by appropriate investigations such as
cytosolic calcium during systole, impairing both electrocardiogram, chest radiograph, echocardiography,
contraction and relaxation. (13) pulmonary artery catheter and biomarkers.
The majority of acute perioperative heart failure Intraoperative and postoperative transoesophageal
occurs in patients who have decreased cardiovascular echocardiography (TOE) and postoperative transthoracic
reserve prior to surgery. In the peri-operative echocardiography should be performed as early as
period, acute heart failure is precipitated by many possible in patients suspected of perioperative heart
triggers- hypertension, tachyarrhythmias, anemia, failure. Echocardiography quickly provides information
hypercoagulability, inappropriate fluid management, on regional or global, right and/or left ventricular
pain, surgical stress and myocardial ischaemia. Other dysfunction, the presence of tamponade, cardiac
causes of perioperative heart failure include acute or thrombi, valvular dysfunction and preload estimation.
chronic valvular heart disease, pulmonary or fat emboli, The role of TOE is important for perioperative
which can be presented as acute right ventricular haemodynamic monitoring and the assessment of the
failure. optimal volume status. (14)
Cardiac surgery may lead to some unique causes of Biomarkers are very useful in less severe acute heart
heart failure. Mechanical complications including failure when the mechanism of postoperative acute
spasm or occlusion of a coronary graft, prosthetic dyspnea is unclear, and when there is an urgent need
paravalvular regurgitation, cardiac tamponade and to discriminate pulmonary infection and pulmonary
pneumo or hemothorax may be seen after cardiac oedema. Currently, the diagnostic role of B-type
surgery. (14) natriuretic peptide (BNP) and N-terminal pro-B-type
natriuretic peptide (NT-pro- BNP) in the perioperative
Preoperative Evaluation
period remains to be demonstrated. These biomarkers
The presence of CHF is one of the most important have the potential to strengthen the diagnosis of acute
factors for predicting postoperative cardiac morbidity perioperative heart failure when used along with
and mortality. According to the most current AHA/ history, physical exam and other diagnostic tools.
ACC guidelines, if signs or symptoms of acute
Patients with pulmonary hypertension and RV
decompensated HF are present, elective surgery is
dysfunction are at extremely high risk for noncardiac
contraindicated.

surgery. Preoperative right heart catheterization and Mechanical circulatory assistance may be required
careful optimization with inodilators and inotropes may preoperatively in extremely sick patients who have
be required before taking these patients for noncardiac to undergo major noncardiac surgery. Preoperative
surgery. (11) insertion of intra-aortic balloon pump (IABP) has
been shown to be useful in the prevention of major
Hemodynamic Monitoring
adverse cardiac events (MACE) in patients with severe
The choice of monitoring depends on the stage of HF, cardiac dysfunction undergoing high-risk noncardiac
the patient’s comorbid conditions, and the complexity surgery. This strategy is justified in emergent or urgent
of the surgical procedure. Invasive arterial blood noncardiac high-risk surgery, patients undergoing
pressure monitoring is beneficial in stage NYHA III/IV cancer surgery and patients with inoperable CAD. An
HF patients. Arterial catheters also allow monitoring of IABP augments cardiac function by improving coronary
blood gases, electrolytes, lactate levels, and hematocrit perfusion and decreasing afterload. Left ventricular
as required. assist devices such as the Impella LP 2.5 (LVAD;
Abiomed Inc., Danvers, MA), a miniature intracardiac
Central venous access allows CVP measurement assist device have been used to support the circulation
and administration of inotropes and vasopressors if during noncardiac surgery. Independent support of the
necessary. circulation is an advantage of assist devices over IABP
Transesophageal echocardiography (TEE) monitoring is in patients with HF. (11)
indicated in surgeries in which extensive fluid shifts are Perioperative heart failure in cardiac surgery
expected (aortic vascular and major thoracic surgery).
It can diagnose new RWMA, valvular dysfunction, and More than 20% of patients are expected to have acute
provide information about volume status. cardiovascular dysfunction in the perioperative period
of cardiac surgery.
Although the role of pulmonary artery catheterization
is contentious, it can be very useful in a complex Classification of acute heart failure by European
perioperative haemodynamic situation. The diagnosis Society of Cardiology/American College of Cardiology
of severe acute heart failure is suspected by the Foundation/American Heart Association is not
association of low cardiac index (<2.2 l/min/m 2), applicable to the perioperative period of cardiac
low mixed venous saturation (<60%) and elevated surgery.
pulmonary capillary wedge pressure (>18 mmHg).
Risk stratification is increasingly used in open-heart
Success depends on accurate measurement, correct surgery to help adjust available resources to predicted
interpretation, and proper application of PAC outcome.
hemodynamic data. Knowledge of the perioperative
Indicators of major clinical risk in the perioperative period
team on how to use the information in combination
are: unstable coronary syndromes, decompensated HF,
with the data obtained from other monitoring
significant arrhythmias and severe valvular disease.
modalities such as TEE, arterial blood gas, stroke volume
variation (SVV), and mixed venous oxygen saturation Clinical risk factors include history of heart disease,
is the key for the management of these patients. (14) compensated HF, cerebrovascular disease, presence
of diabetes mellitus, renal insufficiency and high-risk
Immediate Preoperative Preparation
surgery.
Patients in refractory HF may require optimization
EuroSCORE predicts perioperative cardiovascular
of their hemodynamic status preoperatively with
alteration in cardiac surgery well, although in those
invasive monitoring, vasodilators, and inotropic therapy
older than 80 years it overestimates mortality. (15)
(milrinone or dobutamine).
General Overview in lying flat. If the surgical procedure requires more than
sedation, neuraxial or general anesthesia can be used.
In perioperative AHF, a differential diagnosis must be
established as resuscitation measures are initiated. Select surgical procedures (eg, arteriovenous fistula
Proper diagnosis allows definitive treatment through creation) can be well managed with regional nerve
the use of specific therapies. For example, patients blocks. Cohen and colleagues studied the influence
with perioperative acute heart failure secondary to an of the type of anesthesia on the outcome of patients
acute MI, reperfusion via angioplasty, stenting or bypass with CHF after lower extremity vascular surgery. The
grafting will be necessary. Acute mitral regurgitation type of anesthesia had no impact on the incidence
from a MI causing acute heart failure might require of combined cardiac events, death, MI, death or MI
urgent surgical repair. combined, unstable angina, or CHF.
At the same time, appropriate resuscitation measures Anesthetic Drugs and HF
must be undertaken. The concept of the golden hour
Titration of anesthetic drugs to the hemodynamic goal
for acute heart failure management is very important,
is more important than the anesthetic drugs chosen.
and medication administration must be started within
However, anesthesiologists must be aware of the
minutes of diagnosis. (14)
hemodynamic effects of all anesthetic drugs they are
The list below highlights the general approach to planning to use. Intravenous induction in patients with
perioperative acute heart failure management: a low cardiac output should be performed carefully
because of a slow circulation time. The concentration
• Develop differential diagnosis for cause, treat
of volatile agents must be titrated carefully because
lesions amenable to treatment
of their cardiodepressant effects as well as their
• Initiate resuscitation measures: maximize increased speed of onset. The addition of nitrous oxide
oxygenation/ventilation, control postoperative is associated with significant myocardial depression and
pain/tachycardia, correct acid-base and should be avoided in HF patients.
electrolyte abnormalities
Hemodynamic Goals and Management
• Evaluate and optimize preload, afterload,
The goals for patients in NYHA Stage III and IV HF are
contractility, heart rate and rhythm
to maintain normal sinus rhythm, adequate preload,
• Preload – volume load vs. diuresis based heart rate, and contractility while avoiding afterload
on evaluation of volume status mismatch. These patients rely on normal sinus rhythm
• Afterload – if high, consider dilation with and new onset arrhythmia or LBBB can lead to acute
nitroglycerine, sodium nitroprusside; deterioration. (11)
if low consider augmentation with Cardiac output in patients in end-stage HF is dependent
norepinephrine on increased sympathetic response and their increased
• Contractility – utilize inotropic agent baseline heart rate. They have fixed stroke volume and
• Establish stable heart rate and rhythm. depression of sympathetic compensatory responses
during induction can lead to severe hypotension and
• Utilize mechanical assistance for patients even cardiac arrest.
resistant to above measures.
Assessment of preload and maintenance of euvolemia
Anesthetic Technique (11) are the most challenging aspects of the perioperative
The type of anesthesia administered depends on the management in HF patients. Fluid administration
nature of surgery. Patients with CHF may have difficulty should be titrated to maintain adequate preload while

preventing pulmonary edema or worsening mitral or • Volume status should be repeatedly assessed
tricuspid regurgitation because of annular dilation. to ensure that the patient is not hypovolaemic
Direct visualization and estimation of the ventricular while under vasopressors (15)
volume (left ventricular end-diastolic volume) by TEE is
used during high-risk procedures. Static parameters like Catecholamines
CVP and pulmonary capillary wedge pressure to define All catecholamines have positive inotropic and
volume status are of limited value in patients with HF chronotropic effects. In a comparison of epinephrine
because of the altered ventricular compliance and with dobutamine in patients recovering from CABG,
volume-pressure relationships although their trends they had similar effects on mean arterial pressure,
over time can be useful to guide fluid therapy. Dynamic central venous pressure, PCWP, SVR, pulmonary
parameters of fluid responsiveness such as SVV may vascular resistance, and LV stroke work. Dobutamine
be more useful for that purpose. Currently, there is no
increased heart rate more than epinephrine.
gold standard monitor to assess fluid responsiveness
in these patients. More research is needed in this area. Epinephrine, dobutamine and dopamine all
(11) increase myocardial oxygen consumption (MVO 2)
postoperatively. However, dobutamine causes matching
Significant increase in afterload is poorly tolerated
increase in coronary blood flow, suggesting that
and leads to reduction in cardiac output in patients
the other agents may impair coronary vasodilatory
with HF. Anesthetic medications and vasodilators can
reserve postoperatively. Commonly encountered
synergistically cause significant reduction in systemic
vascular resistance in patients with fixed cardiac output side effects associated with epinephrine use include
with impairment of coronary and end organ perfusion. hyperlactateaemia and hyperglycaemia. (15)
Optimal management of afterload is challenging. Phosphodiesterase III inhibitors
Pharmacological Management of LV dysfunction, Phosphodiesterase III inhibitors, such as amrinone,
especially after cardiac surgery milrinone or enoximone, are all potent vasodilators
In case of myocardial dysfunction, the following that cause reductions in cardiac filling pressures,
inotropes are used pulmonary vascular resistance and SVR; they are
commonly used in combination with β1-adrenergic
• Among catecholamines, low-to-moderate agonists. Compared to dobutamine in postoperative
doses of dobutamine or epinephrine can be low CO, phosphodiesterase III inhibitors caused a less
used: they both improve stoke volume and pronounced increase in heart rate and decreased
increase heart rate while PCWP is moderately the likelihood of arrhythmias. Phosphodiesterase III
decreased; catecholamines increase myocardial inhibitors decrease LV wall tension without increasing
oxygen consumption MVO2, despite increases in heart rate and contractility,
• Milrinone, a phosphodiesterase inhibitor, in striking contrast to catecholamines. The limiting
decreases PCWP and SVR while increasing stoke factor is usually reduction in systemic BP due to drop
volume; milrinone causes less tachycardia than in SVR.
dobutamine
Levosimendan
• Levosimendan, a calcium sensitizer, increases
Levosimendan has been recommended for the
stoke volume and heart rate and decreases SVR
treatment of acute HF and was recently used for the
• Norepinephrine should be used in case of low successful treatment of low CO after cardiac surgery.
blood pressure due to vasoplegia to maintain The effects of levosimendan have been compared to
an adequate perfusion pressure those of dobutamine and milrinone. Compared to

dobutamine, levosimendan decreases the incidence The general rationale for using mechanical circulatory
of postoperative atrial fibrillation and myocardial support (MCS) in patients with CS is to restore adequate
infarction, ICU length of stay, acute renal dysfunction, systemic perfusion pressure, to allow the ventricle time
ventricular arrhythmias and mortality in the treatment to recover. Over the past decades, innovation in this
of postoperative LV dysfunction. field has changed CS management.
In summary, the above-mentioned inotropic agents To date, there is no universal consensus on indications
can be started either alone or in combination with an for MCS in AHF. (16) However, the following are the
agent from another class (multimodal approach) in most common indications:
myocardial depression.
• Postinfarction CS
Pulmonary Hypertension and HF
• Fulminant myocarditis
Patients with pulmonary hypertension and RV
dysfunction deserve special precautions. Pulmonary • A c u te l y d e c o m p e n s a te d c h ro n i c H F
hypertension secondary to elevated left atrial pressure unresponsive to inotropic agents
significantly increases anesthetic risk for cardiac and
• Inability to wean from cardiopulmonary bypass
noncardiac surgery especially with severe pulmonary
hypertension. (15) after cardiac surgery
Acute right HF can occur on induction. In case of severe • Graft failure after heart transplantation
acute right heart failure, a cardiac surgeon should be • Post-cardiac arrest.
available in the room for emergency institution of CPB
if necessary. Invasive arterial blood pressure monitoring Available devices for MCS are:
is established and inotropes should be started before
• Intra-aortic balloon pump (IABP)
induction of anesthesia, if necessary.
• Extracorporeal life support (ECLS)
The hemodynamic goals in this situation are maintenance
of adequate systemic blood pressure to maintain RV • Ventricular assist devices (VADs)
perfusion, avoidance of myocardial depression, and
RV afterload mismatch (avoid increase in pulmonary Current European guidelines recommend considering
vascular resistance). Avoid hypoxia, hypercarbia, the use of a percutaneous assist device for MCS
acidosis, light anesthesia and hypothermia, as these in refractory CS to provide for a quick and easy
can all acutely increase pulmonary artery pressures. initiation, with no preference for device selection
Pulmonary vasodilators can be used in patients with (recommendation IIa C). (16)
severe pulmonary hypertension and right heart
Intra-aortic Balloon Pump
failure. Inhaled pulmonary vasodilators are of benefit
in the setting of systemic hypotension as they avoid The IABP is the most current and less expensive form
the systemic vasodilation caused by intravenous of MCS. It functions as a volume displacement device.
vasodilators. The inflation and deflation of the balloon, synchronized
Mechanical Circulatory Support (MCS) with the cardiac cycle, improve peak diastolic pressure
and coronary blood flow while reducing aortic pressure,
In the event of acute heart failure or cardiogenic afterload and myocardial oxygen consumption. It is
shock (CS), which is refractory to inotropes and easy and fast to deploy and does require some cardiac
vasopressors, mechanical circulatory support (MCS) function to be effective.
can be considered.

Extracorporeal Life Support (ECLS) or extracorporeal • Patients in cardiogenic shock represent an

membrane oxygenation (ECMO) extremely high-risk group in whom mortality
has remained high despite revascularization
Extracorporeal life support in the venoarterial
and pharmacologic therapies. Early placement
configuration can completely replace cardiopulmonary
of an appropriate MCS may be considered in
function and is indicated for severe forms of CS and
those who fail to stabilize or show signs of
refractory cardiac arrest. Blood is withdrawn via the
improvement quickly after initial interventions
venous system (usually the femoral vein or right
atrium) and pumped through an oxygenator, where • MCS may be considered for patients undergoing
gas exchange of oxygen and carbon dioxide takes place. high- risk PCI, such as those requiring
It is then returned to the arterial system (usually the multivessel, left main or last patent conduit
femoral artery or ascending aorta). It requires careful interventions, particularly if the patient is
monitoring of anticoagulation and is conceived for inoperable or has severely decreased ejection
short or mid- term support, carrying a not negligible fraction or elevated cardiac-filling pressures
rate of complications (typically, bleeding at the site
• In the setting of profound cardiogenic shock,
of cannulation or lower limb ischemia), which rises
intra- aortic balloon pump (IABP) is less likely
exponentially with the duration of support.
to provide benefit than continuous flow pumps
Ventricular Assist Devices (VADs) including the Impella CP and Tandem Heart.
ECMO may also provide benefit, particularly
Ventricular assist devices are continuous flow pumps
for patients with impaired respiratory gas
connected to the patient’s circulation that replace the
exchange
function of the left heart, right heart, or both. Pumps
may be centrifugal or axial. Percutaneously implanted • Patients with acute decompensated heart
VADs (intravascular or extracorporeal) are intended for failure may benefit from early use of
temporary, short-term use, while surgically implanted percutaneous MCS when they continue to
(intracorporeal or paracorporeal, axial or centrifugal) deteriorate despite initial interventions. MCS
VADs are for mid- or long-term use. Thus, the latter are may be considered if patients are candidates
not the first choice for MCS in AHF. for surgically implanted ventricular assist
device (VAD) or if rapid recovery is expected
The 2015 SCAI/ACC/HFSA/STS Clinical Expert Consensus
(e.g., fulminant myocarditis or stress-induced
Statement on the Use of Percutaneous Mechanical
cardiomyopathy)
Circulatory Support Devices in Cardiovascular Care, also
endorsed by the Cardiological Society of India provided • MCSs may be used for failure to wean off
the following consensus-based recommendations cardio-pulmonary bypass, considered as
based on the anticipated hemodynamic effects and an adjunct to high-risk electrophysiologic
risks, clinical outcomes data as well as knowledge gaps. procedures when prolonged hypotension is
(17) anticipated or, rarely, for valvular interventions
Recommendations made were as follows: • Severe biventricular failure may require use of
both right- and left-sided percutaneous MCS
• Percutaneous MCS provides superior
and venoarterial ECMO. Certain patients
h e m o d y n a m i c s u p p o r t co m p a re d to
may respond to left ventricular assist device
pharmacologic therapy. This is particularly
(LVAD) implantation with inotropes and/or
apparent for the Impella and Tandem- Heart
pulmonary vasodilators to support the right
devices
heart. MCS may also be considered for isolated

acute right ventricular failure complicated by Cardiology ,Volume 3, Issue 2, Pages 43-48. June
cardiogenic shock 2013
• Registries and randomized controlled trials 5. Teerlink JR, Alburikan K, Metra M, Rodgers JE.
comparing different strategies in different Acute decompensated heart failure update. Curr
clinical scenarios are critically needed Cardiol Rev. 2015;11(1):53-62.
• Early analyses suggest cost-effectiveness 6. David M Viau,Javier A Sala-Mercado,Marty D
of MCS for emergent use in comparison to Spranger,Donal S O’Leary,Phillip D Levy. The
surgical ECMO or VAD support, and for elective pathophysiology of hypertensive acute heart
use in comparison to IABP. Further data are failure. Heart 2015;101:1861–1867
necessary.
7. Gelzinis TA. New Insights Into Diastolic Dysfunction
Conclusion and Heart Failure With Preserved Ejection
In conclusion, anesthesia management for patients Fraction. Semin Cardiothorac Vasc Anesth. 2014
with acute heart failure undergoing cardiac and Jun;18(2):208-17)
noncardiac surgery is challenging and should be 8. Ponikowski P Jankowska EA. Pathogenesis and
carefully planned. A multidisciplinary approach clinical presentation of acute heart failure. Rev Esp
involving the cardiologist, anesthesiologist, cardiac Cardiol (Engl Ed). 2015 Apr;68(4):331-7
surgeon, and intensivist provides the most benefit to
these patients. Preoperative optimization, intensive 9. Ponikowski P Jankowska EA. Pathogenesis and
perioperative monitoring and careful hemodynamic clinical presentation of acute heart failure. Rev Esp
management can reduce perioperative risk and improve Cardiol (Engl Ed). 2015 Apr;68(4):331-7
outcome of these high-risk patients after cardiac and
10. Mebazaa A, Pitsis AA, Rudiger A, Toller W, Longrois
noncardiac surgery.
D, Ricksten SE, Bobek I, De Hert S, Wieselthaler
References G, Schirmer U, von Segesser LK, Sander M,
Poldermans D, Ranucci M, Karpati PC, Wouters
1. Kurmani S, Squire I. Curr Heart Fail Rep. Acute
P, Seeberger M, Schmid ER, Weder W, Follath F.
Heart Failure: Definition, Classification and
Clinical review: practical recommendations on
Epidemiology.2017 Oct;14(5):385-392.
the management of perioperative heart failure in
2. Huffman MD, Prabhakaran D. Heart failure: cardiac surgery. Crit Care. 2010;14(2):201
epidemiology and prevention in India. Natl Med J
11. Gelzinis, Theresa Anne MD; Subramaniam,
India. 2010 Sep-Oct;23(5):283-8.
Kathirvel MD. Systolic Heart Failure and Anesthetic
3. Sandeep Seth, Suraj Khanal, Sivasubramanian Considerations. International Anesthesiology
Ramakrishnan, Namit Gupta, Vinay K Bahl. Clinics, Volume 50(3), Summer 2012, p 146–170
Epidemiology of acute decompensated heart
failure in India : The AFAR study (Acute failure 12. Mentz RJ,, O’Connor CM. Pathophysiology and
registry study). Journal of the Practice of the clinical evaluation of acute heart failure. Nat Rev
Cardiovascular Sciences 2015:Vol 1, Issue 1, 35-38 Cardiol. 2016 Jan;13(1):28-35
4. Srikant Banumathy, V. Dayasagar Rao, Laxmikant 13. Gelzinis TA. New Insights Into Diastolic Dysfunction
Joshi, Usha Govindarajan . Etiology of congestive and Heart Failure With Preserved Ejection
heart failure in Indian population – An acute care Fraction. Semin Cardiothorac Vasc Anesth. 2014
study of 500 cases. Journal of Indian College of Jun;18(2):208-17

14. Sabri Soussi, Kais Chatti, and Alexandre Mebazaa. 17. Rihal CS, Naidu SS, Givertz MM, Szeto WY, Burke JA,
Management of perioperative heart failure. Curr Kapur NK, Kern M, Garratt KN, Goldstein JA, Dimas
Opin Anesthesiol 2014, 27:140 – 145 V, Tu T; Society for Cardiovascular Angiography
and Interventions (SCAI); Heart Failure Society
15. Mebazaa A, Pitsis AA, Rudiger A, Toller W, Longrois
of America (HFSA); Society for Thoracic Surgeons
D, Ricksten SE, Bobek I, De Hert S, Wieselthaler
(STS); American Heart Association (AHA); American
G, Schirmer U, von Segesser LK, Sander M,
College of Cardiology (ACC). 2015 SCAI/ACC/HFSA/
Poldermans D, Ranucci M, Karpati PC, Wouters
STS Clinical Expert Consensus Statement on the Use
P, Seeberger M, Schmid ER, Weder W, Follath F.
of Percutaneous Mechanical Circulatory Support
Clinical review: practical recommendations on
Devices in Cardiovascular Care (Endorsed by the
the management of perioperative heart failure in
American Heart Association, the Cardiological
cardiac surgery. Crit Care. 2010;14(2):201
Society of India, and Sociedad Latino Americana
16. Plácido R, Mebazaa A. Update: Acute Heart Failure de Cardiologia Intervencion; Affirmation of Value
(VII): Nonpharmacological Management of Acute by the Canadian Association of Interventional
Heart Failure. Rev Esp Cardiol (Engl Ed). 2015 Cardiology-Association Canadienne de Cardiologie
Sep;68(9):794-802. D’intervention). Catheter Cardiovasc Interv. 2015
Jun;85(7):E175-96.

MCQ
1. Estimated prevalence of Heart failure in India 4. Indications for MCS in AHF except:
a. 5-6/1000 population a. Postinfarction CS
b. 1-2/ 500 population b. Ustable angina
c. 2–3/1000 population c. Acutely decompensated chronic HF
d. 5/ 10000 population unresponsive to inotropic agents
2. Cardiogenic shock comprises of: d. Inability to wean from

cardiopulmonary bypass after cardiac
a. Tachycardia, tachypenia and increased surgery
JVP
b. Severe peripheral hypoperfusion, low
blood pressure and low urine output
c. Hepatomegaly, sweating and basal
creps
3. Regarding perioperative TOE which one of the
following sentence suits correctly
a. To find out structural lesion and

Ejection fraction
b. All patients undergoing major surgery
c. Volume status alone
d. Haemodynamic monitoring and the
assessment of the optimal volume
status
4 (B) 3 (D) 2 (B) 1 (C)

Answers

12 Adverse Events and Improving Safety In and
Out of OR Anesthesia and Sedation
Associate Professor of Anaesthesia Keira P. Mason

Boston,USA
Learning Objectives Description

1) To construct anesthesia plans for the safe Creating a safe, positive experience is the goal of
management of medically challenging patients every anesthesia provider in and outside of the
who present in the Non-Operating Room operating room, but past data has suggested that Non-
Anesthesia environments. Operating Room Anesthesia (NORA) environments are
2) To define and create systems for dealing with not without increased risk. Anticipating difficulties,
and anticipating emergencies, as well as learning creating and defining systems to deal with emergencies,
from mistakes. implementing known professional guidelines, and
having a current knowledge of recent outcome
3) To identify the data and outcomes to determine
literature are keys to success.
whether anesthesia and sedation in the NORA
environment carries a higher risk for adverse
outcomes than in the OR.

Adverse Events and Improving Safety in and 130
out of or Anesthesia And Sedation Keira P. Mason
MCQ
1. The most common complications due to 4. The following statement is false regarding
sedation outside OR is related to fasting during NORA
a. Airway a. Preoperative fasting is not as
b. Cardiorespiratory arrest important as in patients preparing for
elective surgery
c. Aspiration
b. Clear fluids are allowed 2 hours before
d. PONV
induction
2. The leading sector requiring anesthesia/ c. prolonged fasting can cause
sedation outside OR is hypocalcemia in children
a. Gastrointestinal suite d. solids regarded as a meals must be
b. MRI withheld for at least 8 hours.
c. CT suite 5. Guidelines for Non Operating Room

Anesthesia includes all except
d. Cath Lab
a. Should follow standard anesthesia
3. The requirements for nonanesthesia
monitoring
personnel to administer NORA includes
b. Provision for adequate illumination
a. Trained in preanesthetic assessment
of patients c. Equipments and drugs to provide CPR
should always be available
b. Trained in cardiopulmonary
resuscitation d. Should not be administered by non
anesthesia personnel
c. Trained in use of anesthetic and
resuscitation drugs
d. All of the above
5. (d) 4. (a) 3. (b) 2. (a) 1.(a)

Answers

13 Basics of Mechanical Ventilation
Professor and HOD Arunkumar AS

Saveetha Medical College
Chennai
Key points
Ø There is little evidence of an ideal mode of ventilation

Ø Control, cycle, trigger, breath and flow patterns are essential elements to be understood for the optimal
use of ventilators
Ø In pressure controlled modes, the flow pattern is always decelerating whereas in volume controlled
modes, the flow pattern is constant, decelerating or sinusoidal
Ø A decelerating flow pattern is probably the most effective flow pattern
Ø Pressure control does not guarantee minute ventilation, and therefore requires more monitoring by the
operator
Ø Inverse ratio ventilation improves oxygenation, but it tend to cause CO2 retention
Ø A collapsed airway is tremendously difficult to reinflate: leading to a huge increase in the work of
breathing & oxygen consumption
Ø Rapid shallow breathing index as reflected by frequency (breaths/minute)/Vt (liters) is an accurate
predictor of weaning outcome
Ø Phasic opening and closing of lung units causes release of cytokines and reinforcement and amplification
of the local and systemic inflammatory response
Ø FiO2 of greater than 50% should be avoided provided the PaO2 is acceptable i.e. more than 60 mmHg.
Ø Every time a patient is disconnected from a ventilator, the lungs derecruit and will not inflate with re-
instatement of previous ventilator settings. A recruitment maneuver is then required.
Ø Nerve, muscle and neuromuscular junction (NMJ) abnormalities may affect over 90% of patients
ventilated for more than seven days.
Introduction invasively or non-invasively.

Respiratory failure is caused by failure to ventilate, Failure to oxygenate may occur as a result of:
characterized by increased arterial carbon dioxide
• Decreased alveolar oxygen tension (due to
tension, or failure to oxygenate, characterized by
decreased inspired O2 tension or increased
decreased arterial oxygen tension. The treatment for
CO2 tension)
failure to ventilate is to increase the patient’s alveolar
ventilation (the rate and depth of breathing), either by • Reduced O2 diffusion capacity (due to interstitial
reversing the cause or by using mechanical ventilation; edema or fibrosis, or thickened alveolar walls)

Basics of Mechanical Ventilation 132 Arunkumar AS
• Ventilation perfusion mismatch (due to loss Flow is controlled by an array of sensors and
of functional residual capacity and alveolar microprocessors. Conventionally, inspiration is active
collapse/consolidation) and expiration is passive (although modern ventilators
The treatment for failure to oxygenate is restoration have active exhalation valves).
and maintenance of lung volumes, using recruitment Modes of ventilation describe the primary method
maneuvers and increased baseline airway pressures of inspiratory assistance. A machine generates and
(PEEP/CPAP). Imposed ventilatory workload is increased
regulates the flow of gas into the lungs, flow continues
by loss of lung compliance and inspiration/ventilation
until a predetermined volume has been delivered or
is usually supported to reduce O2 requirements and
increase patient comfort. airway pressure generated. Flow reverses, when the
machine cycles into the expiratory phase. The message
Residents are baffled by the variety of different to do this is either
ventilatory modes and arguments regarding the relative
merits of one over another. In truth, there is little • Preset time
evidence that there is an ideal mode of ventilation. For • Preset tidal volume
any patient, it is the same pressure-volume curve that • Preset percentage of peak flow
governs the lung mechanics, what differs is the way in
which gas flow achieves this. The science of mechanical Mechanical breaths may be
ventilation is to optimize pulmonary gas exchange; the • Controlled (the ventilator is active and the
art is to achieve this without damaging the lungs.
patient passive)
This short review will try to demystify ventilators. A brief • Assisted (the patient initiates and may or may
overview of mechanical ventilators will be followed not participate in the breath)
by ventilatory strategies in some of the commonly
encountered problems in the ICU. The rate, pattern and duration of gas flow control the
interplay between volume and pressure.
What is a mechanical ventilator?
In volume controlled modes, a desired tidal volume
A mechanical ventilator is a machine that generates a is delivered at a specific flow (peak flow) rate, using
controlled flow of gas into a patient’s airways. Oxygen constant, decelerating or sinusoidal flow patterns:
and air are received from cylinders or wall outlets, the the airway pressure generated may be higher than is
gas is pressure reduced and blended according to the
desirable.
prescribed inspired oxygen tension (FiO2), accumulated
in a receptacle within the machine, and delivered In pressure controlled modes, flow occurs until a
to the patient using one of many available modes of preset peak pressure is met over a specified inspiratory
ventilation. period, the flow pattern is always decelerating: the tidal
The central premise of positive pressure ventilation is volume may be lower than that desired. Moreover,
that gas flows along a pressure gradient between the as pulmonary mechanics change, so too does the
upper airway and the alveoli. The magnitude, rate and delivered tidal volume.
duration of flow are determined by the operator. Flow
is either Classification of ventilators
• Volume targeted and pressure variable The classification of ventilators refers to the following
• Pressure limited and volume variable. elements:
The pattern of flow may be either • Control: How the ventilator knows how much
flow to deliver
• Sinusoidal (which is normal)
• Decelerating o Volume Controlled (volume limited,
• Constant volume targeted) and Pressure Variable

o Pressure Controlled (pressure limited,
pressure targeted) and Volume
Variable
o Dual Controlled (volume targeted

(guaranteed) pressure limited)
• Cycling: How the ventilator switches from

inspiration to expiration: the flow has been
delivered to the volume or pressure target -
how long does it stay there?
o Time cycled - such in in pressure

controlled ventilation
o Flow cycled - such as in pressure

support Fig 1: Pressure triggering.
o Volume cycled - the ventilator cycles • Breaths are what causes the ventilator to cycle
to expiration once a set tidal volume from inspiration. Thet may be
has been delivered: this occurs in
volume controlled ventilation. If an o Mandatory (controlled) - which is
determined by the respiratory rate
inspiratory pause is added, then the
breath is both volume and time cycled o Assisted (as in assist control,
synchronized intermittent mandatory
• Triggering: What causes the ventilator to
ventilation, pressure support)
cycle to inspiration. Ventilators may be time
triggered, pressure triggered or flow triggered. o Spontaneous (no additional assistance
in inspiration, as in CPAP)
o Time: the ventilator cycles at a set
frequency as determined by the • Flow pattern: constant, accelerating,
controlled rate. decelerating or sinusoidal (Fig 2)
o Pressure: the ventilator senses the o Sinusoidal: this is the flow pattern
patient’s inspiratory effort by way of seen in spontaneous breathing and
a decrease in the baseline pressure. CPAP
(Fig1) o Decelerating: the flow pattern seen
o Flow: modern ventilators deliver in pressure targeted ventilation:
inspiration slows down as alveolar
a constant flow around the circuit
pressure increases (there is a high
throughout the respiratory cycle (flow-
initial flow). Most intensivists and
by). A deflection in this flow by patient
respiratory therapists use this pattern
inspiration, is monitored by the in volume targeted ventilation
ventilator and it delivers a breath. This also, as it results in a lower peak
mechanism requires less work by the airway pressure than constant
patient than pressure triggering. and accelerating flow, and better
distribution characteristics
o Constant: flow continues at a constant o Accelerating: flow increases
rate until the set tidal volume is progressively as the breath is
delivered delivered. This should not be used in
clinical practice.
Fig 2: Flow patterns
• Mode or Breath Pattern: There are only a few (Fig 4). The patient receives a breath of this type
different modes of ventilation irrespective of actual minute ventilation requirement.
The “interactive” element of this mode is merely
o CMV: Conventional controlled
that the patient receives a breath when they want
ventilation, without allowances
one, nothing else. The advantage of this mode is that
for spontaneous breathing. Many
patients can breathe spontaneously without working.
anesthesia ventilators operate in this
The patient is fully rested on the ventilator, except for
way
triggering, assuming that the peak flow is adequate.
o Assist-Control: Where assisted breaths The problem with this mode is that there is no weaning
are facsimiles of controlled breaths component, and patients tend to hyperventilate as they
emerge from sedation.
o Intermittent Mandatory Ventilation:
Which mixes controlled breaths and
spontaneous breaths. Breaths may
also be synchronized to prevent
“stacking”
o Pressure Support: Where the patient

has control over all aspects of his/her
breath except the pressure limit
o High Frequency Ventilation: Where

mean airway pressure is maintained
constant and hundreds of tiny breaths
are delivered per minute.
Volume Assist Control

In volume assist-control (often labelled “volume
control”), patients may receive either controlled or
assisted breaths (Fig 3). When the patient triggers Fig 3: Volume-assist control, the patient can receive
the ventilator, he/she receives a breath of identical controlled or assisted breaths – all identical
duration and magnitude as the mandatory breath

For the ventilator to interact with the patient, it must in against a valve), these had the problem of placing
sense that the patient is making a spontaneous effort an unnecessary workload on breathing and have been
– a trigger – and address this by delivering a breath. replaced with flow triggers (“flow by”): a continuous
The original triggers were negative pressure sensors (a flow of gas travels around the breathing system,
negative pressure is generated by the patient sucking inspiration deflects this flow and triggers the ventilator.

Fig 4: Breath pattern in volume assist control ventilation. Note the decelerating flow pattern with a peak flow
of 70 l/min, tidal volume of 700ml. Left panel - the patient is receiving controlled breaths at a rate of 12 per
minute. On the right the patient is receiving assisted breaths – can you discern the small downward deflection
of the patient triggering just prior to inspiration? In all breaths the tidal volume is identical.
(Synchronized) Intermittent Mandatory Ventilation

Intermittent mandatory ventilation was developed as
a method of partial ventilatory support to facilitate
liberation from mechanical ventilation. A demand valve
was placed in the breathing system, through which the
patient could take a spontaneous breath (the gas for this
breath is derived from a reservoir bag), without having
to breathe through the various valves and apparatus of
the ventilator. The patient could breathe spontaneously
while also receiving mandatory breaths (Fig 5, 6). As the
patient’s respiratory function improved, the number of
mandatory breaths was decreased, until the patient was
breathing unassisted on CPAP. In SIMV, if the patient
takes a spontaneous breath within the control breath
window, the two are synchronized (Fig 7, 8).
Fig 5: IMV controlled breaths

Fig 6: IMV spontaneous breaths Fig 7: Synchronized intermittant mandatory

ventilation
Fig 8: Breath pattern in SIMV
Unfortunately, there were two problems with this without assistance through an endotracheal
system tube and open a demand valve – a difficult
prospect with normal lungs, a serious burden
• It was possible for the patient and the
with an acute lung injury.
ventilator to inspire in series, thus “stacking”
one breath on top of another, leading to high The first problem was solved with the development
airway pressures of micro-processor technology: the ventilator was
fitted with a sensor that synchronized the patient’s
• The workload of spontaneous breaths remained
spontaneous breaths (up to the mandatory rate) in a
quite high –the patient still has to inspire
manner similar to assist-control. The problem of the In pressure support, the patient triggers the ventilator
excessive effort of the spontaneous efforts was solved and a pressure-limited breath is delivered: the patient
by introducing an assisted spontaneous breathing determines the rate, the duration of inspiration and
mode– “pressure support” ventilation. the tidal volume. The physician can determine how
much work the ventilator can take from the patient,
by altering the pressure limit (Fig 9).
Fig 9: SIMV plus Pressure Support plus CPAP. Note the two different types of breath: the characteristic flat
topped pressure limited breath (center) delivers a similar volume to the mandatory breaths, but in a shorter
time, as determined by the patient.
So when SIMV is used, the patient receives three higher in constant flow patterns rather than the other
different types of breath: two. This suggests that this pattern will cause more
shearing injury to the lung parenchyma. Therefore, a
• The controlled (Mandatory) breath
decelerating flow pattern is probably the most effective
• Assisted (synchronized) breaths flow pattern – it ensures peak flow early in inspiration,
while simultaneously minimizing flow during the phase
• Spontaneous breaths, which can be pressure of the inspiratory cycle in which the patient is least
supported. likely to need it.
Flow Patterns Peak Flow
Flow of gas is calculated in liters per minute. The normal The easiest rule of thumb to follow is that a patient
flow pattern of gas moving in and out of the lungs is requires a peak flow (PF) roughly four times that of the
sinusoidal. In volume control ventilation, a variety of minute ventilation (if the MV is 15 liters, the patient
different wave patterns can be used. In clinical practice, requires a PF of >60 liters). However, if the patient
constant and decelerating flow patterns are used; is breathing spontaneously, then bedside adjustment
the latter is preferred. In constant, decelerating and is required to ensure that flow matches patient
sinusoidal flow patterns, the inspiratory flow rate is efforts. The peak flow should be set slightly higher if a
equal to the peak flow rate, but the mean flow rate is

decelerating waveform pattern is being used, and, in means that stiff, noncompliant lung units (long time
particular, those with airflow obstruction. constants) which are difficult to aerate are more likely
to be inflated. Pressure control is also useful in patients
Pressure Controlled Ventilation
whose airway cannot be fully sealed – children, patient
Pressure control refers to the type of breath delivered, with bronchopleural fistulae etc
not the mode of ventilation. In pressure control, a
Patients can breathe spontaneously on pressure control
pressure limited breath is delivered at a set rate. The
as long the inspiratory time has not been unduly
tidal volume is determined by the preset pressure limit
prolonged. The trigger mechanism is the same as in
(Fig 10). This is a peak pressure rather than a plateau
volume control. The key advantage of pressure targeted
pressure limit (easier to measure). The flow waveform
ventilation is unlimited flow in inspiration to satisfy the
is always decelerating in pressure control: this relates to
patient’s demands. The harder the patient draws in, the
the mechanics of targeting airway pressure: flow slows
greater the pressure gradient, and the higher the flow.
as it reaches the pressure limit. Gas flows into the chest
along the pressure gradient. As the airway pressure rises Pressure control does not guarantee minute ventilation,
with increasing alveolar volume, the rate of flow drops and therefore requires more monitoring by the
off (as the pressure gradient narrows) until a point is operator. The minute ventilation is a complex mix
reached when the delivered pressure equals the airway of the peak pressure, the Ti, the lung and chest wall
pressure: flow stops. The pressure is maintained for the compliance, resistance in the airway and from other
duration of inspiration. The combination of decelerating thoracic structures. If there is a rapid change in the
flow and maintenance of airway pressure over time compliance, then the patient may hypoventilate and
become hypoxic.
Fig 10: Volume control vs pressure control ventilation in the same patient. Note that both modes achieve the
same tidal volume, but the peak pressure is considerably lower in pressure control

Advanced Pressure Control Modes • To protect the lungs against injury during
phasic opening an closing of atelectatic units.3
Inverse ratio ventilation
• To assist cardiac performance, during heart
One of the ways of improving oxygenation is to increase
failure, by increasing mean intrathoracic
the duration of inspiration. The longer the inspiratory
time (Ti), the better the oxygenation benefit. When the pressure.
inspiratory time is longer than the expiratory time, it What is the physiological rational in using PEEP ?
becomes inverse ratio ventilation. Even though inverse
ratio ventilation improves oxygenation, it tend to cause The Functional Residual Capacity (FRC) is the lung’s
CO2 retention. However, this is usually well tolerated physiologic oxygen reserve.. It is the lung volume at the
by most patients (Permissive hypercapnia). Patients end of a passive expiration. At this point, the tendency
on inverse ratio ventilation also need to be heavily for the lungs to collapse inwards is balanced by the
sedated or paralysed to suppress their spontaneous tendency for the chest to spring outwards.
respiratory efforts. This helps to achieve optimal patient
ventilator synchrony. However, abolishing spontaneous The functional residual capacity is determined by the
respiratory efforts and over use of muscle relaxants compliance of the lung and chest wall. Compliance is
is associated with the development of critical illness the rate of change of volume in response to pressure.
myopathy.1 Anything that reduces the outward mobility of the chest
wall reduces its compliance: examples of this are severe
Airway pressure release ventilation (APRV) obesity or constrictive bandages. Likewise, anything
This is a new method of enabling patients to breathe that reduces the volume of the lungs reduce their
spontaneously on inverse ratio ventilation. In compliance, examples of this are pulmonary edema,
conventional ventilation, the baseline airway pressure fibrosis, consolidation or increased intra-abdominal
is the PEEP or CPAP level, and ventilator cycling involves pressure. Loss of chest wall or lung compliance causes
application of positive pressure to a higher airway reduced FRC.
pressure level: the purpose of cycling is CO2 removal.
The idea of APRV is that the ventilator cycles between Exhalation below FRC cause dynamic airway collapse,
two different levels of CPAP – an upper pressure level trapping air in the alveoli. The closing volume (CV) is
and a lower level. The two levels are required to allow the point at which dynamic compression of the airways
gas move in and out of the lung. The key element of begins. The CV increases with age, smoking, lung
APRV is that the baseline airway pressure is the upper disease, and body position (supine>erect). When the
CPAP level, and the pressure is intermittently “released” closing volume is above the FRC, airway collapse occurs
to a lower level, thus eliminating waste gas. during tidal respiration. This will prevent cyclical gas
flow affecting alveolar ventilation. If cyclical gas flow
PEEP
stops, true airway collapse (atelectasis) will ensue: the
Although it is the most ubiquitous form of ventilatory contents of the alveoli will gradually be reabsorbed
support, positive end expiratory pressure (PEEP) (this is enhanced by the use of high FiO2 – absorption
remains a large area of confusion for most physicians. atelectasis).
For a start, the term PEEP is an anachronism, as
the positive pressure is actually applied throughout In pathological conditions, or where tidal volumes are
the respiratory cycle and is more correctly termed low or where the patient does not sigh or yawn, airways
“continuous positive airway pressure” (CPAP) may remain collapsed throughout the respiratory
cycle: this lead to a situation whereby lung units may
There are three purposes to using PEEP be ventilated but not perfused (low V/Q) – shunt and
• To prevent derecruitment, by returning the venous admixture.
functional residual capacity to the physiologic In effect: any condition that causes 1. A reduction in
range.2 lung volumes, FRC, chest wall compliance or, 2. An
increase in closing volume, will cause a reduction in completely deflated balloon: it’s really difficult to inflate
physiological oxygenation reserve, airway collapse initially, then you feel a give and the rest is easy to
and atelectasis. The most common culprit is the inflate. A more appropriate approach would be to let
endotracheal tube, which, by increasing the resistance the balloon (alveolus) deflate to just above the point
to both inspiration and expiration, reduces FRC and where inflation becomes easy (the lower inflection point
increases closing capacity. of the pressure-volume curve), then reinflation is much
less work. This is the concept behind PEEP (Fig 11). The
A collapsed airway is tremendously difficult to reinflate:
objective of using PEEP is to restore Functional Residual
leading to a huge increase in the work of breathing
capacity. It would be appropriate to apply a PEEP level
& oxygen consumption. It is like trying to inflate a
which is above the lower inflection point (4).
Fig 11: PEEP applied at the lower inflection point Prevents alveolar collapse
Excessive PEEP can cause three distinct problems: output. This may lead to a reduction in blood
pressure and pooling of blood in the abdomen
• Alveolar overdistention which could lead to
and peripheries. Conversely, in severe heart
barotrauma
failure, this may be beneficial.
• Excessively high alveolar pressures may
Initiating & Managing the Ventilator
compress the blood vessels which surround the
airspaces, causing an increase in dead space Mechanical ventilation affords patients four main
(wasted ventilation) benefits:
• Increased intrathoracic pressure as a result of • Applied work of breathing
PEEP/CPAP will reduce the pressure gradient • Improved oxygenation
along which blood returns to the heart. • Improved ventilation
This reduces right ventricular preload, right
• Airway ‘protection’ and improved toilet
ventricular output and ultimately cardiac
Initial ventilator setup should be tailored to the reason meet certain criteria, a trial of spontaneous breathing
that the patient needed to be intubated in the first (positive pressure flow mode or T-piece) is undertaken.
place. The parameters that require input are: If patients pass the trial, they are extubated. Patients
who do not pass the SBT will be reassessed to identify
• Mode
and treat any reversible factors and undergo daily SBTs
• Respiratory Rate (only for forms of intermittent
if they continue to meet the criteria.
mandatory ventilation)
• Tidal volume or inspiratory pressure depending Patients receiving mechanical ventilation for respiratory
on mode failure should undergo a formal assessment of
• FiO2 discontinuation potential if the following criteria are
• PEEP satisfied:
The choice of mode and settings for other parameters • Evidence of some reversal of the underlying
should be made with an eye towards correcting cause of respiratory failure
the underlying respiratory problem that resulted in • Adequate oxygenation: PaO2/ FIO2 - 150–200
intubation. Patients can worsen on a ventilator if the
required PEEP - 5–8 cm H2O, FIO2 -0.4–0.5,
interaction between them and the machine is not
and pH - 7.25
monitored. A feedback cycle should be established after
the patient has been intubated: • Hemodynamic stability as defined by the
absence of clinically important hypotension
Change a parameter→ Observe patient → Monitor
for data and requiring no vasopressors or only low-dose
vasopressors (eg, dopamine or dobutamine <
After intubation and initial ventilator settings are made, 5mcg/kg/min)
monitoring the patient includes observing for changes
in: • Patient is able to initiate an inspiratory effort.
• Vital Signs Patients who tolerate a 30–120 minutes SBT should

• SaO2 promptly be considered for ventilator-discontinuation.
• Mental status changes If the patient fails an SBT, determine the reasons the
• ABG patient continues to require ventilatory support. Once
the reversible causes of failure are corrected, an SBT
Depending on results, changes in ventilator settings
should be performed every 24 hours.
should be made.
Rapid shallow breathing index as reflected by frequency
Weaning
(breaths/minute)/VT (liters) is an accurate predictor
Mechanical ventilation is a life-sustaining therapy of weaning outcome. A threshold of less than 105, is
fraught with side effects. The successful removal of MV widely accepted for weaning a patient of the ventilator.
at any time is associated with a higher survival rate. The advantages of the f/VT ratio as a weaning predictor
Therefore, removing the patient from the ventilator as are that it is easy to measure and not dependent
soon as possible is in the patient’s best interest. The best on patient cooperation and effort. The f/VT ratio is
approach to weaning patients from MV involves a team evaluated while patients were breathing spontaneously
approach of all caregivers (physician, nurses, respiratory through an endotracheal tube. A bedside spirometer is
therapist, physical therapist and nutritionists). The used to measure VT. It is important to understand that
team uses a weaning protocol that gives the nurses
no index has proven to be ideal and highly predictive
and/or the respiratory therapist the authority to start
of weaning.
a daily screening of ventilated patients. If patients

Criteria Description
Adequate oxygenation (eg, PO2 >60 mm Hg on FIO2 >

Objective measurements
0.4; PEEP <5–10 cm H2O; PO2/FIO2 >150–300);
Stable cardiovascular system (eg, HR <140; stable BP; no

(or minimal) pressors)
Afebrile (temperature < 38°C)
No significant respiratory acidosis
Adequate hemoglobin (eg, Hgb >8–10 g/dL)
Adequate mentation (eg, arousable, GCS >13, no

continuous sedative infusions)
Stable metabolic status (eg, acceptable electrolytes)
Subjective clinical Resolution of disease acute phase; physician believes

assessments discontinuation possible; adequate cough
* Hgb = hemoglobin; HR = heart rate; GCS = Glasgow coma score.
Table 1 : Criteria for weaning
Troubleshooting Ventilator Alarms

Alarms alert the clinician of a potential hazard to the be treated immediately. The flow diagrams (Flowcharts
patient and should be given immediate attention. There 1 & 2) given below is a rough guide to the most likely
may be a problem with the patient or the ventilator. It cause of the problem and can be used to rectify the
has to be identified and the preventable cause should same in majority of the patients.

Distress on ventilator
Bag ventilate with 100% oxygen
Patient No relief
Comfortable
Airway
Obstruction
Yes No
Tube block
suction
tube Change Respiratory Cardiac Other
CNS Abdomen Posture

Collapse Monitor
Endobrochial tube BP, CVP, I/O
Pneumothorax
Diuretic
Nebulisation
Relief No relief
Cardiac ?Pneumonia
Failure
Flow chart 1
Ventilator
Alarms
Minute Respiratory
Pressure O2
Ventilation Rate
High Low High Low High Low High Low
s Leak s Secretions s Oxygen supply

s High Resp Rate s Low Resp Rate Failure
s Bronchospasm
s Increased Triggering s Increased Triggering s Leak s Neurogenic cause s Hypoventilation s O2 Sensor defect
s Endobronchial tube
s Alt Settings s Alt Settings s Ventilator Failure s Low set trigger s High set trigger
s Pulmonary Edema
s Low compliance s Alt Settings s Pain
s Pneumothorax
s Increased s Collapse
Resistance
Flow chart 2

Issues in the ventilatory management of the • Absorption atelectasis – as the FiO2 increases, the
critically ill alveoli that are well ventilated rapidly empty of
oxygen along the concentration gradient (into the
Ventilator Induced Lung Injury blood), their volume falls and they are vulnerable
to collapse.
Ventilator induced lung injury is caused by volutrauma
and excessive use of oxygen. It occurs when the lung It appears that FiO2 of greater than 50% should be
is directly damaged by the action of mechanical avoided provided the PaO2 is acceptable i.e. more than
ventilation. Macroscopic injuries associated with the 60 mmHg.
ventilation of patients with ARDS have been described
for decades: pneumothorax, pneumomediastinum, Recruitment maneuvers (RM)
pneumoperitoneum, associated with alveolar rupture Recruitment and derecruitment are terms used
from overdistension. The term historically applied to to describe the number of open /collapsed alveoli
this situation was “barotrauma”. This word expressed respectively. Lung alveolar derecruitment induced by
the tendency towards alveolar overdistension when the reduction in tidal volume is now well documented
high inspiratory pressures are applied. However, and represents the price of lung protective ventilatory
the paradigm has shifted somewhat in recent years strategies. Hence, recruitment maneuvers are used to
away from pressure induced to volume induced lung reinflate collapsed alveoli. A sustained pressure above
injury – “volutrauma”. This term recognizes that the tidal ventilation range is applied, and PEEP is used
alveolar overdistension is more likely to occur as a to prevent derecruitment. To optimize lung compliance
result of excessive volume, than excessive pressure. with modern low tidal volume ventilation strategies, the
If normal lungs are exposed to tidal volumes of 10-15 lung needs to be recruited and compliant. Many “sticky”
ml/kg, there is parenchymal inflammation, increased lung units will not reopen in the normal tidal volume
vascular permeability, accumulation of fluid in the lung and protective pressure range. Every time a patient
and alveolar space and atelectasis. However, there is disconnected from a ventilator, the lungs derecruit
is more to ventilator induced lung injury than just – whole segments of the lung will collapse, and will
overdistension. It is believed that the phasic opening not inflate with re-instatement of previous ventilator
and closing of lung units causes release of cytokines settings. A recruitment maneuver is then required.
and reinforcement and amplification of the local and
systemic inflammatory response.5 Limiting the extent Two factors influence whether or not recruitment
of volume expansion certainly curtails this, as does maneuvers are successful: the pressure applied must
the prevention of phasic opening and closing of lung be in excess of the current plateau pressure, and the
units – keeping the lungs open with PEEP. Undoubtedly, pressure must be sustained, in order to inflate lung
the best way to heal an injury is to rest it, and this is units with long time constants. The most effective
also true of the lungs. The less the lungs are forced method of doing this is to apply PEEP to the airway.
to expand-collapse, the less likely the chance of lung The best way to perform a recruitment maneuver
injury. The ultimate question therefore is – should we remains undetermined. One of the accepted procedure
initiate full tidal volume ventilation (i.e. the lungs are is to apply a PEEP of 40 cm H2O for a period of 40
not permitted to deflate at all). This can be achieved seconds. Following the period of sustained inflation,
using high frequency oscillation. the ventilation settings are returned to previous levels.
It is not necessary to increase the PEEP, as the lung
The other notable source of lung injury is, of course, volumes from the same amount of PEEP as before
oxygen. High FiO 2 can cause lung injury by two should be higher. This is explained by hysteresis (Fig
mechanisms: 12). A successful procedure will result in improved
• Formation of oxygen free radicals which are oxygenation, reduced end-tidal CO2 and improved
cytotoxic compliance. (Fig 13 A, B)

Fig 12: Hysteresis. For a given inflation pressure the lung volume is larger during exhalation than inspiration
A B
Fig 13 A: Lungs before recruitment maneuver Fig 13 B: Lungs after a successful recruitment
Role of spontaneous breathing unventilated lung units. Another possible mechanism

is the increase in cardiac output associated with the
Experimental data suggest that interfacing between
periodic decreases in intrathoracic pressure observed
spontaneous breathing and mechanical ventilation
during spontaneous breathing . This may support
is a critical determinant of the effects of ventilatory
the perfusion of nondependent high Va/Q and dead
support on Va/Q matching. It is postulated that during
space regions. In contrast, full ventilatory support in
spontaneous breathing, the diaphragmatic contractions
anesthetized and paralyzed patients has been shown
augments distribution of ventilation to dependent well
to promote formation of atelectasis in dependent
perfused regions of the lungs. 6 In contrast mechanical
lung regions, which considerably contributes to Va/Q
breaths increase ventilation in already well ventilated
mismatch and intrapulmonary shunting.
and poorly perfused lung areas. Spontaneous breathing
also decreases intrapulmonary shunting. This is because Positive-pressure ventilation can also affect systemic
spontaneous breathing completely recruits previously hemodynamics and regional blood flow distribution,

with potentially deleterious effects on organ function. neuromuscular blocking agents 1. Nerve, muscle
The kidney and the gut are two such areas which are and neuromuscular junction (NMJ) abnormalities
prone for hypoperfusion and hypoxia in the critically may affect over 90% of patients ventilated for more
ill. Studies have shown better intestinal blood flows, than seven days. The majority of patients develop
especially in the mucosal and submucosal regions when a polyneuromyopathy, with either neuropathy or
spontaneous breathing is preserved.7 Renal blood flow myopathy predominating, depending on the individual
and GFR is also shown to be higher when spontaneous case. This may be unpredictable. It seems feasible that a
breathing is preserved.8 neuropathy will lead to disuse and hence to a myopathy,
and that an acute myopathy will lead to conditions
Patient-Ventilator Dysynchrony
in which a neuropathy progresses. Hence, except
Dysynchrony is a term used to describe the common in certain cases (outlined below) it is impossible to
observation of a patient “fighting” the ventilator. The pinpoint the initial pathology. Neuromuscular blocking
basic mechanism of patient-ventilator asynchrony agents (NMBA) are the drugs most often implicated in
is the mismatching between neural inspiratory the development of myopathy. The worst offender is
and mechanical inspiratory time. Alterations in vecuronium, presumably as a result of accumulation
respiratory drive, timing, respiratory muscle pressure of its active metabolites (risk factors being renal
and respiratory system mechanics influence the failure, acidosis, elevated magnesium concentration
interaction between the patient and the ventilator. and female sex), but others, such as atracurium, have
If the patient is undersedated and is uncomfortable been implicated. Aminoglycosides prolong the effect
with the endotracheal tube, dysynchrony may occur. of NMBAs, and therefore have been implicated in
In the majority of cases, failure to synchronize is due the development of myopathy in conjunction with
to inadequate flow delivery from the ventilator. If NMBAs. Corticosteroid excess, such as in Cushings
the flow of gas is inadequate, the patient increases syndrome, cause a proximal myopathy in their own
negative inspiratory attempts to increase tidal volume. right, and, in conjunction with critical illness and the
As these attempts are ineffective, there will be gross drugs mentioned above increase the incidence of acute
derangements in arterial blood gases. This occurs in necrotising myopathy.
volume control modes. In pressure control, flow is
Simple preventative measures that can be undertaken
unlimited – the reason is that flow is related to the
include
pressure gradient between the upper and lower airway
– a deeper attempted inspiration makes the pressure • Avoiding high doses of corticosteroids, use
in the alveoli more negative in relation to the upper of the lowest effective dose required, and to
airway (this is true also in normal individuals), and the wean them as quickly as possible
pressure gradient is larger – and the flow greater.
• Using muscle relaxants sparingly in the ICU
Critical illness polyneuropathy / myopathy and when required, to use it as intermittent
boluses. This has been shown to limit the total
Neuromuscular weakness commonly develops in the
dose
setting of critical illness. This weakness delays recovery
and often causes prolonged ventilator dependence. An • Metabolic factors: Hypophosphataemia and
axonal sensory-motor polyneuropathy, critical illness hyperglycaemia are associated with muscle
polyneuropathy (CIP), is seen in up to one third of weakness and should be avoided. It seems
critically ill patients with the systemic inflammatory prudent to correct all other electrolyte
response syndrome (usually due to sepsis). An acute abnormalities.
myopathy, critical illness myopathy (CIM), frequently
There is no specific treatment for any of these disorders,
develops in a similar setting, often in association with
and management should address correcting the
the use of corticosteroids and/or nondepolarizing
factors above, along with physiotherapy, psychological

support and aggressive nutritional support. A recent ventilation a contributing factor? Am J Respir
study showed that strict glycemic control (80 – 110 Crit Care Med 1998 157. 1721–1725.
mg/dl) decreased the incidence of neuropathy by 46%
6 Putensen C, Mutz NJ, Putensen-Himmer G,
in critically patients (9).
Zinserling J. Spontaneous breathing during
References ventilatory support improves ventilation-
perfusion distributions in patients with acute
1 Hund E. Myopathy in critically ill patients.
respiratory distress syndrome. Am J Respir
Crit Care Med. 1999 Nov;27(11):2544-7.
Crit Care Med. 1999 ; 159 (4 Pt 1):1241-8.
2 Halter JM, Steinberg JM. Positive end-
7 Hering R, Viehofer A, Zinserling J, Wrigge H,
expiratory pressure after a recruitment
Kreyer S, Berg A, Minor T, Putensen C.: Effects of
maneuver prevents both alveolar collapse and
spontaneous breathing during airway pressure
recruitment/derecruitment. Am J Respir Crit
release ventilation on intestinal blood flow in
Care Med. 2003 Jun 15;167(12):1620-6.
experimental lung injury. Anesthesiology. 2003
3 Muscedere JG, Mullen JB, Gan K, et al: Nov;99 (5):1137-44
Tidal ventilation at low airway pressures can
8 Hering R, Peters D, Zinserling J, Wrigge H, von Spiegel
augment lung injury. Am J Respir Crit Care
T, Putensen C: Effects of spontaneous breathing
Med 1994 149:1327–1334.
during airway pressure release ventilation on renal
4 Björn Jonson, Jordi Mancebo Laurent Brochard perfusion and function in patients with acute lung
et al: Pressure–Volume curves andcompliance in injury. Intensive Care Med. 2002 Oct;28(10):1426-
acute lung injury evidence of recruitment above 33.
the Lower Inflection Point Am J Respir Crit Care
9 Van den Berghe G, Wouters P, Weekers F et al :
Med 1999;159:1172–1178.
Intensive insulin therapy in the critically ill patients.
5 Arthur S. Slutsky , Lorraine N. Tremblay N Engl J Med. 2001 Nov 8; 345 (19):1359-67.
Multiple System Organ Failure. Is mechanical

MCQ
1. Cycling in pressure support ventilation is done 4. The mode of ventilation which enables the
by patient to breath spondaneously on inverse
ratio ventilation is
a. Time
b. Flow a. APRV
c. Pressure b. PCV
d. Volume c. VCV
2. The flow pattern that is associated with low d. IMV

peak airway pressure and better V/Q is 5. Excessive PEEP can result in
a. Accelerating a. Barotrauma
b. Decelerating b. Increase in Dead space
c. Constant c. Reduction in preload
d. Sinusoidal d. All of the above
3. RSBI of less than -------is widely accepted as
better predictor of weaning
a. 20
b. 30
c. 50
d. 105
5. (d) 4. (a) 3. (d) 1. (b) 2. (b)

Answers

14 Morbidly Obese Parturient :
Challenges for the anesthesiologist. What is new?
Professor of Anesthesiology, Bhavani Shankar Kodali

Chief of Obstetric Anesthesiology,
Chief Safety Officer, Anesthesiology
Assistant Director, Maryland Anesthesiology Simulation Program
Baltimore, USA
Key points
Ø Obesity can have negative effects on pregnancy course and outcomes, including increased rates of
pregnancy-induced hypertension, gestation diabetes, cesarean delivery, hemorrhage, fetal macrosomia,
preterm birth and stillbirth.
Ø The most clinically significant ventilator effects include decreases in functional residual capacity (FRC),
residual volume (RV) and expiratory reserve volume (ERV).
Ø Neuraxial analgesia represents the most effective option for pain control and is of particular benefit in
obese patients.
Ø Epidural catheter placements in morbidly obese parturient require more attempts, take more time,
are less likely to result in adequate analgesia for delivery and more likely to fail outright and require
replacement.
Ø A double neuraxial catheter technique has been described in which a lumbar spinal catheter and
thoracic epidural catheter are placed for intraoperative and postoperative anesthesia in case of supra-
umblical midline incision in supermorbid obese.
Ø The incidence of difficult laryngoscopy in the obstetric population has been reported to be greater than
8%.
Ø In obese parturients, NC/TMD may have the best combined sensitivity and specificity for identifying
difficult laryngoscopy.
Ø Risk of aspiration exists during both induction and emergence of general anesthesia, necessitating rapid
sequence induction and careful emergence and extubation at the end of the procedure.
What is New? Rates of obesity have been increasing exponentially

for the past several decades, with an estimated 1.46
Morbidly obese pregnant women have become a billion overweight and 602 million obese adults
common encounter in our practice worldwide. In the United States, approximately 36% of
We have become better in managing them for labor adults are overweight or obese, and this prevalence is
and delivery higher among women. Depending on the population
Morbidity and mortality are decreasing and hence they studied, there is an approximately 20% incidence of
keep coming with more weight obesity in pregnancy. The management of morbidly
Management requires understanding of pathophysiology obese women during pregnancy presents a challenge
of morbidly pregnant women
Morbidly Obese Parturient : Challenges for the 150 Bhavani Shankar Kodali
anesthesiologist. What is new?
to obstetric and anesthesia providers alike. This is and therefore, both increase overall demand on the
mainly due to frequently co-morbid disease states cardiovascular system. Heart rate, stroke volume,
including hypertension, diabetes, cardiovascular and cardiac output and blood volume increase with both
thromboembolic disease. However, obesity itself obesity and pregnancy. Cardiac output (CO) is increased
can have negative effects on pregnancy course and 30-50 ml/min for each additional 100g of adipose tissue.
outcomes, including increased rates of pregnancy- Pregnancy further increases CO up to 50%. Endothelial
induced hypertension, gestation diabetes, cesarean dysfunction which accompanies obesity as a result of
delivery, hemorrhage, fetal macrosomia, preterm birth, higher levels of leptin, insulin and other inflammatory
and stillbirth. mediators predisposes obese patients to hypertension
The World Health Organization classifies obesity as a result of increased systemic vascular resistance
according to body mass index (BMI) which is defined (SVR). Pregnancy, on the other hand, tends to decrease
as weight in kilograms divided by the square of height SVR, and these changes may offset. Pulmonary vascular
in meters. Overweight is defined as BMI greater than resistance (PVR) and pulmonary artery pressure (PAP)
or equal to 25, with obesity further categorized into are also increased as a result of obesity due to potential
three categories – class 1 (BMI 30-34.9 kg/m2), class left ventricular hypertrophy and dysfunction, increased
2 (BMI 35-39.9 kg/m2), and class 3 (BMI > 40 kg/m2). pulmonary blood flow, and sleep apnea with resulting
chronic hypoxia. While pregnancy itself does not affect
Physiologic Changes of Obesity and Pregnancy
systolic or diastolic function, obesity can impair both,
Cardiovascular changes leading to heart failure and other sequelae. Table 1
summarizes the physiologic effects seen in obesity and
Both obesity and pregnancy increase the amount of
pregnancy as well as the anticipated combined effects.
tissue requiring perfusion as well as oxygen demand;
Pregnancy Obesity Combined

Heart rate ↑ ↑↑ ↑↑
Stroke volume ↑↑ ↑ ↑
Cardiac output ↑↑ ↑↑ ↑↑↑
Systemic vascular ↓↓ ↑ or ↓
resistance
Mean arterial pressure ↑ ↑↑ ↑↑
Systolic function ↔ ↔ or ↓ ↔ or ↓
Diastolic function ↔ ↓ ↓
Central venous pres- ↔ ↑ ↑↑
sure
Pulmonary wedge ↔ ↑↑ ↑↑
pressure
Table 1: Physiologic Changes of the Cardiovascular System Associated with Pregnancy and Obesity

Respiratory changes both pregnancy and obesity result in restrictive type

ventilator patterns. Oxygenation can be impaired
The respiratory system is considerably affected by
by both obesity and pregnancy if the FRC falls below
both obesity and pregnancy. The most clinically
the closing capacity (CC), resulting in shunting and
significant ventilator effects include decreases in
ventilation/perfusion mismatching. Both pregnant
functional residual capacity (FRC), residual volume
and obese patients also tend to have lower baseline
(RV) and expiratory reserve volume (ERV) as a result
arterial oxygen partial pressures (PaO2), with this change
of cephalad diaphragm movement due to the gravid
amplified in morbidly obese parturients. Finally, both
uterus in pregnancy and abdominal and chest wall
pregnancy and obesity can be associated with difficult
adiposity seen in obesity. These changes combined
airways as a result of capillary engorgement with
with increased oxygen consumption also seen in both
mucosal edema or soft tissue adiposity respectively.
pregnancy and obesity lead to rapid desaturation during
These airway changes can lead to the development of
apneic episodes. Tidal volume and minute ventilation
obstructive sleep apnea in both populations. For a full
increase during pregnancy as a result of progesterone’s
list of the physiology effects of obesity and pregnancy
effects on the medullary respiratory centers. Overall,
on the respiratory system, see Table 2.
Pregnancy Obesity Combined

Tidal volume ↑ ↓ ↑
Respiratory rate ↑ ↔ or ↑ ↑
Minute volume ↑ ↓ or ↔ ↑
Expiratory reserve ↓ ↓↓ ↓
volume
Residual volume ↓ ↓ or ↔ ↓
Functional residual ↓↓ ↓↓↓ ↓↓
capacity
Total lung capacity ↓ ↓↓ ↓
Compliance ↔ ↓↓ ↓
V/Q mismatch ↑ ↑ ↑↑
Table 2: Physiologic Changes of the Respiratory System Associated with Pregnancy and Obesity

Gastrointestinal changes disease, congestive heart failure, stroke, pulmonary

embolism, asthma, gallbladder disease, chronic back
Both obesity and pregnancy result in increased
pain, depression and gastroesophageal reflux disease.
intraabdominal pressure, decreased gastrointestinal
A comorbidity with particular influence on anesthetic
motility and decreased lower esophageal sphincter
management is obstructive sleep apnea (OSA). OSA is
tone, putting morbidly obese parturients at greater
more common in obese patients in general; however
risk of pulmonary aspiration of gastric contents.
the definition of OSA in pregnancy is not widely agreed
Changes in gastric volume and gastric pH associated
upon and so the exact prevalence is unknown. Changes
with obesity and pregnancy are less clear, with some
associated with pregnancy and labor have varying
studies showing higher volumes of more acidic fluid
effects on the physiology of OSA, with weight gain and
while others show no difference. Co-morbid diabetes is
airway swelling potentially worsening symptoms while
frequently diagnosed in this patient population, which
increased minute ventilation and side-sleeping may be
is also associated with delayed gastric emptying.
protective.
Endocrine changes
Fetal Morbidity & Mortality
Diabetes mellitus and gestational diabetes are both
Maternal obesity also has implications for fetal
more common among obese parturients compared to
morbidity and mortality. Fetuses born to morbidly
those of normal weight. This most likely results from
obese mothers have higher odds of fetal macrosomia,
increased levels of inflammatory mediators which
with ORs 1.9 and 2.4 for birth weight greater than 4000g
results in insulin resistance and hyperglycemia.
and 4500g respectively. This higher incidence of fetal
Hematologic Changes macrosomia also increases the risk of shoulder dystocia
in the delivery of these infants. Furthermore, the odds
Both pregnancy and obesity are independently of poor obstetric outcomes for the fetus are greater,
associated with hypercoagulability, venous stasis, including higher incidence of large for gestational
and endothelial injury and together they combine to age, fetal distress, meconium aspiration, intrauterine
dramatically increase risk of venous thromboembolic fetal demise and early neonatal death. Congenital
events. Obesity increases the levels of plasminogen malformations such as neural tube defects and cardiac
activator inhibitor-1 which prevents fibrinolysis, leptin anomalies are also more frequent in these infants.
which encourages platelet aggregation, interleukin-6
which increases the production of coagulation factors Labor & Vaginal Delivery
by the liver and C-reactive protein which activates
Impact on Labor Progress
platelets. Venous stasis results from increased
intraabdominal pressure caused by both the gravid The progress of normal labor seems to be related to a
uterus as well as abdominal adiposity. patient’s BMI. Morbidly obese parturients experience
slower centimeter by centimeter labor progress
Morbidity & Mortality
with resultant longer latent and active phases of
Maternal Comorbidities associated with obesity and labor as well as higher chance of cesarean delivery
pregnancy performed for abnormal labor. A large multicenter
trial conducted in the United States showed that
Obesity is associated with a number of comorbidities morbidly obese nulliparous women took more than
which can complicate the care of the parturient. The two hours longer to progress from 4cm to 10cm
relative risk of diabetes mellitus type II in obese women dilation while multiparous women took approximately
is 12 times that of controls of normal BMI and waist one hour longer. These same results of slower labor
circumference. Obesity is additionally associated with progress were demonstrated for both spontaneous and
increased incidence of hypertension, coronary artery
induced labor. This may be due to higher incidence of imaging in the obese population may not be able to
fetal macrosomia in obese mothers, higher rates of identify depth to the epidural space because of lack
induction, and/or dysfunctional uterine contractility of ultrasound penetration, the midline can often be
or poor myometrial response to oxytocin. Zhang et al. identified which can provide some useful information.
{Zhang, 2007} showed that the myometrium of obese The sitting position is preferred by many practitioners
parturients at the time of cesarean delivery contracted for neuraxial placement in obese women because
with less force and frequency and demonstrated less of improved identification of midline and shorter
calcium flux when compared to control women of distance from skin to epidural space in this position.
normal BMI. Thus obese parturients have a significantly After successful placement of an epidural, patients
increased risk of cesarean delivery, driven primarily by should subsequently be repositioned in the lateral
failed or obstructed labor. In an attempt to quantify this position before securing the catheter. This is because
increased risk of cesarean delivery among overweight redistribution of subcutaneous adipose tissue in the
and obese women, Chu et al. conducted a meta-analysis back may lead to an increased distance from skin to
of 33 studies in which they found unadjusted OR of epidural space and thus dislodgement of the catheter
cesarean delivery of 1.46 (1.34-1.60), 2.05 (1.86-2.27), from the epidural space. If unsecured at the skin, the
and 2.89 (2.28-3.79) among overweight, obese and catheter can instead be drawn in from the outside,
morbidly obese patients respectively. Another study preserving the depth residing within the epidural space.
looking at greater than 16,000 patients found that the
Because of these many anatomical and positioning
rate of cesarean delivery in nulliparous women was
challenges associated with maternal obesity, epidural
47.4% versus 20.7% in those with a BMI less than 30.
catheter placements on average require more attempts,
The odds ratio of having an operative vaginal delivery
take more time, are less likely to result in adequate
was also higher among morbidity obese patients
analgesia for delivery, and more likely to fail outright
compared to controls, with an OR 1.7 (1.2-2.2).
and require replacement. Although data is conflicting,
Anesthetic Management inadvertent dural puncture may be more common in
obese patients as a result of these technical difficulties.
Neuraxial analgesia represents the most effective
Whether or not adjustments should be made to
option for pain control and is of particular benefit in
epidural dosing in morbidly obese patients remains
obese patients given the higher rates of macrosomia,
unclear; although, data suggests that higher weight and
shoulder dystocia, operative vaginal delivery, and
BMI are likely associated with greater cephalad extent
cesarean delivery (which may be emergent). A positive
of neural blockade. Finally, the decision of whether to
correlation between BMI and the severity of labor pain
utilize standard epidural or combined spinal-epidural
has also been demonstrated. Technical challenges
(CSE) technique for labor analgesia in obese parturients
associated with neuraxial placement in this population,
is practitioner-dependent. The primary goal of goals of
however, are numerous. These challenges include
neuraxial anesthesia in morbidly obese parturients are
adipose tissue obscuring palpation of spinous processes
to provide patient comfort but also to ensure a properly
and intervertebral spaces, greater depth of the epidural
functioning catheter in the high likelihood (compared
space which exaggerates needle inaccuracies and
to lean patients) that operative vaginal or cesarean
presence of fat pockets which may cause false loss
delivery are necessary. Avoidance of general anesthesia
of resistance. Useful techniques to help mitigate
in this patient population is of utmost importance
these challenges may include use of visible anatomic
because of the higher chance of encountering a difficult
landmarks including the seventh cervical vertebrae
airway. Both the epidural and CSE techniques offer
and gluteal cleft, elicitation of patient feedback on
advantages and disadvantages in this respect. The
perceived needle position, as well as ultrasound
CSE technique indirectly confirms correct positioning
imaging prior to neuraxial placement. While ultrasound
of the epidural needle and may be associated with
higher initial success rates and decreased need for certainly possible, but identifying the epidural space
catheter replacement. On the other hand, the epidural with a larger-gauge epidural needle may be technically
catheter inserted with a CSE technique is unable to be easier, which can be followed with a needle-through-
tested for reliability until the spinal anesthetic wears needle technique for intrathecal (IT) injection. Also,
off. For this reason, some practitioners prefer standard CSE offers the advantage of extending the time frame
epidural technique so that a solid and bilateral epidural of anesthesia should the duration of surgery be
anesthetic level can be confirmed from the outset. As prolonged, which is commonly the case with morbidly
previously mentioned, this standard epidural technique obese parturients. The ability to prolong blockade
may be associated with higher catheter failure rate. can help to avoid the need to convert to general
anesthesia and manipulate the airway, which as has
Cesarean Delivery
been stated previously is more likely to pose difficulty
Operative Variables with intubation. In patients with super-morbid obesity
(BMI > 50 kg/m2), occasionally a supra-umbilical vertical
Many operative variables can be affected by a midline incision is required due to the large abdominal
parturient’s BMI including operative time, blood loss pannus. In these cases, a double neuraxial catheter
and the need for uterotonics. Hood et al. showed technique has been described in which a lumbar
that cesarean delivery operative times for morbidly spinal catheter and thoracic epidural catheter are
obese patients, which they defined as those weighing placed for intraoperative and postoperative anesthesia
greater than 300 lbs, and controls were 76.7 ± 31.2 respectively. The spinal catheter offers the advantage
and 47.1 ± 14.4 min, respectively. Similarly increased of reliable re-dosing compared to the epidural placed
operative times were demonstrated by Perlow et al., as part of a CSE technique, which remains untested
who reported that 48.8% of morbidly obese women until intraoperatively.
had an operative time >60 minutes, compared to 9.3%
of controls. In this same study, 34.9% of morbidly Deciding on the dose of local anesthetic for intrathecal(IT)
obese women had and estimated blood loss of >1000 or epidural administration in the morbidly obese
ml during their cesarean delivery, while only 9.3% of parturient can be challenging. On one hand, there
controls surpassed this cut off. In a related finding, is data to suggest that morbidly obese patients have
morbidly obese women are also more likely to require decreased CSF volume, which is associated with greater
administration of uterotonics following delivery. cephalad extent of neural blockade for any given IT
dose. On the other hand, erring too low on the local
Anesthetic Management anesthetic dose may increase the risk of inadequate
Regional Anesthesia block and need for conversion to general anesthesia if
a single-shot technique is used. Furthermore, despite
In the obese parturient, regional anesthesia is preferred the proven concept of CSF volume effecting cephalad
over general anesthesia for cesarean delivery. If a spread, dose-finding studies in the obstetric population
labor epidural is in situ, the catheter can be used for have failed to demonstrate differences in ED50 or ED95
conversion to surgical anesthesia. If cesarean delivery of local anesthetics for cesarean delivery in morbidly
is elective, or if a parturient has no epidural or a poorly obese versus nonobese patients. Data regarding extent
functioning catheter, both spinal anesthesia and of cephalad blockade with epidural dosing is also
CSE are options in the morbidly obese population. conflicting; however, this is less of an issue as epidural
CSE, however, may be advantageous for multiple local anesthetic can be titrated to effect.
reasons. Depending on the distribution of adipose
tissue and specifically the degree of adiposity at the Neuraxial morphine with or without the additional of a
site of neuraxial placement, longer needles may be lipid soluble opioid (ex. fentanyl) is typically administered
required. Spinal placement using a longer needle is in addition to the local anesthetic for cesarean delivery.

Dosing regimens are usually not adjusted for BMI; Airway manipulation for cesarean delivery is further
however, carefully postoperative monitoring for complicated by higher risk of aspiration in the obstetric
respiratory depression is particularly important in and obese populations. Aspiration prophylaxis is
the morbidly obese patient (see “Postoperative Care” recommended to mitigate this risk. Both non-particulate
section). antacids and H2 receptor blockers have been shown to
increase gastric pH, while metoclopramide significantly
General Anesthesia decreases both nausea and vomiting when compared to
When general anesthesia is required, a thorough airway placebo. However, due to the extremely low incidence
assessment is of utmost importance, as the incidence of aspiration events, none of these medications have
of difficult laryngoscopy in the obstetric population has data to support improved patient outcomes. Risk of
been reported to be greater than 8%, with a reported aspiration exists during both induction and emergence
incidence of 1 in 390 for failed intubations. Multiple of general anesthesia, necessitating rapid sequence
aspects of obesity and pregnancy, including airway induction (unless difficult airway is anticipated) and
edema, enlarged breasts, greater anteroposterior chest careful emergence and extubation at the end of the
diameter, and larger neck circumference, make difficult procedure.
airway more likely and difficult intubation is significantly Induction of general anesthesia should be preceded
associated with greater BMI. One study reported an by adequate denitrogenation (“preoxygenation”) as
incidence for difficult intubation as high as 33% in both pregnancy and obesity predispose to rapid oxygen
women weighing greater than 300 lbs. Predictors desaturation and hypoxemia. There is evidence to
of difficult intubation which have been evaluated in suggest that both eight deep breaths over 1 minute
obstetric populations include modified Mallampati (8DB) and tidal volume breathing for 3 minutes are
score (MMT), upper lip bite test, thyromental distance, equally effective in achieving ETO2 > 90%, with the 8DB
ratio of height to thyromental distance (RHTMD), method having the advantage of ability to perform
sternomental distance, mandible protrusion, neck more quickly in emergent situations. Unless difficult
circumference and ratio of neck circumference to intubation is anticipated, rapid sequence induction is
thyromental distance (NC/TMD). Savva et al. found indicated in pregnant patients undergoing cesarean
that the MMT alone was neither sensitive nor specific delivery. A combination of hypnotic and neuromuscular
in predicting difficult intubation. While Honarmand et blocker is typically administered for induction. Dosing of
al. found RHTMD to have the highest sensitivity, positive propofol (2-2.5 mg/kg) or thiopental (4-5 mg/kg) should
predictive value and negative predictive value compared be based on lean body weight (difference between
to other variables tested. In obese parturients, however, total body weight and fat mass). Succinylcholine (1-
NC/TMD may have the best combined sensitivity 1.5 mg/kg) is the neuromuscular blocker of choice in
and specificity for identifying difficult laryngoscopy. obese parturients, with dosing based on total body
Positioning on the operating room table can be utilized weight. If rocuronium (1.2 mg/kg) is chosen for rapid
to optimize laryngoscopic view, with a ramped position sequence intubation, the dose should be based on
providing best alignment of the oral, pharyngeal and ideal body weight, and sugammadex (16 mg/kg) should
tracheal axes. While retraction of a large panniculus be immediately available to reverse the NMB should
may be necessary for surgical exposure, placement of unanticipated difficult airway arise. Specifically in
these retractors should be used with caution, especially the case of the morbidly obese parturient, additional
prior to intubation, as cephalad retraction of adiposity airway equipment including video laryngoscope,
may hinder laryngoscopy and can also be associated fiberoptic scope, various endotracheal tube sizes and
with hypotension, ventilation difficulties and fetal supraglottic airway devices, should be available in case
compromise. of emergency.

Maintenance of anesthesia is usually accomplished morphine as part of their anesthetic. Although

with volatile agent or propofol infusion with or without there is some data to suggest that respiratory
nitrous oxide. While pregnancy is associated with depression following IT morphine administration
decreased minimum alveolar concentration (MAC), occurs more commonly in morbidly obese patients,
obesity does not affect MAC any further. Desflurane the incidence is still remarkably low. In women who
or sevoflurance may be the preferred volatile agents receive general anesthesia, parenteral opioids are
in obesity as they are less lipid soluble, and therefore commonly required postoperatively, and are usually
are associated with quicker times to extubation at the administered via patient-controlled analgesia (PCA).
end of the case. Functional residual capacity (FRC) is Minimizing opioids in order to mitigate the risk of
decreased by both pregnancy and obesity, and these respiratory depression can typically be achieved
patients may require higher positive end-expiratory by use of multimodal analgesic regimens, which
pressure and frequent recruitment maneuvers to can include nonsteroidal anti-inflammatory drugs,
prevent atelectasis and hypoxemia. At the end of the acetaminophen, gabapentin, local wound infiltration,
procedure, complete neuromuscular blockade reversal and transversus abdominis plane (TAP) blocks. In
should be confirmed and the patient should be fully the general obstetric population, TAP blocks are
awake prior to extubation. Obese parturients are at not effective at reducing pain scores or opioid
greater risk of airway obstruction following extubation, consumption when combined with IT morphine;
and careful monitoring of oxygen saturations should be however, they may be beneficial in patients who
continued into the postoperative period. did not receive neuraxial opioids. The performance
of TAP blocks may be challenging or impossible in
Postoperative Care
patients with excess abdominal adiposity.
Women who undergo cesarean delivery under
regional anesthesia typically receive neuraxial

MCQ
1. Technical challenges associated with neuraxial 3. What are the most clinically significant ven-
placement in this population: tilator effects include decreases in functional
residual capacity (FRC), residual volume (RV)
a. adipose tissue obscuring palpation of
and expiratory reserve volume (ERV) as a
spinous processes
result of
b. intervertebral spaces
a. Cephalad diaphragm movement and
c. greater depth of the epidural space
abdominal, chest wall adiposity seen
which exaggerates needle inaccuracies
in obesity
d. presence of fat pockets which may
b. Large abdomen
cause false loss of resistance
c. Closing capacity more than FRC
e. All of the above
d. Increased adipose tissue deposition
2. Morbid obesity BMI of:
4. 4. Incidence of failed intubation in obstetric
a. 20-25 population
b. >40
a. I in 1380
c. >50
b. 1 in 390
d. 30-34.9
c. 1 in 570
d. 3 in 390
4 (B) 3 (A) 2 (B) 1 (E)

Answers

15 Principles and Protocols of
Enhanced Recovery after Major Surgery (ERAS)
Chairperson, Jayashree Sood

Department of Anaesthesiology, Pain & Perioperative Medicine,
Sir Ganga Ram Hospital, New Delhi
Key points
Ø The aim of ERAS protocols is to reduce the surgical stress and improve the patient’s metabolic milieu
Ø The key principles of the ERAS protocol include preoperative counselling, preoperative nutrition,
avoidance of preoperative fasting and carbohydrate loading and preoperative standardised anaesthetic
regime and early mobilization
Ø Providing carbohydrate loading prior to surgery decreases preoperative thirst, hunger and patient
anxiety.
Ø Abstinence of smoking or alcohol for atleast 1 month decreases the incidence of pulmonary and wound
complications and improves organ function.
Ø Prophylaxis with intravenous antibiotics covering both aerobic and anaerobic bacteria should be
administered 30-60 minutes before incision.
Ø Fluid therapy needs to be balanced to avoid both hypovolemia and hypervolemia.
Ø Postoperative enteral feeding should be encouraged as early as possible, while use of intravenous fluids
should be minimised.
Ø Routine use of nasogastric tube is discouraged and it should be removed prior to end of anaesthesia.
Ø Postoperative analgesia is managed used a multimodal approach with minimal use of systemic opioids.
Ø Early mobilisation of patient after surgery may prevent chest infection and insulin resistance, improve
muscle strength and decrease the incidence of DVT.
Introduction
A protocolized approach to patient care decreases the recovery. Implementation at an institute level needs
complication rate and enhances recovery. Enhanced the constitution of a multi-disciplinary team with
recovery after surgery (ERAS) protocols or “fast-track” representatives from all specialities involved in patient
surgery programme is an amalgam of multimodal care. ERAS- guidelines were initially developed by
patient care pathways applied to care of surgical Henrik Kehlet in the 1990’s for improving patient
patient in the perioperative period. The aim of ERAS outcome after colorectal surgery, but currently these
protocols is to reduce the surgical stress and improve guidelines have been extended and developed for
the patient’s metabolic milieu, so as to expedite the biliary- pancreatic surgery, gastric resection, radical
patient to his preoperative functional status. The cystectomy, pelvic surgery, onco-gynaecology surgery
aim of ERAS is to reduce the surgical impact on the and oesophagectomy. The key components of ERAS
metabolic and endocrine response leading to early protocols can be divided into the preoperative,
intraoperative and postoperative period.

Principles and Protocols of 160 Jayashree Sood
The key principles of the ERAS protocol include: • Preoperative standardised anaesthetic regime
and analgesic regime (epidural and non opioid
• Preoperative counselling
analgesia)
• Preoperative nutrition
• Avoidance of preoperative fasting and • Early mobilization
carbohydrate loading upto 2 hours
Key Components
Preoperative Intraoperative Postoperative
• Preadmission information, • Standard anaesthesia • Postoperative analgesia

education and counselling protocol • Postoperative nutrition
• Preoperative optimization • Fluid management • Glucose control
• No Bowel preparation and haemodynamic
• Urinary drainage
monitoring
• No prolonged fasting • Prevention of Ileus
• Prevention of PONV
• Minimal preanaesthetic • Early mobilisation
medication • Avoid nasogastric
intubation • Audit
• Antimicrobial prophylaxis
and skin preparation • Preventing hypothermia
• Avoid drainage of
peritoneal cavity
• Surgical technique -
laparoscopic
Table 1: ERAS Protocol
Preoperative Components
1. Preadmission information, education and counselling
Patients should be counselled in the preoperative period regarding the surgical and anaesthetic procedure both
verbally as well as in written form.
2. Preoperative Optimisation
Nutritional status should be optimized. Preoperative physical rehabilitation may be beneficial to patients in
terms of improving postoperative recovery. Abstinence of smoking or alcohol for atleast 1 month decreases the
incidence of pulmonary and wound complications and improves organ function.
3. Avoidance of Mechanical Bowel Preparation
Mechanical bowel preparation (MBP) is not routinely indicated as it causes dehydration, dyselectrolytemia and
prolonged ileus after colonic surgery, causes liquefaction of faecal matter resulting in spillage of bowel contents
resulting in infection associated with risk of anastomotic leak.

4. Avoid Prolonged Preoperative Fasting and Provide monitoring. Maintenance of anaesthesia should
Carbohydrate Loading be done using short acting inhalation agents such
as sevoflurane or desflurane. Total intravenous
Short period fasting after ingestion of clear liquids is
anaesthesia (TIVA) with propofol can also be used as it
safe and more acceptable to patients. The traditional
has the added advantage of reduced incidence of PONV.
practice of fasting from midnight prior to surgery
In elderly patients, the use of bispectral index (BIS)
aggravates metabolic stress resulting in hyperglycaemia
monitoring to titrate anaesthesia depth can enhance
and insulin resistance. The current guidelines allow
recovery from anaesthesia.
clear liquids until 2 hours before surgery and solid intake
until 6 hours before surgery. Providing carbohydrate Adequate attention to airway management and
loading prior to surgery decreases preoperative thirst, ventilation is essential to reduce the incidence of
hunger and patient anxiety resulting in decreased postoperative pulmonary complications such as chest
insulin resistance and reduced protein catabolism. infection and lung injury.
5. No Pre-anaesthetic Medication Use of regional blocks along with general anaesthesia
(GA) not only attenuates the stress response but
Preoperative education should be preferred over the
also decreases intraoperative and postoperative
use of sedative/anxiolytic medications as they can
systemic opioid consumption, thereby prompting
cause impairment of postoperative cognitive function
rapid awakening. Intraoperative glucose monitoring is
resulting in decreased early mobility and ability
important as hyperglycaemia increases the incidence
to eat and drink. If required, short acting sedative
of postoperative complications.
premedication should be administered.
2. Fluid Management and Haemodynamic Monitoring
6. Thromboembolism Prophylaxis
Fluid therapy needs to be balanced to avoid both
Mechanical thromboprophylaxis using compression
hypovolemia and hypervolemia. Hypovolemia results
stockings and intermittent pneumatic compression
in hypoperfusion of vital organs resulting in end-organ
devices along with pharmacological prophylaxis
damage, hypervolemia on the other hand causes
with low molecular weight heparin (LMWH) or
bowel oedema and increased interstitial lung water.
unfractionated heparin decrease the incidence of
If hypotension persists after ensuring normovolemia,
venous thromboembolism (VTE).
vasopressors should be used.
7. Antimicrobial Prophylaxis and Skin Preparation
Goal directed fluid therapy (GDFT) is being practised
Prophylaxis with intravenous antibiotics covering both now. The main aim of GDFT is to maintain a balance
aerobic and anaerobic bacteria should be administered between global tissue oxygen delivery and consumption.
30-60 minutes before incision. Hair clipping, as
GDFT is guided using the minimally invasive cardiac
compared to hair removal and skin cleaning with
output monitors. In patients undergoing major surgery,
chlorhexidine alcohol decreases the incidence of SSI.
the use of oesophageal doppler (OD) device, targeted
Intraoperative Components fluid therapy based on changes in stroke volume (SV)
has demonstrated a lower incidence of acute kidney
1. Standard Anaesthesia Protocol injury, decreased rate of infection, faster return of
Anaesthesia drugs and techniques allowing rapid bowel function and possible improved survival after
recovery should be preferred. Short- acting drugs like surgery.
propofol, in combination with short acting opioids such Other minimally invasive cardiac output monitors which
as fentanyl or remifentanil should be used. Muscle use arterial waveform analysis (e.g. LiDCO, Edwards
relaxation should be titrated using neuromuscular
Vigileo) are also commonly used. These functional 6. Surgical technique

haemodynamic monitors measure various dynamic
variables such as stroke volume variation (SVV) and Laparoscopic or minimally invasive surgery
pulse pressure variation(PPV), in addition to SV, to improves patient outcome as compared to the open
guide fluid therapy. technique. Laparoscopy is associated with decreased
inflammatory response, immunosuppression,
Postoperative enteral feeding should be encouraged as perioperative stress and length of hospital stay. It
early as possible, while use of intravenous fluids should promotes early patient mobilisation and decreased
be minimised. analgesic requirement.
3. Preventing Hypothermia Postoperative Components
Hypothermia (core body temp < 36°C) should be 1. Postoperative Analgesia
actively prevented by using forced-air warming
blankets, heated mattresses under the patients and Postoperative analgesia is managed used a multimodal
warming of intravenous fluids. approach with minimal use of systemic opioids. For
patients undergoing open abdominal surgery, Thoracic
Avoiding hypothermia prevents various complications
epidural analgesia (TEA) is considered to be the gold
such as intraoperative bleeding, acidosis, shivering,
standard for providing postoperative analgesia.
myocardial ischaemia and postoperative wound
infection. Intraoperative normothermia should be LA can also be administered peripherally by using
maintained. techniques such as transversus abdominis plane (TAP)
block, rectus sheath block and wound catheter.
4. Avoidance of Postoperative Drains and Nasogastric
Tube TAP block has been used both in open and laparoscopic
Routine use of nasogastric tube is discouraged and surgeries with a reduction in pain score and opioid
it should be removed prior to end of anaesthesia. requirement.
Nasogastric tube increases GE reflux and also prolongs Placement of wound catheter where in multihole
the period of ileus resulting in abdominal distension and catheters are placed in the preperitoneal space at the
basal hypoventilation. A combination of these factors time of closure of surgical incision. The catheter is used
has been shown to increase the incidence of fever, for administration of LA by either bolus or continuous
atelectasis and pneumonia and can hinder mobilisation.
infusion.
5. PONV
The analgesia provided by central and peripheral nerve
PONV is one of the most distressing postoperative blocks can be supplemented with NSAIDs, paracetamol
symptoms and leads to delayed hospital discharge. and tramadol.
General measures used to avoid PONV are: avoidance of
2. Urinary Drainage
inhalation agents, use of propofol TIVA, regional blocks,
minimising preoperative fasting and preoperative use of Early removal of urinary catheter has been shown
carbohydrate containing fluids. Antiemetic prophylaxis to decrease urinary tract infection rate. In patients
should be done using multimodal drug regimen, as receiving thoracic epidural analgesia (TEA), the catheter
the effect is more when more than 2 antiemetics are can be removed, regardless of usage and duration of
used in combination. The commonly used drugs are: TEA. For patients requiring prolonged duration (> 4 days)
cholinergic, dopaminergic (D2), serotonergic (5-HT3) of urinary catheterisation, suprapubic catheterisation
and histaminergic (H1). is superior to transuretheral catheterisation.

3. Prevention of Ileus 7. Audit

Postoperative ileus delays hospital discharge. It can Clinical outcomes including readmission rates and
be prevented by use of TEA, avoiding fluid overload compliance to various ERAS strategies should be
and nasogastric decompression. There is no role of regularly audited. Reeadmission rates should not
prokinetic drugs in preventing ileus. Drugs shown exceed 10%.
to be effective in enhancing gut function are: oral
Conclusion
magnesium, bisacodyl and alvimopan (µ-opioid
receptor antagonist).Perioperative use of chewing gum Implementation of multimodal patient care pathways as
has also shown to be quite effective in preventing ileus. incorporated in the ERAS protocol can improve patient’s
clinical outcome after major abdominal and pelvic
4. Early Postoperative Nutrition surgery. While ERAS pathways are considered standard
Early enteral feeding should be encouraged in the of care for colorectal surgery, more data is required to
postoperative period as it decreases the risk of authenticate them for major urological as well.
infection. The patients should consume atleast 1200- The 3 main component on which ERAS is established
1500 kcal/day. To achieve preoperative nutrition goals, are evidence based perioperative care processes,
oral nutrition supplement can be used for short term. multimodal and multi-professional team work and a
Immunonutrition with arginine, glutamine and omega-3 continuous audit.
fatty acids has been found to be beneficial.
Development of ERAS pathways have highlighted the
5. Glucose Control importance of perioperative care.
Hyperglycaemia and insulin resistance increase the Ability to achieve a reduced hospital stay, patient
rate of complications and morbidity after major satisfaction and reduced rates of complications have
abdominal surgery. Postoperative normoglycemia demonstrated a new powerful tool.
can be maintained by using TEA, preoperative
References
carbohydrate loading, early postoperative enteral
nutrition, maintenance of fluid balance and early O Ljungqvist, M Hubner. Enhanced recovery
mobilisation. after surgery—ERAS—principles, practice and feasibility
in the elderly. Aging Clinical and Experimental Research
6. Early Mobilisation 2018; 30(3): 249–52.
A structured mobilization plan should be in place, Melnyk M, Casey RG, Black P, Koupparis AJ. Enhanced
patient should be seen by physiotherapist. Although recovery after surgery (ERAS) protocols: Time to change
early mobilisation may not have any direct benefits, it practice? Can UrolAssoc J 2011;5:342-8.
may prevent chest infection, insulin resistance, improve
muscle strength and decrease the incidence of DVT. Sood J, Nethi S. Enhanced Recovery After Surgery
(ERAS). Year Book of Anaesthesia 2016.

MCQ
1. All of the following are part of the ERAS pro- 4. Measures to reduce PONV are all of the fol-
tocol except? lowing except?
a. fasting periods a. Avoidance of inhalational agents
b. Prevention of PONV b. Avoidance of preoperative
c. Minimal preanaesthetic medications carbohydrate containing fluids
d. Good postoperative analgesia c. Use of TIVA
2. Which of the following is a part of intraopera- d. prophylaxis

tive protocol of ERAS? 5. All of the following are true regarding ERAS
except?
a. Use of positive fluid balance
b. Preference of open surgical a. Prokinetic drugs have a major role in
procedures to laparoscopic procedures preventing postop ileus
c. Avoidance of nasogastric tube b. Hyperglycemia and insulin resistance
increase rate of complications after
d. Routine use of postoperative drain
surgery
3. When should antibiotic prophylaxis be admin- c. Readmission rates should not exceed
istered according to ERAS? 10% after discharge
a. Just before skin incision d. Suprapubic catheter is preferred to
b. 30-60mins before incision transurethral catheter for patients
requiring prolonged periods of
c. Immediately after skin incision catheterization
d. 2 hours before incision
5. (a) 4. (b) 3. (b) 2. (c) 1. (a)

Answers

16 Anaesthesia for Total Joint Arthroplasties
Senior Consultant & Academic Director, Balavenkatasubramanian J

Ganga Hospital & Medical Centre,
Coimbatore.
Key points
Ø Patients coming for joint arthroplasties pose certain specific challenges to the anaesthesiologists due to
decrease in organ reserves associated with ageing, comorbidities, polypharmacy, etc.
Ø The most important prehabilitation measures includes chest physiotherapy, nutrition, muscle
strengthening exercises, haematinics and erythropoietin administration
Ø It is best to continue low dose aspirin (if the patients were already on the same, for vascular accidents)
in the perioperative period and all the other antiplatelets could be stopped preoperatively based on
their half lives
Ø The commonest electrolyte imbalance noticed in the elderly patients include hyponatremia and
hypokalemia
Ø Albumin levels less than 2.0 gms% indicate poor preoperative nutritional status and increased morbidity
in the postoperative period including poor wound healing
Ø Intermittent pneumatic compression device for 96 hours in the postoperative period and early
ambulation are advocated to decrease the incidence of DVT
Introduction excision surgeries involving the joints and Avascular

necrosis of Hip following long term steroid therapy.
Anaesthesia for Joint Replacement surgeries are on
the rise in India. The degenerative changes which Pre-anaesthesia Care & Prehabilitation:
happens with ageing and the increasing number of
All these patients have to be throughly evaluated in
ageing population have contributed to this raise. The
the preanaesthesia clinic. Preoperative prehabilitation
commonest Joint replacement surgeries are the Knee,
has become the order of the day and has been found
Hip, Shoulder and Elbow.
to decrease the morbidity and may be the mortality
Majority of these cases are due to degenerative after Joint replacement surgeries. The most important
disorders and common after the 6th decade of life. factors would include chest physiotherapy, nutrition,
These cases pose certain specific challenges to the muscle strengthening exercises, haematinics and
anaesthesiologists due to decrease in organ reserves erythropoietin administration.
associated with ageing, comorbidities, polypharmacy
It is crucial to assess the organ function, mainly the
and decrease in the activity of daily living. However,
cardiorespiratory reserve and the renal functions. Many
joint replacement surgeries are also performed in
of these patients will be on long term NSAID’S and hence
younger patients and the common causes include
it is mandatory to evaluate the renal function. Many of
connective tissue disorders like Rheumatoid Arthritis
these patients will be on antiplatelet agents, it is truly
and Ankylosing Spondylitis, Post traumatic, Post tumour
vital to evaluate and understand the reason for being

Anaesthesia for Total Joint Arthroplasties 166 Balavenkatasubramanian J
administered antiplatelets. If antiplatelest were being decreasing the central sensitization for the nociceptive
administered due to previous vascular accidents, it is stimulus. The preemptive analgesia suggested includes
best to continue low dose aspirin in the perioperative Paracetamol 1 gram, a NSAID and Pregabalin 75 mg the
period and all the other antiplatelets could be stopped day prior to surgery. Several studies have also found
preoperatively based on their half lives. Patients on oral benefit in instituting preoperative nerve blocks like
anticoagulants have to be monitored for the INR and Adductor canal block, Femoral Block and ipack as a part
surgery could be undertaken when the INR is equal of preemptive analgesia.
to or less than 1.5. When the oral anticoagulants are
Preoperative Decrease in Bioburden
stopped prior to surgery, it is mandatory to start them
on Low Molecular Weight Heparin. If they are on Preoperative chlorhexidine bath the day prior and on
long term diuretics, we need to continue them in the the day of surgery has found to decrease the bioburden
perioperative period and at the same time monitor in the patient body and have been thought to be an
the Serum Electrolytes. The commonest electrolyte important factor in decreasing the surgical site infection
imbalance noticed in the elderly patients include
hyponatreamia and hypokalemia. Premedication
Preoperative Haemoglobin levels need to be optimized Premedication is individualised. Anxiolytics and proton
and a haemoglobin of 10 gms% would be an ideal pump inhibitors advocated. Preferable to avoid opioids.
preoperative target. Preoperative Albumin is yet Preinduction Monitoring
another important indicator. Albumin levels less than
2.0 gms% indicate poor preoperative nutritional status The pre induction monitoring would include Noninvasive
and increased morbidity in the postoperative period Blood pressure , Pulse, Heart rate, Electrocardiogram
include poor wound healing. It is also imperative to and temperature.
normalize the glycemic levels and blood pressure.
Zero Hour Medication
Preoperative Echocardiogram and Electrocardiogram
for cardiac evaluation and Doppler study of the deep The medications to be given at the time of beginning the
veins to rule out existing DVT are pertinent. procedure include Intravenous antibiotics, antiemetics,
paracetamol, tranexamic acid and ketorolac.
Radiological evaluation of the cervical spine is needed
if we plan for general anaesthesia and lumbar spine Anaesthesia Strategies
if we are planning for neuraxial block, to evaluate the
The possible anaesthesia strategies would include the
degenerative changes in cervical spine and lumbar
following :
spine. Several of these patients have degenerative
scoliosis and neuraxial block administration might be Total Knee Replacement
difficult. With the advent of ultrasound, preoperative
scanning of the spine helps us to plan the neuraxial General anaesthesia/ spinal anaesthesia/combined
block with increased success rates. spinal epidural anaesthesia/lumbar and sacral plexus
block
Assessment of airway is very important in patients with
connective tissue disorders as many of them might Total Hip Replacement
have fused spine and may warrant the use of awake General anaesthesia/ spinal anaesthesia/combined
fibreoptic for endotracheal intubation. spinal epidural anaesthesia/lumbar and sacral plexus
Pre-emptive Analgesia block
Preemptive analgesia has found to be useful, though Total Shoulder Replacement

few studies have challenged its benefit. The use of General Anaesthesia/ General Anaesthesia
preemptive analgesia is based on the concept of + Interscalene Block/ General Anaesthesia +
Suprascapular+Axillary block/ General Anaesthesia+ 3) Bone Marrow Implantation Syndrome
Small volume supraclavicular block
Intraoperative hypoxia and hypotension could be
Total Elbow Replacement because of bone marrow implantation syndrome. The
pulmonary ventilation perfusion mismatch happens
General Anaesthesia/ General Anaesthesia + Nerve due to embolisation of marrow and cement. In
Block/ Brachial Block either Interscalene or Subclavian haemodynamically compromised patients, it is better
perivascular or Cotoclavicular or Infraclavicular to avoid cement or use very small quantity of cement
Intraoperative Position 4) Tourniquet
Total Knee Replacement is done in supine position. Whenever tourniquet is used, it is essential to record
the time and the advocated time for upper limb is 90
Total Hip Replacement is done in supine with 30 degrees minutes and for the lower limbs is 120 minutes. The
pelvic tilt or lateral position. When in lateral position, advocated tourniquet pressure should be 100 mm Hg
caution to be exercised in padding the pressure points. more than the systolic pressure
Total Shoulder Replacement is done in sitting, semi 5) DVT
reclining and lateral position. When positioning the
patient from supine to sitting, it is imperative to do Patients undergoing Total Knee and Hip replacement
it slowly with corresponding monitoring of blood surgeries are highly prone for developing DVT and it is
advocated to start the pneumatic compression device
pressure. Sudden change in position from supine to
in the intraoperative period itself
sitting can produce significant hypotension. It is also
very important to consider intra-arterial pressure Postoperative Concerns
monitoring with the transducer at the tragus level for
1) Pain
major shoulder surgeries. This would aid us to learn
about the cerebral and retinal perfusion. Pain is the most important concern in patients with
joint replacement surgery. The current advocacy is
Total Elbow replacement is done in the lateral position
to use multimodal pain relief using a combination of
and it is imperative to pad the pressure points. Paracetamol, NSAID, Pregabalin, Regional analgesia,
Intraoperative Concerns Opioids and Tramadol. With increasing use of opioid
free anaesthesia and analgesia, intravenous ketamine,
1) Blood Loss lignocaine and dexmedetomedine have been used.
It is advocated to use blood conservative strategies 2) Nausea & Vomiting
including using antifibrinolytics like tranexamic
3) DVT
acid. Close monitoring of blood loss and adequate
replacement is crucial. The blood loss could be more Intermittent pneumatic compression device for 96
than 30 percent of blood volume in redo total hip hours in the postoperative period and early ambulation
replacements. Autologus predonation and acute are advocated to decrease the incidence of DVT. The
normovolaemic haemodilution would aid in autologus chemoprophylaxsis will include low molecular weight
transfusion. heparin, antiplatelets and anticoagulants.
2) Hypothermia 4) Electrolyte imbalance, commonest is hypona-

traemia and hypokalemia.
Hypothermia is very common because of the operating
room temperature. Hence it is advocated to use 5) Hypoxia, is due to basal atelectasis, imperative
temperature conservation through online fluid warming to put them on incentive spirometry and chest
physiotherapy. Hypoxia at times could be because
and patient warming device like bear hugger
of pulmonary embolism as well.
6) Blood loss and replacement has to be done increased residual urine volume resulting in
diligently, especially in redo joint replacements, Postoperative urinary infection.
where the postoperative blood loss in the drains
are very high. 10) POCD: postoperative cognitive dysfunction is
common in the elderly patients undergoing joint
7) Constipation, it is imperative to start them on replacement surgeries. It is important to rule
laxatives out hyponatraemia, hypoxia, hypoglycaemia,
hypercarbia, hypotension and hyperammonaemia
8) Urinary retention and catheterization, it is
preferable to avoid cathetrisation, considering Conclusion
the bactraemia that is associated with the same.
Joint replacement surgeries are being performed more
9) POUR: Postoperative Urine Retention- This than before. Appropriate preanaesthesia evaluation,
phenomenon is increasingly being recognized prehabilitation, selective intraoperative strategies including
in the detrusor muscles as they undergo
blood conservation strategies and regional anaesthesia,
stretching and become weak and it takes a
good postoperative care and early mobilization have
long time to regain the good muscle tone.
The bladder atony that happened results in resulted in very good clinical outcomes.

MCQ
1. Pt on antiplatelets /anticoagulant following is 4. About bone marrow implantation syndrome
false all are true except
a. Best to continue low-dose Asprin a. Embolisation by marrow / cement
b. Stop all other antiplatelets according b. Pulmonary ventilation and perfusion
to half-life mismatch
c. Surgery can be under taken if INR is c. Tend to happen in hemodynamically
less than or equal to 1.5 compromised patients
d. Pt can be continued on oral d. None of the above
anticoagulant for surgery
5. Maximam advocated time of torniqet applica-
2. Use of pre emptive analgesia is based on tion of upper limb
concept of
a. 60 min
a. Pain gate theory
b. 90 min
b. Increase use of opioid
c. 120 min
c. Decreased central sensitization of
nociceptive stimulus d. 360 min
d. None of the above

3. Anaesthetic strategy for total shoulder re-
placement may include all except
a. GA+ Interscalene block

b. GA
c. Lumbar epidural
d. GA+ supra clavicular block+Axillary
block
5.(b) 4.(d) 3.(c) 2.(c) 1.(d)

Answers

FOCUS SESSIONS
17 BASIC STATISTICS FOR THE ANAESTHESIOLOGISTS
Professor, Bala Bhaskar S

Vijayanagar Institute of Medical Sciences,
Karnataka
Key points
Ø Statistics is a field of assumptions and relations, not decisions and final validations.
Ø The observations of interest in a research study are referred to as variables.
Ø Confounding factor is something other than the thing being studied, that could be influencing the
results seen in a study.
Ø In a skewed distribution, the median is a better measure of central tendency.
Ø In a normal distribution, 95% of the population lies within 1.96 standard deviations.
Ø Standard Error is the Standard Deviation (SD) of sample means.
Ø The Confidence Interval is an estimate to provide a range that is likely to include the true value.
Ø It is important not to draw too many conclusions from the p value; there may not be correlative practical
implications of p values on either side of the chosen p value.
Ø Type I error in any hypothesis test is fixed traditionally at 5%, and type 2 error at 20%.
Data, Variables and Measurement some characteristic, or quality, and are referred to as
qualitative data. They cannot be quantified. The second
The Variables
type of data includes those, which are measured on a
During research, the many outcomes and observations numerical scale and are referred to as quantitative data.
as defined in the methodology are observed and noted
Numerical / Quantitative Variables
for the sample studied. The types of data are specifically
defined during the planning stage and will determine There are 2 subtypes – discrete or continuous
which statistical tests will eventually be used. They
Discrete Data take a countable number of values or
could be related to the patient clinical status, monitored
distinct values or have only intermittent values over a
parameters, laboratory tests or others (manikin,
range. The scale units are limited to integers. Example-
simulations, field studies, etc.). They are identified in a
Number of patients admitted to a hospital, number of
manner to make them measurable in as precise (free of
deaths recorded in a particular area, number of attacks
random errors) and accurate (free of systematic errors)
of diarrhoea in a child during a year etc.
manner as possible. This makes them ‘valid’ and helps
to be analyzed statistically. Continuous Data can take any value over a particular
range. They are quantified on an infinite scale. The scale
In general, these observations of interest in a research
units are not specific integers but have decimals. The
study are also referred to as variables, in that they
number of possible values of body weight, for example,
can have different values (i.e. they can vary). Basically,
is limited only by the sensitivity of the machine that is
there are two types of data / variables. The first
used to measure it. Continuous variables are rich in
type of data includes those, which are defined by
Basic Statistics for the Anaesthesiologists 174 Bala Bhaskar S
information. Example- Height, Weight, Age, Level of e.g. Smoking status can be recorded as smoker/non-
protein in blood, Body temperature, Pulse beat etc. smoker (categorical data), heavy smoker/light smoker/
ex-smoker/non-smoker (ordinal data), or by the number
Discrete variables can have a considerable number of
of cigarettes smoked per day (discrete data).
possible values, and can resemble continuous variables
in statistical analyses and can be equivalent for the Studies generally include more than one type of
purpose of designing measurements. data. For example, in a study comparing analgesia
characteristics of bolus vs. patient controlled analgesia
Categorical / Qualitative Variables
for major surgery, the following may be recorded: pain
There are 2 subtypes - ordinal and nominal score (0-4 scale, 0 = no pain, 1 = mild pain, 2 = moderate
pain, 3 = severe pain and 4 = unbearable pain- these
Ordinal data have an order, are measured in categories are ordinal data); incidence of respiratory depression
that are ranked in terms of a graded order (or in (categorical data); total morphine consumption
categories that have specific order). The differences (continuous data) and serum cortisol level (continuous
among the categories are not necessarily equal and data).
often are not even measurable. The symbols assigned
to represent the categories are not important as long Methodological Classification of Variables
as the ranking system is preserved. Ordinal scale are
It is necessary to identify the variables that will be
easy to use, may not require any sophisticated device,
involved in the research project being designed, mainly
and in many times easily understood by all.
the independent and the dependent variables.
Examples: Pain score (0 = no pain,1 = mild pain, 2 =
Independent (predictor) variable is/ are the one/ones
moderate pain 3 = severe pain, 4 = unbearable pain),
that is varied or manipulated by the researcher- any
Extent of Motor block (Bromage Scale Gr 0 - Gr 3),
variable whose value determines that of others; it
Patients status or condition- unimproved, stable, or
represents the treatment or experimental variable that
improved, Age- Child, Adult and Old.
is manipulated by the researcher to create an effect
Nominal data are measured on scales of names, on the dependent variable. Dependent variable is the
numbers or other symbols to assign each measurement response that is measured. It represents a response,
to one of the limited number of categories that behaviour, or outcome that the researcher wishes to
cannot be ordered one above the other. Example- predict or explain.
Measurement of Blood type – A, B, AB, O., Gender
“(Independent variable) causes a change in (Dependent
– male or female, Outcome of a Disease – Survival,
Variable) and it isn’t possible that (Dependent Variable)
Death, Diagnosis as Hepatitis, Cirrhosis, etc., Site of
could cause a change in (Independent Variable).”
Malignancy- lung, mouth, breast, or ovary, Occupation
– Farming, Business, Labour, Service etc. The categories Example-1. A study comparing two local anaesthetics
of a nominal scale must be exhaustive and mutually on duration of analgesia: The independent variable is
exclusive; each measurement must fall into only the use of two LAs and the dependent variable is the
one category. Within any category, the members are duration of analgesia.
assumed to be equivalent (not superior or inferior) with
2. Comparison of two doses of dexmedetomidine
respect to the characteristic being scaled.
(Dex) to attenuate intubation responses: Independent
Dichotomous data have only two possible values (e.g. variable- the dose of dexmedetomidine , the dependent
dead or alive) whereas polychotomous data have variable is the blood pressure/ heart rate changes.
more than two categories, according to the type of Confounding variable (third variable) is a ‘confounding
information they contain. factor’ - something, other than the thing being studied,
that could be influencing the results seen in a study)
The same variable can be expressed in different ways
which has to be identified and discussed.
Uniformity of Distribution of Data
The distribution (Fig 2) of data could be uniform around the central area (when mean, median, mode assume
same value) or non-uniform with mean, median and mode not aligned as the same value. In a skewed distribution,
the median is a better measure of central tendency.
Long tail on the right Long tail on the Left
Fig 2: Data Distribution

The uniform distribution is referred to as the Gaussian / symmetrical distribution; it is a symmetrical bell-shaped
curve with a mean (μ) of 0 and a standard deviation (sigma-σ), of 1. This is also known as the z distribution. (Fig
3a). The non-uniform distribution is referred to as the Non Gaussian distribution or asymmetrical distribution
(Fig 3b). The data representation and statistical test applied varies with Gaussian vs. Non-Gaussian data. Gaussian
Data has better validity with respect to statistical tests.
Standard Deviation
Fig 3: a. Gaussian Distribution (Mean SD) b. Non Gaussian Distribution [Median- Range (IQR)]

Statistical Significance – p value and CI a. The data can be plotted on a graph and distribution
assessed.
The choice of a specific cutoff point for a p-value or
degree of confidence for CI, as mentioned already is b. Difference between the mean and median values of
arbitrary but conventional (p-value of 0.05, 95% CI); variable are checked- if the difference is more than
there is no particular reason why a different p-value, 1.5%, or the SD is more than 40%, it represents non
eg. 0.02 and a corresponding 98 % CI could not be the Gaussian distribution (Mathematical)
standard for calling a result “statistically significant”.
3. If the Distribution is Gaussian: Data is more
Different values may be targeted based on the
amenable to statistical analysis and parametric tests
importance of the hypothesized outcome; for example,
are applied.
minimal p and maximal CI may need to be targeted in
mortality related studies. If the Distribution is non Gaussian: Non-normal,
or skewed, data can be transformed so that they
It is important not to draw too many conclusions from
approximate a normal distribution- commonly by
the p value; there may not be correlative practical
log transformation, whereby the natural logarithms
implications of p values on either side of the chosen p
of the raw data are analysed to calculate a mean
value. The value of 0.001(rather than 0.05) need not be
and standard deviation (Data transformation). The
clearly indicative of a result of the study being tightly
antilogarithm of the mean of this transformed data is
restricted to avoid results occurring by ‘chance’. Also,
known as the geometric mean. One of the ‘goodness
marginally higher value eg. 0.06 need not also mean
of fit’ tests, Kolmogorov- Smirnov or Shapiro-Wilk
that the errors have possibly been higher, leading to
tests is applied for this test to see if the transformed
higher rates of events occurring by chance. Despite
data approximate to a normal distribution. If they
this loss of predictability, it is common and common
do, they can then be analysed with parametric
sense to take very small p-values as stronger evidence
tests. If the Non Gaussian characteristic stays, non-
in support of a hypothesis than p-values close to 0.05.
parametric tests are applied.
Choosing the Statistical Test
4. Check what type of variables to compare?
The following factors influence the choice of the test
A. Numerical Data B. Categorical Data
(the basic tests are covered).
5. Check whether the data are Related or Unrelated?
1. Type of variable considered and how they are
measured: Related means comparison within the same
Numerical / Quantitative (Discrete / Continuous, group, of a variable, before or after an event or
normally Mean & SD) intervention- also called ‘dependent variable’
comparison. Unrelated means comparison of
Categorical / Qualitative (Ordinal / Nominal, variables, between groups- also called ‘independent
normally proportions -frequencies / percentages) variable’ comparison.
2. Distribution of Data: Gaussian or non Gaussian 6. Define X – the number of groups and Y- Normal
Gaussian distribution is demonstrated either a. or non-normal distribution and choose one of the
graphically, b. by comparing the values of mean statistical test as per the figures below (Fig.6, 7)
and Median / Mean and SD

Sample Size and Power Hypothesis and Errors
Sampling is the process of selecting a group of people Before the study is started, while methodology is
from a larger population and subjecting that group for created, assumptions are done with respect to the
the research. The study outcome is then extrapolated outcomes. The assumptions, for example, can be that a
to large population group as research cannot be viable/ new analgesic as compared to a standard analgesic has
economical/ethical to be conducted in the bigger SAME outcomes or has IMPROVED outcomes (duration
population/group. of analgesia). Such assumptions / hypotheses are
referred to as Null hypothesis (assumes no difference
What is the Correct Sample size? : The sample size has between the control and the study group) or Alternative
to be adequate; smaller size will not reflect significant, hypothesis (assumes that there is a difference among
true & valid differences in outcome. Larger size will be the groups, or there is some association between the
difficult, time consuming, uneconomical and unethical. predictor and the outcome). Majority of studies in
It is also represents a number, beyond which additions anaesthesia use alternate hypothesis as new drugs,
are quite unlikely to change the conclusion. routes, doses, new techniques, devices, etc., are
studied.
Thus, Under sampling:
The Errors
• May not achieve statistical significance
• Results may not be consistent when trial is The hypothesis need not be and will not be always be
repeated correct because there can be some errors, reflected
• Questionable validity of research. in the form of false positives or false negatives. For
example, in a study comparing spinal bupivacaine and
Larger sampling:
ropivacaine (30 sample size each) for post operative
• May show statistical significance even if the analgesia, the assumption could be that ropivacaine
clinical significance is minimal ‘produces longer duration of sensory block’ as
• Unnecessary exposure of population to new compared to bupivacaine, by about 25%.
drug Let us check with one group; if 22/30 patients in
• Greater economical and ethical burden. Ropivacaine group had prolonged analgesia, it could
There are numerous formulae for sample size be that 20/22 had actual prolongation (true positives)
calculation but can now be obtained from statistical but 2/22 (false positives) reported prolongation but
software easily. Basics principles and considerations this could be because of errors/chance. This incorrect
related to sample size calculation are discussed below. claim of statistical significance (false positives) is a
Type 1 error (α); the probability of Type I error in any
1) The Primary Outcome Criteria hypothesis test is FIXED traditionally at 0.05 or 5% (CI=
2) The Hypothesis / Assumptions and Errors (Alfa, 95%).
Beta, Power and CI) If 8/30 patients in Ropivacaine group showed reduced
3) Effect Size duration compared to Bupivacaine group, it could be
that 5/8 had actually reduced duration (true negatives)
4) Measure of Primary Outcome: Mean, Proportion, but 3/8 (false negatives) reported reduction, could be
percentages because of errors / chance. This incorrect claim of no
Primary Outcome Criteria statistical significance (false negative) is a Type 2 error
(β); probability of Type II error in any hypothesis test
Aim for only one primary outcome measure Eg: Study is FIXED traditionally at 20%.
on post operative analgesia – Primary Outcome
measure can be duration of analgesia or 24 hour The impact of a false positive error (Type I) is more
analgesic requirement (only one chosen) detrimental than that of false negative (Type II) error;

hence, the error rate of Type I error (α, at 5%) is www.openepi.com is a totally free website and is user
customarily set lower than Type II error (β, at 20%). friendly.
When we say that we allow up to 20% of false negatives, Statement of Sample Size Calculation: When all above
that means this 20% should have been positives, but criteria as required for sample size calculation are
only 80% is shown as positives. This is the basis of Power obtained and used for calculation, the sample size is
of a study; a power of 80% means that the hypothesis calculated and a statement as below is made. Example:
would definitely be correct in 80/100 instances. Greater
“Assuming a duration of analgesia of 150 min and
the power, greater the likelihood of true +ve outcomes
standard deviation of 15 min in first group, keeping
and lesser the false negatives. That is, the probability
power at 80% and confidence intervals at 95% (alpha
of minimizing the type 2 error, represented as the error at 0.05), a sample of 24 patients would be required
complement of β; 1-β (100-20)=80% (traditionally). to detect a minimum of 20% (30 min) difference in the
Effect size duration of analgesia between the two groups. We
included 27 patients in each group to compensate for
This is the minimum difference that the investigator wants possible drop outs.”
to detect between the groups. This can be obtained from
pilot study, previous studies, clinical judgement or expert Summary
advice. Continuing with the previous example, we can Statistics is a field of assumptions and relations, not
assume the duration of sensory block with ropivacaine to decisions and final validations. Knowledge about the
be longer than that with bupivacaine by 30% (or 60 mins). basic principles of statistics is useful so that the right
This is called the ‘effect size’. input of right data is provided to the bio statistician.
Measure of Primary Outcome Wrong analysis of right data can lead to wrong outcome
decisions. It is advised to involve the Bio-statistician
Define primary outcome in terms of mean/proportion/ from planning stage of the study itself.
percentages. Example: Duration of sensory block as
Understanding the types of variables, the distribution
Mean- 216 ± 34 min, Antiemetic efficacy- Incidence
of the data, the errors, the basics of descriptive and
of PONV as percentages / proportions- 30% or 60/200
inferential statistics will help in choosing the best
patients.
statistical tests. Sample size calculation should take
Calculation of Sample Size into consideration the type of variable, the groups,
the hypothesis, type 1 and type 2 errors along with the
The parameters mentioned above are used as input for primary outcome parameter with effect size.
calculation of sample size using formulae or software.
The formulae are incorporated into the software either References
online or offline and the input values are provided. The
1. Paul S Myles, Tony Gin. Statistical Methods for
software / online system will display the sample size. Anaesthesia and Intensive Care. Butterworth-
Software for the calculation of sample size for different Heinemann.2000
designs of study are available at
2. Garg R. Methodology for research I. Indian J
http://powerandsamplesize.com Anaesth 2016;60:640-5
www.openepi.com
3. Bhaskar S B, Manjuladevi M. Methodology for
www.stata.com
research II. Indian J Anaesth 2016;60:646-51
www.spss.com
www.poweranalysis.com 4. Ali Z, Bhaskar S B. Basic statistical tools in research
www.nmaster.com and data analysis. Indian J Anaesth 2016;60:662-9
5. Das S, Mitra K, Mandal M. Sample size calculation:
The last one is available from the Department of
Basic principles. Indian J Anaesth 2016;60:652-6
Biostatistics of CMC Vellore for use with Windows OS.
MCQ
1. WHICH OF THE FOLLOWING DESCRIBE THE 4. the middle value of an ordered array of num-
MIDDLE PART OF GROUP OF NUMBERS? bers is
a. Measure of variability a. Mode
b. Measure of central tendency b. Mean
c. Measure of association c. Median
d. Measure of shape d. Midpoint
2. the mean of a distribution is 23, the median is 5. the sum of the deviations about the mean is
24, and the mode is 25.5. It is most likely that always
this distribution is:
a. Range
a. positively skewed
b. Zero
b. symmetrical
c. Positive
c. asymptotic
d. Negative
d. negatively skewed
e. Total standard deviation
3. which of the following divides a group of data
into four subgroups?
a. Percentiles
b. Deciles
c. Median
d. Quartiles
e. Standard deviation
5. (b) 4. (c) 3. (d) 1. (b) 2. (d)

Answers

18 Renal Replacement Therapy
Professor, Anjan Trikha

All India Institute of Medical Sciences
New Delhi
Key points
Ø Renal replacement therapy replaces the normal excretory functions of the kidney to maintain
intracellular and extracellular milieu and remove toxins.
Ø Indications for renal replacement therapy - Acidosis, Electrolyte abnormalities (hyperkalemia), Ingestion
(of toxins), Overload (fluid), Uremic symptoms.
Ø Removal of solutes, water, toxins, electrolytes and correction of acid base balance during renal
replacement therapy is achieved by the process of diffusion or convection or a combination of both
Ø Advantages of peritoneal dialysis include technical simplicity, hemodynamic stability and lack of need
for anticoagulation or vascular access
Ø In intermittent hemodialysis, solute clearance occurs mainly by diffusion, whereas volume is removed
by ultrafiltration.
Ø Continuous renal replacement therapies have become the preferred modality for managing
hemodynamically unstable patients with kidney failure
Ø Slow continuous ultrafiltration is an alternative mode of renal replacement therapy that is used to
control fluid balance in patients with cardiac and renal diseases that cannot be managed by diuretics
Ø The choices of vascular access for hemodialysis - right internal jugular >femoral> left internal jugular >
subclavian vein.
The normal function of the kidneys is to maintain acid- pneumonic AEIOU (all vowels in the English language)
base balance, regulate electrolyte balance and excrete - Acidosis, Electrolyte abnormalities (hyperkalemia),
toxins. Renal replacement therapy is a treatment Ingestion (of toxins), Overload (fluid), Uremic
regimen that replaces the normal excretory functions symptoms.
of the kidney to maintain intracellular and extracellular
Acid-base control - Severe Acidosis
milieu and remove toxins. Renal replacement therapy
can be given by – kidney transplantation, peritoneal Ions alterations Solutes control - Refractory
dialysis, intermittent hemodialysis, and continuous hyperkalemia, hypercalcemia
renal replacement therapy. The present lecture would
not focus on renal transplantation. Indications for Uremia
initiation of renal replacement therapy are shown Table 1: Absolute Indications for initiations of renal
in Table 1 and Table 2. An easy way to remember replacement therapy
indications for renal replacement therapy is a

Renal Replacement Therapy 184 Anjan Trikha
Volume removal in patients with fluid overload when medical management fails
Drug intoxications –Sodium valproate, lithium, salicylates, theophylline, alcohol
Sepsis for immunomodulation
Rhabdomyolysis
Severe Hypernatremia
Hyperthermia
Table 2: Relative Indications for initiations of renal replacement therapy
There are no universally accepted levels of urea, Peritoneal Dialysis

creatinine, potassium or pH or decreased level of
In peritoneal dialysis, the patient’s peritoneum is
glomerular filtration rate at which to start the therapy.
used as a semi-permeable membrane for removal of
The absolute values may vary on case basis.
solutes by diffusion. A dialysate solution with a high
Removal of solutes, water, toxins, electrolytes concentration of glucose is administered into the
and correction of acid base balance during renal peritoneal cavity through a catheter where it remains
replacement therapy is achieved by the process of for a prescribed period of time, allowing solutes to
diffusion or convection or a combination of both. diffuse from blood in the capillaries into the dialysate.
Diffusion is defined as the movement of the solute The saturated dialysate is then drained and discarded,
across the semipermeable membrane along a and fresh dialysate reintroduced. High concentrations
concentration gradient. In renal replacement therapies, of dextrose are used in the dialysate to create an
a filter containing semipermeable membrane is placed osmotic gradient for ultrafiltration. Advantages of PD
in the extracorporeal circuit through which the blood include technical simplicity, hemodynamic stability,
and lack of need for anticoagulation or vascular access.
flows. During this passage of blood, the toxic molecules
Disadvantages of peritoneal dialysis are – surgical need
pass through this semi permeable membrane and ‘get
of insertion with inherent complications of leakage
filtered’ depending upon the size of the pores on the
and malfunction, possible respiratory compromise
membrane and the weight of the molecules. Most toxic
due to abdominal pressure from the installed dialysate
molecules diffuse from high concentration in blood to
and hyperglycemia. In addition, this modality is
low concentration across the membrane. The major
contraindicated in patients after abdominal surgery
determinants for the efficiency of diffusion are the with surgical drains. This modality is less effective in
concentration of solute, molecular weight, and blood patients with poisoning, hyper catabolic states, and
flow rate. Small molecules such as urea diffuse fast and pulmonary edema. However, it is useful as a domiciliary
therefore used as the marker of efficacy, whilst larger procedure as continuous ambulatory peritoneal dialysis
molecules such as albumin and protein-bound drugs
diffuse slowly. Convection is a process of movement Intermittent Hemodialysis
of the solute across a semipermeable membrane by In intermittent hemodialysis, solute clearance occurs
the drag of the solvent along the hydrostatic pressure mainly by diffusion, whereas volume is removed by
gradient. The bulk movement of fluid pulls the solutes ultrafiltration. Blood and dialysate are circulated on
along with it. This kind of convective transport is the opposite sides of a semipermeable membrane
independent of solute concentration gradients across in a counter - current direction resulting in diffusive
the membrane. This process is also called ultrafiltration. solute removal. Decisions regarding dialysis duration
It helps in clearance of middle and large molecules. and frequency are based on patient metabolic control,
volume status, and presence of any hemodynamic

instability. Advantages include rapid solute and volume modalities of continuous renal replacement therapies
removal. This results in rapid correction of electrolyte use diffusion, convection, or a combination of both
disturbances, such as hyperkalemia, and rapid removal for solute clearance. Unlike Intermittent Hemodialysis,
of drugs or other substances in fatal intoxications this is performed continuously (8 - 24 hours per day)
in a matter of hours. IHD also has a decreased need with a typical blood flow of 100 to 300 mL/min and
for anticoagulation as compared with other types of a dialysate flow of 17 to 40 mL/min. It is performed
RRT because of the faster blood flow rate and shorter most commonly through a venovenous vascular access.
duration of therapy. The patient undergoes such a Continuous renal replacement therapies are classified
dialysis 3-6 times a week with a session lasting 3- 4 based upon the vascular access type and mechanism
hours. The blood flow rate through the machine is of solute or fluid removal Table 3.
between 300 – 400 mL/min and a dialysate flow rate of
Hybrid therapies are also used which combine
500 to 800 mL/min. The main disadvantage is the risk
intermittent hemodialysis and continuous renal
of systemic hypotension caused by rapid electrolyte
replacement therapy; this technique is known as
and fluid removal. Rapid solute removal from the
slow low-efficiency daily dialysis. Slow continuous
intravascular space can cause cerebral edema and
ultrafiltration is an alternative mode of renal
increased intracranial pressure.
replacement therapy that is used to control fluid
Continuous renal replacement therapies balance in patients with patients with cardiac and renal
diseases that cannot be managed by diuretics. Table
Continuous renal replacement therapies have become
4 shows the comparison of modalities of continuous
the preferred modality for managing hemodynamically
renal replacement therapies.
unstable patients with kidney failure. The different
Slow continuous ultrafiltration [SCUF]

Continuous veno-venous hemofiltration [CVVH]
Continuous arterio-venous hemofiltration [CAVH]
Continuous venovenous hemodialysis [CVVHD]
Continuous arterio-venous hemodialysis [CAVHD]
Continuous venovenous hemodiafiltration [CVVHDF]
Continuous arteriovenous hemodiafiltration [CAVHDF]
Table 3: The common modalities of CRRT
Vascular Access catheter tip improves flow; therefore, perhaps not

site, but length remains a more important feature of
The site of insertion of the vascular cannula is crucial
vascular access. Optimal flow rates are obtained with
to the success of renal replacement therapies, as
the catheter tip in the right atrium for internal jugular
this treatment is impossible without adequate blood
lines and within the inferior vena cava for femoral
flows, and poor flows risk premature filter clotting.
access.
The preferred choices in the priority of preference are
- right internal jugular, femoral, left internal jugular and Both continuous renal replacement therapies and
lastly subclavian. The subclavian is the least preferred intermittent hemodialysis are complementary
anatomical position because of the higher rate of strategies. The choice of modality is individualized
stenosis formation during chronic use. Position of the based on patient characteristics (physiological status,

hemodynamics), available expertise and infrastructure that are available. Continuous renal replacement therapies
offer better tolerability of treatment as the removal of fluid occurs slowly. It also minimizes the fluctuations in
metabolites, resulting in fewer osmolality changes and lower incidence of cerebral edema.
Name IHD SLEDD CRRT
Mechanism and mole- Dialysis – mostly low Small + middle mole- Small + middle mole-
cules removed molecular weight cules cules
Ambulatory patients
Critically ill patients Critically ill patients
Use with renal failure, Hy-
Hyperkalemia Non-ambulatory
perkalemia
Blood flow 300 – 400 mL/min 100 – 150 mL/min 150 – 200 mL/min
500 mL/min 100-200 mL/min CVVHF: nil
Dialysate flow
or 30 L/h or 6-12 L/h CVVHDF: 1 L/h
Low
(but increased clearance
Efficiency High Moderate
of high VD molecules
over time)
Urea clearance (mL/
150 80 30 (CVVHDF)
min)
Poor
Hemodynamic stability Good Good
(hypotension common)
Duration 3-4 h 2 – 3 times a week 6-12 h daily Continuous (24h/filter)
Fistula or vascular cath-
Fistula or vascular cath-
Access eter Vascular catheter
eter
Usually not needed

Anticoagulation Not needed Important
Dialysis Dysequilibrium Can occur

N/A N/A
Syndrome
Risk of rebound if high
VD Unclear effects on drug
Drugs and toxicology Slower removal
Better for low VD pharmacokinetics
Table 4: Comparison of Modalities of Renal Replacement Therapy

IHD = intermittent hemodialysis, CRRT = continuous renal replacement therapy, SLED = sustained low-efficiency
dialysis or SLEDD = sustained low-efficiency daily dialysis, VD = volume of distribution

References and Further Readings 3. Connor MJJ, Karakala N. Continuous Renal Re-
placement Therapy: Reviewing Current Best
1. MD GV, MD ZR, MD CR. Renal Replacement
Practice to Provide High-Quality Extracorpore-
Therapy. Critical Care Clinics. Elsevier Inc; 2015
al Therapy to Critically Ill Patients. Adv Chronic
Oct 1; 31(4):839–48.
Kidney Dis. 2017 Jul;24(4):213–8.
2. Gaudry S, Hajage D, Schortgen F, Martin-Le-
4. Lisa Gemmell, Robert Docking, Euan Black. Re-
fevre L, Pons B, Boulet E, et al. Initiation
nal replacement therapy in critical care. BJA
Strategies for Renal-Replacement Therapy in
Education, 2017 Volume 17, Issue 3, 1 March,
the Intensive Care Unit. N Engl J Med. 2016
Pages 88–93.
Jul;375(2):122–33.

MCQ
1. Absolute indications of RRT are all, except? 4. Dialysis disequilibrium syndrome can occur
in?
a. Fluid overload
b. Rhabdomyolysis a. SLEDD
c. Sodium valproate intoxication b. IHD
d. Hypothermia c. SCUF
2. Main disadvantage of Intermittent Hemodial- d. CAVHDF

ysis? 5. Which is a hybrid therapy combining IHD and
CRRT for critically ill patients?
a. Hyperkalemia
b. Hypernatremia a. CVVHD
c. Systemic hypotension b. SCUF
d. Pulmonary edema c. CAVH
3. Which is the least preferred vein for vascular d. SLEDD

access in CRRT?
a. Subclavian vein
b. Femoral vein
c. Right IJV
d. Left IJV
5.(d) 4.(b) 3.(a) 2.(c) 1.(d)

Answers

19 INTRA OPERATIVE HYPOXEMIA
Professor & Head, Bhimeswar MV

Siddhartha Medical College,
Vijayawada
Key points
Ø The four main causes of tissue hypoxia are hypoxemic hypoxia, stagnant hypoxia, anemic hypoxia and
histotoxic hypoxia
Ø Intraoperative hypoxemia can be due to problems with the oxygen delivery systems or with the patients
Ø Children, parturients, elderly and obese patients have a greater propensity for development of
intraoperative hypoxemia
• Stagnant or Circulatory Hypoxia

Introduction
This is due to reduced cardiac output and increased
Hypoxemia is defined as a condition where the arterial
non-pulmonary shunting leading to decreased
oxygen tension (PaO2) is below normal (Normal PaO2
blood flow to the tissues
is 80-100 mmHg). Hypoxia is defined as the failure of
oxygenation at the tissue level. Though both the terms • Anaemic Hypoxia
are used interchangeably, they are not synonymous.
Hypoxia and hypoxemia may or may not occur together. This is due to reduced tissue oxygenation as a
Generally, the presence of hypoxemia suggests Hypoxia. consequence of low Hb leading to decreased
However, hypoxia may not be present in patients with Oxygen carrying capacity of blood.
Hypoxemia, if the patient compensates for low Pao2 • Histotoxic Hypoxia
by increasing O2 delivery. This is achieved by either
increasing the cardiac output or decreasing the tissue This is due to inability of the tissues to utilize
oxygen consumption. Conversely, the patients who are oxygen.
not hypoxemic may be hypoxic if oxygen delivery to
Intra Operative Hypoxemia
tissues is impaired or if tissues are unable to use oxygen
effectively. Nevertheless, hypoxemia is by far the most There are several causes for intraoperative hypoxemia.
common cause of tissue hypoxia. Maintaining adequate For practical purposes, the causes may be broadly
oxygenation of the patient is the prime responsibility of divided into
the anesthesiologist during the perioperative period.
• Problems with oxygen delivery System
Tissue Hypoxia
• Problems with the patient
The four causes of tissue hypoxia are
Problems with Oxygen delivery system
• Hypoxemic Hypoxia
The problems with the O2 delivery system may be
This is due to the disorders causing low PaO2 due
• At the level of central oxygen supplies
to insufficient oxygen reaching the blood
• At the level of pipeline distributing system
Intra Operative Hypoxemia 190 Bhimeswar MV
• At the level of oxygen cylinders attached to • Substitution of non-oxygen cylinder at the O2
anaesthesia machine yoke
• At the level of anaesthesia machine • Erroneously filled O2 cylinder
• At the level of anaesthesia ventilator • Insufficiently opened cylinder
• At the level of anaesthesia circuit Problems at the level of the anesthesia machine
• At the level of endotracheal tube
• Incorrect setting of flow meter
Problems at the level of central O2 supplies • Use of fine O2 flow meter instead of course
• Liquid O2 tank may be filled with nitrogen or flow meter
argon • Crack in the O2 flow meter tubes
• Incorrect tanks may be placed at the central • Transposition of rota meter tubes
supply manifold • Leak in the machine
• Decreasing O2 level at the liquid O2 tank
Problems at the level of the anesthesia ventilator
• Gas leak at the manifold
• Inadequate pressure at the central supply • Incorrect ventilator settings
• Empty cylinders • Low tidal volume
• Depleted cylinders • Low respiratory rate
• Failure to change to secondary supply or • Inadequate minute volume
reserve supply when primary supply fails • Power failure
• Failure of master alarm system • Driving gas failure
• Disconnection of tubing
Problems at the level of pipeline distributing system
• Wrong connection of tubing
• Leak in the O2 pipelines • Failure to switch on the ventilator
• Contamination of Gases • Failure to resume ventilation after a period of
• Cross connection of pipelines (during purposeful apnoea
construction or repair)
Problems at the level of the anesthesia circuit
• Not connecting O2 hose to the terminal unit
• Connecting wrong hose to the terminal unit • Disconnection (most common cause)
of O2 pipeline • Leak
• Not connecting the O2 hose to the anesthesia
Problems at the level of endotracheal tube
machine
• Connecting wrong hose to the O2 yoke • Esophageal intubation
• Inadvertent switching of Schrader adapter on • Endobronchial intubation
piped lines • Accidental extubation
• Terminal units labelled wrongly • Tube kinking
• Wrong outlet connectors installed • Tube obstruction
Problems at the level of O2 cylinders attached to the • Cuff herniation
anesthesia machine • Cuff rupture
• Tube obstructing opening of right upper lobe
• Empty cylinders
bronchus
• Depleted cylinders

Problems with the patient Atelectasis
Intra operative hypoxemia may occur because of the Atelectasis is a condition of alveolar collapse. It may
usual changes that occur during anesthesia or due to be micro atelectasis, macro atelectasis or lobar collapse
intra operative complications. depending on the degree of alveolar collapse. This lead
to V/Q mismatch, R-L shunting and arterial hypoxemia.
• Hypoventilation
Atelectasis may occur due to airway secretions,
• Reduced functional residual capacity compression by packs, wedge and prolonged surgical
• Increased airway resistance procedures in unusual positions. Auscultation may
• Atelectasis reveal crepitations with diminished air entry. PEEP may
• Absorption atelectasis be useful in such situations.
• Diffusion defect Absorption atelectasis
• Shunt
Alveolar collapse can occur when the patient is getting
• I n h i b i ti o n o f h y p o x i c p u l m o n a r y high FiO2. When PAO2 rises, the rate at which O2 moves
vasoconstriction from the alveoli to the capillary blood increases. When
• Poor oxygen delivery to tissues the absorption rate is more than the inspired flow of
• Increased oxygen demand gases, the lung unit collapses. Absorption atelectasis
occurs when FiO2 is high; V/Q is low; time of exposure
Hypoventilation of lung unit with low V/Q ratio to high FiO2 is long and
A spontaneously breathing anesthetized patient CvO2 is low.
may hypoventilate due to drug induced respiratory Diffusion Defect
depression (sedatives, narcotics). In a patient who is
paralyzed and ventilated, hypoventilation may occur Even though adequate oxygen is supplied to the alveoli,
due to inadequate IPPV. there may be a defect at the alveolar level which
prevents its absorption into blood. This may occur
Reduced functional residual capacity with thickened alveolar membrane, thickening of air-
Induction of anesthesia causes a reduction in FRC by blood interface (alveolar-capillary block), inflammation,
15-20%. Maximum reduction in FRC occurs within the edema, fibrosis or loss of alveolar surface area. E.g.
first few minutes of induction. Reduction in FRC is seen sarcoidosis and emphysema.
equally in both spontaneous breathing and controlled Shunt
ventilation. The decrease in FRC continues in the post
operative period also. The reduction in FRC is more in • Inadequate ventilation
obese patients. Application of PEEP may compensate
• Absorption Atelectasis
the decrease in FRC.
• Airway secretions-blockage of alveoli
Increased airway resistance • Pulmonary aspiration
During anesthesia, increase in airway resistance may • Pulmonary edema
occur due to i) reduction in FRC ii) decrease in caliber • Inhibition of HPV-vasodilators (SNP, NTG)
of airways iii) endotracheal intubation (ETT decreases
the size of the trachea by 30-50%) iv) anesthesia • Inadequate perfusion
apparatus v) Pharyngeal obstruction (e.g snoring) in an • ASD/VSD
unintubated patient. vi) laryngospasm vii) obstruction • Patent foramen ovale
of ETT by secretions, kinking, cuff herniation viii)
• Pulmonary embolism
bronchospasm.

Inhibition of hypoxic pulmonary vasoconstriction (HPV) • Pre-existing conditions
When PAO2 decreases in a region of lung, pulmonary • Cardio-pulmonary dysfunction
vasoconstriction occurs at that particular region. This • Morbid obesity
hypoxic pulmonary vasoconstriction is a protective • Hypoventilation
phenomenon. HPV diverts blood flow from the hypoxic
regions of the lung to better ventilated normoxic regions • Patient position
thus decreasing V/Q mismatch maintaining P aO 2, • Pneumoperitoneum
inhibition of HPV may lead on to arterial hypoxemia. • Tracheal tube obstruction
Factors which inhibit HPV are inhaled anesthetics, • Inadequate ventilation
vasodilators (SNP, NTG), hypocapnia, hypothermia and
• Intrapulmonary shunting
thromboembolism.
• Decreased FRC
• Poor oxygen delivery to the tissues
• Endobronchial intubation
• Systemic hypoperfusion (hypovolemia) • Pneumothorax
Embolus • Emphysema (subcutaneous/mediastinal)
• Sepsis – acute lung injury • Pulmonary aspiration of gastric contents
• Local problems (cold limb, Reynaud • Reduced cardiac output
phenomenon, sickle cell disease)
• Hemorrhage (trocar injury)
• Increased oxygen demand • IVC compression
• Malignant hyperpyrexia • Impaired venous return
• Shivering • A r r hy t h m i a ( H y p e rca r b i a o r i n h a l e d
• Sepsis anesthetics)
• Myocardial depression (drug induced/acidosis)
Intra operative hypoxemia during specific situations
• Reduced cardiac output
Hypoxemia can occur any time during anesthesia, • CO2 embolism
induction, maintenance or reversal. It can occur When hypoxemia occurs during laparoscopic surgery,
preoperatively, intra or postoperatively. It can make the operating table and patient straight; give
occur during intubation or extubation. Hypoxemia 100% O2. Release pnuemo-peritoneum. Switch off
may develop during general anesthesia or regional the volatile anesthetics. Check the tube position; find
anesthesia. It may occur in unintubated as well as out the cause of hypoxemia. In cases of refractory
intubated patients. It may develop in spontaneously hypoxemia or high airway pressure, convert to open
breathing patients or controlled ventilation patients. procedure. In patients with pulmonary dysfunction,
It can occur due to pre-existing conditions or due to pre-op ABG may be done and intra-operative radial
intra operative complication. Hypoxemia can occur catheterization may be considered.
during any type of surgical procedures. Certain specific
Pneumothorax
situations are given below although the list is not
complete. Pneumothorax may develop in polytrauma patients,
chest trauma patients, in emphysematous patients
Hypoxemia during Laparoscopic Surgery is very during IPPV, after central venous cannulation (IJV/
common. The mechanism of hypoxemia during SCV), after supraclavicular brachial plexus block.
laparoscopic surgery may be Spontaneously breathing patient may present with
dyspnea, tachycardia, tachypnea and hypotension.

In a patient who is on controlled ventilation, lung fatigue and apnoea. Premature infants have deficient
compliance decreases; reservoir bag becomes tight; surfactant. They are prone for Respiratory Distress
peak airway pressure increases. Chest expansion is Syndrome. Because of the difference in the airway
decreased. There is diminished air entry on auscultation anatomy, there may be intubation difficulty. Mask
and hyperresonance on percussion. The condition may ventilation is also difficult. Endobronchial intubation
be confused with bronchospasm or hyperinflation in and accidental extubation are possible.
COPD patients. Chest X-ray confirms the diagnosis
Hypoxemia in Parturients
by the presence of air in the pleural cavity and lung
collapse. X-ray chest may not be always possible in the Pregnant women have a reduced FRC by 20%. Oxygen
intra operative setup. Prompt diagnosis is essential reserve is decreased. Oxygen consumption is increased
because tension pneumothorax collapses the lung; by 20%. Parturients are more prone for precipitous
gas occurs. Immediate intervention should be done by fall in PaO 2 even after a brief period of apnoea.
inserting an IV cannula in the second intercostal space (Failed endotracheal intubation is more common in
at the midclavicular line. Definite treatment is with an obstetric patients than in surgical patients). Difficulty
intercostal drainage. in intubation, delayed intubation and pulmonary
aspiration of gastric contents may worsen the situation,
Pulmonary edema
regional anesthesia is preferable. Preoxygenation
Pulmonary edema may result from i) increase in preload is a must before induction of GA. Rapid sequence
(fluid overload). ii) Decrease in myocardial contractility intubation with Sellick’s maneuver is to be done. In
(CCF) ii) increase in capillary permeability (sepsis, ARDS, case of failed intubation, algorithm for failed intubation
neurogenic pulmonary edema, high attitude pulmonary should be followed and alternate plan for oxygenation
edema) iv) Negative pressure pulmonary edema (relief should be readily available. Oxygenation should be
of upper airway obstruction). During early stages, fluid monitored continuously.
accumulation occurs in the interstitial space. Airway
Hypoxemia in elderly patients
pressure increases. Lung compliance decreases. In the
later stages, fluid floods into the alveoli. Management is Elderly patients coming for anesthesia are more prone
aimed at identifying the cause and treating it. Steps are for hemoglobin desaturation
taken to decrease the preload, improve the myocardial
contractility, restore normal sinus rhythm, treat sepsis, • Compromised respiratory system
increase FiO2 and apply PEEP. Loss of lung elastin, reduced thoracic compliance,
Hypoxemia in children reduced alveolar surface area, increased residual
volume, loss of vital capacity, impaired efficiency
Neonates and infants are prone for more rapid of gas exchange, increased work of breathing.
desaturation during anesthesia. Small diameter of
airways increases the airway resistance. (Resistance is • Compromised cardio-vascular system
inversely proportional to the radius raised to the fourth • There is decreased requirement of IV induction
power. Chest wall and airway are highly complaint. agents, opioids, benzodiazepines and inhalational
Negative intra thoracic pressures partly maintained. agents
Each breath is accompanied by functional airway
closure. Oxygen consumption is 2-3 times as high as • Prolonged drug effect is seen after sedatives
in adults. In premature infants, work of breathing is 3 narcotics and muscle relaxants.
times that of the adult. Children acquire type 1 muscle
Hypoxemia in obese patients/bariatric surgery
fibres in respiratory muscles only at the age of 2. Only
type 1 muscle fibres are capable repeated exercise. Hypoxemia in obese patients is due to difficult mask
Hence, neonates and premature infants go in for early ventilation, difficult laryngoscopy, difficult intubation,

decreased lung volumes and capacities. Hence, • Begin OLV with Vt=10 ml/kg iv
preoxygenation is less effective in obese patients. • Adjust RR so that PaCO2=40 mmHg
Time for desaturation after safe apnoea (Apnoeic
• Monitor oxygenation and ventilation continuously.
oxygenation reserve) is reduced. FRC is further reduced
in supine position and still further decreased with • If severe hypoxemia persists
induction of anesthesia. Airway resistance is increased. • Non-dependent lung CPAP
Obese patients are prone for pulmonary aspiration of
gastric contents. They are more sensitive to depressant • Dependent lung PEEP
effects of hypnotics and opioids. Parenteral or neuraxial
• Intermittent two lung ventilation
opioids carry potential fatal/near fatal respiratory
misadventure. There may be associated cardiovascular • Clamp pulmonary artery as soon as possible
abnormalities, COPD, pulmonary hypertension, RVH,
RVF, corpulmonale etc. • Other causes of hypoxemia should not be forgotten
(e.g.) Depleted O2 supply, malposition or obstruction
The following factors should be considered of DLT, decreased cardiac output or conditions which
• Preoperative polysomnography (Definitive increase O2 consumption (shivering, hyperthermia)
diagnosis for obstructive sleep apnoea syndrome Hypoxemia during orthopedic procedures
is polysomnography)
Hypoxemia is not uncommon during or after orthopedic
• Supine room air SpO2
surgical procedures.
• Room air ABG
• Pulmonary function test The possible causes may be
• Preop respiratory preparation (cessation of • Difficulty in intubation in cases of ankylosing
smoking, antibiotics, bronchodilators, breathing spondylitis, rheumatoid arthritis, fracture cervical
exercises) spine, prior cervical spine fusion and congenital
• Antacid premedication deformities of cervical spine
• Avoidance of sedative premedication • Unusual positions during surgery (e.g. prone, sitting,
• Awake intubation lateral decubitus, fracture table) à ETT migration,
• Induction and recovery in upright position kinking, dislodgement
• Post-op semi-recumbent position • Lateral position for prolonged periods may produce
• Intense post op monitoring and nursing care dependent lung hypoventilation
• Oxygen therapy alone may not be sufficient. • Upper airway edema in long procedures may result
Prophylactic CPAP/BiPAP may be necessary in post-operative respiratory dysfunction
• Early mobility
• Associated rib injury in polytrauma patients
Hypoxemia during one lung ventilation
• Pulmonary embolism (Fat, thrombus, bone cement,
Hypoxemia occurs in almost all cases during one lung bone marrow, air)
ventilation. The reason for hypoxemia is ventilation- • Upto 75% of fracture femur patients may
perfusion mismatch, because the non-dependent develop DVT
lung is not ventilated but continues to get perfused.
Following are the measures taken to maintain • 10-15% of patients with long bone fracture
oxygenation during OLV. develop fat embolism
• Two lung ventilation as long as possible • Hypoxemia due to bone cement embolism may
• High FiO2=1.0 persist for 5 days post operatively

• Pneumothorax may develop after supraclavicular • High cardiac output is seen in CLD patients. The
brachial plexus block for upper limb surgical transit time in pulmonary capillaries is less and thus
procedures the O2 uptake is low. Poor DLCO is seen in cirrhotic
patients.
• Major blood loss or fluid overload
Hypoxemia at high altitude
• Hypoventilation due to sedatives during regional
anesthesia Anesthesiologists who work at high altitudes above
the sea level should be aware of decrease in PaO2.
• Transient fall in CVO2 is seen after tourniquet release
This is because of the low barometric pressure and
Hypoxemia in renal disease proportionately lower PiO2. One should be aware of this
when resuscitating and transporting a patient in aircraft.
Arterial hypoxemia may be observed during or after
dialysis. It is seen with both acetate and bicarbonate Diffusion hypoxia (Fink’s effect)
dialysates. It may be due to
Diffusion hypoxia occurs at the end of general
• Hypoventilation: Acetate removes the carbon anesthesia when N2O: O2 is switched off and when
dioxide load and bicarbonate dialysis suppresses the the patient is allowed to breathe air. Nitrous oxide is
respiratory drive due to an increase in bicarbonate 31 times more soluble than nitrogen. For every one
molecule of nitrogen entering into blood from alveoli,
• V/Q mismatch may also contribute to post-dialysis 31 molecules of nitrous oxide enters into alveoli from
hypoxemia, which is similar in patients with or blood. The alveolar oxygen is diluted and hypoxemia
without lung disease results. This is more common during the first 5-10
• Reduction in intra vascular volume and cardiac minutes of recovery. Administration of 100% O2 is
output can also cause hypoxemia. essential to overcome the situation.
However, the main reason for hypoxemia is Diagnosis of Hypoxemia

hypoventilation. PAO2 decreases: P (A-a) O2 does During early days of anesthesia, defective oxygenation
not change; PaCO2 increases. This should be born in of the patient was identified by cyanosis and dark
mind when a patient on dialysis comes for anesthesia blood in the surgical field. Cyanosis occurs when the
especially for short surgical procedures under LA with deoxygenated hemoglobin is > 5g/100 ml. Appreciation
spontaneous breathing. Treatment is with oxygen of bluish discoloration of skin and mucus membrane
supplementation. is a subjective phenomenon. Cyanosis is usually
Hypoxemia in liver disease observed when the Hb saturation is less than 85%. This
corresponds to a PaO2 of 45-50 mm Hg in adults and
Hypoxemia is common in chronic liver diseases patients 35-40 mm Hg in infants. Cyanosis may be observed
e.g. cirrhosis of liver. Reasons include when there is no hypoxemia e.g. methemoglobinemia,
sulfhemoglobinemia. Cyanosis may not be apparent in
• Ascites and pleural effusion may interfere with gas
the presence of anemia or peripheral vasoconstriction.
exchange by restricting ventilation
Appreciation of dark blood is again a subjective
• Many of these patients smokes; COPD may produce
phenomenon. Sometimes it may be too late to
V/Q mismatch and abnormal gas exchange.
appreciate dark blood. By the time dark blood is
• Repeated episodes of pneumonia observed, irreversible damage would have already
occurred.
• CLD patients have a decreased HPV response.
Hence, there is increased blood flow to poorly Several monitors are used now to detect hypoxemia.
ventilated lung units Pulse oximeter is the most commonly used one. Other

monitors include, oxygen analyser (FiO2 monitor), • Consider using a mask instead of ETT
ABG, ScvO2. Other monitors which may be useful in • Find out the exact site of leak or block
indirectly identifying the cause of hypoxemia includes
capnography, airway pressure monitor etc. • Decreased FRC
Assessment of oxygenation UU Hyper inflate gently with PEEP
• Measurement of inspired gas with an oxygen • Absorption atelectasis

analyzer UU Decrease FiO2
• Assessment of hemoglobin saturation with a pulse UU Remove secretions
oximeter and observation of skin colour.
• Increased airway resistance (bronchospasm)
Hypoxemia management
UU Deepen anesthesia
Management of hypoxemia is aimed at identifying the UU Add volatile anesthetics (halothane/
cause and treating it. General measures include the sevoflurane)
following UU Stop the precipitating drug (Histamine
releasing drug like atracurium)
• Expose the chest, breathing circuit and all airway
UU Salbutamol nebulization
connections
UU Inj.Aminophylline 5mg/kg bolus followed
• Give 100% O2 (FiO2=1.0) by 0.5-1mg/kg/hr infusion
• Hand ventilate (Switch off anesthesia ventilator);
Give few large breaths • R-L shunt
• Get the feel of the bag UU Cardiovascular support
• Confirm FiO2. If the FiO2 is not at the set level UU Increase SVR: Lifting the legs, vasopressors
• Look at cylinder colour code. Whether the cylinder (noradrenaline), IVF
has O2 or is it depleted UU Decrease PVR; Remove PEEP, avoid high
intra thoracic pressure
• Confirm that the pipe line connections are all right.
UU Maximize FiO2, nitric oxide
• If in doubt about the gas in the cylinder or if there
is doubt about cross connection of pipelines – Use • Hypovolemia
a separate cylinder supply
UU IVF, Blood
• Consider replacing the anesthesia machine with
another one • Increased O2 demand
• As a last resort, think of disconnecting the machine UU Give 100% O2
and ventilate with an AMBU bag
• Confirm the ETT position • Pneumothorax
• Auscultate and confirm bilateral equal air entry UU ICD
• Rule out endobronchial intubation
• Methemoglobinemia
• Rule out ETT kinking, obstruction (Secretions,
mucus, blood or foreign body). Insert a suction • 100% O2
catheter or bougie or FOB. Remove the secretions. • Inj. Methylene blue 1-2 mg IV
Consider changing the ETT
• Check whether the ventilator pattern is correct Prevention of hypoxemia
• Use a Bain’s circuit instead of circle system • Before every anesthetic, anesthesia machine
• Try a self-inflating bag (AMBU bag) check-up should be properly carried out. This
should include check-up for emergency ventilation • Optimization of co-morbid conditions
system, high pressure system, low pressure system,
• Continuous vigilance is the price of safety
scavenging system, breathing system, manual
and automatic ventilating system and monitoring • High degree of suspicion is to be maintained
system.
Conclusion
• Use anesthesia machine with O2 pressure failure
alarm and hypoxic guard To conclude, the occurrence of Intra Operative
Hypoxemia is an emergency situation, which requires
• O2 flow meter tubes placed downstream immediate intervention. If the hypoxemia is severe and
sustained, it can be life threatening. It is always better
• Check valve to prevent flow of gases from the
to prevent hypoxemia rather than treating it. However,
machine to the cylinder or pipeline
if hypoxemia occurs, it should be promptly diagnosed
Minimum mandatory O2 flow and managed.
• Cylinder should always be kept closed when pipeline References
in use. Cylinder should be used to a reserve in case
1) Race 2012: Intra Operative Hypoxemia –
if pipeline supply fails
Ponnambala Namasivayam S – Page: 159-168
• Pressure gauge (cylinder or pipeline) should be 2) Intra Operative Hypoxemia - DM Anderson, MD.,
observed repeatedly during use Decision making in Anaesthesiology : An algorith-
• Always use FiO2 monitor mic Approach http://books.google.co.in
3) Calzia E. Rademacher P.Alveolar Ventilation and
• Careful check-up should be carried out after
pulmonary blood flow, the V(A)Q concept, Inten-
installation, alteration, repair of pipelines and after sive Care Med 29.1229-1232, 2003
construction and civil work
4) Bamber J.Airway Crises, Cur Anaesthesia Critical
• Master alarm system should be installed and Care 14 (1):2-8, 2003
maintained to warm about depletion of central O2
supply 5) Hedensiema G.Rohen HU. Atelectasis formation
during anesthesia: causes and measures to pre-
• Ensure correct placement of ETT vent it. J CIIn Monil 16-329 335, 2000
• ASA monitoring standards should be followed 6) Godart G.Rey C.Prat A. et al: Atrial right-to-left
shunting causing severe hypoxemia despite nor-
• Adequate pre-operative investigations and mal right sided pressures. Report of 11 consecu-
assessment tive cases corrected by percutaneous closure, Evr
Heart J 21 (6):483-489, 2000
• Proper pre-operative preparation of patient

MCQ
1. Induction of anaesthesia causes reduction in 4. Hypoxemia can be prevented by all except?
______?
a. Machine check
a. TV
b. Oxygen failure alarm
b. MV
c. Oxygen flowmeter tube placed
c. FRC upstream
d. PEEP d. Hypoxia guard
2. What can occur if a patient is getting high 5. What is Fink’s effect caused due to?
FiO2?
a. Oxygen
a. Diffusion hypoxia
b. Nitrogen
b. Absorption atelectasis
c. Carbon dioxide
c. Diffusion defect
d. Nitrous oxide
d. Hypoventilation
3. Factors inhibiting hypoxic pulmonary vasocon-
striction are all except?
a. Hypocapnia
b. Hyperthermia
c. Inhaled anaesthetics
d. Thromboembolism
5.(d) 4.(c) 3.(b) 2.(b) 1.(c)

Answers

20 Pain Management Strategies after Thoracotomy Surgeries
Associate Professor, Gyorgy Frendl

Harvard Medical School,
Brigham and Women’s Hospital.
After this presentation you should be able to: pulmonary morbidities, DVT, AKI and atrial
fibrillation, RV failure)
1) Understand the role of immediate and long-
term postoperative pain (and its effective • Design appropriate pain management (together
management) in post-thoracotomy outcomes with surgeons and other consultants) strategies to
mitigate the risk of peri-operative morbidities
2) Better assess the health status of patients
planning to undergo thoracic surgical procedures • Identify patients at high risk for increase need
of pain medications
3) Appropriately risk stratify patients. Identify those
at high risk for peri-operative mortality and • Identify patients at high risk for post-operative
morbidity (including pulmonary morbidities, DVT, pain due to the surgical approach (example:
AKI and atrial fibrillation, RV failure) sternotomy vs. thoracotomy)
4) Design appropriate pain management (together • Identify patients with low tolerance for
with surgeons and other consultants) strategies IV or oral opioids with increased risk for
to mitigate the risk of peri-operative morbidities perioperative morbidities if opioids are used
5) Understand the importance of using opioid- Defining perioperative risks
sparing pain management strategies in order to
Of the many variables relevant (see figure below), ASA
improve outcomes and reduce the risk of opioid
class is the best predictor of postoperative morbidity
addiction.
and mortality.
Goal
Design the best pain management strategies to enable NSQIP Risk Predictor Website
the best outcomes for your patients after thoracic
surgical procedures
Approach
Design the best anesthetic management appropriate for
the patient’s procedure, comorbidities, prior functional
status and perioperative risks for morbidities and
mortality.
Thought process
• Assess both the overall and cardio-pulmonary
health status of patients
• Risk stratify patients. Identify those at high risk for
peri-operative mortality and morbidity (including

Pain Management Strategies 200 Gyorgy Frendl
after Thoracotomy Surgeries
Present issues and future directions of chest surgery Complex anesthetic planning
• Pulmonary complications are the highest in the Plan on implementing an opioid-sparing multi-modal
peri-operative setting and have not improved acute pain management strategy
significantly (particularly high for thoracic surgery • Consider regional anesthesia (alone or with GA),
patients) minimize narcotics
• Pulmonary function of thoracic surgical patients • Use a multi-modal approach to analgesia
almost never improves immediately after surgery.
Pain can be a major contributor • Tylenol [IV or PR/PO]
• Non-pulmonary complications (A Fib, DVT and AKI, • Gabapentin

RV/LV dysfunction) are most frequent for thoracic • IV Lidocaine, postop lidocaine patch
and cardiac surgical patients
• Liposomal bupivacaine
• New diagnostic guidelines for lung carcinoma
require CT and biopsies for many more patients • US-guided regional (paravertebral, intercostal)
blocks / catheters
• Cancer care improvements are dictating procedures
(bronchoscopy, re-biopsies, EBUS, etc.) for very ill • Epidural catheter
stage III and IV cancer patients (often with ASA III
• Recommend minimally invasive surgical procedures
or IV status) commonly with poor functional status

A comprehensive blueprint for planning of the anesthetic strategy
Approaches to pain management • Dexmedetomedine (alpha-2 agonist, like

clonidine), proven antihypertensive effects,
• Minimize surgical/peri-operative pain as well as sedative and anxiolytic properties and
long-term neuropathic pain (modifiable by surgical analgesic qualities. Weak anesthetic, opioid
approaches and techniques; thoracotomy vs. sparing, likely ineffective alone.
minimally invasive thoracoscopy) • Intravenous Lidocaine (may be potentiated
by Dexmedetomidine)
• Manage short-term intra and post-operative pain
• Regional anesthetic/analgesic techniques (US-
• Oral medications (Tylenol, gabapentin, oral
guided or not)
opioids, NSAIDs, etc)
• Thoracic epidural (pure local analgesic or
• Intravenous medications combined with low dose narcotic)
• Opioids (short and long acting) • Paravertebral block or catheter(s)
• NSAIDs • Proximal intercostal block or catheters
• Tylenol • Intercostal (distal) nerve block
• Ketamine • Intra-procedural injection of liposomal
bupivacaine (mostly by the surgeons)

• Manage long-term post-operative pain; post- • Nerve blocks – intercostal nerve or dorsal
thoracotomy pain syndrome (PTPS) (often root ganglion block (temporary)
neuropathic in nature; intercostal neuralgia is • Cryo- or radiofrequency ablation (for severe
caused by inflammation, damage or compression cases)
to the intercostal nerves). Forty to fifty percent of • Severe cases may require an implant of
patients may experience persistent pain following a spinal cord or peripheral nerve stimulator
thoracotomy, and as much as 30 percent of patients References
may continue to experience the pain for four to five
years after the surgery or even permanently 1. RA Meguid et al. Annals of Surgery, July 2016,
264(1):23-31
• Pharmacological management:
2. Allan Gottschalk et al. Anesthesiology, V 104, No
• Nerve-stabilizing medications 3, Mar 2006
• Tricyclic anti-depressants (Amitryptiline,
Nortryptiline, Desipramine) 3. J Richardson et al. Br. J. Anaesthesia 83(3):387-392;
• A n ti - c o n v u l s a n t s ( G a b a p e n ti n , 1999
carbamapezime, oxcarbazepime) 4. Saeki H, Ishimura H, Higashi H, et al. Postoperative
• NSAIDs management using intensive patient-controlled
• Long-acting opioids epidural analgesia and early rehabilitation after
an esophagectomy. Surg Today 2009;39:476-80.
• Non-somatic treatments
10.1007/s00595-008-3924-2 [PubMed] [Cross Ref]
• Rehabilitation (Physico-therapy)
5. Buise M, Van Bommel J, Mehra M, et al. Pulmonary
• Cognitive-behavioral treatment
morbidity following esophagectomy is decreased
• Psychological treatment
after introduction of a multimodal anesthetic
• Interventional pain management regimen. Acta Anaesthesiol Belg 2008;59:257-
61. [PubMed]

6. C e n s e H A , L a ga r d e S M , d e J o n g K , e t 9. Michelet P, D’Journo XB, Roch A, et al. Perioperative

al. Association of no epidural analgesia with risk factors for anastomotic leakage after
postoperative morbidity and mortality after esophagectomy: influence of thoracic epidural
transthoracic esophageal cancer resection. J analgesia. Chest 2005;128:3461-6. 10.1378/
Am Coll Surg 2006;202:395-400. 10.1016/j. chest.128.5.3461 [PubMed] [Cross Ref]
jamcollsurg.2005.11.023 [PubMed] [Cross Ref]
10. Yokoyama M, Itano Y, Katayama H, et al. The effects
7. Neal JM, Wilcox RT, Allen HW, et al. Near-total of continuous epidural anesthesia and analgesia
esophagectomy: the influence of standardized on stress response and immune function in
multimodal management and intraoperative fluid patients undergoing radical esophagectomy. Anesth
restriction. Reg Anesth Pain Med 2003;28:328-34. Analg2005;101:1521-7. 10.1213/01.
[PubMed] ANE.0000184287.15086.1E [PubMed] [Cross Ref]
8. Flisberg P, Törnebrandt K, Walther B, et al. Pain 11. Dureja GP (2017) Intercostal Neuralgia: A Review. J
relief after esophagectomy: Thoracic epidural Neurol Transl Neurosci 5(1): 1076.
analgesia is better than parenteral opioids. J
Cardiothorac Vasc Anesth 2001;15:282-7. 10.1053/
jcan.2001.23270 [PubMed] [Cross Ref]

MCQ
1. Best predictor for post operative morbidity 4. All are part of acute pain management of
and mortality in patients undergoing thorac- thoractomy pain except
tomy
a. Paravertebral block
a. ASA grade
b. Intra procedural liposomal
b. Steroids usage Bupivacaine
c. Age c. Thoracic epidural
d. Number of procedure d. Spinal cord implants
2. Highest number of complications in perioper- 5. Post thoractomy pain syndrome is often be-
ative setting ofthoractomy cause of
a. Pneumonia a. Pectoral nerve damage
b. AF b. Intercostal neuralgia
c. RVF c. Injuries to pleura
d. AKI d. None of the above
3. Complex anaesthetic plan for thoractomy pain
management includes all except
a. Regional anaesthesia
b. Post operative lidocaine patch
c. Gabapentin
d. High dose opioid
5.(b) 4.(d) 3.(d) 2.(a) 1.(a)

Answers

21 Fluid management in children
Professor, Neerja Bhardwaj

PGIMER,
Chandigarh.
Key points
Ø The objective of intraoperative infusion therapy is to maintain/re-establish the child’s normal

physiological state
Ø Perioperative fasting times for children should be as short as possible to prevent patient discomfort,
dehydration and ketoacidosis
Ø Use of hypotonic fluids is no longer recommended because it increases the risk of developing
hyponatremia postoperatively
Ø Glucose administration is recommended only in those patients at increased risk for hypoglycaemia such
as neonates, children receiving hyperalimentation and those with endocrinopathies
Ø Balanced isotonic electrolyte solution with 1–2.5% glucose is recommended for maintenance therapy
Introduction in a normal child. In the past, fluid management in

children has undergone multiple changes ranging
Children undergoing surgery require administration
from administration of hypotonic fluids to the present
of fluids to meet requirements of fluid deficits,
understanding of the advantages of isotonic fluids.
maintenance fluid requirements and fluids to maintain
For a safe fluid therapy in children two aspects of fluid
an adequate tissue perfusion as well to counteract
management are important to consider: the need for
the effects of anaesthetics. These deficits include –
glucose and the sodium content of the infusion solution.
preoperative deficits (fasting, gastrointestinal, renal or
cutaneous losses), haemorrhage and third space losses. Historical basis of fluid management in children
The objective of intraoperative infusion therapy is to
Since the last decade the standard fluid management
maintain or re-establish the child’s normal physiological
guidelines for hospitalized children were based on the
state (normovolemia, normal tissue perfusion, normal
Holliday and Segar formula. The 4/2/1 formula was
metabolic function, normal electrolytes, and acid–base
designed based on the understanding that paediatric
status). Maintenance therapy represents the fluids
water maintenance needs parallel energy expenditure:
and electrolyte requirements needed by the average
100 mL/100 kcal for the first 10 kg of body weight,
individual with a normal intracellular fluid (ICF) and ECF
50 mL/100 kcal for 11–20 kg, and 20 mL/100 kcal for
volumes over a 24 hour period. Thereby, maintenance
every kilogram of body weight above 20 kg. They also
therapy is the provision of fluid and electrolytes to
proposed 3mEq/100 kcal sodium (Na) per day and
replace anticipated physiological losses from breathing,
2mEq/100 kcal potassium (K) per day as maintenance
sweating and urine output.
electrolyte requirements based upon the electrolyte
The type of fluid administered should be based on composition of breast and cow’s milk. Based on this,
characteristics of the fluid compartments present hypotonic fluid was identified as the ideal maintenance

Fluid Management in Children 206 Neerja Bhardwaj
fluid choice in hospitalized children, leading to the use had been NPO for at least 6 to 8 hours. However, based
of 0.225% and 0.45% saline in paediatric population. on the liberalization of fasting guidelines allowing
clear fluids for up to 2 hours, the amount of IV fluids
However, since the past 20 years there has been
required to cover for preoperative fluid deficit may be
a growing awareness that administration of these
less. Also, irrespective of the fasting recommendations
hypotonic solutions can lead to hyponatremia especially
of 2hours the child may be fasting for >6 hours in
in children undergoing surgery. Although the reported
certain situations. The guidelines recommend that
incidence of postoperative hyponatremia has varied
the perioperative fasting times for children should
from 11 to 31%, nearly all studies consistently show
be as short as possible to prevent patient discomfort,
that postoperative patients have an increased risk of
dehydration, and ketoacidosis. If preoperative and
developing hyponatremia.
postoperative fasting times are short, perioperative
The need of glucose administration to compensate intravenous fluid therapy is not required in children
for preoperative fasting depends on the number of beyond neonatal age who drink sufficient volumes
hours the child is kept fasting. The concentration of and undergo short procedures (<1 hour) with a venous
dextrose required has seen a change from use of 5% to access in place. If the child is fasting for >6hours
use of 1-2% dextrose solutions to avoid intraoperative appropriate volume of fluid can be administered.
hyperglycemia.
The need for glucose during maintenance fluid
Physiology of fluid requirement therapy: Hypoglycemia vs. hyperglycemia
Intraoperatively fluids are administered to replace In the paediatric population both hypoglycemia and
preoperative deficits, meet maintenance requirements hyperglycemia is hazardous.
and replace the ongoing losses occurring during the
Hypoglycemia
surgical procedure. Most anaesthesiologists use either
normal saline (NS) or Ringer lactate (RL) as the fluid of Glucose is essential for the normal brain to function.
choice for both maintenance and for the deficit fluid Severe hypoglycemia, can adversely affect the central
replacement. There is no controversy regarding the rate nervous system, especially in neonates. Depending
at which the maintenance fluid needs to be replaced. on its degree, hypoglycaemia may provoke a counter-
However, it is debatable what amount of fluid is needed regulatory stress response (increase in plasma cortisol,
for the preoperative deficit and the so called “third epinephrine, glucagon and growth hormone); increase
space losses”. regional blood flow with a loss of cerebral vascular
autoregulation and it may alter cerebral metabolism
Role of preoperative fasting time
leading to a shift from glycolytic precursors to Krebs’
It was thought that children develop preoperative fluid cycle intermediates, alteration of ion homeostasis and
deficit because of ongoing insensible fluid losses and acid–base abnormalities. All these changes can lead to
urine output. Based on this, Furman et al proposed clinical symptoms and permanent neuronal damage.
calculating preoperative deficit by multiplying the Initial research in 1970s suggested that children
Holliday and Segar hourly rate by the number of hours become hypoglycemic under anaesthesia. However, it
the patient was NPO. Half of this amount was replaced is now been shown in recent studies that the incidence
during the first hour of surgery followed by other half of preoperative hypoglycemia is between 0% and 2.5%
over next 2 hours. Later, Berry et al suggested that and is usually associated with fast durations from 8 to
children 3 years and younger should receive 25 mL/ 19 hours.
kg, whereas children 4 years and older should receive
Hyperglycemia
15 mL/kg of basic salt solution over the first hour of
surgery. The methods of both Furman et al and Berry In the presence of ischemia or hypoxia, it is speculated
were developed based on the assumption that patients that the impaired metabolism of excess glucose causes

an accumulation of lactate, a decrease in intracellular neonates. Whether such low glucose-containing fluids
pH, and subsequently severely compromised cellular maintain blood glucose levels by initiating catabolism of
function that may result in cell death. Hyperglycemia the body’s own stores is unknown. Datta et al found in
can also induce an osmotic diuresis that may lead to their study that 1% dextrose-containing fluid promotes
dehydration and electrolyte abnormalities. It has also catabolism and insulin resistance, increases acidosis,
been shown that in children, hyperglycemia, especially and may result in rebound hyperglycemia in neonates.
in the presence of an ischemic or hypoxic event, worsens They therefore recommend 2 – 4% dextrose solution
neurologic outcomes as well as increases morbidity and as metabolically suitable.
mortality. Studies have shown that the infusion of 5
to 10% dextrose in the paediatric population leads Risk of hyponatremia
to hyperglycaemia. In three prospective randomized In the past, several studies have reported hospital-
studies, it was seen that using 2 or 2.5% dextrose acquired hyponatremia in healthy children after
solutions raised blood glucose levels during surgery to elective surgery after the infusion of hypotonic
a lesser extent and kept the sugars in the normal range solutions. Administration of a hypotonic solution,
(less than 8.3 mmol/l) than 5% solutions. particularly in hypovolemic children, decreases
Based on above observations there is a growing the serum sodium concentration and serum
consensus that intraoperative dextrose is selectively osmolality. This results in symptoms of headache,
administered only in those patients at greatest risk nausea, vomiting, weakness and lethargy, followed
for hypoglycemia. Also, where dextrose is to be by seizures, cerebral edema, herniation of the
administered one should consider the use of fluids with cerebellar peduncles, aspiration and death in
lower dextrose concentrations (e.g., 1% or 2.5%). The 30% of affected children. Various studies have
populations at highest risk of hypoglycemia include reported 11 to 31% incidence of postoperative
neonates, children receiving hyperalimentation, and hyponatremia and nearly all studies have shown
those with endocrinopathies, in whom monitoring that postoperative patients have an increased risk
blood glucose levels and adjusting the rate of infusion of developing hyponatremia. The reason for the
is also recommended. Routine dextrose administration increased risk of hyponatremia in postoperative
is no longer advised for otherwise healthy children period is related to the release of antidiuretic
receiving anaesthesia. hormone (ADH). ADH (vasopressin), is synthesized
in the supraoptic nuclei of the hypothalamus and
However, neonates require dextrose-containing fluid is released from the posterior pituitary gland.
during surgery because they require 4 – 8ml/kg glucose ADH binds to the vasopressin V2 receptor in the
for brain development. In addition, limited glycogen basolateral membrane of the collecting duct, which
reserve makes the neonate susceptible to hypoglycemia leads to the insertion of aquaporin-2 channels in
without glucose supply. Association of Paediatric the apical membrane and ultimately to increased
Anaesthetists of Great Britain and Ireland consensus water permeability and water reabsorption. The
guidelines and European consensus statement primary stimulus for ADH release is an increase
guidelines recommend intraoperative use of low in osmolality, but many non-osmotic stimuli may
dextrose (1–2.5%)-containing isotonic fluids which have also contribute (Table 1). The ADH levels peak at
been shown to maintain acceptable blood glucose levels 6 – 12 hours after surgery and gradually taper off
and prevent electrolyte imbalances during surgery. over the next 5 days. Kanda et al in their study
Sumplemann et al found that the intraoperative use showed that hyponatremia (<137mEq/L) developed
of an isotonic balanced electrolyte solution with 1% in patients who had both elevated ADH levels and
glucose and a mean infusion rate of 10 ml/kg/h helps received hypotonic 0.6 % saline; elevated ADH levels
to avoid acid-base dysbalance, hyponatraemia, hypo- alone or hypotonic saline alone were not associated
glycemia, ketoacidosis, and hyperglycemia in surgical with hyponatremia.

Hemodynamic stimuli Non-hemodynamic stimuli

Hypovolemia CNS disease
• Brain tumors
• Meningitis, encephalitis
• Head trauma
Decreased effective circulatory blood volume Pulmonary disease
• Cirrhosis • Pneumonia
• Congestive heart failure • Bronchiolitis
• Hypoalbuminemia • Positive pressure ventilation
• Hypoxia
Hypotension Oncological diseases
Postoperative state
Miscellaneous
• Pain
• Nausea vomiting
• Stress
Medications
• Narcotics
• Vincristine
• Cyclophosphamide
Table 1: Non-osmotic causes of ADH release
Role of fluid tonicity and hyponatremia less than approximately 150 mEq/L is considered to be
hypotonic.
Tonicity is a measure of effective osmolality. Solutes
like sodium which have restricted cell-membrane Randomized controlled studies comparing hypotonic
permeability, remain in the extracellular fluid (ECF) IV fluids to isotonic IV fluids in paediatric surgical
compartment and create an osmotic pressure gradient and medical patients have consistently shown that
which drives water movement from the intracellular hypotonic IV fluids are associated with hyponatremia.
fluid (ICF) compartment to the ECF compartment. A recent meta-analysis of ten randomized controlled
Solutes which are freely permeable across cell trials, nine of which included surgical patients,
membranes like dextrose distribute equally between demonstrated a higher risk of hospital-acquired
the ECF and ICF compartments and do not create an hyponatremia when hypotonic IV fluids were
osmotic pressure gradient or drive water movement. administered (RR 2.24, 95 % CI 1.52–3.31). One should
Thus, the tonicity of an IV solution depends primarily on also keep in mind that hyponatremia can occur even
the content of its electrolytes. Normal plasma sodium in patients receiving isotonic IV fluids, related to the
concentration [Na] is 135–145 mEq/L, but the [Na] in presence of high circulating ADH levels. ADH leads to
the aqueous phase of plasma water is approximately the reabsorption of water in the collecting duct and the
150 mEq/L; therefore, fluid with a tonicity (Na + K) of creation of concentrated urine with a urine osmolality of

>100 mOsm/kg. Therefore, when the ECF compartment normal BV, normal tissue perfusion, normal metabolic
is expanded by isotonic fluids in the presence of high function, normal electrolytes, and acid–base status).
circulating ADH, sodium is excreted in the urine and free Small children have a larger ECFV than adults but the
water is retained, leading to hyponatremia. composition of the ECF is similar across all age groups.
Therefore, the same solutions for infusion as for adults
It is therefore recommended that a balanced isotonic
can be used for intraoperative fluid therapy in children.
electrolyte solution with 1–2.5% glucose should be
Table 2 shows the tonicity of various types of fluids
used for the background infusion. The background
available. As compared to ECF, conventional Ringer’s
infusion may be initiated with an initial infusion rate of
lactate solution is somewhat hypotonic (276 instead of
10 ml/kg/h and be adjusted to the actual requirement
308 mOsmol/L), while isotonic sodium chloride solution
during the further course (target: normal ECFV). In
contains too much chloride (154 instead of 95–106
case of children at risk and longer surgeries, blood
mmol/L). Therefore, infusion of large volumes may
sugar levels should be measured regularly and glucose
reduce osmolarity or result in hyperchloremic acidosis.
administration should be adjusted (target: normo-
Infusion of smaller volumes are usually compensated
glycemia and stable acid–base status).
by the children. Balanced isotonic electrolyte solutions
What type of fluid for perioperative fluid therapy? mimic the composition of ECF more closely. In a
direct comparison, they are therefore closer to the
Total body water represents as much as 85% of body physiological range of children, too, and also have
weight in premature infants, 80% in full-term newborns fewer undesirable effects on osmolarity and acid–base
and 65% in infants of 12 months of age compared electrolytes balance. A balanced isotonic electrolyte
to 60% in adults. These age-related changes in TBW solution should be used for fluid therapy (target normal
mainly reflect changes in extracellular fluid volume. ECFV). Preoperative deficits should whenever possible
As compared to adults, small children have a larger already be replaced before anaesthesia is induced. In
extracellular fluid volume (ECFV), larger blood volume patients with circulatory instability, balanced isotonic
(BV), higher metabolic rate, and higher fluid turnover electrolyte solutions without added glucose can be
rate relative to their body weight. The objective of given as repeat-dose infusions of 10–20 ml/kg until the
intraoperative infusion therapy is to maintain the desired effect is achieved.
normal physiological state in children (normal ECFV,
Fluid Na Cl K. Ca. Mg. Buffer. Osmolarity. Tonicity in

vivo
(mEq/L) (mEq/L) (mEq/L) (mEq/L) (mEq/L). (mEq/L). (mOsm/L)

D5 0.225% saline. 34. 34. 329 Hypotonic
D5 0.45% saline. 77. 77 432 Hypotonic
Lactated Ringer. 130. 109 4. 3 Lactate 28. 273. Hypotonic
Plasmalyte. 140. 98. 5 3 Acetate 27; Gluconate 23 294. Isotonic
0.9% saline. 154. 154 308 Isotonic
D5 0.9% saline. 154. 154 560. Isotonic
Table 2: Composition of various IV fluids available

Conclusion 4) Gueli SL, Lerman J. Controversies in pediatric
anesthesia: sevoflurane and fluid management.
Perioperative fluid administration in children should Curr Opin Anaesthesiol 2013; 26: 310 – 17.
focus on safety and efficacy. The objective of fluid
therapy is to maintain child’s normal physiological 5) Sumplemann R, Mader T, Denhardt N, Witt L, Eich
state (normovolemia, normal tissue perfusion, normal C, Osthaus WA. A novel isotonic balanced electro-
metabolic function, normal acid- base- electrolyte lyte solution with 1% glucose for intraoperative
fluid therapy in neonates: results of a prospec-
status). For this, the perioperative fasting times
tive multicentre observational postauthorisation
should be as short as possible to prevent patient safety study (PASS). Pediatr Anesth 2011; 21:
discomfort, dehydration, and ketoacidosis. A balanced 1114 – 8.
isotonic electrolyte solution (BS) with 1–2.5% glucose
is recommended for the intraoperative background 6) Datta PK, Pawar DK, Baidya DK, Maitra S, Aravin-
infusion to maintain normal glucose concentrations and dan A, Srinivas M et al. Dextrose-containing in-
to avoid hyponatremia, hyperchloremia, and lipolysis. traoperative fluid in neonates: a randomized con-
trolled trial. Pediatr Anesth 2016; 26: 599 – 607.
Additional BS without glucose can be used in patients
with circulatory instability until the desired effect is 7) Sumpelmann R, Becke K, Brenner S, Breschan C,
achieved. The additional use of colloids (albumin, Eich C, Hohne C, et al. Perioperative intravenous
gelatin, hydroxyethyl starch) is recommended to fluid therapy in children: guidelines from the As-
recover normovolemia and to avoid fluid overload when sociation of the Scientific Medical Societies in
crystalloids alone are not sufficient and blood products Germany. Ped Anesth 2017; 27: 10 – 18.
are not indicated. 8) APA Consensus Guideline On Perioperative Fluid
Management In Children. V 1.1 September 2007
References
© Apagbi Review Date August 2010.
1) Bailey AG, McNaull PP, Jooste E, Tuchman JB.
9) Su€mpelmann R, Becke K, Crean P et al. Europe-
Perioperative Crystalloid and Colloid Fluid Man-
an consensus statement for intraoperative fluid
agement in Children: Where Are We and How Did
therapy in children. Eur J Anaesthesiol 2011; 28:
We Get Here? Anesth Analg 2010; 110: 375 – 90.
637–639.
2) Oh GJ, Sutherland SM. Perioperative fluid man-
10) NICE guidelines [NG29]: Intravenous fluid thera-
agement and postoperative hyponatremia in chil-
py in children and young people in hospital; Pub-
dren. Pediat Nephrol 2016; 31: 53 – 60.
lished Dec 2015. https://www.nice.org.uk/guid-
3) Paut O, Lacorix F. Recent developments in the ance/ng29.
perioperative fluid management for the paediat-
ric patient. Curr Opin Anaesthesiol 2006; 19: 268
– 77.

MCQ
1. According to Holliday Segar per day require- 4. Preferred maintainace of concentration of
ments of sodium. As maintenance is glucose in infusate for children at risk of hy-
poglycemia is
a. 3 meq/100kcal
b. 100 meq/100kcal a. 5%
c. 30 meq/100kcal b. 10%
d. 300 meq/100kcal c. 2.5%
2. Intraoperative Dextrose solution is selectively d. 0.5%
administerd for following 5. Osmolarity of plasmalyte is
a. Neonates a. 329 mOsm /L
b. Children on hyperalimentation b. 294 mOsm /L
c. Children with endocrinipathies c. 308 mOsm /L
d. All the above d. 560 mOsm /L
3. Non hemodynamic stimulus for ADH release
all except
a. Head trauma
b. Cirrhosis
c. Pneumonia
d. Hypoxia
5.(b) 4.(c) 3.(b) 2.(d) 1.(a)

Answers

22 The Future of Sedation and Anesthesia
Associate Professor of Anaesthesia Keira P. Mason

Boston, USA
Learning Objectives Description

1) To renew the role of mainstay drugs in the future Significant advances and changes have occurred over
of anesthesia and sedation. the past few years in pediatric anesthesia and sedation,
2) To determine the potential role of non-ASA as the array of procedures, patients, proceduralists,
(American Society of Anesthesiologists) required locations, sedation techniques, approaches, guidelines
physiologic monitoring in tailoring sedation and agents expand quickly. There have recently
delivery. been important changes in specialty guidelines and
statements apropos to sedation both in the United
3) To understand the benefits of ADV 6209, a newly
States and abroad. From the use of chloral hydrate to
approved pediatric anxiolytic.
the recent introduction of AD6209, and those drugs
still in development, the quest for an ideal sedative
with rapid onset, predictable efficacy and a low adverse
event profile, continues.

The Future of Sedation and Anesthesia 214 Neerja Bhardwaj
MCQ
1. Recommendations for Frequency of 4. False about remimazolam
Monitoring of non invasine blood pressure
during conscious sedation is minimum of a. acts on GABA receptors
every b. undergoes dose dependent ester
a. 5min hydrolysis
b. 10min c. follow zero order kinetics
c. 15min d. flumazenil is the antidote
d. 20min 5. ASA guidelines for non operating room

anesthesia includes all except
2. Intravenous and oral dose of midazolam for
sedation are_mg/kg respectively a. adequate and reliable source of
suction
a. 0.5 to 0.7 and 0.05 to 0.1
b. self inflating resuscitator bag to
b. 0.7 to 0.1 and 0.05 to 0.1 administer atleast more than
c. 0.05 to 0.1 and 0.7 to 0.1 70%oxygen
d. 0.05 to 0.1 and 0.5 to 0.7 c. adequate and reliable system for
scavenging
3. In assessing the depth of sedation the ramsay
score forBrisk response to light glabellar tap d. battery powered illumination other
or loud auditory stimulus is than laryngopscopy
a. 3
b. 4
c. 5
d. 6
5. (b) 4. (c) 3. (b) 2. (d) 1.(c)

Answers

23 ELECTROLYTE EMERGENCIES IN ANESTHESIA
Manjot Kaur Anju Grewal

Senior Resident Professor
Dayanand Medical College & Hospital Dayanand Medical College & Hospital
Ludhiana Ludhiana
Key points
Ø The implications of an increase or decrease in the serum levels of electrolytes are dependent on
whether the change occurred gradually or suddenly.
Ø Correction by up to 2 mmol/L/hr is safe in the initial treatment of acute symptomatic hyponatraemic

states.
Ø Hypernatraemia reflects a net water loss or a hypertonic sodium gain, and invariably denotes hypertonic
hyperosmolality.
Ø Total body water deficit, in cases of hypernatremia, should then be corrected with 5% dextrose, with
half given in the first 12-24 hrs, and the rest over the next 24-36 hrs.
Ø Immediate treatment is necessary if plasma potassium concentration exceeds 7 mmol/ litre or if there
are serious ECG abnormalities.
Ø Consider haemodialysis if serum calcium concentrations >4.5–5.0 mmol/l and neurological symptoms,
in patients with heart failure or renal insufficiency
Ø Clinical manifestations of hypomagnesemia overlap with those of hypokalaemia and hypocalcaemia,

with corresponding neuromuscular and cardiovascular symptoms.
+ +
Disorders of sodium (Na ) and potassium (K ) are be done cautiously with an understanding of basic
amongst the most common electrolyte emergencies physiological processes1,2,3
seen by anaesthetists. In general, the implications
Sodium1-3
of an increase or decrease in the serum levels of
electrolytes are dependent on whether the change Sodium balance is related to ECF volume and is
occurred gradually or suddenly. For example, patients regulated by the kidneys in which the volume and
with chronic renal impairment can endure much higher constitution of filtrate reaching the collecting ducts is
levels of hyperkalaemia which otherwise could be fatal if dependent on GFR, sympathetic tone and angiotensin
they occurred over a few hours. However, physiological II acting via the effects of ADH and aldosterone to
processes get deranged irrespective of a sudden or conserve water and sodium. Normothermic extra-
gradual change in serum electrolytes. Moreover, renal losses are minimal (10 mmol/day). Normal range
rapid correction may lead to adverse sequelae. Hence of serum sodium is approximately 135-145 mmol/L;
management of deranged serum electrolytes should however, levels between 125 mmol/L and 150 mmol/L
Electrolyte Emergencies In Anesthesia 216 Anju Grewal
Manjot Kaur
are often asymptomatic. Symptoms appear outside Consideration of the osmotic state of the patient is
this range, with an increasing frequency of nausea, essential in the evaluation of hyponatraemia1:
lethargy, weakness and confusion, and levels above 160
• Normal Osmolarity: Pseudohyponatraemia
mmol/L or below 110 mmol/L are strongly associated
with seizures, coma and death.3 • High Osmolarity: Translocational hyponatraemia
Hyponatremia • Occurs when an osmotically active solute that
cannot cross the cell membrane is present in
Usually patients with a serum sodium concentration
the plasma.
exceeding 120–125 mmol/l are asymptomatic, but
those with lower values may have symptoms, especially • This is also the cause of hyponatraemia seen
if the disorder has developed rapidly.1,4,5 As serum in the TURP syndrome, in which glycine is
sodium and osmolarity fall, water tends to enter the inadvertently infused to cause dilutional
cells causing them to swell. Clinically this is most hyponatremia.
important in the brain. The symptoms are largely
related to dysfunction of the central nervous system • Low Osmolarity: True hyponatraemia
and may include nausea and vomiting, headache, • True hyponatraemia is always a hypo-osmolar
cognitive impairment, lethargy, restlessness, confusion, condition
seizures and coma. Muscle cramps, rhabdomyolysis
and non-cardiogenic pulmonary oedema may also be The next stage is to consider the volume status of the
observed.1,3,6,7 patient (Table below):
Hypovolemic Hypovolemic Euvolaemic Hypervolemic

(renal) (extrarenal)
Diuretic excess Vomiting Glucocorticoid Acute or chronic renal
deficiency failure
Mineralocorticoid Diarrhoea Hypothyroidism CCF
deficiency
Salt-wasting nephrop- Burns SIADH Nephrotic syndrome

athy
Proximal RTA Pancreatitis Many drugs (most Cirrhosis
acting via ADH
pathway)
Ketonuria Trauma Psychogenic polydipsia
Osmotic diuresis Hypotonic fluid replacement post surgery
Causes of hyponatremia1,3

Manjot Kaur
Emergency treatment in hyponatraemia1,3 Rapid correction should be commenced in symptomatic

patients only till symptoms resolve. Correction by up
Acute symptomatic hyponatraemia is a medical
to 2 mmol/L/hr is safe in the initial treatment of acute
emergency. The aim of treatment is to raise plasma
hyponatraemic states. Methods of rapid correction
concentration to 125 mmol / litre gradually over a
might include the administration of furosemide and/
period of no less than 12 h while treating the underlying +
or hypertonic saline, with monitoring of serum Na
cause.
levels hourly. Patients with an underlying chronic
• Keep the rate of correction in any case under 8–12 hyponatremia should be evaluated for fluid status and
mmol/l per day, avoid excessive correction (serum treated prior to scheduling them for elective surgical
sodium 125–130 mmol/l) procedures.1,3
• Strictly avoid NaCl solutions with higher Hypernatremia1-3
concentration
Presence of severe symptoms usually requires an
• Seizures, agitated confusion, coma: permitted initial
acute and large elevation in the plasma sodium
rate of correction 1–2 mmol/l per hour until clinical
concentration to above 158–160 mmol/l.10 Intense
improvement is achieved.1,8
thirst as an important back-up defence may be absent,
• Calculate the correcting factor for hyperglycaemia especially in patients with altered mental status, or with
in hypertonic hyponatraemia: an increase of 5.6 hypothalamic lesions affecting the thirst centre, and
mmol of glucose (100 mg/dl) is associated with a in infants and elderly persons. Non-specific symptoms
fall of 2.4 mmol/l in sodium.1,9 such as anorexia, muscle weakness, restlessness,
• Closely monitor the sodium concentration nausea and vomiting tend to occur early. More
• Treat the underlying illness serious central nervous system dysfunction follows,
with altered mental status, lethargy or irritability,
• Restoration of euvolemia in hypovolaemia stupor or coma. As hypernatraemia reflects a net
• Water restriction and diuretics in hypervolemic water loss or a hypertonic sodium gain, it invariably
states denotes hypertonic hyperosmolality. Often the cause
• Water restriction in euvolemia is evident from the history; measurement of the urine
• V2-receptor antagonists in chronic heart osmolality in relation to the plasma osmolality and
failure, cirrhosis and SIADH1,10,11 the urine sodium concentration help if the aetiology is
unclear, Correction is advisable over 48–72 h with 5%
• Hormonal repletion in deficiency dextrose.1,12
Hypovolemic Hypovolemic (extrarenal) Euvolemic Hypervolemic

(renal)
+
Loop or osmotic diuretics Diarrhoea/vomiting Diabetes insipidus Na ingestion
(cranial, nephro)
Post obstruction Burns Insensible losses Conn’s Syndrome
Intrinsic renal disease Excessive sweating Cushing’s Syndrome
Fistulae Administration of hyper-
tonic saline, Na HCO3
Dialysis against hypertonic dialysate
Causes of hypernatraemia1,3

Manjot Kaur
Emergency treatment in hypernatraemia1,3 efficient than sodium regulation and extrarenal losses
are minimal.1,14-16
Symptomatic hypernatraemia, serum sodium 158–160
mmol/l Hypokalemia1,2,14-17
• Acute hypernatraemia- Reduction in sodium Hypokalaemia (serum potassium less than 3-3.5
concentration by 1 mmol/L/hour without risk mmol/l) leads to anorexia, nausea, muscle weakness,
paralytic ileus and cardiac conduction abnormalities.
• Chronic hypernatraemia- Reduce the serum sodium
In the electrocardiogram, flat or inverted T-waves,
concentration at a maximal rate of 0.5 mmol/L/
ST-segment depression and prominent U-wave are seen.
hour12,13 until a target of 145 mmol/l is reached.1
In severe hypokalaemia (serum K <,2.5 mmol/l), myopathy
• Hypovolaemic hypernatraemia may progress to rhabdomyolysis with myoglobinuria and
acute renal failure, and at serum concentrations of 2.0
• Use isotonic saline to stabilize systemic mmol/l, an ascending paralysis can develop with the risk
haemodynamics of impairment of respiratory function.
• Use 0.45% NaCl or 5% dextrose to correct
water deficit Causes of hypokalaemia1-3
• Euvolaemic or hypervolaemic states: Administer Hypokalaemia is caused by a shift of potassium into

hypotonic fluids, preferably orally or enterally cells, or more commonly by a total body potassium
deficit. Occasionally the two situations may co-exist.
• Consider hormonal and pharmacological therapy
for the specific causes of the dysnatraemia • Intracellular potassium shifting:
• Desmopressin acetate 2–4 mg intravenously in • Excess insulin (exogenous or endogenous)

central diabetes insipidus • Beta-adrenoceptor agonists (such as
• Monitor the sodium concentrations closely endogenous catecholamines or exogenous
The total body water deficit can be calculated based on salbutamol)
the serum sodium and the assumption that 60% of the • Theophylline toxicity
body is water – this deficit should then be corrected
• Acute rise in plasma pH.
with 5% dextrose, with half given in the first 12-24 hrs,
and the rest over the next 24-36 hrs. In the case of • Total body potassium deficit
hypervolaemic hypernatraemia, the removal of excess
• May result from either decreased intake or
sodium is the aim, and loop diuretics or dialysis may
increased losses.
achieve this if the patient has renal dysfunction.1.3
• Diet must be severely deficient in K+ over a long
Potassium 1-3,14-20
period in order to reach a position of clinical
With 98% of total body potassium predominantly hypokalaemia; hence seen most commonly in
an intracellular cation, potassium has a serum alcoholics
concentration of 3.5–5.0 mmol/l. The ratio of • Excessive losses may be either renal or
intracellular to extracellular potassium, created by extrarenal:
active transport, is important in determining the cellular
membrane potential, and is influenced by insulin, beta- - Renal causes include:
adrenergic catecholamines, thyroid hormone, acidosis • Diuretics
and alkalosis. The long-term balance is regulated by
• Mineralocorticoid excess
aldosterone in the kidneys. Potassium regulation is less

Manjot Kaur
• Glucocorticoid excess Causes of hyperkalaemia1-3

• Renal tubular acidosis Type I and II Hyperkalaemia may be due to either an overall increase
• DKA – glucose causes an osmotic diuresis, in total body potassium, or an acute shift of potassium
washing out potassium from the intracellular to the extracellular compartment.
• Vomiting – this is not caused by a loss of K+ in
• Extracellular Potassium Shifts
the vomit; rather, loss of H+ and water lead to
metabolic alkalosis and increased aldosterone • Acidosis – H+ is taken into the cell in exchange
• Ureterosigmoidostomy for K+
• Rare inherited conditions such as Bartter’s and • Insulin deficiency, with hyperglycaemia – note
Gitelman’s Syndromes that this is often found coexistent with a
profound total body potassium deficit
- Extrarenal causes include:
• Digitalis toxicity – due to inhibition of the Na+/
• Inadequate intake K+-ATPase
• Excessive perspiration • Beta-blockers – typically cause only a mild
• Chronic diarrhoea elevation in K+
• Gastrointestinal fistulae • Exercise – Potassium efflux from skeletal
muscle as a result of muscular contraction
Emergency treatment in hypokalaemia
• Suxamethonium administration
Symptomatic hypokalaemia • Fasciculations lead to an efflux of potassium
from skeletal muscle, similar to the effect
• Cardiovascular and close laboratory monitoring
of exercise but more pronounced and more
• Potassium chloride (KCl), up to 20 mmol/l per acute
hour intravenously.17,18 Adapt the infusion rate • A single 100 mg dose may cause the serum
to the severity of the clinical disorder potassium to rise by up to 1.0 mmol/L. If
the patient already has elevated serum
• 10 mmol/l KCl over 5–10 minutes intravenously
potassium, this may be enough to cause a
in life threatening hypokalaemia19
fatal arrhythmia
• Magnesium repletion20 • In patients with denervated muscle, the
usual mechanisms keeping the acetylcholine
• Favour oral potassium repletion as soon as possible
receptors in the synaptic cleft are disturbed,
Hyperkalemia1-3 and they spread out to cover the whole of
the muscle fibre (extrajunctional receptors)
Symptoms of hyperkalaemia are related to impaired
neuromuscular transmission, inducing cardiac and • S u xa m et h o n i u m a d m i n i st rati o n i s
neurological symptoms. Electrocardiographic changes contraindicated in these patients as it
include peaked T-waves, a decrease in, or absence of, causes a much bigger potassium efflux and
P waves, a prolonged PR interval, bundle branch blocks often leads to dangerous hyperkalaemia.
and a sequential progression in widening of the QRS • Excessive potassium input
complex to resemble a sine wave, ventricular fibrillation
• Cellular lysis, as in haemolysis or rhabdomyolysis
and finally asystole. Immediate treatment is necessary +
• Inappropriate prescription of K -containing IV
if plasma potassium concentration exceeds 7 mmol/litre
fluids or supplements is a very important cause
or if there are serious ECG abnormalities.
in hospitalized patients.

Manjot Kaur
• Impaired renal excretion • Expected fall in plasma potassium

concentration: 0.5–1.5 mmol/l
• Decreased GFR – renal failure is the commonest
cause of hyperkalaemia • Careful monitoring of glucose
• Mineralocorticoid insufficiency – this may be • 10–20 mg of nebulized albuterol
due to primary adrenal failure, hyporeninaemic • Effect onset within 30 minutes and a peak
hypoaldosteronism (RTA Type IV), or due within 90–120 minutes
to drugs like ACE inhibitors, ATII-receptor • Expected fall in plasma potassium
antagonists or spironolactone concentration: 0.6–1.0 mmol/l
• Potassium sparing diuretics • Possible resistance in dialysis patients
• Primary renal insults (such as interstitial • 20–60 ml of 8.4% NaHCO3 intravenously—not
nephritis) causing decreased potassium proven unanimously
excretion in the distal tubules and collecting • Haemodialysis
ducts • Furosemide 40–80 mg intravenously or
• Pseudohyperkalaemia ethacrynic acid 50–100 mg intravenously
• Sodium polystyrene sulphonate
• A common cause of spuriously elevated
potassium levels • Oral dose: 20 g with 100 ml of 20% sorbitol
every 4–6 hours
• The most common causes are in vitro
haemolysis, or leaving the tourniquet on for • Effect after 4–6 hours
an extended period prior to blood sampling • Enema: 50 g with 50 ml of 70% sorbitol plus
• It is also seen in patients with highly elevated 100–150 ml of water, retained for at least
white cell or platelet counts, due to secretion of 30–60 minutes, better 2 hours
potassium from these cells prior to laboratory The
+
various therapies commonly used to reduce the
analysis. K level acutely may be divided into two groups: those
that seek to transiently move the potassium to the
Emergency treatment in hyperkalaemia1 intracellular compartment, and those that seek to
remove an overall surplus of potassium from the body.
Hyperkalaemia and ECG abnormalities, acute
hyperkalaemia >6.0 mmol/l Calcium1
• Continuous ECG monitoring Calcium is required for the proper functioning of many
• 10–20 ml of 10% calcium gluconate intracellular- cAMP-mediated messenger systems and
intravenously over 2–5 minutes with abnormal most cell organelle functions, and for extracellular
ECG findings. Effect within 1–3 minutes, lasting processes, muscle contraction, nerve conduction
for 30–60 minutes. Can be repeated if there is and blood coagulation. In calcium homeostasis, the
no effect within 5–10 minutes. Use extreme extracellular calcium ion concentration is kept constant
caution in patients taking digitalis within a narrow physiological range (2.1–2.6 mmol/l or
8.5–10.5 mg/dl; 1 mmol/l approximately equals 4 mg/
• 10 U of regular insulin with 50 ml 50% dextrose dl calcium), regulated by parathyroid hormone (PTH),
intravenously 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], calcitonin,
• No dextrose necessary in hyperglycaemic phosphate and calcium itself through complex feedback
patients. loops, acting on the renal tubular re-absorption, the
• Effect onset within 15–20 minutes and peak intestine and bone. Calcium is essential for structural
within 30–60 minutes, lasting for 4–6 hours. integrity of bony skeleton, coagulation cascade,

Manjot Kaur
neuromuscular function, smooth muscle contraction. 10. Fat embolism

Calcium is 50% Ionic, 40% protein bound and 10% 11. Burns
anion bound.
12. Post thyroid & neck surgery
Hypocalcaemia (Serum calcium less than 8.5 mg/dl) 13. Malignant diseases
Clinical Manifestations ↓ Ca causes delayed awakening 14. Nutritional deficiency
15. Hyperphosphatemia- rhabdomyolysis , tumor lysis
• Neuromuscular syndrome
• Tetany of peripheral or laryngeal muscles 16. Inflammatory conditions
• Muscle weakness & spasm 17. Endocrine disorders-hypoparathyroidism
• Hyperreflexia (↑ excitability)
Emergency treatment in hypocalcaemia
• Parasthesias- circumoral & distal limbs
• Seizures, irritability, depression, psychosis Symptomatic acute hypocalcaemia, ionized Ca <0.7
mmol/l (2.8 mg/dl)
• Chovstek’s sign
• Trousseau’s sign • 200 mg of elemental calcium slowly
• Cardiovascular intravenously over 10–20 minutes (10 ml
calcium gluconate 10% contains 94 mg of
• Hypotension elemental calcium; 10 ml calcium chloride 10%
• Decreased cardiac output (↓ contractility) contain 272 mg of elemental calcium)
• Ventricular ectopic activity • Monitor patients under digitalis
• Reversible heart failure • Calcium solutions are irritating to veins,
and should not contain bicarbonate or
Causes of Hypocalcemia
phosphate
1. Magnesium depletion- by inhibiting PTH secretion • Infusion with 0.5–1.5 mg elemental
& reducing end organ responsiveness to PTH calcium/kg per hour diluted in dextrose or
2. Renal insufficiency-phosphate retention & impaired saline over 4–6 hours
conversion of Vit D to its active form • Expected rise in total serum calcium 0.5–
3. Sepsis, toxic shock syndrome 0.75 mmol/l (2–3 mg/dl)
4. Hypoalbuminemia • Continue with oral supplementation
5. Alkalosis-promotes binding of Ca to albumin, • Check for hypomagnesaemia
which reduces concentration of ionised Ca causing • Consider vitamin D supplementation
symptomatic hypocalcemia. Most commonly • C o r r e c t h y p e r p h o s p h a t a e m i a , n o t
observed with respiratory alkalosis. Infusions of hypocalcaemia in a hypercatabolic state
sodium bicarbonate also cause hypocalcemia • Treat the underlying disease
6. Massive Blood tranfusions-Calcium binding by
citrate anticoagulant in banked blood, transient, Hypercalcemia (Serum Ca >10.5 mg/dl)
resolves when citrate is metabolised by liver & • Calcium increases acetylcholine release from
kidneys (impaired in hepatic or renal failure) presynaptic vesicles, hence increased doses
7. Drugs- Aminoglycosides, heparin, anticonvulsants of non depolarising neuromuscular blockers
8. Pancreatitis-Calcium →saponification of fats required. Hypercalcemia causes hypovolemia-
fluid management. ECG monitoring- PR & QT
9. Liver disease
interval shortening in hypercalcemia.

Manjot Kaur
• G a s t r o i n t e s ti n a l - n a u s e a , v o m i ti n g , • Zoledronate 4 mg as a single short infusion over

constipation, ileus, pancreatitis 5–15 minutes intravenously
• Cardiovascular-hypovolemia, hypotension, • Expected effect after 2 days, median
shortened QT interval, prone to digoxin toxicity duration of action 33 days
• Renal-polyuria, nocturia, nephrocalcinosis • Do not repeat dose until after a minimum
• Neurologic-weakness, confusion, depressed of 7 days or
consciousness, coma • Pamidronate in 500 ml of isotonic saline as a
single infusion over 1–2 hours intravenously.
Causes of hypercalcemia
Expected maximum effect in 2–4 days, median
1. Endocrine-Primary hyperparathyroidism (↑ bone duration of action 2–4 weeks.Do not repeat
turnover) thyrotoxicosis dose until after a minimum of 7 days
2. Renal dysfunction, acute adrenal insufficiency • Serum calcitonin, 4 IU/kg subcutaneously or
3. Malignancy- bone metastasis, Multiple Myeloma, intramuscularly every 12 hours
paraneoplastic syndrome • A d d i ti v e e ffe c t w h e n g i v e n w i t h
4. Elevated vitamin D-vit D intoxication, milk alkali bisphosphonate
syndrome, sarcoidosis, lymphoma • Expected lowering in serum calcium by
a maximum of 0.3–0.5 mmol/l (1–2 mg/
5. Paget’s disease of bone
dl), beginning after 4–6 hours with a nadir
6. Immobilization within 12–24 hours
7. Nutritional, lithium therapy • Effective only in 60–70% of patients,
• Inherited disorders-Familial hypercalciuric possible tachyphylaxis within 2–3 days
hypercalcemia • Consider haemodialysis if serum calcium
• Thiazide diuretics concentrations >4.5–5.0 mmol/l (18–20 mg/
dl) and neurological symptoms, in patients with
Emergency treatment in hypercalcaemia heart failure or renal insufficiency
• Corticosteroids in vitamin D toxicity, multiple
Symptomatic hypercalcaemia (Ca>3.0 mmol/l or >12
myeloma, lymphoma, granulomatous diseases
mg/dl)
• Hydrocortisone 200–300 mg intravenously
• Isotonic saline, 1–2 l intravenously over a for 3–5 days or prednisone 20–40 mg/day
1-hour period, afterwards approximately 4–6 • Onset of action after 3–5 days
l/day intravenously
• Consider cardiovascular status Magnesium1,21-24
• Furosemide, 20– 40 mg intravenously, every 2 Normal serum concentration of 0.74–0.95 mmol/l
hours after correction of dehydration (1.7–2.2 mg/dl; 1 mmol/l = 2.43 mg/dl). Magnesium
• Anticipate potassium and magnesium is essential as a cofactor in numerous enzyme
depletion, consider water, sodium and systems, and is involved in phosphate transfer, muscle
chloride loss contractility and neuronal transmission.21
• Measure urine volume, the urine calcium Hypomagnesemia21.22
excretion and serum calcium concentration
Magnesium depletion should be suspected in chronic
• E x p e c t e d f a l l i n s e r u m c a l c i u m diarrhoea, hypocalcaemia, refractory hypokalaemia and
concentration: 0.25–0.75 mmol/l (2–6 mg/ ventricular arrythmias, particularly during myocardial
dl) after 24 hours ischaemia and cardiopulmonary bypass. Clinical

Manjot Kaur
manifestations overlap those of hypokalaemia and Treatment should be based on discontinuation

hypocalcaemia with corresponding neuromuscular of magnesium intake, counteracting the effect of
and cardiovascular symptoms. As magnesium is vital hypermagnesaemia on excitable membranes with
to carbohydrate metabolism and the generation calcium to reverse cardiac arrhythmias, respiratory
of both anaerobic and aerobic energy, and as it depression and hypotension, and removing magnesium
influences glucose catabolism and insulin sensitivity, from the serum. In severe cases, haemodialysis may
carbohydrate intolerance and hyperinsulinism are be necessary.
observed. Because deficiency has been shown to cause
hypertrigliceridaemia and hypercholesterolaemia as Hence to conclude, electrolyte emergencies occur
well, there is a risk for atherosclerosis. Bone is affected in anesthesia, commonly being hyperkalemia and
by osteoporosis and osteomalacia in chronic disorders. hyponatremia. High clinical suspicion and management
is the key.
Emergency treatment in hypomagnesaemia
References
Severe, symptomatic hypomagnesaemia—seizure or
acute arrhythmia. 1. Eva-Maria Weiss-Guillet, Jukka Takala. Diagnosis
and management of electrolyte Emergencies.
• 4–8 mmol magnesium intravenously over 5–10 Best Practice & Research Clinical Endocrinology &
minutes Metabolism Vol. 17, No. 4, pp. 623–651, 2003
• Infusion with 25 mmol magnesium intravenously
over 12–24 hours 2. Sahir S Rassam,David J CounsellDaniel Perioperative
electrolyte and fluid balance Continuing Education
• Maintainance of the treatment for 3–5 days in
in Anaesthesia, Critical Care & Pain | Volume 5
hypocalcaemic patients
Number 5 2005 doi 10.1093/bjaceaccp/mki042
• Aim to keep the plasma magnesium levels over
0.4 mmol/l (1.0 mg/dl) 3. Freshwater-Turner. Sodium, potassium and the
• Consider and treat associated electrolyte and anaesthetist. World Anaesthesia Tutorial of the Week.
acid–base disorders www.AnaesthesiaUK.com/WorldAnaesthesia.
Hypermagnesemia1,23,24 4. Kumar S & Berl T. Sodium. Lancet 1998; 352:
220–228.
Hypermagnesaemia, as defined by a serum magnesium
concentration above 0.95 mmol/l (2.2 mg/dl), is rare 5. Strange K. Regulation of solute and water balance
and usually iatrogenic after intravenous administration and cell volume in the central nervous system.
of magnesium or after use of antacids and laxatives Journal of the American Society of Nephrology
containing magnesium. The elderly and patients with 1992; 3: 12–27.
renal insufficiency are those most at risk.
6. Trimarchi H, Gonzalez J & Olivero J. Hyponatraemia-
Clinical manifestations include confusion and depressed associated rhabdomyolysis. Nephron 1999;
level of consciousness, muscular weakness, paralysis 82:274–277.
with absence of reflexes and respiratory depression in
severe cases. Hypermagnesaemia causes vasodilatation 7. Ayus JC, Varon J & Arieff AI. Hyponatraemia,
and hypotension. The electrocardiogram shows cerebral oedema, and noncardiogenic pulmonary
bradycardia, complete AV-block and, in the end, oedema in marathon runners. Annals of Internal
asystole. The PR and QT intervals and the QRS duration Medicine 2000; 132: 711–714.
are increased, while the decrease in P wave voltage and 8. Adrogue HJ & Madias NE. Hyponatraemia. New
the T wave peaking show variable degrees. The patients England Journal of Medicine 2000; 342: 1581–1589.
complain of nausea and vomiting.

Manjot Kaur
9. Hillier TA, Abbott RD & Barrett EJ. Hyponatraemia: Council on Potassium in Clinical Practice. Archives
evaluating the correction factor for hyperglycemia. of Internal Medicine 2000; 160: 2429–2436.
American Journal of Medicine 1999; 106: 399–403
18. Kruse JA & Carlson RW. Rapid correction of
10. Gheorghiade M, Niazi I, Ouyang J et al. Vasopressin hypokalemia using concentrated intravenous
V2-receptor blockade with tolvaptan in patients potassium chloride infusions. Archives of Internal
with chronic heart failure: results from a double- Medicine 1990; 150: 613–617
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19. Wingo CSWID, Disorders of potassium balance.
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24. Schelling JR. Fatal hypermagnesemia. Clinical
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practice: a contemporary review by the National

Manjot Kaur
MCQ
1. Common causes of hyperkalemia are any one 4. Hyperkalemic emergencies which
of the following: Interventions can drive potassium into
intracellular space
a. Acute renal failure and Hypertension
b. Renal pathology and Drug therapy a. Administer calcium chloride or calcium
with ACE inhibitors, ARB’s etc gluconate 1–2 g IV.
c. Fluid overload and Drug therapy b. Administer 20–40 mg furosemide IV,
d. None of the above c. Initiate Renal replacement therapy
2. Metabolic Acidosis promotes an extracellular d. Administer 1 ampule of D50 and 10

potassium shift; each 0.1 unit decrease units of insulin IV
in pH is accompanied by an increase of 5. A 60 year old cachexic, alcoholic is admitted
…………………………………..in serum Potassium in ICU for pancreatitis for the past one month
on ventilatory support. He is posted for an
a. 0.4 mmol/L
exploratory laparotomy ..during induction
b. 0.1 mmol/L of anaesthesia, ECG rhythm shows Torsades
c. 0.6 mmol/L de Pointes with loss of palpable pulse. You
initiate high quality chest compressions and
d. 1 mmol/L
rapid defibrillation…Which definitive drug
3. A class-I Obese male with history of therapy should be administered apart from
prolonged immobility due to an underlying Inj. Epinephrine?
neurological injury is scheduled for
a. Inj. Calcium chloride 10% 5–10 mL
debridement of bed sore in prone position.
Which agents are safe to use during induction b. 2 g 50% magnesium sulphate (4 mL; 8
of anesthesia and facilitation of endotracheal mmol) IV over 1–2 min
intubation (Suggamadex is available): c. Haemodialysis
a. Thiopentone, Rocuronium and d. Fluid Boluses and Inj Amiodarone 150
Fentanyl mg IV
b. Propofol, Succinylcholine and
Remifentanyl
c. Thiopentone, Succinylcholine and
Fentanyl
d. Ketamine, Fentanyl and Propofol
5.(b) 4.(d) 3.(a) 2.(c) 1.(b)

Answers

24 Management of increased ICP
Debashish Mahapatra Nibedita Pani

S.C.B. Medical College, Professor,
Cuttack S.C.B. Medical College, Cuttack
Key points
Ø The skull is a noncompliant and closed structure, comprising of brain and interstitial fluid constituting
78%, intravascular blood 12%, cerebrospinal fluid10%.
Ø The Monroe-Kellie hypothesis states the sum of the intracranial volumes of blood, brain, CSF and other
components is constant and that an increase in any one of these must be offset by an equal decrease
in another, or else pressure increases.
Ø Intracranial hypertension is defined as sustained intracranial pressure (ICP) greater than 20 mm Hg for
greater than five to ten minutes
Ø Autoregulation maintains a normal cerebral blood flow (CBF) with a CPP ranging from 50 to 150 mm Hg.
Ø Indications for intracranial pressure monitoring include GCS Score: 3–8 with abnormal CT Scan or
Normal CT Scan Plus 2 factors - Age > 40 years, Motor posturing & Systolic blood pressure < 90 mm Hg
Ø Pathologic ICP waveforms comprises of Lundberg A, B, and C types.
Ø Goals of therapy includes maintain ICP at less than 20 to 25 mm Hg, maintain CPP at greater than 60
mm Hg and avoid factors that aggravate or precipitate rise in ICP.
Ø Prophylactic hyperventilation should be avoided and routine administration of steroids is not indicated
in TBI
Ø Medical management of increased ICP should include sedation, drainage of CSF and osmotherapy with
either mannitol or hypertonic saline
Ø For intracranial hypertension refractory to initial medical management, barbiturate coma or
decompressive craniotomy should be considered.
Introduction rise in pressure caused by any expanding intracranial

volume, is spread equally throughout the intracranial
The skull is a noncompliant and closed structure, cavity [2, 3].The Monroe-Kellie hypothesis states the sum
comprising of brain and interstitial fluid constituting of the intracranial volumes of blood, brain, CSF, and
78%, intravascular blood 12%, cerebrospinal fluid10%. other components is constant, and that an increase in
That is total intracranial volume of 1450 mL: out of any one of these must be offset by an equal decrease
which 1300 mL is brain, 65 mL is CSF, and 110 mL is in another, or else pressure increases. Intracranial
blood [1]. ICP is the total pressure exerted by all the three hypertension is common in course of many neurologic
components within the skull; it reflects the hydrostatic and non-neurologic disorders.Randomized trials
force measured in the brain-CSF compartment. As the have been conducted on few treatment options for
structures are enclosed within a rigid skull and vertebral intracranial hypertension; however, most management
canal, constituting a nearly incompressible system. A recommendations are derived from clinical experience.

Management of increased ICP 228 Nibedita Pani
Debashish Mahapatra
Anatomy and Physiology of CSF Flow

Cerebrospinal fluid is a colorless acellular fluid. It is CSF formed in two lateral ventricles communicates with
produced by the choroid plexus in the lateral, third and the third ventricle through the interventricular foramina
fourth ventricle at a rate of 0.3-0.4ml/min (500ml/day). of Monro. Then it flows into the fourth ventricle
It is formed by filtration of plasma through fenestrated through the cerebral aqueduct of Sylvius. Then the CSF
capillaries followed by active transport of water and continues into the subarachnoid space through three
dissolved substances through the epithelial cells of the outlet foramina: two lateral foramina of Luschka and
blood-CSF barrier.CSF gets absorbed primarily through one median foramen of Magendie.
the arachnoid villi into the superior sagittal sinus.Total
volume of CSF is 125-150 ml.
Functions
• Provides mechanical protection by buoyancy,
to concussive injury. The specific gravity of CSF
(1.007) which reduces the effective weight
of the brain from 1.4kg to 47g (Archimedes’s
principle). This reduction in mass supports
the brain, reduces brain inertia and thereby
protects it against deformation caused by
acceleration or deceleration forces
• It transports hormones and hormone-releasing
factors
Fig 1 : Flow of CSF
• It removes metabolic waste products through
absorption. The normal range for ICP varies with age.
Plasma mmol/l CSF mmol/l • Adults and older children- < 10 to 15 mm Hg

(7.5–20 cm H2O)
Urea 2.5-6.5 2.0-7.0
• Young children - 3 to 7 mm Hg
Glucose (fasting) 3.0-5.0 2.5-4.5
• Term infants -1.5 to 6 mm Hg
Sodium 136-148 144-152 • May be sub atmospheric in newborns [4]
Potassium 3.8-5.0 2.0-3.0 Intracranial pressure more than the normal pressure
corresponds to Intracranial hypertension. Or in adults
Calcium 2.2-2.6 1.1-1.3
it is defined as sustained intracranial pressure (ICP)
Chloride 95-105 123-128 greater than 20 mm Hg for greater than five to ten
minutes in a patient that is not being stimulated.[5, 6]
Bicarbonate 24-32 24-32
• Mild intracranial hypertension - 20 to 30 mm
Protein 60-80g/l 200-400mg/l Hg
• Values more than 20 to 25 mm Hg require
Tab 1 Composition of Plasma and CSF treatment.

Debashish Mahapatra
• Sustained ICP values of greater than 40 mm[7] Pressure autoregulation maintains a normal cerebral
Hg indicate severe, life-threatening intracranial blood flow (CBF) with a CPP ranging from 50 to 150 mm
hypertension. Hg[8-10] and PCO2 20-80mmHg. But autoregulation may
fail after stroke or traumatic brain injury.[11]
Cerebral Pressure Dynamics
• Decrease in CPP results in vasodilation of
In response to increase in intracranial volume initial
cerebral vessels, which allow CBF to remain
compensation occurs by displacement of CSF from
unchanged.
the ventricles and the cerebral subarachnoid space to
spinal subarachnoid space where there is increased • Increase in CPP results in vasoconstriction of
absorption of CSF. Increased ICP causes decrease in cerebral vessels and reduces ICP.
CPP which reduces the formation of CSF. Infants and
children with open fontanels and sutures may be able
to compensate better but will still be susceptible to
acute increases in ICP.
Compliance indicates the brain’s tolerance to rise in
ICP. Intracranial compliance is different from patient
to patient and also varies with type of injury they have
sustained. When the patient’s compliance is exhausted,
as seen with head injury, there is a sharp increase in
the pressure/volume curve, leading to a rapid elevation
in ICP.
Cerebral blood flow
In a normal brain, cerebral blood flow (CBF) is
regulated to supply the brain with adequate oxygen
Fig 2 : Autoregulation of CBF
and substrates. This flow can be increased by certain
physiologic factors like hypercarbia, acidosis and Increase ICP causes movement of CSF into the spinal
hypoxemia which cause vasodilatation. Seizures and sac. There is increases reuptake of CSF and compression
fever increases cerebral metabolic rate which in of venous sinuses. These mechanisms shrink the liquid
turn increases CBF. This excess blood flow leads to volume (CSF and Blood) of the intracranial content.
hyperemia and increased ICP. Measures to decrease
the cerebral metabolic rate, such as hypothermia and
barbiturates,will decrease CBF and thus the ICP.
Cerebral perfusion pressure (CPP) is determined by
mean systemic arterial pressure (MAP) and ICP
CPP=MAP−ICP
where MAP= (1/3 systolic BP)+(2/3 diastolic BP)
CPP can be decreased due to an increase in ICP, a
decrease in blood pressure, or a combination of both
factors.
Fig 3 : Intracranial pressure - volume relationship

Debashish Mahapatra
Stage 1&2 o Idiopathic or benign intracranial

hypertension
Compensation phase. As one of the intracranial
o Other (eg, pseudo-tumorcerebri,
component increases in volume, the other two
pneumoencephalus, abscesses, cysts)
components decrease to keep the intracranial pressure
constant. • Extracranial (secondary)
Stage 3&4 o Airway obstruction
Decompensation phase. When compensatory o Hypoxia or hypercarbia (hypoventilation)
mechanisms are exhausted, small increase in the o Hypertension (pain/cough) or
volumes of intracranial component causes a large hypotension (hypovolemia/sedation)
increase in ICP. The slope of the curve also depends o Posture (head rotation)
on which intracranial component is increasing. The o Hyperpyrexia
slope is steeper if it is blood or CSF as both of them are o Seizures
poorly compressible. If the cause for raised ICP is brain
o Drug and metabolic (eg, tetracycline,
tissue, such as from a tumor, the curve is less steep as
rofecoxib, divalproex sodium, lead
the tissue is compressible. intoxication)
At CPP values less than 50 mm Hg, the brain may not be o Others (eg, high-altitude cerebral edema,
able to compensate adequately, and CBF falls passively hepatic failure)
with CPP.
• Postoperative
Vasodilatory cascade
o Mass lesion (hematoma) Edema
Decreasing CPP results in vasodilatation of cerebral o Increased cerebral blood volume
vessels, this vasodilatation can result in an increase (vasodilation)
in ICP, which further perpetuates the decrease in CPP. o Disturbances of CSF
Intracranial Hypertension - Causes [12] Intracranial hypertension secondary to traumatic brain

injury In patients with traumatic brain injury (TBI),
• Primary: Raised ICP is due to intracranial lesion and
lesions may be heterogeneous, and several factors often
normalisation of ICP depends on rapidly addressing
contribute to increase the ICP [16]
the underlying brain disorder
1. Traumatically induced masses: epidural or subdural
• Secondary: Intracranial hypertension is due to an
hematomas, hemorrhagic contusions, foreign body,
extracranial or systemic process.[13-15]
and depressed skull fractures
• Postoperative: Causes of increased ICP after a 2. Cerebral edema
neurosurgical procedure. 3. Hyperemia owing to vasomotor paralysis or loss of
• Intracranial (primary) autoregulation
4. Hypoventilation that leads to hypercarbia with
o Brain tumor subsequent cerebral vasodilation.
o Trauma (epidural and subdural 5. Hydrocephalus resulting from obstruction of the
hematoma, cerebral contusions) CSF pathways or its absorption
o Nontraumaticintra-cerebral hemorrhage
6. Increase is intrathoracic or intra-abdominal pressure
o Ischemic stroke as a result of posturing, agitation, mechanical
o Hydrocephalus ventilation, or valsalva maneuvers.
Debashish Mahapatra
After evacuation of traumatic mass lesions, the most on awakening in case of tumors. Nausea, and vomiting
important cause of increased ICP is cerebral edema.[16] which is projectile in nature.
Clinical features Signs
Headache is severe (‘worst ever’) and explosive in case Papilledema[17], pupillary dilation and decerebrate
of intracranial haemorrhage, or progressive and worst posturing. Determine the patient’s level of consciousness
with the Glasgow Coma Scale.
Eye opening Verbal response Motor response
Spontaneous 4 Orientated 5 Obeys commands 6
To verbal command 3 Confused speech 4 Localises pain 5
To painful stimulus 2 Inappropriate words 3 Withdrawal to pain 4

None 1 Incomprehensible 2 Abnormal flexion 3
sound
None 1 Abnormal extinction 2
None 1
Tab 2 : Glasgow Coma Scale
Features seen in increased ICP are rapidly deteriorating Progressive

consciousness level, visual disturbances. Diplopia may
The whole disc is involved and splinter haemorrhages
occur due to 3rd, 4th and 6th cranial nerves cranial nerve
may be seen at the disc margin.
palsies. There can be visual obscurations, which are
transient losses of vision lasting a few seconds. They Chronic stage
occur with sudden risein ICP, associated with activities
that increase ICP (coughing, sneezing, bending down, There is gliosis of the optic nerve head and eventually
straining at stool) and relieved by their cessation.It optic atrophy with nerve fiber damage and permanent
is due to compromise of optic nerve head perfusion. visual field defect.
Retinal venous pulsation [17] is seen at the margin Cushing’s triad is seen with critical compression of
of the disc in the normal retina. When ICP exceeds brain, which comprises of increased systolic pressure
venous pressure, this retinal venous pulsation is lost. (including widened pulse pressure), bradycardia and
Papilloedema[17] is swelling (oedema) of the optic nerve irregular breathing.
head due to raised ICP
Further increase in ICP can cause the downward
Acute stage displacement of the brainstem and upper cervical
Edema at the superior and inferior poles of the cord through the foramen magnum. This can cause
disc, absence of spontaneous venous pulsation, and compression on structures that control cardiac and
enlargement of the blind spot. respiratory function.

Debashish Mahapatra
Several brain herniation syndromes [17] superior colliculi. Decrease level of consciousness as the
blood vessels supplying the diencephalon and midbrain
perforating vessels are compromised. Traction on the
pituitary stalk and hypothalamus can lead to diabetes
insipidus.
3. Uncal/Tentorial herniation (lateral) Third nerve
palsy (ptosis, poorly reactive pupil, reduced eye
movements). False localising; ipsilateral hemiparesis
with contralateral third nerve injury and pupil dilatation
(Kernohan’s notch). Depressed level of consciousness
from reticular formation compression. Occlusion of
posterior cerebral artery results in a homonymous
hemianopia.
4.Tonsillar herniation - Neck stiffness as cerebella
tonsils compress against the foramen magnum (as
opposed to meningism from meningitis – beware of
performing a lumbar puncture in the patient with
tonsillar herniation).Increased blood pressure and
Fig 4 : Brain herniation syndromes slowed pulse rate suggests progressive brainstem
1. Subfalcine: This does not put as much pressure on compression. Respiratory arrest will follow persistent
the brainstem as the other types of herniation, but it compression.
may interfere with blood vessels in the frontal lobes. Hutchinson’s pupil is one of the first signs to appear
Presents with abnormal posturing and coma. in increased ICP. There is unilateral pupillary dilatation
2. Tentorial herniation (central) Upward gaze palsy resulting from ipsilateral supratentorial (usually
results from compression on the pretectum and extrinsic) space-occupying lesion.
Fig 5 : Decorticate posturing and Decerebrate posturing

Debashish Mahapatra
Investigations Intracranial pressure monitoring

Imaging should aim to identify intracranial pathology
that requires emergency surgery. An unenhanced head
CT is the test of choice for trauma and most of the cases.
If CT does not explain neurological findings, Magnetic
Resonance Imaging (MRI) may be indicated. Magnetic
resonance imaging is often the preferred imaging
modality for sub-acute neurological insults and seizure.
Transcranial Doppler is a noninvasive procedure that
allows the early detection of raised ICP by measuring
bloodflow velocity in both middle cerebral arteries.
Other investigations
• Jugular venous bulb oxygen saturations (SjvO2,
Fig 6 : Monitoring of ICP
usually 65-75%) reflects the balance between
cerebral oxygen delivery and CMRO2. Low Sjv02 Ventriculostomy catheter
reliably indicates cerebral hypoperfusion. They are surgically placed into the ventricular system,
• Microdialysis catheters are used to measure has low cost and is considered the “gold standard”.Can
glucose, pyruvate, lactate, glycerol, glutamate be used for therapeutic CSF drainage.Access to CSF for
(metabolic variables) in CSF. instilling contrast media/medication, is reliable and has
high accuracy. But it requires frequent recalibration.[16]
• Positron Emission Tomography – The
Disadvantages
distribution of radio labelled water in the brain
is monitored to indicate metabolic activity. Difficulties with insertion into compressed or displaced
ventricles. Gives intermittent pressure measure.
Functional MR imaging techniques
Catheter obstruction.
Kety-Schmidt equation can be used to determine CBF
Microsensor transducer and the fiberoptic transducer
by using an inert carrier gas like 133Xe
in the subdural space or directly into the brain tissue.[16]
Monitoring
Complication
Patients with suspected intracranial hypertension,
Common complication of ventriculostomy catheter
especially secondary to TBI, should have monitoring
placement is infection with an incidence of 5% to 14%
of ICP and monitoring of cerebral oxygen extraction.
colonization. Hemorrhage with an incidence of 1.4%,
Other systemic parameters, includes ventilation, malfunction, obstruction, and malposition.[16]
oxygenation, electrocardiogram, heart rate, blood
pressure, temperature, blood glucose, and fluid Subarachnoid bolt or screw has lower infection rates
intake and output. Pulse oximetry and capnography than ventriculostomy and is quick and easy to placed.
are helpful to avoid unrecognized hypoxemia and It can be used in small and collapsed ventricles and
hypoventilation or hyperventilation. Central venous requires no penetration of brain tissue.[18]
catheter commonly is needed to help evaluate volume
Epidural monitors are passed through the skull and the
status and administration of inotropes. Foley’s catheter optical transducer is rested against the dura in epidural
is inserted to monitor urine output accurately. space. They often are inaccurate, as intracranial

Debashish Mahapatra
pressure gets dampened while transmitting through b. Motor posturing

the dura; thus have limited clinical utility [19]. c. Systolic blood pressure < 90 mm Hg
Indications for intracranial pressure monitoring [20] ICP wave form - Normal tracing of ICP originate from
small pulsations transmitted from the systemic blood
GCS Score: 3–8 (after resuscitation)
pressure to the intracranial cavity. These blood pressure
1. Abnormal admission Head CT Scan pulsations are superimposed on slower oscillation
caused by the respiratory cycle.[21]
a. Hematoma
b. Contusion The normal ICP waveform contains three phases
c. Edema • P1 (percussion wave) represents arterial
d. Herniation pulsations.
e. Compressed basal cisterns
• P2 (rebound wave) reflects intracranial
2. Normal admission Head CT Scan Plus 2 or compliance.
more of the following
• P3 (dichrotic wave) represents venous
a. Age > 40 years pulsations.
Percussion
(Arterial) P1 Tidal
(Rebound) P2
Dichrotic
(Venous) P3
Normal ICP
Low pressure waveform
Non-complaint skull
Fig 7 : Normal ICP waveform
As the ICP increases, cerebral compliance reaches its understood if the change in MAP is cause or effect.
limit. In ICP waveform arterial pulses become more
Lundberg B waves or pressure pulses have amplitude
pronounced, and venous components disappear.
of 50 mm Hg and occur every 30 seconds to 2 minutes.
Pathologic ICP waveforms comprises of Lundberg A,
Lundberg C waves have an amplitude of 20 mm Hg and
B, and C types. Lundberg A waves or plateau waves
are ICP elevations to more than 50 mm Hg lasting 5 a frequency of 4 to 8 per minute; they are seen in the
to 20 minutes. These waves are accompanied by a normal ICP waveform, but high-amplitude C waves may
simultaneous increase in MAP, but it is not clearly be superimposed on plateau waves.[22]

Debashish Mahapatra
Raised ICP
High pressure wave form;
Non-complaint skull
Fig 8 : Waveform when ICP is raised
Intracranial pressure treatment measures fever, severe hypertension, hyponatremia, anemia,

and seizures.
Goals of therapy
1) Maintain ICP at less than 20 to 25 mm Hg. Optimizing venous outflow
2) Maintain CPP at greater than 60 mm Hg by main- Elevation of the head of the bed by 15° to 30°[16]and
taining adequate MAP.
keeping the head in a neutral position. Increasing the
3) Avoid factors that aggravate or precipitate rise in
ICP. head end will decrease ICP but will also decrease CPP, so
higher angles are avoided[24]. Avoid posture increasing
CPP targeted protocols in venacaval pressure like excess flexion of hips.
The conventional way of management of raised ICP Respiratory failure
has been to reduce ICP below 20 mmHg. However,
emerging evidence favours CPP targeted therapy. Respiratory dysfunction is common in patients with
Here measures are taken to achieve an optimum CPP. intracranial hypertension, especially when the cause
In order to maintain adequate supply of oxygen and is head trauma[16].Comatose patients (GCS<8) often
essential nutrient to brain, a certain minimum CPP is have absent airway protective reflexes and respiratory
needed. What should this minimum be and whether dysfunction requiring mechanical ventilation. Hypoxia
this minimum should be adjusted according to the and hypercapnia can increase ICP dramatically[16],
patient’s age remains unclear. A review of available and mechanical ventilation can alter cerebral
studies in paediatric TBI suggests that a CPP between hemodynamics. Optimal respiratory management is
crucial for control of ICP.Mechanical ventilation have
40- 65 mmHg represents an optimum threshold; a CPP
adverse effects on ICP. PEEP, which may be needed to
<40 mmHg is associated with high risk of death.[23]
improve oxygenation, can increase ICP by impeding
General care venous return and increasing cerebral venous pressure
and ICP, and by decreasing blood pressure leading to a
Prevention or treatment of factors that may aggravate
or precipitate intracranial hypertension, obstruction of reflex increase of cerebral blood volume. This is more
venous return (head position, agitation), respiratory in patient with low lung compliance such as associated
problems (airway obstruction, hypoxia, hypercapnia), acute lung injury.

Debashish Mahapatra
Diagram of diagnosis and treatment of intracranial hypertension.

Debashish Mahapatra
Sedation and analgesia Treatment of anemia

Agitation and pain may significantly increase blood Anecdotal cases have been reported in patients with
pressure and ICP. Adequate sedation and analgesia is severe anemia presenting with symptoms of increased
an important adjunct treatment. Opoids are avoided ICP and signs of papilledema, which resolve with
as it may increase ICP.[16] Shorter acting agent like treatment of the anemia.[16]There is increase in CBF,
midazolam is used as it permits interruption of sedation to maintain cerebral oxygen delivery when anemia is
for neurologic examination. severe. A Hb level <7g/dL will be benefitted by blood
transfusion.[16]
Fever increases metabolic rate by 10% to 13% per
degree Celsius and is a potent vasodilator. Fever- Prevention of seizures
induced dilation of cerebral vessels can increase CBF
The risk of seizures after trauma is related to the
and may increase ICP and worsens the neurologic
severity of the brain injury; seizures occur in 15% to
outcome.[16]Fever should be controlled with antipyretics
20% of patients with severe head injury. Seizures can
and cooling blankets. Infectious causes must be sought
increase cerebral metabolic rate and ICP.[16]Sometimes
and treated with appropriate antibiotics when present.
seizures may be subclinical and requires continuous
Blood Pressure electroencephalographic monitoring for its detection.
[16]
Seizure prophylaxis for patients with severe brain
Elevated blood pressure is seen commonly in patients
injury is recommended for the first 7 days after injury.
with intracranial hypertension, especially secondary
to head injury, and is characterized by a systolic blood Hypothermia
pressure increase greater than diastolic increase.
A phase II trial to test safety and efficacy of hypothermia
It is unwise to reduce systemic blood pressure in
in children with TBI did not show a beneficial effect
patients with hypertension associated with untreated
on neurologic outcome, however, a reduction in
intracranial mass lesions because cerebral perfusion is
ICP was evident during the hypothermia treatment
being maintained by the higher blood pressure.[16]When [18]
. There were no significant differences between
pressure autoregulation is impaired, which is common
the hypothermia and no-hypothermia patients with
after TBI, systemic hypertension may increase CBF and
respect to complications viz. arrhythmia, coagulopathy
ICP. In addition, elevated blood pressure may exacerbate
or infection. However, the early hypothermia group
cerebral edema and increase the risk of postoperative
had a trend toward better neurological outcome at
intracranial hemorrhage.Systemic hypertension may
3 and 6 months.[18] A recently completed multicentre
resolve with sedation. If the decision is made to treat
trial by hypothermia paediatric head injury trial
systemic hypertension, the choice of antihypertensive
investigators, Canadian Critical Care Groups found
agent like β-blocking drugs (labetalol, esmolol) or
a detrimental trend with hypothermia. Currently
central acting α-receptor agonists (clonidine), are
therefore, routine induction of hypothermia is not
preferred. Vasodilators like GTN and nitroprusides are
indicated. However, hypothermia may be an effective
avoided as it increases ICP.
adjunctive treatment for increased ICP refractory to
In case of shock, BP must be maintained at levels other medical management.
appropriate for age or restored to ensure adequate
Medical interventions
CPP and prevent further ischemia. Fluid boluses
should be given to the hypotensive neurologically Intracranial hypertension caused by agitation,
injured patient in the sameway as any other patient posturing, or coughing can be prevented by sedation
presenting in shock. Vasopressor support is initiated if and nondepolarizing muscle relaxants that do not
the patient remains hypotensive despite appropriate alter cerebrovascular resistance[18]. Morphine and
fluid resuscitation.
Debashish Mahapatra
midazolam for analgesia/sedation and cisatracurium or Hypertonic saline can be safely given in concentrations
vecuronium as a muscle relaxant can be used. Myopathy ranging from 3% to 23.4%, creating an osmotic force
is associated with the use of neuromuscular blocking to draw water from the interstitial space of the brain
agents specially if its used along with steroids. So parenchyma into the intravascular compartment in
there should be limited use of neuromuscular blocking the presence of an intact blood-brain barrier, reducing
agents by monitoring train-of-four, measuring creatine intracranial volume and ICP [18]. Mannitol is relatively
phosphokinase daily. Neurologic examination cannot contraindicated in hypovolemic patients because of the
be monitored closely in patient receiving sedations and diuretic effects, whereas hypertonic saline augments
muscle relaxants. So, the sedatives and muscle relaxants intravascular volume and may increase blood pressure.
can be interrupted once a day, usually before morning Other situations where it may be preferred are renal
rounds, to allow neurologic assessments. failure or serum osmolality >320 mosmol/Kg.[18] It is
Hyperosmolar therapy given as continuous infusion at 0.1 to 1.0mL/kg/hr, to
target a serum sodium level of 145–155 meq/L. When
Mannitol is the most commonly used hyperosmolar the hypertonic saline therapy is no longer required,
agent for the treatment of raised intracranial pressure. serum sodium should be slowly corrected to normal
Intravenous bolus administration of mannitol decreases values (hourly decline in serum sodium of not more
the ICP in 1 to 5 minutes with a maximum effect at 20 than 0.5 meq/L).
to 60 minutes and its effect on ICP lasts for 1.5 to 6
hours, depending on the clinical condition[16]. Mannitol Hyperventilation decreases PaCO2, which can induce
usually is given as a bolus of 0.25 g/kg to 1 g/kg body constriction of cerebral arteries by alkalinizing the
weight. Patients who have herniated from diffuse CSF. The resulting reduction in cerebral blood volume
brain swelling, could be benefitted by a higher dose decreases ICP[18].Most effective use of hyperventilation
of mannitol (1.4 g/kg)[16]. Mannitol has rheologic and is acutely to allow time for other more definitive
osmotic effects. Immediately after infusion of mannitol, treatments to be put into action. But hyperventilation
there is an expansion of plasma volume and a reduction may cause vasoconstriction and decreases CBF leading
in hematocrit and in blood viscosity, which may increase local cerebral perfusion and worsen neurologic injury.
CBF and on balance increase oxygen delivery to the So prolonged hyperventilation has a detrimental effect
brain. These rheologic effects of mannitol depend on on outcome[18]. And prophylactic hyperventilation
the status of pressure autoregulation[16]. In patients with should be avoided.
intact pressure autoregulation, infusion of mannitol
induces cerebral vasoconstriction, which maintains CBF Barbiturate coma should only be considered for patients
constant, and the decrease in ICP is large. If mannitol with refractory intracranial hypertension because of
is infused with patients with absent auto regulation, the serious complications associated with high-dose
it leads to increases CBF, and the decrease in ICP barbiturates, and because the neurologic examination
is less pronounced.The osmotic effect of mannitol becomes unavailable for several days [18]. Thiopentone
increases serum osmolality, which draws edema fluid is given in a loading dose of 10 mg/kg body weight
from cerebral parenchyma into the intravascular followed by 5 mg/kg body weight hourly for 3 doses.
compartment. This process takes 15 to 30 minutes to The maintenance dose is 1 to 2 mg/kg/h, titrated to
start until gradients are established. Serum osmolarity is maintain a serum level of 30 to 50 μg/mL. EEG burst
optimal when increased to 300 to 320 mOsm. Mannitol suppression is an indication of maximal dosing. It acts
may cross open the blood-brain barrier, and mannitol by decreasing CBF and CMRO2, with an immediate
that has crossed the blood-brain barrier may draw fluid effect on ICP. The reduction in ICP with barbiturates is
into the central nervous system, which can aggravate closely tied to the retention of carbon dioxide reactivity
vasogenic edema resulting in a “rebound” increase in by the brain[18].
ICP.
Debashish Mahapatra
Steroids commonly are used for primary and metastatic ICP. If the brain is diffusely swollen, the ventricles may
brain tumors, to decrease vasogenic cerebral edema. collapse, and this modality then has limited utility.
Focal neurologic signs and decreased mental status due
Decompressive craniectomy
to surrounding edema begin to improve within hours.
[18]
Dexamethasone, 4 mg every 6 hours. For other The surgical removal of part of the calvaria to create
neurosurgical disorders, such as TBI or spontaneous a window in the cranial vault is the most radical
intracerebral hemorrhage, steroids have not been intervention for intracranial hypertension, negating the
shown to have a benefit [25] and in some studies have Monro-Kellie doctrine of fixed intracranial volume.The
had a detrimental effect [26] that routine administration swollen brain is allowed to herniate through the bone
of steroids is not indicated for patients with TBI. window to relieve pressure. Decompressive craniectomy
has been used to treat uncontrolled intracranial
Other: Acetazolamide (20–100 mg/kg/day, in 3 divided
hypertension of various origins, including cerebral
doses, max2 g/day) is a carbonic anhydrase inhibitor
infarction [16], trauma, subarachnoid hemorrhage, and
that reduces the production of CSF. It is particularly
spontaneous hemorrhage. Decompressive craniectomy
useful in patients with hydrocephalous, high altitude
effectively reduces ICP in most (85%) patients with
illness and benign intracranial hypertension. Loop
intracranial hypertension refractory to conventional
diuretics like Furosemide (1 mg/kg/day, q8hrly), has
medical treatment [16]. Brain oxygenation measured by
sometimes been administered either alone or in
tissue PO2 and blood flow estimated by middle cerebral
combination with mannitol[27].
artery flow velocity also are usually improved after
Surgical interventions decompressive craniectomy[28, 29]. Complications include
hydrocephalus, hemorrhagic swelling ipsilateral to the
Resection of mass lesions craniotomy site, and subdural hygroma.[30]
Intracranial masses which produces raised ICP, Effects of anaesthetics agents on ICP
should be removed when possible. Acute epidural
and subdural hematomas are a hyperacute surgical IV agents
emergency, especially epidural hematoma because the
• Thiopentone protect brain from incomplete
bleeding is under arterial pressure. Brain abscess must
ischemia. It suppresses CMR. Helps in free radical
be drained, and pneumocephalus must be evacuated scavenging effects and decrease ATP consumption.
if it is under sufficient tension to increase ICP. Surgical Cerebral autoregulation maintained and CO 2
management of spontaneous intracerebral bleeding is responsiveness intact.
controversial.[18]
• Methohexital: It has myoclonic activity and patients
Cerebrospinal fluid drainage with seizures of temporal lobe origin [psychomotor
CSF drainage lowers ICP immediately by reducing variety] are specifically at risk.
intracranial volume and in long-term by allowing edema • Propofol: It primarily reduce CMR. It decreases
fluid to drain into the ventricular system. Drainage of both CBF and ICP by vasoconstriction. In patients
even a small volume of CSF can lower ICP significantly, with high ICP, there is significant reduction in CPP
especially when intracranial compliance is reduced by following propofol induction. Fentanyl along with
injury. CSF should be removed at a rate of approximately propofol : ablates increase in ICP at intubation. CO2
1 to 2 mL/minute, for two to three minutes at a time. responsiveness and autoregulation is preserved.
An intervals of two to three minutes in between till a Though seizures, dystonic & choriform movements,
satisfactory ICP has been achieved (ICP <20 mmHg). This opisthotonus etc have been reported with its use,
modality is an important adjunct therapy for lowering systematic studies have failed to confirm it.

Debashish Mahapatra
• Etomidate: It causes parallel reduction in CBF and Succinyl Choline

CMR, but the effect varies regionally; more in
Increase ICP in lightly anaesthetized patient, which can
forebrain. Reactivity to CO2 preserved. Some of the
be prevented by deep anesthesia. Defasciculation with
concerns in using etomidate are, adrenocortical
metocurine 0.03 mg/kg or with Vecuronium 0.01mg/kg
suppression, worsening of acidosis,precipitate is recommended. Consider risk/benefit of rise in ICP Vs
generalized epileptic EEG activity in epileptic rapid attainment of paralysis in a given case.
patients. So is avoided in patient with history of
recent seizure. NDMR
• Ketamine: It increases CMR. Secondarily increase Pancuronium- large bolus causes abrupt increase in BP.
ICP. And increases CBF but effect is regionally If autoregulation is defective, it will lead to increase
variable, more pronounced in limbic system. in ICP. Atracuronium can cause histamine release
which can lead to cerebral vasodilation & increase
Inhaled anesthetics ICP, simultaneous decrease in BP leading to reduction
in cerebral perfusion pressure. A metabolite of
At 0.5 MAC, the CMR suppression predominates and atracurium, laudanosine has epileptogenic properties in
net blood flow decreases. At 1 MAC: CMR suppression trials, but it appears highly unlikely that epileptogenesis
is equal to vasodilation, so CBF is unchanged. At dose will occur in humans with atracurium.
beyond 1 MAC, CMR is reduced, but vasodilatory effect
is more predominate, hence blood flow increases and Conclusion
coupling persists, ie. dose related increase in CBF/CMR. Effective treatment of intracranial hypertension involves
Order of vasodilatory potency: Halothane >> Enflurane meticulous avoidance of factors that precipitate or
> Desflurane = Isoflurane > Sevoflurane.Major aggravate increased ICP. When ICP becomes elevated,
impact on CBF & ICP occurs when we exceed 1 MAC. it is important to rule out new mass lesions that should
It will become significant if intracranial compliance be surgically evacuated. Medical management of
is abnormal, it is better to use a predominantly increased ICP should include sedation, drainage of CSF,
intravenous technique until the point of opening of and osmotherapy with either mannitol or hypertonic
cranium & dura. Net vasodilatory effect of isoflurane/ saline. For intracranial hypertension refractory to initial
desflurane & sevoflurane less than halothane; so medical management, barbiturate coma, hypothermia,
if one is to be used. Enflurane is epileptogenic and or decompressive craniotomy should be considered.
there is slight risk with sevoflurane. CO2 reactivity and Steroids are not indicated and may be harmful in the
autoregulation preserved. treatment of intracranial hypertension resulting from
TBI.
Nitrous Oxide
References
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1. Doczi T. Volume regulation of the brain tissue—a
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benzodiazepines, narcotics]. Nitrous with volatile vasomotor paralysis produced by intracranial
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Debashish Mahapatra
MCQ
1. The Monro-Kellie hypothesis explains the 4. A patient is receiving Mannitol for increased
compensatory relationship among the ICP. Which statement is INCORRECT about this
structures in the skull that play a role with medication?
intracranial pressure. Which of the following
are NOT compensatory mechanisms a. Mannitol will remove water from the
performed by the body to decrease brain and place it in the blood to be
intracranial pressure naturally? Select all that removed from the body.
apply: b. Mannitol will cause water and
a. Shifting cerebrospinal fluid to other electrolyte reabsorption in the renal
areas of the brain and spinal cord tubules.
b. Vasodilation of cerebral vessels c. When a patient receives Mannitol we

must monitor the patient for both
c. Decreasing production of fluid volume overload and depletion.
cerebrospinal fluid
d. Mannitol is not for patients who are
d. Leaking Proteins into the brain barrier experiencing anuria.
2. External ventricular drains monitor ICP and 5. A male patient with suspected increased
are inserted where? intracranial pressure (ICP), a most appropriate
respiratory goal is to:
a. Sub arachnoid space
b. Lateral Ventricle a. Prevent respiratory alkalosis.
c. Epidural space b. Lower arterial pH.
d. Right Ventricle c. Promote carbon dioxide elimination.
3. Which patient below with ICP is experiencing d. Maintain partial pressure of arterial
Cushing’s Triad? A patient with the following: oxygen (PaO2) above 80 mm Hg
a. BP 150/112, HR 110, RR 8
b. BP 90/60, HR 80, RR 22
c. BP 200/60, HR 50, RR 8
d. BP 80/40, HR 49, RR 12
5.(c) 4.(b) 3.(c) 1.(b,c,d) 2.(b)

Answers

25 Opioid Free Anaesthesia
Head of Department of Anaesthesia, Subrahmanyam M

Rainbow Hospitals.
Director, Axon Anaesthesia Associates.
Key points
Ø Opioid free anaesthesia came in to practice in order to avoid the well described side effects of opioid
Ø Opioid induced side effects are nausea, vomiting, pruritus, respiratory depression, sleep disordered
breathing, urinary retention, constipation, POCD, postoperative ileus, opioid induced hyperalgesia
Ø Alternatives for opioids are dexmedetomidine, ketamine, local/regional anesthesia, lignocaine infusion,
magnesium sulfate, paracetamol, NSAIDS, dexamethasone
Opioids have been used for pain relief for several opioid use, its risk vs benefits and other alternatives
thousands of years and have contributed to improve the available to provide balanced anesthesia. Enhanced use
quality of life of countless number of patients including of ultrasound guided regional anesthesia techniques,
patients enduring severe postoperative pain and cancer improved monitoring standards and modern surgical
patients. In the past two decades, opioids have been techniques, have paved way to multimodal anesthesia
used increasingly not only for the treatment of various with lower use of hypnotics.
chronic pain conditions but also during the perioperative Why go Opioid free?
period. Use of synthetic opioids began only after the
Second World War. Reports of death of several soldiers Opioid free anesthesia (OFA) and Opioid sparing
during induction of anesthesia (hemodynamically anesthesia are terminologies now in vogue, and they
unstable patients), during the Pearl Harbor Attack,1941 came in to practice in order to avoid the well described
is well known. In 1960, Paul Janssen first described the side effects of opioid use such as nausea, vomiting,
use of fentanyl for its marked hemodynamic stability pruritus, respiratory depression, sleep disordered
in comparison to the then available agents and it thus breathing, urinary retention, constipation, POCD and
found a place for use in sicker patients. Intraoperative postoperative ileus. Some studies highlight the risk
opioids achieve hemodynamic stability. They block of opioid induced hyperalgesia, a phenomenon of
the sympathetic reaction to surgical injury while acute tolerance, which worsens pain and increases
postoperative opioid analgesic consumption. Due to
maintaining blood pressure and heart rate. Currently
the above described side effects, liberal use of opioids
we dispose of very specific drugs to blunt the stress
in day care procedures is not recommended.
response and the sympathetic reaction to the surgical
incision. The advent of opioids led to the concept of Opioids in higher doses have shown to depress or alter
‘Balanced Anaesthesia’, where different drugs were cell mediated immunity. Cell mediated immunity plays
used for different actions viz. analgesics, hypnotics a pivotal role in immunosurveillance and elimination
and relaxants. of cancer cells. Being the main stay of treatment for
cancer pain currently, the potential effects of promoting
With the progress of science and medicine, with the tumor growth, tumor cell aggressiveness, angiogenesis
advent of newer drugs and technology, it is always wise and metastasis need to be borne in mind. Risk vs benefit
to review our clinical practices. Evidence based medicine needs to be considered prior to using high dose of
is the norm today, and hence it is interesting to compare perioperative opioids during oncological surgeries.

Opioid Free Anaesthesia 246 Subrahmanyam M
Many authors using ‘Opioid free anesthesia’ (OFA) have ambulatory surgery. Is this the best approach? Is
shown that actual use of post-operative opioids and opioid-induced hyperalgesia from ultrashort-duration
recovery characteristics are the same or better than in opioids a problem? Several investigations, in both
patients managed by intra-operative opioids. This may surgical patients and volunteers, have shown that high-
seem paradoxical, but has been shown in many studies. dose opioid infusions, particularly remifentanil, are
associated with greater postoperative pain and opioid
Intraoperative opioids are used by many as mandatory
consumption or with post-infusion hyperalgesia. By
to control intraoperative pain. By definition, pain is an
using ultrashort-duration opioids, are we inadvertently
‘unpleasant sensory and emotional experience . . .’
causing more postoperative pain and necessitating
Under anaesthesia, as under other conditions where
greater postoperative opioid use? Is remifentanil
a patient is unconscious the term ‘pain’ should not be
hyperalgesia associated with persistent postoperative
used and replaced by ‘nociception,’ which relates to the
pain? Are we inadvertently encouraging surgeons to
neural processes of encoding and processing noxious
prescribe more take-home opioids? Should we instead
stimuli. Then, are opioids the best way to control
be using long-duration intraoperative opioids that also
intraoperative nociception?
diminish postoperative pain? And perhaps, therefore,
Anaesthesiologists and surgeons face three challenges also diminish postoperative opioid requirements and
in the quest to provide optimum perioperative pain prescribing?
care, particularly within the growing domain of “shared
What can, and what should, anaesthesiologists and
responsibility” for patients’ surgical outcomes with
surgeons do to help address and mitigate the escalating
other physicians and providers. The first challenge
problem of opioid availability, diversion, nonmedical
is provision of adequate perioperative analgesia.
use, and opioid related harm?
Adequate pain relief has been deemed a fundamental
right, but more than 80% of patients report inadequate How do we go opioid free? What are the alternatives?
postoperative pain relief. Acute postoperative pain is a
1) Alpha-2 agonists
major risk factor for chronic postoperative pain, which
occurs in 10 to 50% of patients. The second challenge is Clonidine and dexmedetomidine can be used, with
to minimize or prevent opioid related side effects—the fairly stable hemodynamics. Dexmedetomidine
most serious of which is respiratory depression. The is 7 times more potent than clonidine. It is
third issue is the soaring volume of opioid prescribing, administered by a continuous infusion, and
prescribing patterns, and the accompanying devastating provides hypnosis, sedation and has analgesic
surge in prescription opioid diversion, abuse, addiction, properties. Pretreatment with dexmedetomidine
and overdose especially in USA. The US Centre attenuates the adrenergic response to tracheal
for Disease Control and Prevention (CDC) defined intubation and decreases plasma catechol
prescription drug abuse as an epidemic and one of its concentrations during anesthesia. Intravenous
top five health threats for 2014. In 2011, an estimated infusion of dexmedetomidine results in a
700,000 people in the United States received treatment decrease in minimum alveolar concentration
for misuse of prescription pain relievers, exceeding (MAC) for volatile anesthetic agents and has an
the number for cocaine (511,000) or heroin (430,000) opioid-sparing effect.
and there were 488,000 emergency department visits 2) Loco – regional analgesia / anaesthesia can
involving nonmedical use of prescription opioids. There be achieved with peripheral nerve blocks and
were 64,000 deaths in 2016 (in USA) due to opioid neuraxial techniques such as epidural. When
overdose. administered preemptively, better post-operative
pain scores/ patient satisfaction can be achieved.
During the past decades, there has been a trend,
CNS sensitization and chronicisation of pain
or fashion, toward the use of shorter and shorter
can be avoided. Use of non-opioid adjuvants
duration opioids intraoperatively, particularly in in the local anaesthetic mixture, also prolongs
duration of blockade and minimises use of other 8) Dexamethasone at doses more than 0.1 mg/kg
analgesics. is an effective adjunct in multimodal strategies
to reduce postoperative pain and opioid
3) Preservative free lignocaine infusion
consumption after surgery
Lignocaine has analgesic, anti-inflammatory
and anti hyperalgesic properties. The dose Opioid free anaesthesia in bariatrics
of intravenous lignocaine for analgesia in the
Understanding the altered physiology in an obese
perioperative period is 1–2 mg kg−1 as an initial
bolus followed by a continuous infusion of 0.3– individual, primarily those involving the respiratory
0.5 mg kg−1 h−1. A continuous infusion (without system and cardiovascular system is important.
a bolus) takes 4–8 h to achieve a steady-state
Obesity alters the respiratory system, and the respiratory
plasma concentration. On discontinuation after
changes include obstructive sleep apnea, obesity-
prolonged infusion, the plasma levels decrease
rapidly. The context-sensitive half-time after a hypoventilation syndrome, asthma, and pulmonary
3-day infusion of lidocaine is ∼20–40 min, and hypertension. Lung compliance is decreased, which
there is no accumulation over time in healthy leads to a decreased functional residual capacity (FRC),
individuals. vital capacity, and total lung capacity. The decreased
FRC is a result of a decrease in expiratory reserve
4) Ketamine acts on NMDA receptors in the brain.
Ketamine is an amnesic and provides intense volume (ERV). If the ERV is reduced the tidal volumes
analgesia. The analgesia is profound even at in the lungs are below the closing capacity. A decrease
subanesthetic doses and it can reverse the in ERV leads to small airway closure, ventilation-
tolerance to opioids. perfusion mismatch, right-to-left shunting, and arterial
hypoxemia. Thus, anaesthetising such individuals
5) Magnesium sulphate is not a primary analgesic
pre-disposes them to a higher risk of respiratory
in itself, but it enhances the analgesic actions of
other analgesics as an adjuvant agent. Magnesium complications.
sulfate is a useful drug for perioperative pain Obese patients are more sensitive to the respiratory
treatment by blunting somatic, autonomic and
depressant effect of opioids. Patients may do well
endocrine reflexes provoked by noxious stimuli.
intraoperatively while intubated. However, opioid use
It is administered as a loading dose of 30-50
mg/kg followed by a maintenance dose of 6-20 in the obese patient places the patient at a higher risk
mg/kg/h (continuous infusion) until the end of of requiring post-operative ventilation in order to avoid
surgery. Magnesium reduces the requirement hypoxic episodes. Patients receiving opioids are also
of anaesthetic agents and muscle relaxants. more sedated in the PACU, making incentive spirometry
Intraoperative magnesium use decreases the and early ambulation an impossible task. Opioid-free
pain score postoperatively and hence the opioid general anesthesia is an alternative option to opioid
consumption. use, and studies have shown that both techniques
6) Paracetamol has demonstrated analgesic achieve the same level of pain control but without the
and opioid-sparing properties. In adults, the side effects of the latter.
appropriate dose for preemptive analgesia
is 1,000 mg administered intravenously over Research and updates in the area of Opiod free
approximately 20 minutes. The analgesic anaesthesia:
onset is rapid (within 5 minutes), but the peak
The Postopertative and Opioid Free Anesthesia (POFA)
concentration in plasma occurs at approximately
1 hour. It can be administered pre-operatively trial is the first prospective, randomised, parallel, single-
and can then be repeated 6th hourly. blind, multicentre study of 400 patients undergoing
elective intermediate or major non-cardiac surgery.
7) NSAIDS like Diclofenac and Ibuprofen have The primary outcome measure is the occurrence of
analgesic and opioid sparing properties.

postoperative opioid-related adverse event within the but understanding the mechanism of action helps
first 48 hours after extubation. These are: postoperative the anesthesia provider utilise these drugs to their
hypoxaemia or postoperative ileus or postoperative full potential. Mulier’s technique offers a guideline to
cognitive dysfunction. The POFA trial is specifically alternatives to opioid anesthesia, and many anesthesia
studying OFA using dexmedetomidine. The study providers are sharing their modification of Mulier’s
started in December 2017 and is still ongoing. technique.
MuliMix SOFA
Jan Paul Mulier, a Belgian anaesthesiologist, popularized Society for Opioid Free Anaesthesia is a nonprofit
the “MuliMix” opioid free anaesthesia technique. The organization formed to research, promote and educate
following techniques are used in various combinations anaesthesia professionals and patients on opioid free
to provide opioid free anaesthesia. pain management techniques. The first Annual Opioid
Free Anaesthesia Congress was held in Alabama on
• Sympatholysis, analgesia, and anesthesia (MAC
10th and 11th November 2018, and it brought together
reduction) with dexmedetomidine
pioneers in this field from all over the world.
• Analgesia with low-dose ketamine
Conclusion
• Co-anesthesia and sympatholysis with
With the available evidence favouring opioid sparing
intravenous lignocaine
strategies, it is unclear if total avoidance of perioperative
• Profound neuromuscular blockade maintained opiod use is beneficial. The ongoing POFA randomised
up to the end of surgery and appropriately control trial could throw light in this area and give
reversed information regarding the benefits and safety of opioid
free anaesthesia. The benefits of OFA in terms of
• 0.7 -1.0 MAC desflurane in oxygen/air titrated reduction of opioid-related adverse events, reduction
to entropy or BIS EEG monitoring of global morbidity, reduction of the cost burden
• Magnesium infusion as a further co-analgesic encountered due to opioid-related adverse events, and
reduction in duration of hospital stay would result in a
Example of Mulimix for patient of 70 kg IBW collective benefit for the future. OFA has the potential
to change the current anesthesia practice and to
“The induction & maintenance mixture” 50 cc syringe:
emerge as a new paradigm.
Dexmed 50 mcg = 12.5 ml of dexmedetomidine mixture
Suggested Reading
Ketalar 50 mg = 1 ml of Ketamine
1) Forget P. Opioid-free anaesthesia. Why and how?
Lidocaine 500 mg = 25 ml lidocaine 2% A contextual analysis. Curr Opin Anesthesiol
2018, 31:556–561
NaCl 0.9% up to 50 ml = 11.5 ml
2) Opioid-free anesthesia; a different regard to an-
7 ml for induction, 7ml/h for maintenance, 3,5 ml/kg/h esthesia practice. Lavand’homme, Patricia; Es-
in PACU tebe, Jean-Pierre. Curr Opin Anesthesiol: 2018,
31:556–561
Content of one 50 cc syringe should be enough for
about 6 hours 3) Kharasch ED, Brunt LM. Perioperative Opioids and
Public Health. Anesthesiology 2016, 124: 960-65
The mechanism of action of these adjuncts differs
from one another, thus providing pain management by 4) Boysen PG, Pappas MM, Evans B. An Evi-
dence-Based Opioid-Free Anesthetic Technique
targeting multiple sites in the pain pathway. The ideal
to Manage Perioperative and Periprocedural
combination of these adjuncts may not be perfect,
Pain. Ochsner Journal 2018, 18:121–125
5) Samuels D, Abou-Samra A, Dalvi P, Mangar D and
Camporesi EM. Opioid-free Anesthesia Results in
Reduced Post-operative Opioid Consumption. J
Clin Anesth Pain Med 2017, Volume 1, 3-5.
6) Beloeil H, Laviolle B, Menard C, et al. POFA trial
study protocol: a multicentre, doubleblind, ran-
domised, controlled clinical trial comparing opi-
oid-free versus opioid anaesthesia on postoper-
ative opioid-related adverse events after major
or intermediate non-cardiac surgery. BMJ Open
2018;8:e020873.

MCQ
1. All are side effects of opioids except: 4. Opioid induced hyperalgesia refers to
a. Pruritis a. Opioid tolerance
b. Arrhythmias b. Opioid withdrawal
c. Constipation c. Increased sensitivity to painful
d. Respiratory depression stimulus
2. All are components of Mulimix except: d. sensitivity to painful stimulus

5. Opioid free anaesthetic techniques include all
a. Lignocaine
except:
b. Propofol
a. Dexmedetomidine
c. Dexmedetomidine
b. Ketamine
d. Ketamine
c. Buprenorphine
3. most dangerous complication of opioids
requiring postop monitoring is: d. Paracetamol
a. Abuse potential
b. Postop ileus
c. Vomiting
d. Respiratory depression
5.(c) 4.(c) 3.(d) 2.(b) 1.(b)

Answers

HOW I DO IT?
26 An Update on General Anaesthesia for Caesarean Section
Consultant Anaesthetics, Matthew Winton Gibbs

University of Cape Town and
Groote Schuur Hospital, Cape Town.
Key points
Ø Rapid sequence induction (RSI) with cricoid pressure and endotracheal intubation is still recommended
as the gold standard in pregnant patients
Ø Propofol is now a standard induction agent in healthy patients without haemodynamic compromise
Ø Thrive is a promising means of pre-oxygenation and preventing desaturation during RSI
Ø The incidence of difficult airway in obstetric anaesthesia between 1970 and 2015 remains 1 in 390, so
knowledge of and familiarity with current guidelines is imperative
Ø The risk of awareness in obstetric general anaesthesia is elevated
Ø Rocuronium and sugammadex have been recommended for muscle relaxation and reversal but certain
implications remain including cost and risk of anaphylaxis
Introduction and Brief History reduced to 7.7% with the average number of GA’s per
trainee dropping from 18 to just 4.3
The nature and indications for general anaesthesia (GA)
for caesarean section (CS) has changed over the many Rapid sequence induction for CS
years in which it has been practiced. Before the 1950s,
Although there have been case reports and series
open breathing systems utilising gauze and chloroform
describing the use of supra-glottic devices in GA
were commonly used. Since the introduction of CS, the gold standard still remains rapid sequence
tubocurarine in the subsequent decades, endotracheal induction, due to the increased risk of pulmonary
intubation became routine. From 1959, the combination aspiration. However the risk is probably not as high as
of thiopental, succinylcholine, nitrous oxide and oxygen previously thought. Gastric ultrasound has been used
became standard with the addition of cricoid pressure to demonstrate normal gastric emptying in pregnant
in 1961 and halothane in 1970. Other than the new patients, with minimal residual fluid.4
volatiles, very little has changed in the approach to
general anaesthesia for caesarean section. A recent survey of practice for RSI for CS was undertaken
in 2017 in the United Kingdom 5 to evaluate the
There has been, however, an increased use of regional current practice of rapid sequence induction for
anaesthesia for Caesarean over the intervening years, caesarean section in England. Methods: In 2017, 316
resulting in decreased exposure to GA for CS for many questionnaire surveys were posted to all 158 hospitals
trainees. This is particularly noticeable in more well- with caesarean section capabilities in England. At each
resourced environments, where the GA section rate hospital, one questionnaire was to be completed by the
in some areas has declined from 79% to barely 10%,1 obstetric anaesthetic consultant lead and one by an
dropping even as low as 2.5% in certain institutions.2 anaesthetic trainee. Differences in responses between
Between 1982 and 1998 in Leeds, the use of GA was consultants and trainees, regardless of their place of

An Update on General Anaesthesia for Caesarean Section 254 Matthew Gibbs
work, were compared for all data using the Chi-square Preoxygenation and THRIVE
and the Fisher’s exact tests. Results: One-hundred-and-
eighty complete questionnaires were returned, with Administration of 100% oxygen prior to induction,
an overall response rate of 57%, 98 (54% 90 different replaces nitrogen in the functional residual capacity of
hospitals with CS capabilities responded and revealed the parturient, increasing the oxygen reserve and time
that thiopentone remained the most commonly used to hypoxaemia during apnoea. The use of a tight-fitting
agent (67%), routine intravenous opioids at induction in face mask with 100% oxygen whilst maintaining a patent
9% of all cases but 93% for preeclampsia and that only airway in the period between apnoea and laryngoscopy
17% of respondents routinely used a videolaryngoscope has been advocated. In addition, the anaesthetist may
as the primary airway device. Despite succinylcholine consider the use of nasal prong cannulae at 5 l/min O2
being the neuromuscular blocker of choice (92%), 52% flow to promote apnoeic oxygenation. This has been
of respondents supported a change to rocuronium. successfully used in obese non-pregnant patients to
There remained a significant variation in the practice increase desaturation time to 5.29 ± 1.02 minutes vs.
of RSI for GA CS in the UK. 3.49 ± 1.33 minutes (mean ± SD).7
The use of short acting opioids (e.g. remifentanil, Taking this concept further, Mir and Patel investigated
alfentanil) is advised during intubation especially in the use of high flow, humidified and warmed nasal
high-risk patients like pre-eclamptics, maternal cardiac prong cannulae to prolong the apnoeic period during
disease or neurological disease.6 The maintenance airway manipulation. New high-flow nasal cannulae
of haemodynamic stability is imperative, due to (HFNC) can deliver humidified oxygen at rates of up to
the increased risk of stroke when GA is compared
70 l/min over a prolonged period, providing a glottic
to neuraxial anaesthesia in pre-eclamptic patients.
FiO2 of 1.0 that is well tolerated. In 25 non-pregnant
Transient respiratory depression of the newborn
patients being anaesthetised with difficult airway (9
however can be expected.
obese, 12 with stridor), they were able to demonstrate
Minimum Equipment for Obstetric General Anaesthesia significant protraction in the time before desaturation
(According To OAA) occurred, as airway was maintained by jaw thrust. No
patient desaturated below 90% SaO2, with median
Preparing the theatre for the GA CS remains routine,
and should be standardised as much as possible. A apnoea time of 14 minutes. In two patients where
checklist, as published by the Obstetric Anaesthestists’ the airway was maintained, spectacular results were
Association (https://www.oaa-anaes.ac.uk/General_ achieved, up to 32 and 65 minutes. The rate of increase
Anaesthesia_Checklist) may be of benefit in reducing in end-tidal carbon dioxide was 0.15 kPa/min.8
the risk of human error during a stressful situation. A further randomised control trial in patients undergoing
As per most theatres, a full range of face masks,
RSI, 40 patients were randomised to either FMO2 or
oropharyngeal airways, an array of supraglottic devices
THRIVE. Despite longer apnoea times (248 seconds v
(especially second generation), endotracheal tubes and
123 seconds), there were no differences in maintenance
working laryngoscopes should be available and checked,
of SaO2 or arterial blood gas profiles.9
as well as standard monitoring equipment, gum elastic
bougie and Magill forceps. A videolaryngoscope that A subsequent modelling investigation in pregnancy,
is familiar to the users of the theatre would also be using the Nottingham Physiology Simulator (validated
advantageous. in pregnancy and the investigation of pre-oxygenation
Extra equipment that may be of use includes fibreoptic and apnoea in adults), showed that increasing and
scopes, intubating catheters, surgical cricothyroidotomy maintaining the FiO2 at the open glottis extended the
tools and all the necessary equipment for an awake average time for SaO2 to reach 40% from 4.5 minutes
fibreoptic intubation. A fit-for-purpose ramping pillow to 58 minutes in the non-labouring parturient.10and
should also be available. pre-oxygenated seven models of pregnancy for 3 min

using Fi O2 1.0, before inducing apnoea. We found blocking agents for optimum intubating conditions.
that increasing FiO2 at the open glottis increased the Anaesthetists should be familiar with all aspects of the
time to desaturation, extending the time taken for OAA/DAS guidelines.
SaO2 to reach 40% from 4.5 min to 58 min in the average
Cricoid Pressure
parturient model (not in labour). The greatest increase
was for an FiO2 of 1.0. Although practice varies in other country, evidence still
supports the use of 10 Newtons of force initially then
The use of THRIVE in obstetrics has been limited. A small
increasing to 30 N after induction of anaesthesia.12and
pilot study of 4 pregnant women at term was performed
emphasises: planning and multidisciplinary
by Tan and Dennis, where the pre-oxygenation induction
communication; how to prevent the rapid oxygen
of trigger threshold of FetO2 ≥0.9 proved difficult to
desaturation seen in pregnant women by advocating
achieve. A further prospective study in 73 parturients,
nasal oxygenation and mask ventilation immediately
with the primary outcome being EtO2 >90% after one
after induction; limiting intubation attempts to two;
breath using HFNO.11and mention the potential use of
and consideration of early release of cricoid pressure
high-flow humidified nasal oxygen (HFNO Only 60%
if difficulties are encountered. Because cricoid pressure
of women achieved the recommended target within
can lead to a poor view at laryngoscopy, OAA/DAS
one breath, and 84% achieved FetO2 ≥0.8. The authors
guidelines suggest a low threshold to reduce or release
determined HFNO as being inadequate to preoxygenate
cricoid pressure if intubation proves problematic. If a
term pregnant women. However, the great benefit
supraglottic device is being placed, it must be released.
of THRIVE is prolonging time to desaturation via bulk
Anaesthetists should be ready to reapply cricoid
oxygen flow during apnoea. Further studies need to be
pressure if regurgitation occurs, along with appropriate
performed to elucidate the role of THRIVE in obstetrics.
repositioning and expedient suctioning.
Difficult airway
Awareness in GA For CS
It is well recognised that there is elevated risk of
The 5th National Audit Project in the UK reported a
difficult airway in obstetric patients. Maternal, fetal,
high incidence of intraoperative awareness in obstetric
surgical and situational factors all contribute to the
anaesthesia for caesarean section. The risk factors
increased incidence. An increasing Mallampati score,
include emergency situations, the use of low dose
vascular and oedematous upper respiratory tract
thiopentone, the use of muscle relaxants, obesity,
mucosa also worsen intubating conditions. Increased
omission of opioids at induction and only a very short
oxygen requirements and decreased functional residual
time between induction and surgical induction. 13
capacity accelerate desaturation during apnoea, along
Thiopentone has been implicated as a risk factor for
with the elevated risk of pulmonary aspiration.
accidental awareness and in one survey, was used in
The release of the 2015 joint Obstetric Anaesthetists’ only 3% of anaesthetic inductions but implicated in 23%
Association and Difficult Airway Society guidelines for of awareness reports.
managing the difficult airway in obstetric patients has
Maintenance by volatiles is acceptable practice but
been timely and useful. These guidelines are available
concentrations greater than 1 minimum alveolar
from www.das.uk.com and from www.oaa-anaes.
concentration (MAC) should be avoided due to fetal
ac.uk. Some recommendations include the use of
depression and dose-dependent myometrial relaxation.
gentle face mask ventilation (maximal inflation pressure
Bispectral index monitoring (BIS) is commonly used
<20 cm H2O) with cricoid pressure, as it may reduce
to monitor the depth of anaesthesia but is not yet
the risk of desaturation; early release of cricoid to aid
established in obstetric GA practice. The isolated
laryngoscopy if difficulty is encountered and the use of
forearm technique (IFT) remains the gold-standard but
adequate doses of induction agents and neuromuscular
BIS cannot predict IFT response rates.
Muscle Relaxation it is becoming more widely available and is routinely

used in Japan, where in the eight years since its release
Succinylcholine has been, until recently, the gold
is estimated that sugammadex was administered to
standard for muscle relaxation for RSI due to its rapid
approximately 10% of the total Japanese population.16
onset. It is highly ionised and poorly lipid soluble and
In obstetrics, Nauheimer was the first to describe the
only small amounts cross the placenta.6 Due to its
use of sugammadex in caesarean section patients, with
side-effects and possible life-threatening (but rare)
excellent results.17 It has also been used to reverse
complications, other muscle relaxants have been
prolonged blockade in a parturient with transverse
sought. Rocuronium, since its introduction in 1994, due
myelitis, where neostigmine was ineffective.18 The
to its rapid onset in high (1.2mg/kg) doses, has become
combination of rocuronium and sugammadex has been
popular for RSI in obstetrics. It does not affect neonatal
suggested for routine use in GA for CS in a number of
Apgar-scores or acid-base measurements and provides
influential review articles.6
good intubating conditions in the vast majority of
obstetric patients. This comes with the sacrifice of still
being slower than succinylcholine and a very prolonged
duration of action. Due to the increased risk of difficult
airway and the ‘Can’t Intubate, Can’t Oxygenate’ (CICO)
scenario, many obstetric anaesthetists have been
reluctant to embrace rocuronium.
Sugammadex
Sugammadex is a modified cyclodextrin molecule that However, there are still safety concerns regarding
encapsulates rocuronium and other amino-steroid hypersensitivity and anaphylactic reactions due
neuromuscular agents. It reverses moderate blockade to sugammadex. A recent randomised controlled
17 times faster than neostigmine (with fewer episodes trial in healthy subjects receiving 4 mg/kg, 16 mg/
of partial reversal) and is particularly attractive as it kg or placebo, showed hypersensitivity in alarming
can potentially reverse even deep blockade (i.e. within 6.6% and 9.5% of patients receiving the 4 and 16
five minutes of administration of an RSI at a dose of 16 mg/kg doses respectively.19 In an earlier double-blind,
mg/kg).14 There have also been case reports proposing placebo-controlled study, 448 healthy volunteers were
sugammadex as a treatment for rocuronium induced randomised to receive the same doses as the above
analphylaxis.15 trial, the incidence was 0.7% in the 4 mg/kg group and
4.7% in the 16 mg/kg group.20 On the basis of this work,
The cost of sugammadex is high, about twenty times an incidence of 1:20 mild to moderate hypersensitivity
that of neostigmine at an average reversal dose of reactions could be expected and an alarming 1:150
2-4mg/kg, and eye-watering at 16 mg/kg. However, anaphylaxis incidence at 16 mg/kg. This is in contrast
to Japan, where thousands of cases would be expected. Prescription for a cure. Int J Obstet Anesth 2005;
Although it is the most common cause of perioperative 14: 2–4
anaphylaxis, only 284 cases of anaphylaxis due to
sugammadex have been reported, giving an incidence 3. Johnson R V., Lyons G, Wilson RC, Robinson
of between 1:2500 and 1:34-40000, depending on the APC. Training in obstetric general anaesthesia:
study quoted.16 In the UK, there is only one confirmed a vanishing art? Anaesthesia [Internet] 2000;
case of sugammadex anaphylaxis out of an estimated 55: 179–83 Available from: http://doi.wiley.
64000 administrations.21 Given that succinylcholine com/10.1046/j.1365-2044.2000.055002163.x
and teicoplanin are relatively common causes of 4. Arzola C, Perlas A, Siddiqui NT, Downey K, Ye
perioperative anaphylaxis (11/100000 and 16/100000
XY, Carvalho JCA. Gastric ultrasound in the third
respectively), the true incidence remains unclear but
trimester of pregnancy: a randomised controlled
certainly not at the levels suggested by de Kam and
trial to develop a predictive model of volume
Min. Sugammadex can certainly be used in practice,
assessment. Anaesthesia 2018;
but an awareness of the possibility of hypersensitivity
reactions must in the back of the treating physicians 5. Desai N, Wicker J, Sajayan A, Mendonca C. A
mind. survey of practice of rapid sequence induction for
One other note of caution is the use of sugammadex caesarean section in England. Int J Obstet Anesth
in the CICO situation, where sugammadex proponents [Internet] Elsevier Ltd; 2018; Available from:
emphasise its advantages. Studies suggest that, unless https://doi.org/10.1016/j.ijoa.2018.05.008
stored in theatre and readily available, mean time to 6. Devroe S, Van de Velde M, Rex S. General anesthesia for
administration of sugammadex in a CICO situation was caesarean section. Curr Opin Anaesthesiol [Internet]
6.7 minutes (8.9 minutes to reach a train-of-four of 2015; 28: 240–6 Available from: http://content.
0.9).22 Sugammadex might not save a life in this scenario
wkhealth.com/linkback/openurl?sid=WKPTLP:
as critical hypoxaemia may well have been reached.
landingpage&an=00001503-201506000-00003
Regional Blockade
7. Ramachandran SK, Cosnowski A, Shanks A,
Multimodal analgesia is the standard approach to post Turner CR. Apneic oxygenation during prolonged
CS analgesia. A number of truncal blocks have been laryngoscopy in obese patients: a randomized,
developed including Transversus Abdominis Plane (TAP) controlled trial of nasal oxygen administration.
blocks, Rectus Sheath blocks and Quadratus Lumborum J Clin Anesth [Internet] Elsevier Inc.; 2010; 22:
Blocks. The latter named blocks are increasing in 164–8 Available from: http://dx.doi.org/10.1016/j.
popularity due the coverage of T6-T12/L1 and that jclinane.2009.05.006
both visceral and parietal peritoneum may be covered.
Some early work is encouraging and at least one study 8. Patel A, Nouraei SAR. Transnasal Humidified
shows decreased visual analogue scale scores and 24 Rapid-Insufflation Ventilatory Exchange (THRIVE):
hour morphine consumption when compared to TAP a physiological method of increasing apnoea time
blocks.23 24 Ongoing studies in post CS patients are in patients with difficult airways. Anaesthesia
underway. [Internet] 2015; 70: 323–9 Available from: http://
doi.wiley.com/10.1111/anae.12923
References
9. Mir F, Patel A, Iqbal R, Cecconi M, Nouraei SAR. A
1. Russell R. Failed intubation in obstetrics: a self- randomised controlled trial comparing transnasal
fulfilling prophecy? Int J Obstet Anesth 2007; 16: humidified rapid insufflation ventilatory exchange
1–3 (THRIVE) pre-oxygenation with facemask pre-
2. Lipman S, Carvalho B, Brock-Utne J. The demise oxygenation in patients undergoing rapid sequence
of general anesthesia in obstetrics revisited: induction of anaesthesia. Anaesthesia [Internet]

2017; 72: 439–43 Available from: http://doi.wiley. Available from: http://link.springer.com/10.1007/
com/10.1111/anae.13799 s00101-012-2065-6
10. Pillai A, Chikhani M, Hardman JG. Apnoeic 18. Weekes G, Hayes N, Bowen M. Reversal of
oxygenation in pregnancy: a modelling investigation. prolonged rocuronium neuromuscular blockade
Anaesthesia 2016; 71: 1077–80 with sugammadex in an obstetric patient with
transverse myelitis. Int J Obstet Anesth [Internet]
11. Tan PCF, Millay OJ, Leeton L, Dennis AT. High-flow
2010 [cited 2019 Jan 12]; 19: 333–6 Available from:
humidified nasal preoxygenation in pregnant
http://www.ncbi.nlm.nih.gov/pubmed/20627694
women: a prospective observational study.
Br J Anaesth [Internet] Elsevier Ltd; 2018; 6: 19. Min KC, Bondiskey P, Schulz V, et al. Hypersensitivity
1–6 Available from: https://doi.org/10.1016/j. incidence after sugammadex administration in
bja.2018.08.015 healthy subjects: a randomised controlled trial.
Br J Anaesth [Internet] 2018; 9: 1–9 Available
12. Mushambi MC, Kinsella SM, Popat M, et al.
from: https://linkinghub.elsevier.com/retrieve/pii/
Guidelines Obstetric Anaesthetists’ Association
S0007091218304574
and Difficult Airway Society guidelines for the
management of difficult and failed tracheal 20. de Kam P-J, Nolte H, Good S, et al. Sugammadex
intubation in obstetrics*. Anaesthesia 2015; 70: hypersensitivity and underlying mechanisms: a
1286–306 randomised study of healthy non-anaesthetised
volunteers. Br J Anaesth [Internet] Elsevier Ltd;
13. Pandit JJ, Andrade J, Bogod DG, et al. 5th National
2018; 121: 758–67 Available from: https://doi.
Audit Project (NAP5) on accidental awareness
org/10.1016/j.bja.2018.05.057
during general anaesthesia: Summary of main
findings and risk factors. Br J Anaesth 2014; 113: 21. Savic L, Savic S, Hopkins PM. Sugammadex: the
549–59 sting in the tail? Br J Anaesth [Internet] 2018; 121:
694–7 Available from: www.apsf.org/newsletter/
14. Bailey CR. Sugammadex: when should we be giving
june-2018/
it? Anaesthesia [Internet] 2017 [cited 2017 Oct
2]; 72: 1170–5 Available from: http://doi.wiley. 22. Bisschops MMA, Holleman C, Huitink JM. Can
com/10.1111/anae.13960 sugammadex save a patient in a simulated ‘cannot
intubate, cannot ventilate’ situation? Anaesthesia
15. Spoerl D, D’incau S, Roux-Lombard P, Harr T,
2010; 65: 936–41
Czarnetzki C. Non-IgE-Dependent hypersensitivity
to rocuronium reversed by sugammadex: Report 23. Yousef N. Quadratus lumborum block versus
of three cases and hypothesis on the underlying transversus abdominis plane block in patients
mechanism. Int Arch Allergy Immunol 2016; 169: undergoing total abdominal hysterectomy: A
256–62 randomized prospective controlled trial Naglaa
Yousef. Anesth Essays Res 2019; 3: 1–8
16. Takazawa T, Miyasaka K, Sawa T, Iida H. Current
Status of Sugammadex Usage and the Occurrence 24. Akerman M, Pejčić N, Veličković I. A Review of
of Sugammadex-Induced Anaphylaxis in Japan. Off the Quadratus Lumborum Block and ERAS. Front
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fmed.2018.00044/full
17. Nauheimer D, Kollath C, Geldner G. Modifizierte
Blitzintubation im Kreißsaal. Anaesthesist [Internet]
Springer-Verlag; 2012 [cited 2019 Jan 12]; 61: 691–5

MCQ
1. Respiratory system changes during pregnancy 4. Amount of cricoid pressure in RSI after
are all except induction of anesthesia
a. Tidal volme increase by 40-50% a. 20N
b. Minute volume increases by 20-50% b. 30N
c. FEV1/FVC ratio increases c. 50N
d. FRC decreases by 30% d. 10N
2. Air way changes in pregnancy are 5. Hematological changes in pregnancy are all
except
a. Mallampati score increases by 1 level
during labor a. Increase in factor VII,VIII,IX,X,XII
b. vascular and edematous upper b. RBC volume increases by 45%,plasma
respiratory tract mucosa volume increases by 30%
c. prone for early desaturation c. Decrease in anti thrombin
d. increased risk of pulmonary aspiration d. Increase in fibrinogen and FDP’S
e. all of above
3. Regional blocks in cesarean section are all
except
a. TAP block
b. Rectus sheath block
c. Quadratus lumborum block
d. serratus anterior plane block
5.(b) 4.(b) 3.(d) 2.(e) 1.(c)

Answers

27 Anaesthesia for neonate with tracheo-oesophageal fistula
Professor and HOD, Anila Malde

Lokmanya Tilak Municipal Medical College and General Hospital,
Mumbai
Key points
Ø The incidence of associated defects is high in patients with isolated oesophageal atresia, but least
common in infants with the H-type fistula.
Ø Virtual endoscopy can be used to traverse past stenoses.
Ø An echocardiogram is strongly recommended before surgery to identify cardiac defects and the position
of the aortic arch.
Ø Waterston classification and Spitz classification allows for risk stratification, predicting outcome and
surgical timing.
Ø In infants with significant associated anomalies or sepsis, a definitive repair of an oesophageal lesion
may be too risky.
Ø The ligation of a TOF is urgent, but not emergent, except in the setting of respiratory insufficiency
severe enough to require ventilatory support, especially in the premature infant.
Ø An oesophagoscopy or bronchoscopy is often performed at the start of surgery to confirm the diagnosis,
to assess fistula position and to exclude multiple fistulae.
Ø If there is significant tension at the anastomosis, the neonate should remain paralyzed and the lungs
ventilated mechanically for approximately 5 days postoperatively.
Ø Cardiac anomalies typically are the cause of death in this more complicated cases.
Ø The approach to open repair has been revised to include a muscle-splitting surgical approach that has
decreased dramatically the musculoskeletal complications.
Ø The main anaesthesia complications relate to inadvertent intubation of the fistula or preferential
ventilation of the fistula causing gastric distension and desaturation.
Ø Main anaesthesia goals are to maintain adequate oxygenation, ventilation and avoidance of gastric
distension.
Ø Manual ventilation is recommended as surgical traction can easily occlude the neonate’s soft trachea.
It can be helpful in assessing pulmonary compliance.
Ø Blood clots or secretions may block the ETT, and frequent ET suctioning may be required.
Epidemiology tracheooesophageal fistula (TOF). Although most cases

are sporadic, incidence is 2.4-fold higher in twins.
Oesophageal atresia (OA) is the most frequent
congenital anomaly of the oesophagus, with an Embryology and anatomy
approximate incidence of 1 in 4000 neonates. Greater
Both the oesophagus and the trachea originate from
than 90% of affected individuals have an associated
the median ventral diverticulum of the primitive
Anaesthesia for Neonate with 262 Anila Malde
Tracheo-Oesophageal Fistula
foregut. Oesophageal atresia results when the tracheal • Type B: Oesophageal atresia with proximal
structures assume most of the endoderm, and TOF TOF (1%)
results when the oesophageal and tracheal ridges fail • Type C: Oesophageal atresia with distal TOF
to develop, leaving a communication between the two (84%)
structures. • Type D: Oesophageal atresia with proximal and
Classification and incidences distal TOFs (3%)
• Type E: TOF without oesophageal atresia or
C l a s s i fi c a ti o n o f e s o p h a g e a l a t r e s i a a n d
so-called H-type fistula (4%)
tracheoesophageal fistula according to Vogt.
• Type F: Congenital oesophageal stenosis (<1%)
Type 1: Obliteration of the oesophagus.
Type II: Atresia without fistula. The length of the gap between proximal and distal
Type IIIa: Atresia with proximal fistula. oesophagus is variable, as is the position of fistula (or
fistulae) within the trachea. These anatomical variations
Type IIIb: Atresia with distal fistula.
have important implications for surgical strategy and
Type IIIc: Atresia with proximal and distal fistula. anaesthesia management. In one series, the fistula was
Type IV: Tracheoesophageal fistula (H-type fistula). mid-tracheal in 61 %, at or just above the carina in 33
Gross created a classification system in 1953 (Fig 1) %, cervical in 8 % and bronchial in 1 %. There was more
than one fistula in 3 % of patients. In the “H”-type TEF,
• Type A: Oesophageal atresia without fistula or the fistula is typically in the cervical region, whereas in
so-called pure oesophageal atresia (8%) EA with a proximal fistula, the fistula is usually 1–2 cm
from the blind-ending upper pouch.
Fig 1: Gross classification of congenital anomalies of the trachea and oesophagus. A: OA without fistula. B:
OA with proximal fistula. C: OA with distal fistula. D: OA with proximal and distal fistula. E: TOF with no OA. F:
Oesophageal stenosis. OA, oesophageal atresia; TOF, tracheooesophageal fistula

Associated Anomalies Also, trisomies 13, 21 or 18 and Fanconi syndrome

may be present. The overall incidence of associated
VACTERL: V Vertebral (vertebral malformations, anomalies is approximately 50%. Another 20% to 30%
hemivertebrae); A Anal (imperforate anus, also of infants with tracheoesophageal fistula (TOF) are
midgut malrotation, Meckel’s diverticulum); C Cardiac premature, weighing less than 2000 g.
(VSD, PDA, TOF, ASD, coarctation of aorta); T Trachea
(TOF); E Esophagus (EA); R Renal (renal agenesis, Clinical Presentation
hydronephrosis, renal lobulation); L Limb (radial aplasia, Classically, the neonate with OA presents with copious,
polydactyly, wrist anomalies). As many as 20% to 25% of fine, white, frothy bubbles of mucus in the mouth
infants with oesophageal atresia have at least three of and sometimes, the nose. These secretions may clear
the lesions included in VACTERL. Between 50% and 65% with aggressive suctioning but eventually return. The
of infants with oesophageal atresia with or without a infant may have rattling respirations and episodes of
TOF have at least one additional anomaly. The incidence coughing, choking and cyanosis. These episodes may
of associated defects is particularly high (50% to 70%) be exaggerated during feeding. Aspiration of saliva or
in the group with isolated EA but least common (10%) milk, if the baby is allowed to suckle, can lead to an
in infants with the H-type fistula (Type E). aspiration pneumonitis. In a baby with oesophageal
atresia and a distal TOF, the lungs may be exposed
CHARGE syndrome is associated in 6 % of patients. It
to gastric secretions. Infants with an isolated TOF in
includes coloboma of the eye, heart disease, choanal the absence of OA may elude diagnosis until later in
atresia, retarded growth, ear abnormalities and life when the patients come to medical attention for
deafness. Potentially fatal anomalies e.g. tracheal recurrent pneumonias and refractory bronchospasm.
agenesis or stenosis, laryngeal atresia are uncommon Air from the trachea can pass down the distal fistula
but associated with TOF with OA but not H type fistulas. when the baby cries, strains or receives ventilation. As
a result, the stomach and small intestine can become
Incidence of Associated Anomalies: Cardiovascular-35%;
dilated, which elevates the diaphragm and makes
Musculoskeletal -30%; Gastrointestinal -20%;
respiration more difficult. Occasionally, it can lead
Genitourinary -10%; Craniofacial - 4%.
to an acute gastric perforation, which is often lethal.
The following anomalies also occur with increased The abdomen will be scaphoid if no fistula exists. In
frequency in oesophageal atresia: the delivery room, the affected infant may have the
sonorous seal-bark cough that indicates concomitant
Neurologic defects: Neural tube defects, hydrocephalus, tracheomalacia.
tethered cord, holoprosencephaly
Diagnosis
GI defects: Duodenal atresia, ileal atresia,
hypertrophic pyloric stenosis, OA is usually diagnosed soon after birth when an oral
omphalocoele, malrotation, catheter cannot be passed beyond 10 to 12 cm into
Meckel’s diverticulum the stomach or when the neonate exhibits cyanosis,
coughing and choking during oral feedings.
Pulmonary defects: Unilateral pulmonary agenesis,
Plain radiographs of the chest and abdomen will reveal
diaphragmatic hernia
coiling of a nasogastric tube in the oesophageal pouch
Genitalia defects: Undescended testicles, ambiguous and possibly an air-filled stomach in the presence of
genitalia, hypospadias a co-existing TOF (Fig 2,3). In contrast, pure OA may
present as an airless abdomen.

Fig 4: X ray chest and abdomen PA View of a baby

with OA & TOF with 13 ribs
Computed Tomography (CT) Findings
Fig 2: X ray chest and abdomen lateral View of a baby CT is not typically used in the evaluation of OA and TOF;
with OA & TOF however, CT does allow 3-dimensional (3D) visualization
of the entire length of the oesophagus, complete with
atresias, fistulas and gap length. Virtual endoscopy
can be used to traverse stenoses, unlike traditional
endoscopy.
Ultrasonography
The ultrasonographic finding of an absent or small
foetal stomach bubble in combination with maternal
polyhydramnios is suggestive of OA and/or TOF. The
presence of a dilated blind-ending oesophageal pouch
on a sonogram is suggestive of OA.
Preoperative Management
1) Look for other associated anomalies.
Fig 3: X ray chest and abdomen PA View of a baby 2) An echocardiogram is strongly recommended be-
with OA & TOF fore surgery to identify cardiac defects and the
position of the aortic arch. Every neonate should
have a preoperative echocardiogram to identify
The chest radiograph provides information about the the presence of a congenital heart defect that
cardiac silhouette, the location of the aortic arch and may range from a patent ductus arteriosus or
the presence of vertebral and rib anomalies, as well as ASD/VSD to a hypoplastic left heart. Failure to
the presence of pulmonary infiltrates (Fig 4). be aware of the presence of a congenital heart
defect during one-lung anaesthesia for an OA/

TOF repair could lead to catastrophic complica- 8) A catheter is placed in the oesophagus to drain
tions including hypoxia, hypotension and cardiac saliva and the infant is placed prone in a head-up
arrest. Vascular anomalies (e.g., right aortic arch, position.
2.5% to 5%) that can alter the surgical approach
can be identified, and therefore echocardiogra- 9) Intravenous fluid containing an adequate glucose
phy should be done preoperatively. concentration (i.e., 10% glucose) is administered
at a rate appropriate for the neonate’s gestation-
3) Renal ultrasound should be done. If the neonate al age and weight.
has passed urine (thus excluding bilateral renal
agenesis), then a renal US can be delayed until 10) Prophylactic broad-spectrum antibiotics (eg, am-
after surgery. Look for choanal atresia which may picillin, gentamicin) are intravenously adminis-
cause respiratory distress. tered.
4) Retrognathia is common with CHARGE syndrome, 11) The neonate is kept warm by using an incubator
so be prepared for difficult intubation. or overhead warmer.
5) A tethered cord is usually detectable with ultra- 12) Oxygen therapy is used as needed to maintain
sonography in the newborn period. If present, normal oxygen saturation.
one cannot plan for epidural anaesthesia. 13) In infants with respiratory failure, endotrache-
6) Look for signs of aspiration pneumonitis. It cer- al intubation should be performed. If preopera-
tainly depends upon: Type of TOF/OA, duration tive ventilation is required, inspiratory pressures
between birth and presentation to clinician. 90% should be kept to a minimum.
of cases come to the anaesthesiologist after first Risk Stratification
feed with aspiration pneumonitis and respiratory
distress. Waterston classification, as shown in Table 1, allows for
risk stratification, predicting outcome and surgical timing.
7) For management of anaesthesia, the infant’s
feedings are withheld. There are three important factors which predict outcome
and includes birth weight, associated anomalies and
pneumonia. Spitz classification is also used.
Category Weight Surgical timing
A >2.5 kg Can undergo surgery

1.8‑2.5 kg or pneumonia or congenital Short‑term delay, needs stabilization
B
anomaly before surgery
<1.8 kg or severe pneumonia and
C Requires customized/ staged repair
congenital anomaly
Table 1: Waterson classification
Groups Features Survival (%)

I >1.5 kg, no major cardiac abnormality 98.5
II <1.5 kg or major cardiac abnormality 82
III <1.5 kg and major cardiac abnormality 50
Table 2: Spitz classification
Surgical management of a TOF and poor lung compliance often prevent

delivery of adequate tidal volumes (ventilation escapes
Type of surgery depends on the following three factors
into the esophagus and stomach via the fistula). In
• Weight of the baby such cases, dilation of the stomach may add to the
• Overall clinical condition of neonate respiratory compromise by elevating the diaphragm
and worsening pulmonary compliance. It can also cause
• Upper pouch level
deterioration of cardiorespiratory status and possible
The aim of surgery is to restore continuity of the gastric rupture. Inadvertent intubation of the fistula
oesophagus and ligate the TOF, if present. Surgery is must be excluded in cases of severe gastric distention
usually performed on the first or second day of life if with cardiorespiratory instability. To prevent gastric
the neonate is stable and does not require respiratory distention from ventilation via the fistula, some have
support. Surgery is the definitive management, delay in recommended clamping the distal oesophagus as soon
surgical correction is usually associated with increased as the chest is opened. Decompressive gastrostomy
risk of aspiration from the upper oesophageal pouch. should not be undertaken as a primary intervention as
Reflux of gastric contents from the lower pouch and TOF it will lead to a torrential gas leak via the gastrostomy
is responsible for causing pneumonitis. Early diagnosis and worsening minute ventilation. The child should
and repair results in significant improvement in survival undergo emergency transpleural ligation of the fistula,
outcomes. with delayed division of the fistula and possible repair
of OA at 8–10 days.
In infants with significant associated anomalies or
sepsis, a definitive repair of an oesophageal lesion may Neonates with pure OA or OA with a proximal TOF
be considered too risky, and a limited thoracotomy may often have a long gap between proximal and distal ends
focus on ligation of the TEF followed by placement of of the oesophagus. A feeding gastrostomy is inserted
a gastrostomy. In some cases, such critically ill infants and the length of the gap estimated radiographically
may be mechanically ventilated preoperatively. In these at the time of surgery. If the gap is greater than the
cases, a more definitive surgery may be tolerated within vertical height of three vertebral bodies, upper pouch
suction is continued postoperatively and delayed
24 to 72 hours, when the extent of other anomalies is
primary closure is usually possible by about 12 weeks
defined, cardiovascular stability is established and a
of age; if the gap is greater than six vertebral bodies,
clear surgical plan has been defined. The gastrostomy
a cervical oesophagostomy is often fashioned and the
provides a reliable system to decompress the stomach,
oesophagus repaired at a later date. Oesophageal
minimizing the risk for regurgitation into the lungs, and
replacement surgery is occasionally required.
in cases in which definitive surgery is delayed, allows
nutrition via enteral feedings, thus avoiding intravenous An oesophagoscopy or bronchoscopy is often performed
alimentation. at the start of surgery to provide absolute confirmation
of the diagnosis, to assess the position of the fistula if
It may be preferable to divide the fistula and place
present, and to exclude multiple fistulae. A variety of
a feeding gastrostomy in a neonate with severe
techniques have been described to identify fistulae
comorbidities such as a duct-dependent cardiac
in neonates: rigid bronchoscopy, esophagoscopy or
anomaly. Primary oesophageal repair can be performed
flexible fiberoptic bronchoscopy via the tracheal tube.
6–12 weeks after cardiac surgery.
The advantage of using a small flexible bronchoscope is
The ligation of a TOF is urgent, but not emergent, that the scope may also be used to assess the position
except in the setting of respiratory insufficiency severe of the tip of tracheal tube, to pass through the fistula
enough to require ventilatory support, especially in to assist the surgeon in identifying the fistula during
the premature infant. In this setting, the presence surgery and to assess the airway at the end of surgery
to exclude a residual blind-ending tracheal pouch and
the severity of the tracheomalacia near the fistula. tube must be fixed in place, because it has a tendency to
become dislodged. This tube should be clearly marked
The traditional approach to repair of OA/TOF is to preclude accidental removal postoperatively. If there
extrapleural via a right posterolateral thoracotomy with is significant tension at the anastomosis, the neonate
the neonate placed in the lateral decubitus position should remain paralyzed and the lungs ventilated
with a roll under the chest to facilitate surgical access. mechanically for approximately 5 days postoperatively.
The posterior mediastinum is approached via the 4th A gas leak from the upper pouch during oesophageal
and 5th intercostal spaces and the extrapleural route, anastomosis should raise suspicion of an upper
gently compressing the right lung. The approach is pouch fistula. Dissection of the upper pouch helps to
delicate and time consuming but reduces morbidity identify a proximal fistula, if one is present, and allows
from an anastomotic leak, should one occur. If a right mobilization of the oesophagus to minimize tension of
arch is confirmed on preoperative echo, a left-sided the repair. Typical surgical time: 2 to 4 hours for primary
approach should be considered and a double aortic arch repair of TOF/OA.
may be approached via the standard right thoracotomy.
In some cases, the distal portion of the oesophagus
If the child becomes unstable, a transpleural approach
is either absent or too short to reach the proximal
may be used. Dividing the azygous vein is necessary to
segment. Type C (OA with a TOF between the distal
find the subjacent fistula, branching off the posterior
oesophagus and the trachea) commonly includes a
aspect of the trachea (Type C). The right bronchus,
gap short enough to allow a primary repair, and Type
aorta, and (rarely) left bronchus may be mistaken
A(OA) is least commonly associated with such a gap.
for this structure. Test occlusion of the fistula is good Usually, at some point preoperatively, the gap between
practice to ensure that the right lung can still be the proximal and distal oesophagus is estimated, but
inflated and that a vital structure (e.g., the pulmonary no highly reliable technique is available to accurately
artery or main bronchus) has not been clamped in measure this distance. Simple radiographic contrast
error. Division of the fistula may dramatically improve studies (“unstressed”) may allow imaging of the
ventilation; until this moment it is sometimes necessary proximal end of the oesophagus, but the risk for aspira
to operate in short 3- to 5-minutes. bursts, relaxing tion must be considered. Specifically, to minimize the
lung and mediastinal retraction for 1–2 minutes. when risk, only a small amount of diluted, nonionic contrast
saturations descend to critical levels. The integrity of should be inserted into the proximal pouch by an
tracheal repair can be checked by instilling warm saline experienced paediatric radiologist. Hyperosmolar
in the chest during a sustained inflation to identify an cont rast such as gastrografin should be avoided,
air leak by the presence of air bubbles. because pulmonary aspiration of such material may
elicit chemical pneumonitis and associated pulmonary
The anaesthetist may be asked to help identify the oedema. If a gastrostomy has been placed, images can
distal end of the proximal pouch within the thorax be obtained with metal dilators inside the proximal
by manipulating the Replogle tube from above. The and distal pouches. In general, a gap smaller than
distance from the mouth to the distal tip is noted. two vertebral bodies implies that a primary repair is
Only catheters of this length should be used for suction appropriate. If the gap is between two and six vertebral
in the postoperative period. The lower oesophagus bodies, a delayed anastomosis might be considered,
should not be aggressively mobilized in order to avoid and if greater than six vertebral bodies, some would
devascularization, as this may cause later problems with suggest that primary anastomosis is impossible. In
oesophageal motility. some series, OA with a long gap is defined in terms of
centimeters between the two ends. A gap of longer than
Once the two ends of the oesophagus are approximated,
2.5 cm is sometimes considered the starting point for
the anaesthetist usually passes a fine transanastomotic
the category of long-gap OA. Some refer to long-gap
nasogastric tube before the anastomosis is fashioned to
OA as either 3 cm or more than two vertebral bodies.
allow enteral feeding in the postoperative period. This
A staged procedure, initial gastrostomy with deferred The known cardiac abnormality is also considered
thoracotomy may be used in babies < 1 kg, those with a relative contraindication considering impaired
pure OA or with more critical associated anomalies. The oxygenation during thoracoscopic approach, right aortic
survival rate in this group is lower but in the range of arch is an anomaly where anatomy is distorted and it is
80 to 95 percent. Cardiac anomalies typically are the difficult to work in a small space during TREAT. Similarly,
cause of death in this more complicated cases. long gap atresia and gap more than vertebral length are
difficult to handle at the time of anastomosis. Patient
Traditionally, in the setting of planned delayed surgery,
is placed in semi‑prone position with placement of
surgeons have ligated the fistula and inserted a
pad underneath right pectoral region so as to tilt chest
gastrostomy in the newborn. In the past, some surgeons
by 15° to opposite side. Table is tilted by 15° reverse
have opted to exteriorize the upper pouch through an
Trendelenburg position.
oesophagostomy, but this approach has been widely
abandoned. The gastrostomy provides a route for Borruto and colleagues reported in a meta-analysis,
enteral nutrition until surgical repair of the atresia. In no differences in complications or operative time.
most cases, definitive repair is undertaken between 3 Although no difference in the rate of postoperative
and 6 months of age, depending on the infant’s status leaks was noted between open and thorascopic repairs,
(e.g., growth and cardiorespiratory status) and the a subanalysis of the stricture rate demonstrated a higher
opinion of the surgeon. At that time, ideally, the two rate in the group who had undergone an open repair.
oesophageal segments are either directly anastomosed, In addition, thoracoscopy has not been associated with
as the native oesophagus allows superior function fewer days of postoperative ventilation, lower need for
compared to an interposed bowel segment or gastric analgesic agents, shortened NICU stay or decreased
tube graft. time to first feed. However, at a mean age of 3.8 years
(1 to 7 years), chest asymmetry and scoliosis (54%)
was more frequent in the open repair group (Lawal
Repair of TEF is classically performed through open
et al. 2009). The approach to open repair has been
thoracotomy, but there are various postoperative
revised to include a muscle-splitting surgical approach
concerns which include pain because of major incision,
that has decreased dramatically the musculoskeletal
splinting of diaphragm thereby delayed weaning,
complications.
postoperative pulmonary complications, scoliosis,
elevation or fixation of the shoulder, asymmetry of Anaesthetic Management
chest wall, large scar and cosmetic concerns.
Anaesthetic considerations include general factors
Over the past two decades, thoracosopic repair of relating to the thoracotomy or thoracoscopic surgery
tracheoesophageal fistula and esophageal atresia in neonates and the high incidence of comorbidity.
(TREAT) has emerged as an acceptable and even Specific considerations include airway management
preferred surgical approach to repair TOF/OA. A and positioning the tracheal tube in the presence of
major advantage of thoracoscopy is that the fistula is a tracheal fistula. Selective OLV is not usually required
visualized perpendicular to its insertion to the trachea, as the surgeon can easily compress the lung to access
and, consequently, the exact site for ligation is apparent. the fistula. The main anaesthesia complications relate
The visual advantage also improves mobilization of to inadvertent intubation of the fistula or preferential
the oesophageal pouch, especially in the setting of a ventilation of the fistula causing gastric distension and
longer gap. desaturation. As described above, the fistula may vary
in position; two-thirds occur in the mid-trachea and
Low birth weight babies tend to be more sick and
one-third occur at or near the carina. The majority of
tolerate stress such as hypoxia, hypercarbia poorly and
complications have been described with large fistulae,
are not able to sustain prolonged duration of surgery.

particularly when they occur near the carina. relaxation accompanied by cautious, gentle positive
pressure ventilation as needed. In the setting of
Main anaesthesia goals are to maintain adequate
haemodynamic instability in response to either
oxygenation, ventilation and avoidance of gastric
narcotics or an inhalation agent, a neuromuscular
distension. Avoid excessive positive pressure ventilation
blocking agent may be delivered, necessitating support
(PPV) especially before the placement of the Fogarty
of positive pressure ventilation. Inhalational inductions
balloon catheter or the ligation of the fistula.
in neonates can cause major cardiovascular instability.
The degree of prematurity, episodes of aspiration and
An IV induction is quicker (less crying) and may be
associated congenital heart disease (CHD) are most
more stable, allowing for the use of NMBDs to optimize
relevant to anaesthetic management. Limb anomalies
may make venous access and arterial cannulation intubating conditions. Positive-pressure ventilation is
difficult. If there is no tracheo-oesophageal fistula usually successful because the compliance of the lungs
present, then gastric distension during induction of is greater than that of the distended stomach. Gentle
anaesthesia will not occur. mask ventilation with low peak pressure ventilation will
decrease the amount of air that enters the stomach.
Premature babies or those who have aspirated may With normal lung compliance, gentle positive pressure
already be intubated. In this case, the positioning and can be delivered with minimal delivery of inspired
length of the ETT are checked. Ideally, the distal end gases into the stomach via the fistula. Optimally, the
will be distal to the tracheo-oesophageal fistula so that endotracheal tube can be advanced beyond the fistula,
distension of the stomach by ventilation through the but, with the fistula often close to the carina, this often
fistula is avoided. induces single-lung ventilation. In fact, in the absence
Patient should have intravenous access before induction of significant pulmonary dysfunction, this process often
and receive 20 μg/kg atropine (minimum 0.15 mg). The is well tolerated. In all cases, the surgeon should be
Replogle tube (tube in the upper oesophageal pouch) present for induction of anaesthesia. For example, on
is aspirated. rare occasions, the distended stomach may need to
be decompressed emergently (e.g., transcutaneous /
“Awake intubation” is considered by some to be the ultrasound-guided insertion of a catheter or needle).
safest approach to secure the airway in an infant with
TOF. Theoretically, this technique allows appropriate Most advocate inhalational or intravenous induction,
positioning of the endotracheal tube without positive according to personal preference, with muscle relaxant
pressure ventilation and, therefore, minimizes the and gentle mask ventilation before intubating the
risk for gastric distention from inspired gases passing trachea.
through the fistula. However, awake intubation can be
Leakage of gas through the fistula may cause
quite challenging in vigorous infants. It can be traumatic
preferential ventilation of the stomach during
and difficult, and a crying infant will only put more air
PPV, which will decrease the functional residual
into the stomach. In most cases, after mild sedation
capacity (FRC), impair ventilation and oxygenation by
by titrating small doses of fentanyl (0.2 to 0.5 mcg/
diaphragmatic splinting, and increase the chance of
kg) or morphine (0.02 to 0.05 mg/ kg), intubation
aspiration. Clinically, however, this is seldom a problem
of the trachea is accomplished without excessive
and most anaesthetists use a gaseous or intravenous
haemodynamic stimulation or depression. In reality, in
some patients, especially the premature infant, apnoea induction, facilitating tracheal intubation with a non-
accompanies even seemingly minimal sedation. depolarizing relaxant. Irrespective of mode of induction,
ventilation by face mask should be at inflation pressures
Therefore, some prefer an alternative technique less than 10–15 cm H2O.
that includes an inhaled anaesthetic without muscle

Evaluating the upper airway via rigid or fiberoptic does not prevent intubation of a large fistula at the
bronchoscopy may be an integral part of the presurgical/ carina. Alternatively, rigid bronchoscopy (or flexible
intraoperative course of TOF/OA repair. Bronchoscopy bronchoscopy after intubation) may be used to
can aid in detecting the number and location of the demonstrate the precise level of the fistula (or exclude
fistulae as well as assess for tracheomalacia and multiple fistulae) and then plan the intubation strategy.
other anomalies relevant to the surgical procedure. If the fistula is mid-tracheal, the tip of the tracheal tube
Bronchoscopy can also be used to assist in precisely is ideally positioned just below the fistula, with the
placing an endotracheal tube below the fistula. bevel facing anteriorly (to avoid ventilating the fistula
However, this location may be difficult to sustain after since the origin of the fistula is the posterior tracheal
the bronchoscopy (even with careful marking of the wall) and gentle positive pressure ventilation used. If
endotracheal tube, attention to flexion and extension of the fistula is at the carina, the tracheal tube may still
the neck, and other precautions) because of subsequent be placed at the mid-tracheal level, provided the fistula
repositioning for surgery and normal movement of the is small.
endotracheal tube during positive pressure ventilation
The tracheal tube should be fixed carefully and the
and repeated suctioning during surgery. For cases in
position of the tube checked again after positioning for
which rigid bronchoscopy is performed prior to the
surgery to make sure that the dependent lung remains
start of surgery, the choice of anaesthetic induction
ventilated. In the unusual situation of a large fistula at
technique involving spontaneous ventilation and
the level of the carina resulting in preferential gastric
controlled ventilation with muscle relaxation is very
ventilation, some authors suggest passing a 2 or 3 Fr
much dependent on the surgical skill of the operator
Fogarty embolectomy catheter through the fistula into
performing the bronchoscopy.
the stomach via the rigid bronchoscope; the balloon
In addition to the mode of anaesthetic induction, the of the Fogarty catheter is then inflated to occlude the
surgeon and anaesthesiologist must decide if single- fistula. The tracheal tube is positioned alongside the
lung ventilation would facilitate the surgical procedure, Fogarty catheter. This may not be a suitable technique
and if the patient can tolerate the technique. In the if the child is very small or unstable. In such a case, the
newborn, single-lung ventilation implies advancing surgeon should proceed directly to thoracotomy to
the endotracheal tube into the mainstem bronchus of ligate the fistula as quickly as possible. If the stomach
the lung contralateral to the surgical site. If tolerated, becomes very distended before the fistula is occluded,
collapse of the lung may improve surgical exposure, the tracheal tube should be disconnected intermittently
but an unacceptable decrease in oxygen saturation to decompress the stomach via the airway.
can occur in some instances, even with a high FiO2.
In babies with associated significant airway
In this situation, a return to two-lung ventilation is
abnormalities, some prefer to insert the tracheal tube
necessary. Finally, even with initial ideal positioning of
while the baby breathes spontaneously, anaesthetized
the endotracheal tube, ventilation through the fistula
with a volatile agent. ‘Awake intubation’ is seldom
still occurs in some patients, This is especially true if
used because it is difficult, distressing for the baby
high peak airway pressures are required.
and associated with significant oxygen desaturation
Several approaches have been popularized to position and oropharyngeal trauma. Increases in intracranial
the tracheal tube while avoiding intubating the pressure must be considered in a vigorous neonate.
tracheoesophageal atresia. One popular technique is It can contribute to the occurrence of intraventricular
to deliberately intubate the right main bronchus after hemorrhage in premature infants.
general anaesthesia is induced and then withdraw
Occasionally massive gastric distension can occur,
the tube until bilateral air entry is confirmed. This
resulting in respiratory compromise and cardiovascular
ensures the tracheal tube is below the fistula but

collapse, requiring an emergency gastrostomy. Risk Proper positioning of ETT between fistula and carina
of gastric distension is proportional to the size of the is impossible if the fistula connects to the carina or a
fistula. Though, insertion of a gastrostomy may be mainstem bronchus. In these situations, intermittent
lifesaving, it has its own problem. Airflow resistance venting of a gastrostomy tube that has been placed
through the fistula–stomach–gastrostomy may be so preoperatively may permit positive-pressure ventilation
low that ventilation of the lungs becomes impossible. without excessive gastric distention. Even with
The gastrostomy may need to be intermittently clamped adequate positioning of the ETT, in some patients,
and unclamped or left partially clamped. It is critical, and ventilation through the fistula still occurs. In patients
sometimes difficult, to establish an airway in patients without a gastrostomy, gastric distention may impair
with a TOF. Surgeons should be readily available during ventilation. In the preterm neonate with respiratory
the induction should emergent decompression of the distress, this is most problematic. Poorly compliant
stomach be required. lungs and a large distal fistula can mean an easy
egress of ventilatory gases into the stomach with
The presence of a gastrostomy reduces the potential for
reflux of gastric juice during the surgical procedure. If resultant compromise in ventilation. With progressively
a gastrostomy is present, the gastrostomy tube should increasing gastric distension, the stomach may rupture,
be open to air and left at the head of the table under resulting in a tension pneumoperitoneum which
the anaesthesiologist’s observation to avoid kinking further impairs ventilation. The traditional approach
and obstruction. Presence of a gastrostomy may slow in this instance would be to perform an emergency
mask induction, requiring transient partial clamping gastrostomy. However, this often worsens the situation
of the tube. as the sudden reduction in intragastric pressure further
facilitates escape of ventilatory gas through the fistula.
Positioning the tracheal tube Resuscitation in this instance is often ineffective until
leakage of gas through the esophagus is controlled.
Most fistulas lie posteriorly in the mid or low trachea.
Salem and others suggest distal positioning of the ETT, Filston et al have suggested occluding the fistula with a
with the bevel facing anteriorly and the posterior wall Fogarty catheter placed through a bronchoscope. Once
of the ETT occluding the fistula, but this manoeuvre is the infant is adequately anaesthetized, the surgeon is
challenging to achieve and maintain. In practice, we able to perform rigid bronchoscopy with a ventilating
insert the tube ‘too deep’, slowly withdrawing it until bronchoscope, following removal of the ETT. At this
both lungs are ventilated. At this point, it is possible point, the exact location and size of the fistula can be
to confirm the position of the endotracheal tube by determined and it can be occluded using a Fogarty
passage of a flexible bronchoscope through it. balloon catheter. The ETT can then be replaced under
During surgery, inadvertent bronchial intubation is a direct visualization. However, bronchoscopy, itself
possibility because of the low lying tip. Bilateral air entry is quite challenging in newborn, leave aside proper
should be confirmed after intubation and whenever the placement of a Fogarty. Ventilation difficulty is usually
baby is re-positioned. It is important to check proper encountered with a fistula > 3 mm in diameter at or
ETT placement. Accidental right main stem bronchus near the carina. Smaller fistulas or those more than 5
placement of the tracheal tube results in a precipitous mm above the carina are not associated with ventilation
decrease in arterial oxygenation, especially during problems.
surgical retraction of the lung. The use of a cuffed ETT to minimize the risk of gastric
Once positioned, the ETT should be carefully secured. distension and aspiration has been described. Proper
After the patient is positioned in the left lateral placement of the ETT can be confirmed with fiberoptic
decubitus position, reconfirmation of the position of bronchoscope. After intubation, the fiberoptic
the ETT may be necessary. bronchoscope is passed through the ETT and the carina

is visualized. Upon withdrawal of the bronchoscope, if Inadvertent entry of ETT into the fistula, kinking
the fistula is not visualized then the ETT is appropriately of bronchus during surgical manipulation and lung
positioned. If the fistula is visualized, the ETT is advanced retraction can cause drop in oxygen saturation and end-
making sure that its tip remains above the carina. Keep tidal carbon dioxide (EtCO2). The surgeon must stop the
air leak around ETT to a minimum (leak at 18–35 cm procedure while the situation is clarified. The surgeon
H2O) to minimize alterations in ventilation secondary will be able to palpate the tip of the tube in the fistula
to changes in chest and pulmonary compliance. if this is the problem.
In the past, the infant with TOF/OA often underwent Because of these myriad problems with PPV, many
an initial surgical gastrostomy, sometimes under anaesthesiologists recommend an anaesthetic
local anaesthesia, with the thought that this would technique that uses spontaneous ventilation with
decompress the stomach and minimize ventilatory sevoflurane. Alternatively, others believe that paralysis
problems. The thoracotomy was then performed may be a safe and effective alternative, as long as the
several days later. fistula can be effectively isolated by careful positioning
of the ETT. In our experience, sufficient anaesthetization
However, as noted above, a gastrostomy may allow
with sevoflurane of a spontaneously breathing newborn
egress of ventilatory volume through the fistula and out
without compromising blood pressure and oxygenation
of the gastrostomy. In modern practice, the gastrostomy
is rarely possible. This is particularly true in the repair of
is rarely performed primarily, and usually not at all
an oesophageal atresia with tracheooesophageal fistula
except in cases of long - gap OA where prolonged
because this surgery is performed in the lateral position.
healing is required.
A new option, of the general inhalational plus caudal
In patients with a gastrostomy, proper positioning of the
(or thoracic) epidural anaesthetic have been described.
ETT can be monitored by submerging the gastrostomy
Caudally placed catheter can be advanced upto the
tube in a container of water so that gas bubbles are
thorax. Either 0.5–1 ml/kg of 0.25% bupivacaine with
evident during ventilation of the fistula. If gas bubbling
epinephrine (5 µg/mL) or 0.5 ml/kg of 3% chloroprocaine
occurs, the ETT must be repositioned. The gastrostomy
(15 mg/kg) with epinephrine is administered, and the
tube may be left to water seal during the surgery, which
inspired sevoflurane concentration is significantly
allows for continued monitoring for ventilation through
reduced. With this combination, spontaneous
the fistula. Alternatively, the gastrostomy tube can be
breathing can be maintained without haemodynamic
connected to a capnograph. When the ETT is proximal
compromise. In addition, postoperative analgesia can
to the fistula, carbon dioxide is detected. When the ETT
be supplemented.
is distal to the fistula, no expiratory gases are detected.
Intraoperative maintenance
In patients with a gastrostomy, gastric decompression
may serve as a low resistance vent through which Nitrous oxide may distend the stomach, compromising
most of the tidal volume escapes. If this occurs, the ventilation, and is best avoided. Avoid high FiO2 if
gastrostomy tube should be clamped or, as Karl has possible in premature neonates at risk for retinopathy
reported, a retrograde Fogarty catheter can be inserted. of prematurity (ROP). Use air/O2 mixture for ventilation
Although this sounds good, precise positioning is nearly to maintain O2 saturation between 90-95%. At times
impractical in neonates. If at all done, maintenance of they require ventilation with 100% oxygen, despite
this exact position for two hours is almost impossible. the risk of the ROP. Healthy infants may tolerate
Displacement of the balloon can cause complete spontaneous ventilation, but most often neuromuscular
occlusion of the trachea, or high pressure on small blockade is necessary especially once the chest is
pulmonary vessels and/or airways with pulmonary opened and the lungs are retracted. It can be difficult to
blood flow or ventilation compromise. obtain adequate oxygenation, ventilation and surgical

conditions in a spontaneously breathing patient during of oxygen must be closely monitored and adjusted,
open thoracotomy. balancing the risks of oxygen toxicity with those of
hypoxia. Loss of breath sounds and the end-tidal
Use low PIPs to avoid gastric distension by gases passing
carbon dioxide (EtCO2) tracing commonly occurs during
through fistula. Careful adjustment of ventilation will be
surgery secondary to airway obstruction. It may be
necessary during surgical retraction of lung or during
due to the accumulation of secretions or blood in the
insufflation if procedure is done thoracoscopically.
ETT. More often, however, it results from kinking of
Manual ventilation is recommended as surgical traction
the trachea during surgical manipulation. The surgeon
can easily occlude the neonate’s soft trachea. It can
should immediately be instructed to release the
be helpful in assessing pulmonary compliance. IPPV
surgical traction. Cardiac output can fall dramatically
is usually done by hand using a Jackson Rees circuit
if surgical manoeuvres compress major vessels. Good
at a high frequency of 30-40 per minute and low tidal
communication and cooperation with the surgeon
volumes.
are essential. ETT placement may interfere with TOF
Air/O2/opioid (e.g., fentanyl 1–2 µg/kg/h), propofol closure. I have seen inadvertent inclusion of ETT in
or low-dose volatile technique is preferred because sutures while repair of tracheal tear. This was detected
of better hemodynamic stability. Muscle relaxation at the time of extubation as the ETT could not be pulled
(atracurium) is usually necessary. If epidural is used, GA out. Migration of ETT above fistula may lead to leak
drug requirements will be reduced. Once satisfactory through gastrostomy and difficult ventilation. Before
ventilation is ensured, the chest is opened and the the closure of the thoracic wound the lung should be
lungs are retracted. carefully re-expanded in order to avoid unnecessary
postoperative atelectasis
Lung retraction impairs ventilation, especially in infants
with respiratory dysfunction from immature lungs, Fluids
pneumonia or congenital heart disease. Intermittent
Two intravenous cannulas are advisable, though
release of pressure by the surgeon to allow inflation
significant bleeding is uncommon. Third-space losses
of the right lung improves oxygenation and ventilation.
can be replaced with (6–8 ml/kg/h) RL with 5%
Close communication between the surgeon and
dextrose.72
anaesthesiologist is mandatory. The surgeon must
be alerted when this happens but must be given Intraoperative monitoring must be carefully planned.
reasonable time to perform the different stages of A precordial stethoscope should be placed in the
the procedure. Brief periods of desaturation or blood dependent (left) axilla, since obstruction of the
pressure changes must be accepted without alarming mainstem bronchus during surgical retraction is not
the surgeon. uncommon. It also helps in detection of endobronchial
intubation. Surgical retraction can also compress the
Blood clots or secretions may block the ETT, and
great vessels, trachea, heart and vagus nerve. In infants
frequent ET suctioning may be required. Rarely, the
with an unstable cardiorespiratory status or CHD,
ETT may become completely occluded by a clot that
an arterial catheter (umbilical or right radial) should
cannot be removed by suctioning, necessitating
be placed. If an arterial catheter is not available, a
immediate replacement of the tube. This author has
noninvasive device is used. Other monitoring consists
seen two such cases. Because the trachea is a soft
of an electrocardiogram, pulse oximetry and end-tidal
structure in the newborn, surgical manipulation may
gas monitoring. A change in the distance of insertion
kink the airway and further obstruct ventilation. Thus,
of the endotracheal tube of as little as 1 to 2 mm may
interference with adequate oxygenation can occur as a
determine whether the anaesthesiologist is ventilating
result of the patient’s anatomy, operative positioning,
both lungs, one lung or the fistula. Pulse oximeter may
and surgical manipulations. Inspired concentration

give early warning of some problem. A preductal and nerves before wound closure. An intrapleural catheter
postductal location (two pulse oximeters) will diagnose is another means of providing analgesia after open
intracardiac shunting and pulmonary hypertension. The surgery, but this may risk local anesthetic toxicity
patient’s temperature must also be monitored, and owing to rapid absorption from the pleural cavity. I use
efforts must be made to prevent hypothermia. Blood multimodality approach consisting of IV fentanyl 0.5 -1
gas monitoring is recommended to check pH, PO2, µg/kg, rectal paracetamol 30 mg/kg and caudal 0.125%,
PCO2, haematocrit, glucose, electrolytes and possibly 1.25 ml/kg bupivacaine after anaesthetic induction.
coagulation.
Emergence and extubation
Neonates with cardiac disease have a greater incidence
There is a constant debate whether to extubate
of critical events such as desaturation or the need for
the patient or to continue intubation & ventilation.
new inotropic support compared with those without
Extubation has advantage that it minimizes
cardiac disease as well as a 57 % mortality during
manipulation of the anastomosis from the ETT.
the hospitalization for those with ductal-dependent
However, approximately 30% will require reintubation
congenital heart disease. These data underscore the
for clearing of secretions. With laryngoscopy and
need for a preoperative echocardiogram to identify
reintubation there are chances of trauma to the fistula
a possible cardiac defect in all neonates with EA/TEF
site and traction on the oesophageal repair.
and, if a heart defect is present, to discuss the need
for central venous access. Phenylephrine should be Some full-term infants are extubated after simple
prepared to treat a “tet spell” in a neonate with an ligation of a TEF, but this is rare, secondary to
unrepaired tetralogy of Fallot. persistent effects of preoperative pulmonary lesions
(e.g., pneumonia, immaturity and other anomalies)
Pain Management
combined with the residual impact of surgery and
Intravenous opioids are effective for intraoperative and general anaesthesia. In addition, tracheomalacia
postoperative pain management. Generous doses can or a defective tracheal wall at the site of the fistula
be used if there is definite indication for postoperative predisposes to collapse of the airway. Treatment of
ventilatory support. Infusion (fentanyl 2-4 µg/kg/hour; postoperative pain, when combined with the host
remifentanil 0.25-0.5 µg/kg/min) can be started. The of other cardiorespiratory problems of the newborn,
author uses fentanyl in titrated doses for such cases. often requires a period of postoperative ventilation for
Babies who are expected to be extubated, regional at least 24 to 48 hours. The ETT provides a means to
anaesthesia is advantageous to avoid opioids and the suction and expand the lungs during the first 24 hours
risk of postoperative respiratory depression. Providing of greatest risk. Other advantage of ventilation is that
there are no significant vertebral anomalies, a caudal adequate amounts of analgesia can be given.
catheter may be advanced to T6–T7 to supplement the
After repair of “long-gap” OA, tension at the
general anaesthetic and provide excellent postoperative
anastomotic site may predispose to oesophageal
analgesia without the use of opioids and to facilitate
leaks. Postoperative ventilatory support for 5 to 7
extubation. The catheter’s position can be confirmed
days has been recommended to improve the rate of
by injecting low ionic strength contrast medium (0.5 mL
maintaining anastomotic integrity. Sedation to eliminate
Omnipaque 180). Either intermittent bupivacaine (1 to
spontaneous ventilation (i.e., to eliminate negative
2 mL of 0.125% with epinephrine 1: 200,000) can be
intrapleural pressure transmitted to the anastomosis)
administered every 6 to 8 hours or a continuous infusion
should be tailored to the haemodynamic status of the
of chloroprocaine (1.5%) with fentanyl (0.4 µg/mL) can
infant. If deep sedation is not tolerated, neuromuscular
be infused at 0.3 to 0.8 ml/kg/hr. This is only possible
blockade may be indicated, but immobility is often
with good ICU support. Surgeon can block intercostal
accompanied by oedema that may lead to decreased

chest wall compliance and the need for increased (15–20 %), anastomotic stricture (30–50 %), and
positive pressure to maintain adequate ventilatory recurrent fistula (10 %). Tracheomalacia is due to
support. I take the following approach: extubate babies abnormal cartilage in the region of the fistula and
which are good weight, full term without CHD and often produces a typical barking cough. In severe cases,
without intraoperative cardiopulmonary complications, the child may develop recurrent chest infections or
and are normothermic; I continue intubation and “near death” episodes due to acute airway collapse,
ventilation for babies <2 Kgs, premature, hypothermic, and emergency aortopexy may be required in the
with CHD or intraoperative complications or if first few months after repair. An early anastomotic
postoperative adequacy of ventilation is doubtful. They leak may cause a tension pneumothorax; a chest
are weaned from ventilatory support when adequate drain should be inserted and the leak explored and
gas exchange and respiratory effort are demonstrated. repaired. Late complications include gastroesophageal
reflux (severe reflux in 40 %) and recurrent chest
Postoperative Considerations
infections, probably related to gastroesophageal
Nasopharyngeal and oropharyngeal suctioning reflux. Long-term respiratory complications including
catheters should be carefully marked to avoid insertion bronchiectasis may result from aspiration, GERD and
down to the level of the anastomosis. Oral suctioning is chest wall abnormalities. Complications can also occur
performed every half hour for the first day, then every secondary to underlying medical conditions and result
hour or more frequently as necessary on the second in significant morbidity and mortality.
day. Thereafter, it is performed as needed. Suctioning
An anastomotic leak tends to occur 3-4 days after
is required to handle the copious oral secretions that
surgery. This leak has been reported in approximately
can build up in the first day or so after surgery. As the
15% of cases. Pain and distress are often evident.
swelling of the oesophagus settles, the secretions taper.
Signs of sepsis may be present. The chest tube drains
Head extension can put tension on the anastomosis and
saliva. Treatment is supportive; appropriate antibiotics
should be minimized. The chest draining tube is placed
should be used, and the child should be given nothing
in 2 cm of water only to seal it; it is not connected to a
by mouth. Surgery is not indicated, even with huge
suction device, which could encourage an anastomotic
leaks. If the leak persists, oesophagography may be
leak. Antibiotics are continued until the chest drain is
performed with water-soluble contrast material to
removed, and the ETT is suctioned as necessary. Severe
assess its magnitude. The usual protocol is to wait and
forms of tracheomalacia can cause life-threatening
let the leak close. If an extrapleural approach was used,
apnoeic spells, inability to extubate the airway and
the child is usually less ill than with other approaches,
pneumonia.
and the resultant oesophagocutaneous fistula closes
A chest film is required. The child is fed by nasogastric within days. If a transpleural approach was used, then
tube or parenterally for 5-7 days until a contrast study the child is more ill and has an empyema that may
confirms anastomotic integrity. If the oesophagus is require further treatment and drainage.
patent and reasonably sized, the baby may be orally fed;
Recurrent TEF may occur within days; most often, it
starting with expressed breast milk is ideal. Then, the
occurs weeks later. Its incidence has been variously
chest tube is removed. As soon as the baby is feeding
reported as 3-14%. Its first manifestation may be
well, the intravenous line is discontinued, and the baby
pneumonia, although the child may cough and have
can be discharged.
respiratory distress with feeding. The diagnosis is made
Postoperative complications by means of an oesophagography.
Early complications at OA/TOF repair include An open posterolateral thoracostomy in infancy has
tracheobronchomalacia (20–40 %), anastomotic leak been associated with musculoskeletal malformations,

including “winged” scapula and chest-wall asymmetry. Due to the substantial alterations that take place both
Finally, scoliosis has been attributed to both thoracotomy regarding haemodynamics and gas exchange, it is
and congenital vertebral anomalies very useful to use cerebral near-infrared spectroscopy
(Invos) to monitor cerebral oxygenation throughout the
Concerns during conduct of thoracoscopic
procedure. Even if it is clearly possible to perform TOF
tracheoesophageal fistula
repair as a thoracoscopic procedure, the combination
Intubation is done in a similar way as that of open of neonatal anaesthesia with periods of hypoxia,
technique such that ET tube bevel is placed away from pronounced hypercarbia and substantial acidosis may
fistula. Fogarty balloon occlusion method can be used raise concern regarding the risk for brain cell apoptosis
for lung isolation. Left main stem bronchus intubation with potential long-term cognitive and behavioural
may be necessary in large pericarinal fistulae, by problems. This is often not tolerated in sick neonates
techniques as described above. Most of the other with compromised cardio‑respiration. Transient
times, paediatric surgeons do not request for one‑lung hypoxemia and hypercarbia can occur at the beginning
ventilation as nondependent lung is compressed by of procedure due to pressure effects on mediastinal
CO2 insufflation. Neonatal insufflators are also used to contents and collapse of lung. Ventilator parameters
overcome the problem of overdistension of chest cavity. are adjusted, maintaining minute ventilation, so as
to maintain normal oxygenation and ventilation.
Surgery is started with insertion of 5 mm port at Pneumothorax may also be diminished to achieve the
postaxillary line near the tip of scapula, ensuring proper same. Increase in fraction of oxygen is also done to
position of first port in pleural space. Gas insufflation avoid desaturation at this time point. After few minutes,
is started at 0.1–3 L/min flow, maintaining 5 mmHg after the ipsilateral lung is collapsed no pneumothorax
intrapleural space. This will in turn result in an increase pressure is applied. High FiO2 may be required along
in pulmonary vascular resistance secondary to hypoxic with application of positive end‑expiratory pressure
vasoconstriction in the right lung. The positive pressure to maintain saturation above 85%. End‑tidal carbon
in the right hemithorax will also cause a decrease dioxide reading will be unreliable during this period.
in venous return by compression of the vena cava Arterial CO2 will be raised, and must be noted in the
and may also cause direct compression of the right setting of congenital cardiac disease and pulmonary
ventricle. Thus, reductions in cardiac output and blood hypertension. Procedure is started after a stable
pressure are likely to occur during the case. Insufflation condition is achieved.
of CO2 combined with a limited possibility to maintain
adequate alveolar ventilation will result in serious Except in one series by Yomoto, rest all have used
CO2 retention combined with pronounced respiratory CO2 insufflation. In Yomoto’s series under general
acidosis (pH<7.0). This situation is further compounded anaesthesia, a 4-Fr Fogarty catheter was inserted via
by the fact that the measurement of end-tidal-CO2 is a nostril into the trachea, following which tracheal
notoriously unreliable and the CO2 tracing may even intubation was performed with a 3.0-mm tracheal tube.
become absent during parts of the procedure. A well- Flexible bronchoscopy was performed, and the fistula
functioning arterial line is, thus, a prerequisite in this was cannulated with the Fogarty catheter to block the
situation. Desaturation episodes can be considered fistula. After occlusion of the fistula, a tracheal tube
the rule, and to counteract this as much as possible was inserted in the left main bronchus and one-lung
ventilation with 100% oxygen is recommended during ventilation was performed.
the period of OLV.
Analgesia
The combination of hypoxia, hypercapnea and
1. Intercostal nerve block may be placed by
acidosis will add to the increase in pulmonary vascular
surgeons or anesthesiologists at the completion
resistance caused by the atelectasis of the right lung.
of surgery, at levels two dermatomal segment
above and below the surgical incision. It helps 4. Gupta B, Agarwal M, Sinha SK. Recent
provide excellent postoperative analgesia and advances in anesthetic management in repair
helps the child breathe with good respiratory of tracheoesophageal fistula repair. Indian
efforts. Local anaesthetic toxicity is, however, Anaesth Forum 2018;19:XX-XX.
a concern as it is known to be absorbed most
5. Spaeth JP, Lam JE. The Extremely Premature
through intercostal spaces
Infant (Micropremie) and Common Neonatal
2. Port infiltration with local anesthetics may be Emergencies. In: Coté CJ, Lerman J, Anderso BJ,
provided in thoracoscopic approach to provide Eds. Coté and Lerman’s A Practice of Anesthesia
postoperative pain relief. Port site is considered for Infants and Children, sixth edition. Elsevier
most notorious for causing pain; hence, relief https://t.me/Anesthesia_Books).
should be adequate 6. Morton NS, Fairgrieve R, Moores A & Wallace E.
3. Thoracic epidural anesthesia is usually not Anesthesia for the Full -Term and Ex-Premature
required in VATS repair of TEF Infant. In: Gregory GA and Andropoulos DB,
Eds. Gregory’s Pediatric Anesthesia, fifth
References edition. Wiley and Blackwell, John Wiley &
Sons Ltd. 2012
1. Malde AD. Anaesthetic management of
neonatal thoracic surgeries. In: Gandhi 7. Lönnqvist PA. Management of the Neonate:
MN, Malde AD, Kudalkar AG, Karnik HS, Anesthetic Considerations. In: Bissonnette B
Eds. Practical Approach To Anaesthesia For Ed. Pediatric Anesthesia Basic Principles—State
Emergency Surgery. New Delhi, Mumbai, of the Art—Future. Shelton, Connecticut:
Panama City, London: Jaypee Brothers Medical People’s Medical Publishing House—USA;
Publishers (P) Limited; 2011: PP 321-344. ISBN 2011.
978-93-5025-070-9. 8. Ramos CT and Kim PCW. Management of
2. Brett CM and Davis PJ. Anesthesia for General the Neonate: Surgical Considerations. In:
Surgery in the Neonate. In Davis PJ, Cladis Bissonnette B Ed. Pediatric Anesthesia Basic
FP, Eds. Smith’s Anesthesia for Infants and Principles—State of the Art—Future. Shelton,
Children, Ninth Edition. Philadelphia: Elsevier Connecticut: People’s Medical Publishing
House—USA; 2011.
Inc; 2017: PP 597-603.
9. Yamoto M, Urusihara N, Fukumoto K, Miyano
3. C r o s s K , S m i t h J , a n d Wa l ke r I A .
G, Nouso H, Morita K et al. Thoracoscopic
Thoracoabdominal and General Surgery. In:
versus open repair of esophageal atresia
Lerman J Ed, Neonatal anesthesia. New York
with tracheoesophageal fistula at a single
Heidelberg Dordrecht London: Springer; 2015:
institution. Pediatr Surg Int 2014; 30:883–887.
232-237.

MCQ
1. GROSS classification of TOF (TRACHEO 4. Sudden loss of ET CO2 tracing
OESOPHAGEAL FISTULA )type D is intraoperatively can be due to
a. oesophageal atresia with proximal TOF a. Airway obstruction by blood clots
b. oesophageal atresia with distal TOF b. Airway obstruction by kinking of
c. oesophageal atresia with both endotracheal tube
proximal and distal fistula c. Displacement of endotracheal tube
d. TOF without esophageal fistula d. all of above
2. TOF associated with following anomalies 5. According to spitz classification survival rate
except in children with TOF and cardiac anomaly
a. VACTREAL anomalies a. 90%
b. CHARGE syndrome b. 70%
c. FANCONI syndrome c. 50%
d. TURNERS syndrome d. 80%
3. Anesthesia goals in TOF are
a. Maintain adequate oxygenation

b. Maintain adequate ventilation
c. Avoid excessive positive pressure
ventilation
d. All of above
5. (c) 4. (d) 3. (d) 2. (d) 1.(c)

Answers

28 LOW FLOW ANESTHESIA
Professor and HOD, Aruna Parameswari

SRIHER,
Chennai.
Key points
Ø Low flow anesthesia refers to any technique utilizing a fresh gas flow that is less than the alveolar
ventilation
Ø The gas volume that is taken up by the patient has to be delivered into the breathing system, or a
volume deficit would occur
Ø A high fresh gas flow initially ensures sufficient denitrogenation and wash in of the aspired gas
composition into the whole gas containing space
Ø To maintain a safe inspired concentration of about 30% in low flow anesthesia, the fresh gas oxygen
concentration has to be increased to 50%
Ø With low flow, the reduction in anesthetic vapor concentration has to be compensated by a corresponding
increase of the agent’s concentration in the fresh gas, by increasing the vaporiser dial setting
Ø A given volume of the system and a given individual gas uptake assumed, the time constant is inversely
proportional to the fresh gas flow
Ø The reduction of anesthetic gas and vapor consumption, the decrease in atmospheric pollution with
inhalation anesthetics, the improvement of anesthetic gas climate and the significant reduction of costs
are some advantages of LFA
Ø Oxygen analyzers monitor and display the FIO2 and their use during low flow anesthesia would help
identify delivery of hypoxic inspired gas mixture and thus rectify it
Introduction and Theory the use of an even lower flow of 500 ml/min and
introduced the term “Minimal flow anesthesia”.
Low flow anesthesia refers to any technique utilizing a
fresh gas flow that is less than the alveolar ventilation. Baum et al had defined low flow anesthesia as an
The term “low flow anesthesia” was introduced by F. anesthetic technique in which a semiclosed breathing
Foldes, inaugurating an anesthetic technique performed system is used, recirculating atleast 50% of the exhaled
with a fresh gas flow of 1 L/min. R. Virtue recommended air back to the patient after CO2 absorption. This can

Low Flow Anesthesia 280 Aruna Parameswari
be achieved with modern rebreathing systems using a Assuming a constant gas composition circulating within
fresh gas flow less than 2L/min. the breathing system, the total gas uptake, the sum
of oxygen, nitrous oxide and inhalational anesthetic
Low flow anesthesia has also been defined as fresh gas uptake, follows a power function. Initially it is high
flow of less than half the minute volume, usually less and declines sharply during the first 30 min, but it is
than 3 L /min. comparatively low and decreases only slowly during
Baker, in his editorial has suggested the following the following course of anesthesia. This is because the
modification of Simionescu’s classification of flow rates partial pressure difference of anesthetic gases between
the alveoli and blood is initially high but thereafter
of gases into anesthetic circuits:
decreases continuously with increasing saturation
• Metabolic flow: 250 ml/min of blood and the tissues. If the anesthesiologist
• Minimal flow: 250 – 500 ml/min could succeed in approximating the total gas uptake,
anesthesia with a closed rebreathing system would be
• Low flow: 500 – 1000 ml/min
realized.
• Medium flow: 1 – 2 L/min
• High flow: 2 – 4 L/min The Practice of Low Flow Anesthesia
• Very high flow: > 4 L/min Premedication and induction can be done using routine
techniques with no procedure specific requirements for
There is a limit for reducing the fresh gas flow to avoid the practice of low flow anesthesia.
gas volume deficiency. Atleast that gas volume has to
be delivered into the breathing system that is definitely Initial high flow rate
taken up by the patient.
A high fresh gas flow (3 L/min of N2O and 1.5 L/min of O2)
Uptake of oxygen, nitrous oxide and inhalational has to be used in the initial 10 to 15 minutes with 1.5%
anesthetics isoflurane, 2.5% sevoflurane or 4 – 6% desflurane. With
these settings, an expired concentration of 0.7 – 0.8
During the course of anesthesia, oxygen uptake is MAC of the respective agent will be gained. In addition
constant and is given by the Brody formula to a nitrous oxide MAC of about 0.6, corresponding to
a nitrous oxide concentration of 60%, this will result
VO2 = 10 x body weight (kg)3/4
in a common MAC of 1.3, guaranteeing sufficient
More commonly, oxygen uptake can easily be calculated anesthetic depth to tolerate skin incision. A high fresh
as 3.0 ml/kg/min and is about 250 ml/min in a normal gas flow initially also ensures sufficient denitrogenation
adult. and wash in of the aspired gas composition into the
whole gas containing space. If the flow is reduced too
The uptake of nitrous oxide is given by Severinghaus’ early to low values, gas volume deficiency would result
formula compromising adequate ventilation.
VN2O = 1000 x t -1/2 Flow reduction
And the uptake of inhalational anesthetics may be After 10 minutes, the fresh gas flow can be reduced to 1
calculated by Lowe’s formula L/min. With flow reduction, the inspired gas contains a
markedly increased proportion of the exhaled gas which
VAN = f x MAC x λB/G x Q x t -1/2
already had passed the patient’s lung and contains less
where f x MAC is desired anesthetic concentration, oxygen. This decrease in the oxygen content of the gas
fraction of MAC, Q is cardiac output and t is time. mixture can be compensated by increasing the fresh
gas oxygen fraction, which must be higher, the lower
The uptake of nitrous oxide and volatile anesthetics the flow. To maintain a safe inspired concentration
follows a power function. of about 30% in low flow anesthesia, the fresh gas
oxygen concentration has to be increased to 50%.
Also, with flow reduction, the amount of anesthetic concentration is delayed and slow. Towards the end of
vapor delivered into the system is markedly reduced. the anesthesia, a high flow of gas can thus be used to
For example, with a fresh gas flow rate of 5 L/min and flush out the anesthetic agents which accelerates their
sevoflurane vaporizer at 2%, 100 ml/min of sevoflurane washout. The other method is to use activated charcoal,
vapor is added, whereas with a fresh gas flow rate which when heated to 220 deg C, adsorbs the potent
of 1 L/min and sevoflurane at 2%, only 20 ml/min of vapors almost completely. So, a charcoal containing
sevoflurane vapor is added to the circuit. So with low canister with a bypass is placed in the circuit. Towards
flow, this reduction in anesthetic vapor concentration the end of anesthesia, the gas is directed through the
has to be compensated by a corresponding increase activated charcoal canister. This results in rapid recovery
of the agent’s concentration in the fresh gas; 2 vol% and at the same time, reduction in theatre pollution.
of isoflurane and 3 vol % of sevoflurane is used with
Nitrous oxide is washed off towards the end by using
flow reduction. Due to its specific pharmacokinetic
100% oxygen.
properties, only the fresh gas desflurane concentration
can be maintained unchanged. With these standardized Technical requirements for safe conduct of low flow
schemes, the expired anesthetic concentrations will anesthesia
be maintained in the aspired range of 0.7 to 0.8 times
the MAC. Monitoring
Time constant With flow reduction, the composition of the fresh gas
flow does not reliably indicate the composition of the
The time constant is a measure for the time it takes, inspired gas mixture. Thus, monitoring of inspired
that alterations of the fresh gas composition will lead oxygen concentration is absolutely indispensable.
to corresponding alterations of the gas composition The same applies for volatile anesthetics, if fresh gas
within the breathing system. According to a formula flow lower than 1L/min is used. Airway pressure and
given by Conway, the time constant can be calculated
minute volume also need to be monitored to indicate
by dividing the system’s volume (VS) by the difference
the gas filling of the breathing circuit. Sodalime
between the amount of anesthetic agent delivered into
consumption increases fourfold if low flow techniques
the system with the fresh gas (VD) and the individual
are consistently performed. By monitoring inspired CO2
gas uptake (VU).
concentrations, soda lime exhaustion can be reliably
T = VS/ (VD – VU) detected and replaced when necessary.
A given volume of the system and a given individual Anesthetic apparatus
gas uptake assumed, the time constant is inversely
proportional to the fresh gas flow. This marked increase The flow control system must feature needle valves
in time constant has to be taken into account while to measure very low gas flows. The flowmeter tubes
switching from high to low fresh gas flows. Whenever must be calibrated to work reliably even in the low
the gas composition within the breathing system has flow range. The vaporizers must feature fresh gas
to be changed rapidly, the fresh gas flow has to be flow compensation. The rebreathing system has to be
increased for adequately accelerating the wash in of sufficiently gas tight; the leakage must not exceed 100
the newly aspired gas composition. For newer volatile ml/min at a pressure of 20 bar. The reservoir bag or
agents like sevoflurane and desflurane, the time ventilator bellows indicate the volume of the circuit gas.
constants will be significantly shorter as VD can be If the volume of gas entering the circuit is less than the
raised considerably and VU is extremely low. total patient uptake plus any leaks, then the reservoir
bag or bellows will refill less with each breath. This gives
Recovery phase
an indication of the total volume of gas flow needed,
If low flow is maintained, due to the long time constant, while oxygen, nitrous oxide and anesthetic analyzers
the washout and hence the decrease of anesthetic indicate the composition of the circuit contents.

Omission of nitrous oxide 1) Economic
Without nitrous oxide, the conduction of low flow Use of low flow anesthesia reduces the fresh gas
anesthesia is simpler. As only oxygen and anesthetic flow and anesthetic vapor consumption. This
agent are absorbed, total gas uptake is noticeably assumes more significance with the use of newer
reduced and denitrogenation is no longer necessary. By agents like sevoflurane and desflurane which are
eliminating N2O, the breathing system filling is improved more expensive compared to the older inhalational
following the reduction of fresh gas flow. agents, halothane and isoflurane. Also, the low
potency of desflurane mandates the use of more
The omission of nitrous oxide in low flow anesthesia
anesthetic vapor and the amount of consumption
• Facilitates a reduction in fresh gas flow by the with conventional fresh gas flows can significantly
resulting excess in gas volume and, thus, the escalate the costs.
increase in gas volume circulating within the
2) Environmental
breathing system
There are stringent regulations on the maximum
• Reduces the risk of gas volume deficiency
acceptable workspace concentrations of
• Makes it possible to keep the initial high-flow anesthetic gases in USA, Europe and Canada.
phase very short since this is only determined Even with the extremely low anesthetic gas
by the wash in characteristics of the anesthetic concentrations stipulated by the US National
agent used Institute of Occupational Safety and Health
(NIOSH), this can be achieved easily only by the use
• Makes it possible to achieve closed system
of low flow techniques. The use of gas scavenging
anesthesia with conventional anesthetic
systems ensures there is no theatre pollution and
machines in routine clinical practice
permissible workspace levels can be maintained
• Impedes the further use of anesthetic agents as per the requirements.
with high blood solubility, such as halothane,
However, all gases delivered from the anesthetic
since it becomes impossible to deliver
machines are ultimately lost to the atmosphere.
sufficient amounts of these anesthetics into
The chlorinated hydrocarbons (halothane,
the breathing system with the aid of agent
specific vaporizers outside the circuit isoflurane and enflurane) are broken down by
ultraviolet radiation releasing chlorine atoms
• Augments the concern about Compound A that have been shown to deplete the protective
as it becomes possible to use extremely low ozone layer in the stratosphere. Nitrous oxide also
fresh gas flows. Long lasting closed system depletes ozone through nitric oxide production, and
sevoflurane anesthesia should be performed also reflects heat back to the earth, contributing
using calcium hydroxide lime (non – caustic directly to global warming. The inhalational
absorbents) anesthetics are only responsible for 0.1 - 1% of
the global release of chlorofluorocarbons and
Advantages of Low Flow Anesthesia over Conventional
nitrous oxide accounts for only 3 – 12% of global
High Flow Anesthesia
nitrous oxide release; nevertheless it becomes
There are several advantages to the use of low flow the responsibility of anesthesiologists to prevent
anesthesia that are obvious and indisputable and this contribution to environmental degradation.
were listed in the original Waters’ paper namely, the Use of low flow anesthesia would significantly
reduction of anesthetic gas and vapor consumption, decrease this environmental damage. Desflurane
the decrease in atmospheric pollution with inhalation and Sevoflurane are chlorine free, and have less
anesthetics, the improvement of anesthetic gas climate potential for ozone depletion, but may contribute
and the significant reduction of costs. considerably to the greenhouse effect.

3) Improvement of anesthetic gas climate It is axiomatic that if you put little gas into the
breathing system, then little or none will come
Inspiration of cool dry gases impairs mucociliary
out. Due to the failure to flush gases out of the
function, with subsequent microatelectasis,
breathing system, any gases that are introduced
potential for infection, and impaired gas exchange.
but not taken up by the patient or absorbed
Use of low fresh gas flow conserves heat and
chemically will tend to accumulate. Such gases
humidity and improves inspired gas humidification
may be exhaled by the patient, be a contaminant
and temperature and is useful in improving the
of the medical gases or result from a reaction
anesthetic gas climate, especially in places where
with the chemical agents used for carbon dioxide
the practice of using heat and moisture exchangers
absorption.
is not routine.
Substances exhaled by the patient:
4) Efficiency of inhalational anesthesia
These include alcohol, acetone, carbon monoxide
The most striking argument in favor of low flow
and methane. Use of low fresh gas flow is hence
anesthesia is the marked increase in the efficiency
contraindicated in patients who are in uncompensated
of inhalational anesthesia. The efficiency can be
diabetic states, intoxicated, or who are suffering from
calculated by dividing the amount of anesthetic
carbon monoxide poisoning.
agent taken up by the patient (VU) by the amount
of anesthetic agent delivered into the breathing Carbon monoxide is produced as a metabolite of
system (VD). proteins and during low flow anesthesia, there is a
steady and small rise in carboxyhemoglobin. This is
Efficiency = VU/VD
unlikely to exceed 3 – 4% even after several hours.
As the amount of agent delivered into the system
Methane is produced by the action of Methanobacterium
directly depends on the fresh gas flow, the
ruminatum in the large bowels of about 30% of the
efficiency of the inhalational anesthetic technique
population and will equilibrate with the circuit gases
is lesser with use of higher fresh gas flows. This
during low flow anesthesia. It is biologically inert. The
is especially applicable to inhalational agents
amount that accumulates is much less than its lower
with low solubility and anesthetic potency. If
flammability limit. The only issue with methane is that
desflurane, for instance, is used with a fresh gas
it absorbs infra-red light at 3.3 micrometer about 10
flow of 4.5 L/min at an inspired concentration of
times as strongly as halothane. This can lead to a “mixed
6% for a period of 2 hours, the overall efficiency
agent” warning or will cause inaccuracy of the analyser.
will decline to 0.07. Only 7% of the total amount
of agent delivered into the system is really needed Acetone is produced by hepatic metabolism, excreted
and taken up by the patient, whereas 93% is in the expired gas, and equilibrates in the anesthetic
wasted with the excess gas escaping from the circuit. During prolonged anesthesia, blood acetone
breathing system. Only if this agent is applied concentration can increase, especially in patients
with low fresh gas flow rates, the efficiency can with preoperative starvation or increased production
be increased to an acceptable range of about 30%. (diabetes, cirrhosis). Concentrations more than 50 ppm
The use of anesthetic agents with low solubility may cause nausea, vomiting and slow emergence.
and potency can only be justified if judicious use
is made of rebreathing techniques. Contaminants of medical gases:
Disadvantages of Low Flow Anesthesia Potential contaminants of medical gas supplies include
the lethal gases carbon monoxide and nitric oxide.
1) Accumulation of unwanted gases in the breathing More benignly, nitrogen and argon may accumulate
system and cannot be detected by infra-red analyzers. Argon
is biologically and chemically inert.
Products of reaction with absorbents: included the addition of a zeolite. Molecular sieves are
a reusable alternative to soda lime or Baralyme. These
Chemicals used to absorb CO2 may react with volatile
are alumino-silicate zeolites, tetrahedral with 4 – 7
inhalational anesthetics. Trilene was known to break
Angstrom pores, which retain CO2 by Van der Waal’s
down to phosgene (COH2), which is lethally toxic.
forces, and can be regenerated for reuse.
Halothane reacts with soda lime to produce hydrofluoric
acid and bromochlorodifluoroethylene (‘BCDFE’ In 1999, a novel absorbent was introduced (Amsorb)
BrClC=CF2), though no harm has been attributed to this. which contains no strong alkali. Amsorb utilizes
hygroscopic agents to ensure that the calcium hydroxide
Desflurane, enflurane and isoflurane (which contain a
does not become dry. The main claimed benefits of
difluoromethoxy group: F2HCO-) react with dry baralyme
Amsorb are that it produces no CO or compound A,
producing carbon monoxide. More degradation of the
though with the disadvantages of increased cost and
anesthetic agents and more CO production occurs with
reduced efficiency.
increased absorbent temperature, high anesthetic
concentration and with dry absorbent. 2) Danger of hypoxia and hypercapnia
Sevoflurane reacts with sodalime to produce an olefin There is a danger of hypoxaemia if an inspired oxygen
“Compound A” which was considered to pose a risk of concentration of 33% is used in low flow anesthesia
renal toxicity. It is accepted that prolonged sevoflurane using nitrous oxide. This is because with time, the
anesthesia with low fresh gas flows results in protienuria, nitrous oxide uptake decreases, while oxygen uptake
glycosuria and enzymuria. However, this has not been continues, resulting in relatively more nitrous oxide
shown to be associated with any clinical manifestations, in the expired gas, leading to a hypoxic inspired
even in patients with pre-existing biochemical renal mixture. Increasing the inspired oxygen concentration
abnormalities. Much of the laboratory work on renal to 50% prevents this. Also, oxygen analyzers monitor
toxicity was undertaken on rats, where compound A and display the FIO2 and their use during low flow
causes acute tubular necrosis at concentrations in anesthesia would help identify delivery of hypoxic
excess of 250 ppm. It is now clear that these studies are inspired gas mixture and thus rectify it.
invalid due to the marked differences between human
Soda lime is consumed more when low flow anesthesia
and rat renal biochemistry. The generally held view is
is used. A rise in inspired CO2 indicates that absorbent
that compound A has a considerable margin of safety
should be replaced. Monitoring endtidal and inspired
in humans at the concentrations typically found during
CO2 concentration thus helps prevent hypercapnia.
low flow sevoflurane anesthesia (around 15 ppm).
3) Inability to quickly change inspired gas mixture
Due to the above concern, the FDA (USA) has set a 2
L/min lower limit for fresh gas flow during sevoflurane Due to the long time constant with low flow anesthesia,
anesthesia. This was revised to 1 L/min in December any change in the fresh gas flow composition takes time
1997 with a 2 MAC hour exposure limit for fresh gas to be reflected in the inspired gas mixture.
flows between 1 and 2 L/min. Canada and Australia
still have a 2 L/min limit while Switzerland and Israel Conclusion
have adopted the US FDA revised guideline. There are There is a resurgence of low flow anesthesia technique
no flow restrictions in UK. with the introduction of more expensive inhalational
With the discovery that strong alkalis in carbon dioxide agents of low potency and solubility. The advantages
absorbents were responsible for the production of both compared to conventional flow anesthesia are
CO and compound A, manufacturers have taken a lot enormous and the apparent disadvantages are easily
of measures. Removal of all KOH was widely adopted overcome. Understanding the concepts behind low flow
and NaOH levels were reduced. Other approaches anesthesia would allow a safe practice of this technique.

References economics. Best Practice and Research in Clinical
Anaesthesiology 2001; 15: 377-388.
1) Baum JA. Low-flow anesthesia: Theory, practice,
technical preconditions, advantages and foreign 4) Nunn Geoffrey. Low-flow anaesthesia. CEACCP
gas accumulation. J Anesth 1999; 13:166-174. 2008; 8: 1-4.
2) Baxter AD. Low and minimal flow inhalational an- 5) Yumiko Ishizawa. General anesthetic gases and
esthesia. Can J Anaesth 1997; 44: 643-653. the global environment. Anesth Analg 2011;112:
213-7.
3) Baum JA. Nitrous oxide: use in low-flow systems/

MCQ
1. Which of the following fresh gas flow rate 4. According to the FDA in USA, fresh gas flow
refers to metabolic flow? below a particular level is not recommended
when sevoflurane is administeredwith soda
a. 1000 ml/min
lime as CO2 absorbent. What is this minimum
b. 500 ml/min value?
c. 250 ml/min
a. 2 L/min
d. 100 ml/min
b. 1 L/min
2. Which of the following formula are used for c. 500 ml/min
the calculation of uptake of nitrous oxide?
d. There is no such limit
a. Brody’s formula
5. The effects of omitting nitrous oxide in the
b. Lowe’s formula fresh gas flow during low flow anesthesia
c. Baker’s formula includes all except
d. Severinghus’ formula a. Shortened duration of initial high flow
phase
3. Which of the following represents a
contraindication to the use of low flow b. Increased risk of gas volume deficiency
anesthesia with Fresh gas flow < 1 L/min? c. Ecologically safe carrier gas
a. Diabetic ketoacidosis d. None of the above
b. Carbon monoxide poisoning
c. Alcohol intoxication
d. All of the above
5. (b) 4. (b) 3. (d) 2. (d) 1.(c)

Answers

29 Cirrhosis and incidental surgeries
Professor and HOD, Lakshmi Kumar

Amrita Institute of Medical Sciences,
Kochi.
Key points
Ø Cirrhosis is a diffuse hepatic process characterized by fibrosis and progressive replacement of hepatic
parenchyma by abnormal nodules.
Ø Complications of cirrhosis are portal hypertension, ascites, hepatorenal syndrome, hepatic
encephalopathy, hepatopulmonary syndrome, portopulmonary hypertension
Ø The decision to operate will depend upon multidisciplinary assessment and explanation of additional
morbidity if the procedure is considered to benefit the patient.
Ø The severity of cirrhosis is assessed by Child-Pugh-Turcotte scoring system and MELD scoring system
Ø Elective cardiac surgery is contraindicated in Child C as the morbidity is unacceptably high
Ø Intraoperative hypotension is avoided to prevent ischemia of liver
Introduction in the extracellular matrix. While this degree of fibrosis

may be reversible, the occurrence of nodules altering
Awareness of a varied spectrum of liver disease the hepatic architecture is an irreversible process.
has increased in the last two decades. The growing
knowledge of occurrence of subclinical cirrhosis In patients with cirrhosis, splanchnic arterial flow is
amongst patients presenting for incidental surgery increased along with an increase in venous return to
and its potential implications have improved the the liver. The increased resistance to flow across the
scope of management of these patients. Patients sinusoidal vascular bed occurs by fixed changes due to
with established cirrhosis may present for incidental fibrotic nodules and collagen produced by the stellate
malignancy, following trauma or for cardiac or spine cells in the cellular matrix. Due to resistance to inflow
or joint surgery. The decision to operate will depend of portal blood, the nitric oxide produced by endothelial
upon multidisciplinary assessment and explanation of cells is directed to the splanchnic circulation. The lack
additional morbidity if the procedure is considered to of hepatic nitric oxide causes contraction of the stellate
cells contributing to contraction of the hepatic sinusoid.
benefit the patient.
This obstruction to flow from hepatic sinusoids results
Pathophysiology in the development of portal hypertension and
subsequently to opening of portosystemic collaterals.
Cirrhosis is a diffuse hepatic process characterised by
progressive replacement of the hepatic parenchyma by Portal hypertension (clinically significant) is present
abnormal nodules that can evolve over a varied time. when the gradient between the hepatic venous and
Along with this are features due to the development the portal vein gradient is above the normal value of
of portal hypertension and ascites. 3- 6 mm Hg. A person is at risk for the development of
ascites above a gradient of 8 mm Hg and varices above
Fibrosis is the usual inciting event that involves increased 12 mm Hg. The risk of variceal bleed is increased above
amounts of collagen, glycoproteins and proteoglycans a HVPG of 20 mm Hg.

Cirrhosis And Incidental Surgeries 288 Lakshmi Kumar
Ascites results from a combination of increased hepatic picked up only at laparoscopy / laparotomy. Tell tale
lymphatic flow and renal dysfunction. Normally, the evidences may include minimal jaundice, pedal edema,
fluids and plasma proteins diffuse across the sinusoidal hyperpigmentation and wasting of the chest and upper
endothelium and enter the space of Disse. Lymphatic limbs but these are usually seen in more advanced
channels in the portal and central venous channels of disease. The clinical manifestations of cirrhosis may
the liver in turn reabsorb this fluid. When the fluid and include nonspecific symptoms (e.g., anorexia, weight
lymphatic entry exceeds the capacity of the cisterna loss, weakness, fatigue) or signs and symptoms of
chyli to reabsorb, this fluid transduces across the liver hepatic decompensation (jaundice, pruritus, signs of
capsule into the peritoneal cavity. upper gastrointestinal bleeding, abdominal distension
from ascites, confusion due to hepatic encephalopathy).
Systemic Manifestations of Cirrhosis
Laboratory values with unexplained low platelets,
Can an anesthesiologist identify cirrhosis in an elevated prothrombin time or low albumin could be a
asymptomatic patient presenting for incidental pointer for undiagnosed liver disease
surgery? In a well-compensated Child A cirrhosis,
Bonacini cirrhosis discriminant score is useful for
the fibrotic changes in the liver are sometimes
prediction of cirrhosis
Points 0 1 2 3 4 5 6
Platelets x
> 340 280-339 220-279 160-219 100-159 40-99 <40
1000/mm3
AST/ALT > 1.7 1.2 to 1.7 0.6- 1.19 <0.6
INR < 1.1 1.1-1.4 >1.4
Table : Bonacini cirrhosis discriminant score

A score of 7 and above has a likelihood ratio of 9.4 in predicting cirrhosis
Cardiovascular System causes is suggestive of hepatopulmonary syndrome.

Portopulmonary hypertension (PoPH) is the presence
A hyperdynamic circulatory state exists with increased
of elevated portal pressures in the background of
cardiac output and decreased systemic vascular
cirrhosis and is a consequence of constant volume
resistance. Blood pressures usually fall with the onset
overload on the pulmonary vasculature. Unlike the
of cirrhosis and chronotropic incompetence is seen
hypoxemia related to the hepatopulmonary syndrome,
with increasing jaundice. ECG may show prolonged
this is not reversible. Mean pulmonary artery pressures
QT (> 440 msec) suggestive of underlying cirrhotic
above 50 mm Hg in the background of portopulmonary
cardiomyopathy. Echo may show increased ejection
hypertension have a high morbidity and are even
fractions, LVOTO with increasing rate and elevated
considered a conatraindication for transplant.
RVsystolic pressure with advanced cirrhosis. Pulmonary
arteriovenous channels are dilated and in extreme Renal System
situations result in hypoxemia (hepatopulmonary
Extreme splanchnic vasodilatation compromises
syndrome).
renal blood flow and results in an acute kidney injury
Respiratory System with activation of the renin-angiotensin-aldosterone
axis labelled as hepatorenal syndrome. The kidneys
Restrictive lung disease is seen with large volume
are functionally normal and can return to normal
ascites. Pleural effusions secondary to liver disease may
with the correction of renal perfusion. Terlipressin
also occur. Hypoxemia in the absence of explainable
which is splanchnic vasoconstrictor is administered in the rates of correction as pontine myelinolysis can
intravenously in doses ranging from 2-8 mg in 24 occur. The levels of cholesterol, triglycerides and lipids
hours along with albumin as a volume expander often are not a true reflection of the cause for liver failure
effectively restores the renal dysfunction. and merely reflect the inability of the synthetic liver
functions. They may be very low in patients with CLD
Coagulation
and should not give a false sense of protection against
All the clotting factors that are synthesised by the liver coronary artery disease.
are reduced with the exception of factor VIII and vWF.
Scoring systems
Recent evidence suggests that even though the number
of platelets and prothrombin time are deranged, The simplest and most widely used scoring system is
cirrhotics are in a state of balanced coagulation and the Child –Pugh scoring system. Scores 5-6 Child A, 7-9
are at an intrinsically compensated state. With growing Child B and > 9 Child C.
experience, clinicians are comfortable in dealing with
The MELD (model for end stage liver disease) was
patients with platelet number < 50,000/mm3 or INR
introduced as the CTP was subjective on two variables
more than 1.5. The availability of dynamic tests of
and did not include renal dysfunction as a variable. This
coagulation that measure the viscoelastic property of
includes serum creatinine and bilirubin in addition to
the clot improves the margin of safety by providing the
the INR (https://www.mdcalc.com/meld-score-model-
scope for product targetted transfusion.
end-stage-liver-disease-12-older). Although it was
Metabolic & Endocrine introduced to predict survival after TIPS procedure it
is currently used for organ allocation in patients with
Co-existing endocrine abnormalities like NIDDM liver disease(www.unos.org/resources).
needs to be evaluated. HbA1C levels may be unreliably
low because of the shortened RBC half-life. Oral MELD could be used to stratify risk in patients
hypoglycemic agents are best avoided in ESLD and short undergoing non-transplant surgery. In a retrospective
acting insulin is ideal in management. Hyponatremia is study of 140 patients with cirrhosis who underwent
common with ESLD and is due an increase in ECF fluid surgery, a 1% increase in mortality for each one-point
volume. Initial treatment involves fluid restriction with increase in the MELD score from 5 to 20 and a 2%
albumin and a mild diuretic. Hypertonic saline (3%) increase in mortality for each one-point increase in
or AVP receptor antagonists (Conivaptan/Tolvaptan) the MELD score above 20 was observed. A simple
can be used in resistant cases. Caution should be used correlation between Child and MELD scores are MELD
< 10 Child A, 10-14 Child B and > 14 Child C respectively.
Score 1 2 3
Ascites Nil Controlled Uncontrolled
S. Bilirubin (mg/dL) <2 2-3 >3
S. albumin mg/dL >3.5 2.8-3.5 > 3.5
Encephalopathy Nil Grades 1 and 2 Grades 3 and 4
PT (sec above normal) <4 4-6 6
Table 2 : Child Pugh Turcotte scoring system

Indications for surgery in patients with cirrhosis to improve myocardial perfusion prior to transplant.
Challenges are ongoing coagulopathy and the need
The presentation for incidental surgery unrelated
for antiplatelet medications following stenting. While
to cirrhosis would imply some compensation in the
this can increase the chances of GI and variceal bleed,
patients. In contrast, patients who present for surgery
witholding may predispose to stent thrombosis. The
directly or indirectly related to the cirrhotic process
use of radial versus femoral arterial access can minimise
e.g., intracranial bleed for decompression, hernia of
bleeding complications in these patients.
anterior abdominal wall resulting from cirrhosis are
poory compensated and could have poorer outcomes. Abdominal surgery
Factors related to poorer outcome in these patients Gallstones and abdominal wall hernia are common
1) Child C or MELD > 14 surgical conditions as the increased intraabdominal
pressure results in abdominal wall hernia and occurrence
2) Renal dysfunction (primary or secondary to liver
of gall stones. Laparoscopic surgery has been shown to
disease)
be superior to open surgery in cholecystectomy and
3) Pulmonary infections minimises risk of blood loss and length of hospital stay.
4) Poor cardiac reserve (cirrhotic cardiomyopathy/ The morbidity is only marginally higher in cirrhotics
coexistent CAD) than non- cirrhotics (< 2%) and elective laparoscopic
5) Synthetic function derangement (coagulopathy cholecystectomy can be undertaken in Child A and
and albumin < 2.8) B patients with a reasonable margin of safety. Care
6) Hepatic encephalopathy should be taken to ensure that the patients are not
decompensated at the time of surgery. Anesthetics with
7) Acute on chronic liver failure shortest duration should be used and mean arterial
Guidelines on candidacy for surgical procedures pressure maintained to prevent decrease in blood
flow to the liver. Surgical considerations will involve
Cardiovascular Surgery / Intervention open method of port introduction and placement of
As described above, the mileu in cirrhosis is favourable additional ports.
for cardiovascular status with low SVR and low Abdominal wall hernia is a consequence of chronic
cholesterol. The decreased activity levels also decrease ascites and weakness of the muscles of the anterior
occurrence of increased demand and occurence of abdominal wall. Elective repair can be undertaken but
effort angina. Elective CABG can be safely performed the condition may recur as the underlying mechanism
in Child A or MELD < 10 with about 20% incidence
is pressure from chronic ascites. Repair is sometimes
of perioperative morbidity and mortality. Published
undertaken at the time of transplant. Emergent
literature is minimal but there is substantial reduction
conditions are ulceration of the hernia or obstruction
in morbidity in Child A and B in the last 2 decades.
or strangulation of bowel. Ulceration can be safely
CABG can be undertaken in Child A with the usual managed by anterior abdominal wall blocks such
risk. These patients may need more transfusion in the as rectus sheath blocks and outcomes are similar
perioperative period. Vigilance on organ function and to that of the non cirrhotic group. Implications on
multidisciplinary care is needed postoperatively. outcomes are worse if there is involvement of the
bowel with or without peritonitis. General anaesthesia
Elective cardiac surgery is contraindicated in Child C as the
with invasive monitoring is usually indicated for the
morbidity is unacceptably high. The decision to operate
same. Hepatectomy can be safely performed in Child
on Child B will be based on associated comorbidities
A cirrhosis and even a neuraxial blockade is being
and presence or absence of decompensation. The
used for anlagesia with safety. Hepatectomy is usually
morbidity can vary from 20-47%. Cardiac interventions
contraindicated in Child B and higher groups.
are undertaken even in end stage disease as an attempt
Neurosurgery and vecuronium undergo metabolism by phase II
reactions, atracurium and cis atracurium have a non
Neurosurgical procedures carry a high morbidity
end organ linked route of elimination by ester hydrolysis
and surgical indications are spontaneous intracranial
and are considered to be safe for use in liver disease.
hemorrhage, traumatic brain injury, surgery for brain
Rocuronium undergoes hepatic metabolism and will
tumors and spinal instrumentation procedures. In this
have a prolonged duration but sugammadex can be
group, mortality is as high as 34-87 % and should be
safely used in liver disease as its excretion is through
approached with caution.
the kidney.
Intraoperative Anaesthetic considerations
Paracetamol is a weak NSAID that in doses large
The hepatic blood flow is determined by dual flow enough produce hepatotoxicity due to depletion of
through the portal vein and hepatic artery, the two glutathione in the hepatocytes. It can be used in smaller
having a semi reciprocal relationship called the doses or for a shorter time in liver diseases. NSAIDS
hepatic arterial buffer response (HABR). This implies (cox inhibitors) rarely produce hepatotoxicity by an
that a fall in portal vein flow is compensated by an idiosyncratic reaction.
increase in hepatic arterial flow through the release of
Regional anesthesia can produce a fall in MAP and hepatic
adenosine but the converse cannot occur. A fall in blood
perfusion proportional to the height of sympathetic
pressure can reduce the liver blood flow and this can
blockade. This can be corrected by administration
be corrected by drugs that increase the mean arterial
of phenylephrine to correct the MAP. Coagulopathy
pressure (MAP).
associated with liver diseases may prohibit the use of
Isoflurane, Sevoflurane and Desflurane are safe for use regional anesthesia, however a decision on the risks
in patients with increasing order in safety. Propofol, of regional versus a general anesthetic will have to be
Etomidate and Ketamine are lipid soluble with a high decided upon each patient and the experience of the
hepatic extraction ratio. Their duration of action is team and transfusion services and ICU management in
not prolonged and elimination half- lives are similar each institution. Broad guidelines will allow a regional
to normal adults. Dexmedetomidine has a decreased with an INR < 1.5 and platelet counts > 75,000 /mm3. A
half-life and prolonged clearance in patients with spinal anesthetic may be safer than an epidural when
hepatic dysfunction part of which could be due to postoperative coagulopathy is anticipated.
altered protein binding. Caution should be exercised
Fluid management in Liver Surgery
in the dosage as the duration could be prolonged.
Although fentanyl is lipid soluble with a short half-life, The perioperative fluid management is on similar lines
redistribution to storage sites occurs and prolonged for all surgical procedures. Balanced salt solutions
administration results in cumulative effects. Sufentanil are emerging as replacement solutions of choice as
has a similar profile to fentanyl and pharmacokinetics they contain a base of lactate or acetate. Normal
is safe for use in liver diseases. Alfentanil has a saline administration raises concerns regarding
prolonged half-life, almost double that of normal in hyperchloremia and dilutional acidosis. Hyperchloremia
patients with liver diseases and is best avoided in this could increase renal dysfunction by activation of
group. Remifentanyl is metabolised by tissue esterases the renin angiotensin aldosterone axis and by renal
that hydrolyze the ester linkage and its elimination is arteriolar vasoconstriction. In the context of hepatic
independent of liver function and is the safest opioid hypoperfusion or dysfunction, lactate administered
for use in children with liver diseases. extraneously is inadequately broken down in the liver
and lactic acidosis could ensue. Acetate solutions do
Succinylcholine and mivacurium are metabolised by
not interfere with lactate measurements as they have
the enzyme pseudo cholinesterase that is decreased
an extra hepatic metabolism. Additionally, they do
in chronic liver disease, hence the duration of action
not increase gluconeogenesis in the liver and release
can be prolonged in this group. While pancuronium

bicarbonate faster than lactate containing solutions risk of large volume transfusion. Renal replacement
and may be superior in diabetics and in situations therapies and nitric oxide and extracorporeal circuits
where lactate measurements are followed as markers may be needed for the critically ill patient.
of tissue perfusion.
References
Starches have fallen in disrepute after several studies
have shown a higher incidence of renal dysfunction 1) Wolf D.C. Cirrhosis, Updated July 30, 2018,
https://emedicine, medscape.com.
in sepsis. Gelatins are possible alternatives although
concerns regarding anaphylaxis and coagulation 2) Goldberg E, Chopra S. Cirrhosis in adults: Etiolo-
remain. Albumin is the colloid of choice in liver gy, clinical management and diagnosis. www.up-
dysfunction but at high cost; availability and potential todate.com, last updated on September 5, 2018.
disease transmission remain as concerns. 3) Pandey CK, Karna ST, Pandey VK, Tandon M, Sin-
Postoperative Care ghal A, Mangla V. Perioperative risk factors in pa-
tients with liver disease undergoing non hepatic
Patients need to be cared for in multidisciplinary surger..World J Gastrointest Surg 2012; 4(12):
ICU and vigilance for any postoperative signs of 267-274 .
decompensation. Paracetamol can be used with safety
4) Rothenberg DM, O’Connor CJ, Tuman KJ. Anaes-
in slightly lowered doses. NSAIDS are avoided and thesia and the Hepatobiliary system. Adult Sub-
opioids are used judiciously. The use of peripheral nerve specialty Management. Chapter 73.pg .2244-60
blocks and abdominal wall blocks may reduce opioid Miller’s Textbook of Anaesthesia.8th edition. Ed-
requirements. itor. Ronald D. Miller, Associate Editors. Eriksson
LI, Fleischer LA, Weiner- Kronish JP, Young WL.
Conclusion Publishers. Churchill- Livingstone- Elsevier.
Cirrhotic patients have an improved profile following 5) Clinical Anesthesia, 6th Edition
surgery in the last two decades following better Copyright ©2009 Lippincott Williams & Wilkins
understanding and availability of new techniques for Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting,
detection and management of complications. Patients Robert K.; Cahalan, Michael K.; Stock, M. Christine
may present with multisystemic complications and Section VII - Anesthesia for Surgi-
awareness of the spectrum of symptoms increases cal Subspecialties: Chapter 48 - Hepat-
scope of treatment. Dynamic tests of coagulation and ic Anatomy, Function, and Physiology
availability of procoagulant concentrates minimizes Brian S. Kaufman J. David Roccaforte

MCQ
1. Bonacini cirrhosis discriminant score includes 4. Cardiovascular changes in cirrhosis includes
the following except all except
a. Platelets a. Increased responsiveness to beta
b. Albumin agonists
c. INR b. Increased cardiac output
d. Serum transaminases c. Decreased systemic vascular
resistance
2. Major criteria to confirm the diagnosis of HRS
include all except: d. Increased heart rate
5. Risk of ascites occurs at HVPG above
a. A low GFR as assessed by serum
creatinine >1.5 mg/dL a. 4mm Hg
b. Absence of shock or treatment with b. 6 mm Hg
nephrotoxic drugs
c. 8mm Hg
c. No sustained improvement in renal
function after oral diuretic withdrawal d. 12 mmHg
d. <500 mg/day proteinuria with

ultrasonographic evidence of
parenchymal renal disease
3. False about pharmacokinetics in liver disease
a. Total apparent volume of distribution

of thiopentone at the steady state is
unchanged
b. Plasma clearance of fentanyl is
significantly low
c. Clearance of thiopentone depends on
hepatic blood flow
d. Half life of morphine and its
metabolites is prolonged
5. (c) 4. (a) 3. (c) 2. (d) 1.(b)

Answers

VIDEO SESSIONS
30 Ultrasound guided Chest wall blocks
Professor and Head, Sivashanmugam T

Mahatma Gandhi Medical College and Research Institute,
Puducherry.
Key points
Ø The major blocks for anterior and anterolateral chest wall are the PEC I block, PEC II block, and SPB
Ø PEC I block aims to anesthetize the pectoralis muscles, PEC II block and SPB also anesthetizes the skin,
muscles and axilla
Ø In PEC I block, the drug is deposited in the myofascial plane between Pectoralis major and minor
Ø PEC II block is a modified PEC I block, where the drug is deposited deep to pectoralis minor, in addition
to PEC I
Ø In Serratus plane block, the drug is deposited in the myofascial plane between Latissimus Dorsi and
Serratus Anterior muscle
Introduction cord (root value of C8, T1) of brachial plexus

respectively. Lateral pectoral nerve courses
The major blocks for anterior and anterolateral chest
between Pectoralis major and minor and
wall are the pectoral nerve blocks (PECS): PEC I block
supplies them. Medial pectoral nerve courses
and PEC II block, and serratus plane block (SPB). They
below the Pec minor, pierces it to supply
were described by R. Blanco (1-4).
Pec minor and lower part of Pec major. Ansa
Chest wall is comprised from anterior to posterior by: Pectoralis is a loop of communication between
the two aforementioned nerves.
1) Skin: supplied mainly by T1-T6 intercostal nerves
(anterior and lateral cutaneous branches) • Intercostal muscles- supplied by T1-T6
intercostal nerves.
2) Subcutaneous fat with breast tissue
3) Muscles (Fig 1 and 2) • Serratus anterior muscle- In the lateral chest
wall, supplied by the long thoracic nerve.
• Pectoralis major and minor- supplied by lateral
and medial pectoral nerves. They are branches • Ribs: supplied by T2-T6 intercostal nerves
of lateral (root value of C5,C6,C7) and medial

Ultrasound Guided Chest Wall Blocks 298 Sivashanmugam T
Fig 1: Muscles of chest wall
Fig 2: Muscles of chest wall after reflecting the pectoralis major muscle
While the PEC I block aims to anesthetize the pectoralis anaesthetizes Pectoralis major. The nerves have a
muscles, PEC II block and SPB also anesthetizes the skin, constant course with thoracoacromial vessels.
muscles and axilla.
Technique
PEC I
Patient Position
Anatomical basis
Supine with arm abducted and head turned away.
Drug is deposited in the myofascial plane between
Operator and USG machine
Pectoralis major and minor. It aims to block lateral
and medial pectoral nerve- both course between With the patient in the supine position, the operator
the Pectoralis major and minor (1). It essentially stands at the head end of the patient, and the

ultrasound machine is positioned ipsilateral to the side Transducer is moved laterally until the anatomy of the
to be examined and directly in front of the operator thoracic wall at the level of the third to fourth ribs is
visualized (5).
Probe selection
Method 2
High-frequency (13–15 MHz) linear array transducer.
Transducer is positioned in the transverse orientation
Sonoanatomy and reference point (Fig 3)
medial to the coracoid process with its orientation
Method 1 marker directed laterally. The medial end of the
transducer is directed towards the sternum (4).
Ultrasound transducer is positioned over the middle of
clavicle, its orientation marker directed cephalad and PECS-I plane is identified between the posterior surface
distal end of the transducer is directed slightly laterally. of the pectoralis major muscle and the anterior surface
of the pectoralis minor muscles at the level of fourth
The clavicle and ribs are visualized as hyperechoic rib. The pectoral branch of the thoracoacromial artery
structures with underlying acoustic shadows. is seen as a hypoechoic and pulsatile structure within
the PECS-I plane.
Fig 3: PEC I block is given in plane between pectoralis major (pM) and Pectoralis minor (pm). PEC II block the
second injection is between pectoralis minor (pm) and serratus anterior muscle (sm)

Injection technique Probe selection
Needle can be inserted in-plane to the desired plane High-frequency (13–15 MHz) linear array transducer.
at the level of fourth rib.
Sonoanatomy and reference point (Fig 3)
Drug volume and concentration
• Transducer is placed and moved similar to PEC I
20-30 ml of 0.25% bupivacaine.
• The first plane is identified between the
Outcome posterior surface of the pectoralis major
• Essentially blocks most of Pectoralis major but muscle and the anterior surface of the
not all the quadrants pectoralis minor muscles and second plane is
identified between the posterior surface of the
• Nil cutaneous supply pectoralis minor muscle and the outer surface
• Axilla not covered of the serratus anterior muscle.
Application Injection technique
Breast expanders and subpectoral prosthesis Needle can be inserted in-plane or out-of-plane to the
desired plane at the level of third and fourth rib.
PEC II block
Drug volume and concentration
Anatomical basis
Between Pec major and minor: 10 ml of local anesthetic
• It is a modification of PEC I block. The first and between Pec minor and serratus anterior: 20 ml
injection is in the myofascial plane between of local anesthetic.
Pectoralis major and minor. Second injection
is performed deep to pectoralis minor in the Outcome
plane between Pec minor and serratus anterior
Essentially blocks the skin over lateral half of chest in
• Aims to block Lateral and Medial pectoral addition to the Pectoralis major and minor muscles,
nerves, third to sixth intercostal nerves, serratus anterior muscles. It also blocks the axilla.
intercostobrachial nerves and the long thoracic
Application
nerve (2)
• Analgesia for breast surgeries
• It anaesthetizes the skin in addition to the
muscles of the chest. • Axillary clearance
• Pace maker implantation
Technique • Analgesia for VATS
Patient Position SERRATUS PLANE BLOCK
Supine with arm abducted and head turned away. Anatomical basis
Operator and USG machine The drug is deposited in the myofascial plane between
With the patient in the supine position, the operator latissimus dorsi and serratus anterior muscle.
stands at the head end of the patient, and the Aims to block second to ninth intercostal nerves,
ultrasound machine is positioned ipsilateral to the side intercostobrachial nerves, the long thoracic nerve and
to be examined and directly in front of the operator thoracodorsal nerve (3).

Thoracodorsal artery is seen in this plane. is the serratus plane. Local anesthetic can also
be deposited below the serratus anterior in
Technique the deep block. Thoracodorsal artery is seen
Patient Position in this plane. Transducer is moved cranially till
the inferior margin of teres major is seen.
Lateral with arm abducted.
Injection technique
Operator and USG machine
Needle can be inserted in-plane to the desired plane
With the patient in the lateral position and with the at the level of fifth and sixth rib.
side to be scanned uppermost, the operator stands
behind the patient, and the ultrasound machine is Drug volume and concentration
positioned on the contralateral side and directly in 20-30 ml of local anesthetic
front of the operator
Outcome
Probe selection
• Essentially blocks the skin over lateral aspect
High-frequency (13–15 MHz) linear array transducer. of chest wall in addition to the Pectoralis
Sonoanatomy and reference point (Fig 4) major and minor muscles, serratus anterior
and latissimus dorsi muscles
• Transducer is placed longitudinal at lateral
chest wall near posterior axillary line at the • Also blocks the axilla.
level of fifth and sixth rib Application
• Transducer is moved posteriorly to identify the • Analgesia for breast surgeries
thick serratus anterior muscle overlying the
sixth rib and the latissimus dorsi muscle lying • Axillary clearance
superficial. The myofascial plane between two • Anterior rib fractures
Fig 4: In Serratus plane block local anesthetic is injected between the latissimus dorsi muscle (LD m) and
serratus anterior (Serr m) or deep to serratus muscle
Complications 3. Blanco R, Parras T, McDonnell JG, Prats-Galino
A. Serratus plane block: a novel ultrasound-
• Common to all chest wall blocks. guided thoracic wall nerve block. Anaesthesia.
• Hematoma 2013;68:1107–1113.
• Pneumothorax
4. Blanco R. Thoracic interfascial nerve blocks:
• Local anesthetic systemic toxicity PECS (I and II) and serratus plane block,
References musculoskeletal ultrasound for regional
anaesthesia and pain medicine. In: Karmakar
1. Blanco R. The ‘pecs block’: a novel technique MK, ed. 2nd ed. Hong Kong: Department of
for providing analgesia after breast surgery. Anaesthesia and Intensive Care, The Chinese
Anaesthesia. 2011;66:847–848. University of Hong Kong; 2016:377–82.
2. Blanco R, Fajardo M, Parras MT. Ultrasound 5. Hadzic A. 2017. Hadzic’s textbook of regional
description of Pecs II (modified Pecs I): a novel anesthesia and acute pain management. 2nd
approach to breast surgery. Rev Esp Anestesiol Ed. McGraw-Hill: New York. p 650–60.
Reanim. 2012;59:470–475.

MCQ
1. Nerve supply of skin of chest wall 4. The following is the target in Pecs II block:
a. T2-T5 a. Between pectoralis major and minor
b. T1-T5 muscles
c. T3-T5 b. Between pectoralis minor and the
serratus anterior muscles
d. T1-T6
c. Between serratus anterior and
2. Following are true regarding anatomical basis
latissimus dorsi muscles
of PEC 1 block except
d. Below teres major muscle
a. Drug is deposited in myofascial plane
between Pec maj and Pec minor 5. The following are true regarding anatomical
basis of PEC 2 block except
b. Aims to block lateral and medial
pectoral nerves a. Aims to block Lateral and medial
c. It anesthetizes both Pec Major and Pec pectoral nerves
minor b. 3rd to 6th intercostals nerves
d. Nerves have a constant course with c. intercostobrachial nerves
thoracoacromial vessels.
d. doesn’t block the long thoracic nerve
3. The following are indications of PEC1 or PEC2
except
a. Lattismusdorsi flap reconstruction

b. Portacath insertion
c. Sentinel biopsy
d. Breast expander surgery
4.(a,b) 5.(b) 3.(a) 2.(c) 1.(d)

Answers

31 Lung isolation techniques
Professor and Head, Gopinath R

Department of Anesthesiology
NIMS, Hyderabad
Lung separation is done when there is a need to lungs. DLT allows suctioning from the isolated lung, and
ventilate one lung only. One lung ventilation (OLV) can application of continuous positive airway pressure if
be accomplished by using an endobronchial tube or by required to improve oxygenation. Ventilation of either
blocking ventilation of the contralateral lung. or both lungs can be easily achieved.
Double-lumen endotracheal tubes (DLT) have been Double-lumen endotracheal tubes may be challenging
used in thoracic anesthesia for lung separation and to place in patients with difficult airways, cannot be
one-lung ventilation (OLV) for more than 50 years, since used routinely used for postoperative ventilation and
the report of Carlens and Bjork in 1950. They provide since they are large and relatively stiff may have a higher
excellent operating conditions when sized and placed propensity for trauma after insertion, which may result
correctly, and allow access to both ventilated and in postoperative hoarseness and/or vocal cord lesions.
collapsed lungs for secretion clearance, independent
Indications
ventilation and bronchoscopic inspection.
Absolute indications
OLV is a standard method to improve surgical exposure
for lung surgery and can be used for esophageal, 1. Isolation of each lung to prevent contamination of
cardiovascular and orthopedic procedures on the a healthy lung (eg, infection, massive hemorrhage)
verterbrae. OLV is also used to prevent soiling from
the contralateral lung, which may occur in cases of 2. Control of distribution of ventilation to only one
suppurative lung disease, pulmonary hemorrhage or lung (eg bronchopleural/bronchopleural cutaneous
bronchoalveolar lavage, or to prevent air leak of the fistulas, unilateral cyst or bullae, major bronchial
pathologic lung in cases of bronchopleural fistula or an trauma/disruption)
emphysematous bulla or cyst. 3. Unilateral lung lavage
Expertise in both laryngoscopy and fiberoptic 4. Video-assisted thoracoscopic surgery (VATS)
bronchoscopy (FOB) are necessary prior to placement
of OLV devices. Lung separation can be achieved with Relative indications
a left-sided double-lumen endobronchial tube (left
1. Thoracic aortic aneurysm
DLT) to ventilate the left lung via the bronchial lumen
2. Pneumonectomy
or the right lung via the tracheal lumen. Right DLTs
are used less frequently because of anatomical and 3. Lung volume reduction
technical reasons. Bronchial blockers allow the isolation 4. Minimally invasive cardiac surgery
of a lung (or a segment of a lung) using a single-lumen 5. Upper lobectomy
endotracheal tube. 6. Esophageal procedures
Various methods of methods of lung separation include 7. Lobectomy (middle and lower lobes)
DLT placement, bronchial blocker and single-lumen 8. Mediastinal mass resection
endobronchial tube placement of which the placement 9. Thymectomy
of DLT is the most common way of separating the two
10. Bilateral sympathectomies

Lung isolation techniques 306 Gopinath R
Contraindications right-sided and left-sided versions. For smaller adults
and children, smaller size tubes are available (32-Fr left-
1. Difficult airway
sided and 28 Fr).Tubes of one size smaller and larger
2. Small patients
should be available during the procedure.
3. Airway lesion or tumor
The bronchial tip of a properly sized double-lumen
endotracheal tube should have a diameter 1-2 mm
smaller than the left main bronchus. It is important to
review computed tomography scans prior to planning
for placement of a right sided tube. General guidelines
to determine size are:
1. Female shorter than 160 cm size: 35-Fr tube
2. Female taller than 160 cm size: 37-Fr tube
3. Male shorter than 170 cm size: 39-Fr tube
4. Male taller than 170 cm size: 41-Fr tube
OR
1. Very small person 28F
2. Small person 35F
3. Medium size person 37Fr
4. Large size person 39Fr or 41Fr
Fig 1: Anatomy of the Lung
Tube Selection
Double-lumen endotracheal tubes are available in
various sizes (35 Fr, 37 Fr, 39 Fr and 41 Fr) in both
Table 1: DLT selection based on CT

Tube Insertion Using fibreoptic bronchoscopy - the flexible fiberoptic
bronchoscope is passed down the tracheal lumen, the
Double-lumen endotracheal tube can be placed
tracheal cuff is deflated and pulled back until the carina
under direct laryngoscopy, via tube exchanger or over
is seen. At this juncture, the tracheal cartilaginous rings
fiberoptic bronchoscope.
are anterior and the tracheal membrane is posterior.
With direct laryngoscopy the distal, bronchial curvature Next the tube is advanced until the bronchial blue tip
is kept with the concavity facing upwards. After the tip enters the left main stem.
passes through the glottis, the stylet is removed and
At this point, the blue bronchial balloon is inflated with
the tube is advanced and rotated 90 degrees with the
1-3 ml of air until the blue cuff is visible in the left main
proximal pharyngeal concavity upwards (towards the
stem. A portion of the blue cuff should be seen seated
side to be intubated) and advanced until resistance is
in the left main stem.
felt; this depth is usually between 28-30 cm.
After positioning the patient laterally, the tube should
The tracheal cuff is inflated, breath sounds are
be checked again to ascertain that it is not displaced.
auscultated and end-tidal CO2 is noted on the capnogram
The tube can either become malpositioned by coming
to ascertain placement of the tube in the airway.
Fig 2: Flexible bronchoscopic placement and positioning of right-sided DLT. A: The FB is passed through the bronchial lumen into the
right mainstem bronchus. The patency, length, and anatomy of the right bronchial tree are evaluated. B: The FB is withdrawn inside
the bronchial lumen. The tip of the FB is placed at the proximal end of the slit of the bronchial cuff rotated 90 degrees to the right
and the tip is angulated anteriorly towards the lateral wall of trachea. C: The tube and FB are then advanced together inside the
right mainstem bronchus until the orifice of the right upper lobe comes into view through the slit of the bronchial cuff. D: The FB is
advanced 2 to3 mm through the bronchial slit inside the right-upper-lobe bronchus to visualise its three segments. E: The FB is passed
through the tracheal lumen to check the position of the bronchial cuff and the opening of the left mainstem bronchus.
out or advancing to a deeper level. When patient There are multiple methods available to confirm
position is changed to lateral, the tube can be displaced, placement, including radiographic verification,
mainly due to extension of the neck. auscultation, fiberoptic visualization and various
clinical tests such as selective capnography and use
Position Verification
of underwater seal. Currently, the use of multiple
This step is very important because correct placement methods for confirmation of correct tube placement
is of paramount importance for patient outcome. is widely considered to be the standard of care.
The correct placement might be partially confirmed Auscultation and fiberoptic examination are used
already if fiberoptic bronchoscope was used during most commonly.
tube placement.

Auscultation by Alliaume et al showed that malposition was present
in 78% of left-sided double-lumen endotracheal tubes
Auscultation is a widely available first-line test. After
and 83% of right-sided double-lumen endotracheal
placement of the double-lumen endotracheal tube, the
tubes. Auscultation should always be supplemented
tracheal cuff is inflated and ventilation is attempted.
with fiberoptic evaluation and repeated each time the
The patient should have bilateral breath sounds and
patient is repositioned.
end-tidal CO2 should be noted on capnogram confirming
placement in the airway. Fiberoptic Bronchoscope
Next, the tracheal lumen is clamped and opened to The fiberoptic bronchoscope first is advanced through
room air. The bronchial cuff is inflated with minimal the tracheal lumen to confirm that the bronchial tube
volume to stop the leak (2 mL of air). At this point, is placed in the desired bronchus. For the left bronchus,
confirmation of separation of lungs can be done with the cuff should be ideally placed 5 mm below the
air bubble leak test. One-sided breath sounds should carina. It is crucial to identify the right bronchus. The
be heard, only over the desired lung field. right main bronchus gives off the right upper lobe
bronchus, which is the only one that has 3 orifices in it.
Next, with the bronchial cuff inflated, the tracheal
Then examination through the bronchial tube is done
lumen is unclamped and reconnected, the bronchial
to assure tube patency and determine margin of safety.
lumen is clamped and ventilation is attempted through
Therefore, orifices to both upper and lower lobes must
tracheal lumen. If the tube is positioned correctly,
be identified. Identification of those bronchi confirms
breath sounds should be heard over contralateral
correct placement of a left-sided tube.
hemithorax. Then the bronchial lumen is unclamped
and reconnected and bilateral breath sounds should be Troubleshooting
audible again. This concludes auscultation for correct
If the double-lumen endotracheal tube is malpositioned,
placement.
it may be in the correct bronchus but too deep, in the
Auscultation is not very reliable, however. Smith et correct bronchus but too shallow, or in the wrong
al showed that 48% of blindly placed double-lumen bronchus. Table 2 presents physical examination
endotracheal tubes were malpositioned. Another study findings for both correct and incorrect positions.
Procedure Too Deep Too Shallow Wrong Bronchus Correct Position

Both lumen Breath sounds
ventilated Breath sounds heard Breath sounds heard Breath sounds heard
heard on the left
on the left and right on the left and right on the left and right
Both cuffs up and right
Clamp right
lumen Breath sounds heard Breath sounds heard Breath sounds heard Breath sounds
Both cuffs on the left on the left and right on the right heard on the left
inflated
Clamp left
lumen No breath sounds or No breath sounds or No breath sounds or Breath sounds
Both cuffs severely diminished severely diminished severely diminished heard on the right
inflated
Clamp left
lumen Breath sounds
Breath sounds heard Breath sounds heard Breath sounds heard
heard on the left
Deflate on the left on the left and right on the right
and right
bronchial
Table 2: Troubleshooting Left-Sided Double-Lumen Endotracheal Tube Placement

Bronchoscopy is of great value in troubleshooting tube specific situations for which the use of a right-sided tube
malposition and will help to position the tube. is warranted, including compression of left mainstem
bronchus by external/internal mass, aneurysm of
Even a correctly placed tube can relocate at any time.
thoracic descending aorta, left lung transplant, left-
Surgical maneuvers and patient repositioning can
sided sleeve resection, left-sided pneumonectomy and
result in tube dislodgement, which can manifest as
left-sided tracheobronchial disruption.
sudden change in compliance and airway pressures
and decrease in tidal volume. Physical examination Right-sided double-lumen endotracheal tubes are
and fiberoptic verification should be undertaken and designed differently because the right bronchus is
correct placement of the tube confirmed or changed shorter than the left bronchus. These tubes have a cuff
if necessary. with a slot in it to facilitate right upper lobe ventilation.
The right-sided tube is much more challenging to place.
Right-Sided DLT Placement
Most of the failures in correct placement stem from not
A left-sided double-lumen tube is preferred for both confirming the placement after the patient is moved.
right- and left-sided procedures. However, there are
Fig 3: Left and right sided DLT
Unable to intubate with DLT Double Lumen tube with Integrated Camera
The DLT usually has a larger outer diameter than the VivaSight-DL is the new generation of Double Lumen
normal endotracheal tube. Thus there are occasions Tubes with integrated high-resolution camera making
when intubation with a DLT can be difficult. Inability to placement of the DLT fast and effective and providing
extend the neck, a full set of teeth and limited mouth continuous visual monitoring throughout the procedure.
opening are usually causes for concern. Malpositioning and dislocation are easily detected with
the real-time high resolution video image transmitted
1. Attempt to place DLT. Use stylet in bronchial lumen to the aView monitor. Studies reported faster tracheal
to curve DLT in similar way to the normal ET intubation rate and higher success rate at first attempt
for VivaSight. VivaSight tubes may cause soft tissue
2. Intubate with appropriate size tube exchanger. Pass
trauma such as bleeding, hematoma, edema and
exchanger up bronchial lumen and pass tube over erythema. Sore throat and dysphonia also reported.
exchanger with laryngoscope in place. Twisted the Due to the outer thickness, smaller-sized double-lumen
tube as it goes in can help it to pass into the trachea tube may be necessary. Other disadvantages: melting
3. Abandon DLT and use a bronchial blocker due to the heat of light source before insertion and
sudden shutdown without warning.

Other tubes (by AMBU) for SLV also include VivaSight-SL the ET tube separately and simultaneously with the
with integrated high-resolution camera together with pediatric bronchoscope. An ET tube of 7.5mm or larger
the endobronchial blocker, VivaSight-EB. is required. The tip of the blocker has a loop of suture
through which the bronchoscope can be placed. This
allows the scope to guide the blocker into the correct
bronchus.
Fig 4: Vivasight - DL
Bronchial Blockers Fig 6: A: Cuff of Arndt bronchial blocker inflated with 3 ml of air.
Notice the elliptical shape and potentially broad contact area with
Bronchial blockers are another means to provide one
the isolated bronchus. B: Multiport adapter with FOB and Arndt
lung ventilation by using a balloon catheter inflated blocker in place. Notice the coupling of the blocker and scope
to occlude the bronchus of the lung being operated provided by the distal wire loop of the blocker.
upon. This method is useful when a DLT cannot not be
placed such as smaller airway, in situations of difficult
intubation, in an already intubated patient when the • Fogarty Catheter
risk of re-intubation is high, or when the patient is
tracheostomised.
There are three methods of establishing OLV by a
bronchial blocker. These are by using an Arndt Blocker,
a Univent tube, a Fogarty catheter or the EZ blocker
• Arndt Blocker
Fig 7: A: Proximal end of Fogarty embolectomy catheter

demonstrating rapid, replaceable wire stylet. B: Distal end of
Fogarty catheter. The balloon is inflated with 3 ml of air. Notice the
relatively spherical shape.
Fig 5: Arndt bronchial blocker. The pilot balloon for the cuff has a
syringe attached. Notice the wire loop at the distal end, designed One lung ventilation can be achieved by placing
for direct coupling with a FOB. The multiport adapter, which comes a Fogarty catheter into the airway outside of the
packaged with the blocker, is in the center of the picture. endotracheal tube. An 8-14 or 8-22 Fogarty is ideal. The
useful maneuver is to manually bend the tip by about
The Arndt blocker is a balloon catheter that comes 20 degrees which allows the catheter to be directed
with a special adapter allowing the catheter to enter into the correct bronchus.

• Univent Tube • The E-Z Blocker
The EZ-Blocker® consists of a 7 Fr polyurethane catheter
containing four lumina. Two of these lumina are
for inflation of the cuffs; the other two can be used
for additional oxygen supplementation to the non-
inflated lung, or suctioning. The distal part of the BB
ends in a Y shape, consisting of two 4 cm long distal
extensions, each with a polyurethane spherically
Fig 8: Univent tube. A: Retractable blocker extended somewhat beyond
distal end of tube for display. The pilot balloon for the blocker has a shaped cuff. The extensions are fully symmetrical and
smaller syringe attached than the pilot for the cuff or the endotracheal colored differently (blue and yellow) for identification
tube. B:Closeup of the blocker inflated with 3 ml of air. Notice that it
has a somewhat more spherical shape than the Arndt cuff, potentially
purposes. The EZ-Blocker® is supplied with an adaptor,
applying more pressure to the isolated bronchus. the EZ-Multiport Adaptor ®, which is designed for
connection to ventilation devices, introduction of the
The Univent tube is a specially designed endotracheal EZ-Blocker® and a fiberoptic- or video bronchoscope
tube where the bronchial blocker is contained within a or a suction catheter. The blocker is introduced and
separate lumen within the wall of the tube. positioned under direct vision using a bronchoscope.
Steps in placing the Univent Tube The symmetrical design facilitates introduction and
1.) An adult or smaller bronchoscope is made available positioning of the device with the extensions in both
and in working order main stem bronchi. When the proper position is
reached, the cuff in the main stem bronchus of the
2.) The patient is intubated with the Univent tube. The non-ventilated lung can be inflated and lung isolation
tube should be no lower than the mid-portion of the is achieved. Owing to its Y shape, the blocker remains
trachea in position.
3.) Bronchoscopy of the airway is performed
4.) The bronchoscope is pulled back to just distal to
the end of the Univent tube and the balloon catheter
is advanced into the desired mainstem bronchus.
Positioning and inflation are the same as with the Arndt
and Fogarty blockers.
Fig 10: E-Z blocker
Troubleshooting
Unable to get blocker down correct side
1) Make sure endotracheal tube is well above carina to
allow blocker access to each side
2) If using Fogarty catheter as blocker, be sure just the
tip is angulated by about 20 degrees.
3) Turn patient’s head to the side opposite the side the
blocker is supposed to go down
4) Tighten the loop on the Arndt blocker where the
bronchoscope flexes to allow it to direct the blocker.
Fig 9: Placement of Univent tube
Lung separation and the difficult airway Children and Adolescents
If placement of a DLT or Bronchial blocker is problematic, Patients who develop thoracic disease later in
one must consider the safety and need for lung childhood and adolescence typically present with
separation. Surgical preference alone is an insufficient infection, malignancy and musculoskeletal deformities.
reason to jeopardize a patient. An anterior mediastinal mass, due to the potential
complications of complete airway compression and
Bronchial blockade is always an option when a DLT
cardiovascular collapse is a life threatening condition
cannot be placed, but the airway is accessible to
requiring general anesthesia.
endotracheal intubation. Examples include patients
with very limited mouth opening or in whom only a Techniques for Lung Isolation in Infants and Children
nasotracheal intubation is possible. For a patient with
Manual Retraction
a tracheostomy, lung separation can be obtained with a
BB through an endotracheal tube or tracheostomy tube, A common method employed to obtain adequate
with a conventional DLT or with short DLTs intended for exposure for thoracic surgery in infants and small
tracheostomies. children is by open thoracotomy with manual retraction
of the operative lung performed by the surgeon. This
A fiberoptic bronchoscope must be available, and the
method allows for conventional dual lung ventilation
anesthesiologist must be familiar with both normal and
with the use of a standard endotracheal tube. Manual
abnormal airway anatomy.
retraction can also be used during Video Assisted
Videolaryngoscopes are replacing bronchoscopes as the Thoracoscopic Surgery (VATS) allowing for two
first choice for accessing the difficult airway. lung ventilation; however single lung ventilation is
preferable.
Airway exchange catheters
Single Lung Ventilation Techniques
An airway guide or airway exchange catheter (AEC) is an
essential piece of equipment for thoracic anaesthesia. A) Single Lumen Endotracheal Tubes
A gum elastic bougie, an Aintree catheter (Cook
A single lumen endotracheal tube (ETT) is perhaps
Critical Care) or other guides facilitate direct tracheal
the simplest method of obtaining lung isolation. The
intubation with an endotracheal tube and the Frova
technique for placement is straightforward and can be
intubating catheter (Cook Critical Care) has been used
accomplished with standard intubating equipment. With
for placement of DLTs in patients with Cormack–Lehane
this technique, the ETT is advanced into the mainstem
grade II or III views during laryngoscopy.
bronchus of the lung to be ventilated until breath
Techniques for Single Lung Ventilation in Infants and sounds on the operative side disappear. The ETT can be
Children advanced blindly, or a fiberoptic bronchoscope can be
used to guide or confirm placement. The angulation of
Indications
the right mainstem bronchus is significantly less acute
Diseases of the chest that may require lung isolation than that of the left making the right side technically
for surgery easier for mainstem intubation.
Neonates and Infants B) Balloon Tipped Bronchial Blockers
Congenital anomalies of the thoracic cavity that present There are multiple balloon-tipped bronchial blockers
in the neonatal period requiring surgical intervention available including the Arndt endobronchial blocker,
are tracheal stenosis, pulmonary sequestration, Fogarty embolectomy catheter, Cohen endobronchial
congenital diaphragmatic hernia, tracheoesophageal blocker, Coopdech bronchial blocker and EZ-blocker as
fistula, congenital lobar emphysema, vascular ring etc. described for adults.

Troubleshooting hypoxemia during single lung 5. Pass soft suction catheter down tube to ensure
ventilation there is no obstruction from secretions.
Single lung ventilation creates a large intrapulmonary 6. Lastly, if hypoxemia remains after the above steps
shunt as the non-ventilated lung is still being perfused have been taken, the surgeon should be informed
without oxygenation; therefore, some degree of and the operative lung should be re-inflated.
desaturation is to be expected. Patients with chronic
References
lung disease of the operative lung typically tolerate
single lung ventilation better than patients with two 1. Techniques for single lung ventilation in infants
healthy lungs. In the former situation, perfusion to the and children. Jaida Fitzgerald, Faye Evans,
diseased lung is chronically decreased and preferentially Paediatric Anaesthesia, Tutorials. October
guided to the healthy lung; therefore, when single lung 2015.
ventilation is initiated there is a smaller intrapulmonary
shunt fraction. 2. Advances in lung isolation techniques. Wanda
M.Popescu. Anesthesiology News. Guide to
In the setting of hypoxemia, a methodical evaluation of airway management 2014.
potential causes should be sought. The following are
basic steps that can be taken sequentially to evaluate 3. An Update on the use of Bronchial blockers.
and treat hypoxemia during single lung ventilation: Campos JH.CurrOpinAnaesthesiol 2007; 202:
27-31.
1. Place patient on 100% FIO2
4. Lung separation and the difficult airway. J. B.
2. Evaluate position of tube or blocker by auscultation Brodsky. British Journal of Anaesthesia 103
for breath sounds or via fiberoptic bronchoscopy (BJA/PGA Supplement): i66–i75 (2009).
if available. The placement of the tube or blocker
should be verified after every change in patient 5. Lung isolation techniques. Martin Ma,Peter D
positioning. Slinger,UpToDate. May 2016.
3. Apply CPAP to the non-dependent lung. A level 6. A six-month evaluation of the VivaSight™
of CPAP between 5-10 mmHg typically does not video double-lumen endotracheal tube after
interfere with surgical conditions and will help to introduction into thoracic anaesthetic practice
decrease shunt fraction. at a single institution.Rapchuk IL, Kunju S,
Smith IJ, Faulke DJ.Anaesth Intensive Care.
4. Apply low levels of PEEP to the dependent lung. 2017 Mar;45(2):189-195.
Avoid high levels of PEEP as this can divert blood
flow away from the dependent lung due to increases
in intrathoracic pressure.

MCQ
1. Absolute indications of DLT include all of the 4. Troubleshooting hypoxemia during OLV
following except includes the following except
a. Isolation to prevent contamination a. Placing patient on 100% fio2
b. Control of distribution of ventilation to b. Applying cpap to dependent lung
any one lung
c. Passing soft suction catheter down
c. VATS tube to ensure there is no obstruction
d. Lung volume reduction from secretions.
2. Following steps are true regarding DLT d. Evaluate position of tube or blocker by
insertion with fibreoptic bronchoscope except auscultation for breath sounds or via
fiberoptic bronchoscopy if available.
a. tracheal cuff is deflated & pulled back
5. Following are the available DLT sizes except
until carina is seen
b. tube is advanced until the bronchial a. 35
blue tip enters the LT main stem b. 39
c. Blue cuff should not be visible in Lt c. 37
main stem
d. 42
d. Bronchial balloon is inflated
3. Regarding Fogarty catheter useful maneuver
is to manually bent the tip by about _____
a. 10 degrees
b. 30 degrees
c. 20 degrees
d. 40 degrees
5. (d) 4. (b) 3. (c) 2. (c) 1.(d)

Answers

32 Interventional Pain Procedures in Head & Neck
Director, Pain Management Centre, Muralidhar Joshi

Virinchi Hospitals,
Hyderabad.
Interventional pain management is the discipline of However, there are a group of patients who respond
medicine devoted to the diagnosis and treatment of excellently to the interventions like coeliac plexus
pain related disorders principally with the application block, stellate ganglion block, intercostal block, lumbar
of interventional techniques in managing subacute, sympatholysis etc. Often, patient feels better for some
chronic, persistent and intractable pain, independently weeks, before complaining of same symptoms. Some
or in conjunction with other modalities of treatment of them develop a new site of pain because of other
(NUCC definition). pathology. Sometimes the pain specialist feels out of
place after he runs out of ideas. In view of all these
In the last two decades, interventional management
possibilities, it is preferable to limit the interventions
of both acute and chronic pain has become more
to a particular subpopulation of patients who do not
popular mainly because of side effects associated with
do well with conservative treatment.
the pharmacological agents and probably the patient
feels a magic injection can get rid of pain once for all. Before taking up the patient for procedure, it should be
Nevertheless, one should not forget that interventions made clear to the patient about the procedure, possible
are not free from any kind of side effects. There are benefits, anticipated side effects, percentage of success
limitations in using the procedures for any kind of etc. Informed consent has to be obtained. The patient
pain. The underlying pathology, reversible stage of should share responsibility for decision-making and must
illness, accessibility to neural structures, competence understand the risks and the fact that complications do
of the pain specialist and other factors can make the occur. If there is any need for admission or sedation,that
difference between the success and failure. also should be explained. Whenever any intervention is
planned, always insist for an attendant to accompany
There are large numbers of patients both in acute
the patient to hospital. Many clinicians have ended
and chronic pain groups who benefit from these
in trouble by not taking these precautions. Maintain
interventions. The immediate relief from pain makes
a record of all interventions if possible by radiologic
many patients feel comfortable. The attendants get
imaging (wherever it is possible), it helps for any future
relieved of psychological pressure whatever they might
references.
be facing. The clinician leaves the hospital on a positive
note that his patient is doing well. The percentage of However, the attractive option of finding a one-time
success varies anywhere from 50% to 70% depending solution for the agonising pain drives the clinicians
on the selection of patients and the competence of pain to search for newer remedies. In this direction,
specialist. Patients with malignancy and associated interventional pain management has come as a big step
pains do not do well with the interventions that often. for the medical community. Expecting an interventional
The reasons for the same could be different types of procedure to solve all these problems is not at all
pain located over different parts of body (fracture justified. One should not forget that the underlying
rib, osteoporosis, muscle cramp, tumour infiltration, pain continues to harm the body relentlessly. Newer
intestinal obstruction, gastritis, undernutrition, gadgets like radiofrequency and cryoablative systems
constipation, insomnia…). Expecting the interventions have become valuable modalities. The pain mediated
to sort out all these pains is not justified. Many of them through the autonomic nervous system responds very
do well with opioids and other supportive medications.
Interventional Pain Procedures in Head & Neck 316 Muralidhar Joshi
well to neuroablative procedures (like stellate ganglion Ideally, proper preparation for any intervention
block, coeliac plexus block, lumbar sympathetic begins at the visit before the procedure (Prithviraj
block and others). The pain mediated because of 2006). The patient is much more likely to remember
somatic structure involvement is a bit difficult to treat discharge instructions and expected side effects if they
interventionally. The difficulty arises because of attempt are explained during a visit when the patient is not
to preserve the function of that part of body. apprehensive about the imminent procedure, what side
effects may be expected and potential complications.
It might be ideal for doing all procedures in a place
Discussions of the realistic expectations of the proposed
where resuscitation facilities are available. Problems
intervention should be held before any procedure.
can come from various quarters like apprehensive
The goals of blockade and the number of blocks in
patient, exaggerated effects to sedation, intravascular
a given series differ with each pain syndrome and
injection and various others. It is not advisable also to do
these variables should be discussed, when possible,
the procedures in sitting position in view of possibility
at visits before the actual blockade. Patients are much
of syncope, hypoglycemia and infirm patients. All
less likely to experience frustration or despair if they
these points are considered to prevent catastrophes.
understand before what can be expected. If the cause
If a designated pain procedure room is present, that is
of pain is unclear and the intended block is considered
ideal. Sometimes the clinician might be forced to share
diagnostic, a complete explanation allows the patient
the area with other doctors. Procedure close to spinal
to record valuable information on the effectiveness of
cord and brain where in catheters might be used can
the procedure. Procedures not involving much of local
be done in operating room. This is for ensuring sterility.
anaesthetics or other agents may not require a fasting
The basic principle of any therapy is “do no harm” and patient. One can allow them to have light food upto
interventions are no exception. The clinician should be 2–3 hours before procedure. But procedures involving
well versed with anatomy and pathophysiology. Imaging sedation and major intervention should have a fasting
modalities like Fluoroscopy/CT/USG have revolutionized patient (6 hours of fasting). These patients should be in
the interventional procedures in view of its precision. the operating room with a vascular access. Placement of
These options are easier and simpler to use. They an intravenous line before the block is not mandatory
increase comfort for clinician and patient along with at all pain clinics, but it facilitates use of IV sedation,
offering more safety. Always equip the interventional when indicated, and provides access for administration
areas with crash cart, suction, defibrillator, medications, of resuscitative drugs should a complication occur. For
monitors and trained personnel. For safe practice, anxious patients and in teaching institutions when
always appreciate feel of tissues (ligament, muscle, the operator is inexperienced or when “hands on”
bone, potential space). View fluoroscopy in two angles teaching is expected, pre-block sedation through an
and save images. Watch for contrast spread; when in IV line is beneficial. Situations wherein there can be
doubt, always pause. Consult professional colleagues change in heart rate (like using adrenaline), change in
and cancel procedure if necessary. Sometimes aspiration blood pressure (following sympatholysis) or any other
of needle for blood and CSF may not be reliable. Watch parameters, it is preferable to monitor heart rate,
for response to injection like pain, hypotension, cerebral blood pressure, O2 saturation. Always be in touch with
symptoms, sensory loss, motor loss etc. There can patient who is lightly sedated by constantly conversing
be complications like allergy, medication side effects, with him. If these precautions are taken, you will not be
bleeding, infection, nerve damage, pneumothorax, doing any harm to patient, if not helping him.
spinal cord/brain stem/brain injury and death. The
Conclusion
complications risk will increase linearly with situations
like elderly, obesity, chronic medical conditions, post Although fluoroscopy has revolutionized the precise and
surgical anatomy and most important of all these is an accurate practice of interventional pain management,
inexperienced interventionist. radiation safety training is required for any physician

who uses fluoroscopy in his practice. Of late, use of References
USG has increased the safety margin for patients going
• ASIPP. Comprehensive Evidence-Based
for interventions as part of pain management. We will
Guidelines for Interventional Techniques in
discuss more about head & neck interventions during
the Management of Chronic Spinal Pain. Pain
the session.
Physician 2009; 12: 699-802. ISSN 1533-3159.
• Prithviraj. Stellate ganglion block. Indpain
2006; 20; 2; 12-19.

MCQ
1. The pain mediated through the autonomic 4. Complication of Superficial Trigeminal Nerve
nervous system responds well to Blocks are all except
neuroablative procedures
a. Intravercular injection
a. True
b. Hematoma
b. False
c. Seizures
2. Pain mediated because of somatic structure
involvement is a bit difficult to treat d. Eyeglobe damage
5. Cervical Radiculitis can be treated by all
a. True except
b. False
a. Physical activity modification
3. Fusion of inferior cervical ganglion with the
first and sometimes with second thoracic b. NSAIDS
ganglion is called c. Cervical Epidural Steroid Injection
a. Sphenopalatine ganglion d. Cervical Sympathetic Chain Block
b. Stellate ganglion
c. Cervical Sympathetic Chain
d. Celiac Plexus
5.(c) 4.(c) 3.(b) 2.(a) 1.(a)

Answers

BREAKFAST SESSIONS
33 Acid base physiology
Shrirang Bamne Jigi Divatia

Senior Resident, Professor & Head,
Tata Memorial Hospital, Mumbai. Tata Memorial Hospital, Mumbai.
Key points
Ø Normal acid-base balance depends on the cooperation of at least two vital organ systems: the lungs
and the kidneys.
Ø The principal extracellular buffer system is the carbonic acid/bicarbonate pair.
Ø Disturbances that affect the PaCO2 primarily are called respiratory disturbances, and those that affect
the HCO3-primarily are called metabolic.
Ø Compensation for a respiratory disturbance is metabolic and compensation for a metabolic disturbance
is respiratory.
Ø Hypokalemia tends to perpetuate a metabolic alkalosis, and hyperkalemia a metabolic acidosis.
Ø Increased Anion Gap (AG) metabolic acidosis is due to acids whose anions are not normally measured
by routine electrolyte determinations whereas normal anion gap acidosis is due to abnormalities in
chloride homeostasis.
Ø If a normal AG hyperchloraemic metabolic acidosis is present, the cause can be determined by examining
the urine strong ion difference (SID).
Ø Anion gap is proportional to the plasma albumin concentration, hypoalbuminemia will lower the
baseline anion gap.
Ø Routine administration of sodium bicarbonate to correct the acidemia is not recommended.
Introduction a daily production of approximately 15,000 mmol of

carbon dioxide (CO2) and 50 to 100 mEq of hydrogen
Acid-base homeostasis is defined by the pH of blood
and by the conditions of the acid-base pairs that ions (H +), from the catabolism of carbohydrates,
determine it. Normally, arterial plasma pH is maintained fats and proteins. An appropriate response to this
between 7.35–7.45. The determinants of blood pH acid load is essential as the range of extracellular
can be grouped into two broad categories, respiratory H + concentration compatible with life (150 to 15
and metabolic. Respiratory acid-base disorders are nmol/L and respective pH of 6.8 to 7.8) is fairly
disorders of carbon dioxide (CO2) homeostasis whereas
narrow. Disorders of the acid–base system and the
metabolic acid-base disorders comprise all other
conditions affecting the pH. appropriate management are best understood by
examining the equation for the bicarbonate–carbon
Acid-Base Disorder dioxide buffer system:
Acid-base, electrolyte and metabolic disturbances are H2O + CO2 ↔ H2CO3 ↔ H++ HCO3-
common in medicine. The average individual generates
Acid Base Physiology 322 Jigi Divatia
Indeed, critically ill patients often suffer from compound concentration or pH, the direction of the compensation
acid-base and electrolyte disorders. Successful must be the same as the direction of the primary
evaluation and management of such patients requires disturbance. Thus, consumption of bicarbonate will be
recognition of common patterns (e.g., hypokalemia accompanied by hyperventilation and a consequent
and metabolic alkalosis) and an ability to recognize one reduction in PaCO2.
disorder from another.
A simple acid-base disturbance is considered to consist
Acid-Base Homeostasis of the primary disturbance and its normal compensation.
A complex acid-base disturbance consists of more than
Normal acid-base balance depends on the cooperation one primary disturbance. In order to detect complex
of at least two vital organ systems: the lungs and the acid-base disturbances, one must be familiar with both
kidneys. The gastrointestinal (GI) tract also is involved the direction and magnitude of normal compensation.
in many acid-base disturbances. More than one metabolic disturbance may coexist (e.g.,
Normal Acid-Base Physiology metabolic acidosis and metabolic alkalosis), but only
one respiratory disturbance is possible at a time.
The “normal” range of pH in clinical laboratories is
7.35 to 7.45 pH units, the actual pH in vivo varies Effect of Acidosis on Organ Systems
considerably less. This tight control is maintained by a
Cardiovascular System
complex homeostatic mechanism involving buffers and
the elimination of volatile acid by respiration. • Myocardial suppression, decreased inotropy, hy-
The principal extracellular buffer system is the carbonic potension
acid/bicarbonate pair. The equilibrium relationships of
• Conduction defects, arrhythmias, hypotension
the components of this system are as follows:
• Arterial vasodilation and venous vasoconstric-
H2O+CO2H2CO3 HCO3- + H+
tion, hypotension
From these relationships, the Henderson-Hasselbalch
Oxygen Transport
equation is derived:
• Decreased oxygen hemoglobin affinity
pH = pK + log10/ αCO2*PaCO2
In this equation, αCO2 is the solubility coefficient of • In late course, decreased 2,3 DPG  Change in
CO2 (0.03), and pK is the equilibrium constant for this previously decreased oxyhemoglobin affinity
buffer pair (6.1).
A low pH by itself decreases the affinity of haemoglobin
Rearrangement yields the for oxygen. However, by inhibiting the production of
2,3-DPG, an acidic environment inhibits the activity
Henderson equation: H+ = 24* PaCO2/HCO3- of diphosphoglycerate mutase and promotes a more
It is apparent from this equation that disturbances “normal” glycolytic pathway, thus inhibiting the
in the proton concentration of the extracellular fluid production of 2,3-DPG and favouring the production of
(ECF) (and blood) may be due to disturbances in the ATP; this is used as a homeostatic mechanism. Thus in
numerator, the denominator or both. late stage, low pH increases the affinity of haemoglobin
Disturbances that affect the PaCO2 primarily are called for oxygen.
respiratory disturbances and those that affect the HCO3- The interaction of these two competing actions results
primarily are called metabolic. Acid-base homeostasis
in a useful homeostatic mechanism.
depends on compensation for a primary disturbance.
Compensation for a respiratory disturbance is metabolic Neuromuscular
and compensation for a metabolic disturbance is
respiratory. Furthermore, it is clear from the previous • Respiratory depression
equations that in order to mitigate the change in proton • Decreased sensorium
Metabolic Disorder • Seizures
• Protein wasting • Respiratory depression
• Bone demineralization
Metabolic
• Catecholamines , PTH , aldosterone secretion
• Insulin resistance 1) Hypokalemia
Electrolytes 2) Hypophosphatemia
3) Hypocalcemia
• Hyperkalemia
• Hypercalcemia 4) Impaired enzyme functioning
• Hyperuricemia Simple acid-base disorders
Gastrointestinal
Simple acid-base disorders result in predictable
• Emesis changes both in terms of carbonic acid equilibrium and
Effect of Alkalosis on Organ Systems physiologic compensation. Table 1 below outlines the
observed changes in bicarbonate, PaCO2 and arterial
Cardiovascular System
standard base excess (SBE) seen with simple acid-base
• Increased calcium entry, increased contractility disorders.
Oxygen transport When measured acid-base variables fall outside the
• Increased oxyhemoglobin affinity ranges shown in the table, the acid-base disorder
• In the late stage, increased 2,3 DPG and change in should be considered complex. The table also shows
increased oxyhemoglobin affinity the expected compensatory changes that accompany
Neuromuscular simple acid-base derangements. A failure of normal
compensation leads to the development of a complex
• Increased neuromuscular excitability
acid-base disorder.
• Encephalopathy
Acid-base disorder Primary disturbances compen- Required compensation Duration SBE mmol/L
sation required for
compensa-
tion
Metabolic acidosis Decreased HCO3- Decreased 1.5*HCO3- +8 +/- 2 12-24 hrs < -3
(<22) PaCO2
Metabolic alkalosis Increased HCO3-(>26) Increased 0.7*HCO3- + 21 +/- 2 12-24 hrs >+3
PaCO2
Acute respiratory Increased PaCO2(>45) Increased 1 mmol increase in HCO3- for ev- Within 6 hrs 0
acidosis HCO3- ery 10 mm Hg increase in PaCO2
Chronic respiratory Increased PaCO2(>45) Increased 4 mmol increase in HCO3- for ev- More than 5 0.4*(PaCO2-
acidosis HCO3- ery 10 mm Hg increase in PaCO2 days 40)
Acute respiratory Decreased Decreased 2 mmol decrease in HCO3- for ev- Within 6 hrs 0
alkalosis PaCO2(<35) HCO3- ery 10 mm Hg decrease in PaCO2
Chronic respiratory Decreased Decreased 5 mmol decrease in HCO3- for More than 7 0.4*(PaCO2-
alkalosis PaCO2(<35) HCO3- every 10 mm Hg decrease in days 40)
PaCO2
Table 1. Simple Acid –base disorder
Complex acid-base disorders Individuals with normal ventilatory capacity eliminate
this abnormal acid load through the lungs, thus the
A complex acid-base disorder is diagnosed by first
examining the pH. If the pH is<7.35, at least one type term volatile acid.
of acidosis is present and if the pH is >7.45, at least one The remainder of the daily acid load, about 1 mmol/
type of alkalosis is present. The values of compensatory kg body weight per day, derives from metabolism
changes shown in the above table should be used to
of phosphate- and sulfate-rich protein (yielding
determine if a complex disorder is present.
phosphoric and sulfuric acid).
Examples:
These nonvolatile or fixed acids are buffered, primarily by
• A simple metabolic acidosis will manifest as a extracellular bicarbonate under normal circumstances.
SBE less than 3 mmol/L, a plasma bicarbonate
concentration <22 mmol/L and PaCO2 = 1.5 × bi- The four main mechanisms used in an attempt to
carbonate + 8 or 40 + SBE (either formula has a maintain homeostasis in this setting are as follows:
range of ± 2). If the arterial PaCO2 is outside this
range, a secondary respiratory acid-base disorder • Extracellular buffering primarily via HCO3
is present (respiratory alkalosis if PaCO2 is lower • Intracellular and bone buffering (buffers up to
than expected and respiratory acidosis PaCO2 is 55% to 60% of the acid load)
higher than expected).
• Renal excretion of H+ and regeneration of bicar-
• A simple chronic respiratory acidosis will man-
ifest as a pH <7.35, a PaCO2 >6kPa (45 mmHg). bonate
The plasma bicarbonate concentration should be • Removal of CO2 by alveolar ventilation.
equal to [4*(PaCO2–40) / 10] + 24 and the SBE
should equal 0.4 × (PaCO2 –40). The ranges are In metabolic acidosis, these secreted protons must
again ±2. be buffered in the tubule lumen in order to allow
Metabolic Acidosis elimination of the daily fixed acid load within the
physiologic constraint of the minimum urinary pH. The
Definition And Classification urinary buffers are composed of the filtered sodium
A metabolic acidosis is a process that, if unopposed, salts of the phosphoric acid and ammonia, which is
would cause acidemia (a high hydrogen ion concentration synthesized in the proximal tubule and acidified in
or low pH of the blood) by reducing the extracellular the collecting duct to form ammonium (NH4+). Under
bicarbonate concentration. conditions of acid loading, the normal kidney reabsorbs
all the filtered bicarbonate in the proximal tubule.
The extracellular bicarbonate concentration may be
reduced by either addition of acid and consequent Many factors modify the kidney’s capacity to regulate
consumption of bicarbonate, or by primary loss of acid-base balance. For example, renal ammonia
bicarbonate. genesis is stimulated by acidemia and inhibited by
An appropriate response to this acid load is essential alkalemia except for hypokalemic metabolic alkalosis,
because the range of extracellular H+ concentration and thus participates in a homeostatic feedback loop.
compatible with life (150 to 15 nmol/L and respective Hyperkalemia inhibits and hypokalemia stimulates renal
pH of 6.8 to 7.8) is fairly narrow. ammonia genesis. Hypokalemia further stimulates acid
secretion by activating the Na+-H+ exchanger in the
Disorders of the acid–base system and the appropriate
management are best understood by examining the proximal tubule and the H+/K+-ATPase in the collecting
equation for the bicarbonate–carbon dioxide buffer duct. Finally, aldosterone stimulates both proton and
system: K+ secretion in the collecting duct. For these reasons,
hypokalemia tends to perpetuate a metabolic alkalosis,
H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3- and hyperkalemia a metabolic acidosis.

Metabolic acidosis can be caused by excessive kidneys are functioning normally in a patient with a
production of fixed acid, decreased renal secretion of metabolic acidosis, the urine SID should be negative.
fixed acid or loss of bicarbonate, either through the
If a patient has an increased AG metabolic acidosis,
kidney or through the intestine. The net effect of any of
looking for an osmolar gap might help determine the
these processes is a reduction in the blood bicarbonate
aetiology.
concentration.
The plasma anion gap helps to distinguish among the M Methanol
various causes of metabolic acidosis. (Table 2) U Uraemia
D DKA, alcohol ketosis, starvation
When metabolic acidosis is diagnosed, the anion gap ketosis
(Na+ + K+ – Cl- _ HCO3-) should be calculated. Increased
P Paraldehyde
AG metabolic acidosis is due to acids whose anions
are not normally measured by routine electrolyte I INH
determinations (e.g. lactate, ketones, toxins) whereas L Lactates
normal anion gap acidosis is due to abnormalities in E Ethylene glycol
chloride homeostasis. In the case of an increased AG, S Salicylates
the change in SBE should be equal to the increase in
Table 2. Increased AG metabolic acidosis
the AG from its normal value.
If the change in SBE is larger than the change in the Iron overload can lead to increased anion gap acidosis
AG, a concomitant hyperchloraemic acidosis is also by cellular injury, increasing lactates by circulatory
present. If the AG is increased, the anion should be collapse and proximal renal tubular injury
sought and when possible, its concentration compared Causes of Normal anion gap acidosis
to the change in the AG.
• RTA (type 1,2,4)
Strong ions such as lactate produce a 1:1 decrement
• Diarrhea
in the AG for each mmol/L (mEq/L) increase in their
concentration. When the increase in the AG is larger • Small bowel and pancreatic drainage
than the increase in strong ions, other acids must be
• Parenteral infusion
present.
• IV saline infusion Clinical management
AG is often calculated in all patients routinely to avoid
missing a concealed metabolic acidosis. But alkalemia There are two important pitfalls in the interpretation
can increase the AG by as much as 3–5 mmol/L (mEq/L) of the anion gap.
by altering the charges on plasma proteins. Alkalemia
1) Anion gap is proportional to the plasma albumin
may also induce mild hyperlactatemia by stimulating
concentration, hypoalbuminemia (common in
phosphofructokinase activity. critically ill patients) will lower the “baseline” an-
If a normal AG (hyperchloraemic) metabolic acidosis is ion gap (by approximately 2.5 mmol/L for each g/
present, the cause can be determined by examining the dL decline in the albumin concentration). Thus,
profound hypoalbuminemia may falsely lower
urine strong ion difference (SID). (Strong ions are those
the anion gap, and thus mask a high anion gap
that are present in the dissociated state at physiological
acidosis.
pH). Strong cations include Na+ and K+ and major strong
anions include Cl- . The difference between strong Corrected AG for hypoalbuminemia equals
cations and anions make the strong ion difference AG +2.5*(4.0-albumin levels)
(SID). In conditions of acidosis, the normally functioning 2) Alkalemia increases the anion gap by causing lac-
kidney excretes more Cl- than Na+ and K+. Hence if the tate generation and by titrating plasma buffers,

most notably albumin. Thus, in respiratory alka- In many cases, a metabolic acidosis is a manifestation
losis, the bicarbonate concentration will be low in of an underlying pathology. Routine administration
compensation, and the anion gap may be elevat- of sodium bicarbonate to correct the acidemia is not
ed, giving a false impression of a high anion gap recommended. Identify and treat the underlying cause
metabolic acidosis by inspection of the electro- of metabolic acidosis whenever it is possible
lytes alone.
Causes of lactic acidosis may be due to increased
If bicarbonate is lost e.g., through diarrhea or production or decreased clearance (from liver, kidney).
hydrochloric acid is gained (e.g., renal tubular acidosis Increased production of lactates and decreased
or administration of unbuffered amino acid solutions), clearance in combination is present clinically in most of
the bicarbonate concentration falls with a proportionate the patients. Increased lactate production can occur due
increase in the plasma chloride concentration; thus the to (A) Tissue hypoxia (B) Underlying disease process,
anion gap is unchanged. (C) Drugs and toxins (D) Inborn error of metabolism
If bicarbonate is lost in buffering an organic acid such A) Tissue hypoxemia from
as lactic acid or a ketoacid, the decrement in the
bicarbonate concentration is more or less matched by • shock
an increase in the anion gap. • very severe anemia
• very severe hypoxemia
In post hypocapnic metabolic acidosis, bicarbonate
falls in compensation for a chronic respiratory alkalosis. • carbon monoxide poisoning
When “normal” ventilation is restored, the pH falls until B) Underlying disease process
bicarbonate can be retained, giving the appearance of
a hyperchloremic metabolic acidosis. This shows the • Sepsis
importance of history and observation over time in the • Liver failure
analysis of acid-base status. • Thiamine deficiency
Dilutional hyperchloremic acidosis is seen in patients • Malignancy
who are rapidly resuscitated with large volumes of • Pheochromocytoma
isotonic saline solution. The acidosis traditionally has • Diabetes
been attributed to dilution of blood bicarbonate.
C) Drugs and toxins
Osmolar gap is the difference between the measured
• Ethanol
serum osmolarity and the calculated serum osmolarity.
• Methanol
A gap of more than 10 mOsmol/l is indicative of the • Paracetamol
presence of a toxin that increases osmolarity. Alcohols • Epinephrine
(methanol and ethylene glycol) typically cause (raised)
• Salbutamol
anion gap metabolic acidosis with an increased osmolar
gap. • Propofol
• Nucleoside analogue reverse tran-
Osmolar gap = Measured serum osmolarity– scriptase inhibitors
Calculated serum osmolarity • Biguanides
The formula for calculating the serum osmolarity is • Ethylene glycol
• Salicylate
2 (Na+ + K+) + Glucose (mmol/L) + BUN (mmol/L)
• Nitroprusside
[when glucose and BUN are in mg ,then to convert it to • Isoniazide
mmols, the formula is • Cyanide
2 × Na+ glucose/18 +BUN/2.8 mg/dL] • Xylitol

• Sorbitol Chronic metabolic acidosis (e.g. chronic renal failure)
• Fructose requires therapy to increase the SID (these ions are
“strong” because their ionization state is independent
D) Inborn error of metabolism of pH). Oral sodium bicarbonate therapy is most
• Glucose 6 phosphatase deficiency commonly used. Patients with proximal or Type IV
• Fructose 1,6 diphosphatase deficiency RTA rarely develop life-threatening acidosis, while
• Deficiency of enzymes of oxidative patients with distal RTA may. In addition, distal RTA
phosphorylation may be associated with hypokalemia. Sometimes,
severe response to treatment depends upon cause for
• Pyruvate carboxylase deficiency
metabolic acidosis and degree of underlying disorder
The physiological response to a metabolic acidosis is to causing it. (Table 3)
hyperventilate and reduce PaCO2. This is generally the Metabolic alkalosis
safest way to treat acute metabolic acidosis.
Metabolic alkalosis is a process leading to accumula-
Treatment of acute metabolic acidosis with sodium
tion of extracellular bicarbonate that, if unopposed,
bicarbonate has not been shown to be beneficial and will result in an increase in the plasma pH (alkale-
may be harmful (by increasing intracellular pH, increased mia). It can be caused either by a gain of bicarbonate
activation of phosphofructokinase, more production of or a loss of fixed acid from the ECF.
pyruvate from glycolysis and this in presence of tissue
hypoxemia or inhibitors of oxidative phosphorylation, Patients with intravascular volume depletion, or
diverts the pathway to production of lactates and those who are slow to wean secondary to depressed
bicarbonate and also causes hypocalcemia), so if at all respiratory drive (resulting in compensatory hyper-
soda bicarbonate required is for pH of 7.00 and below carbia) may have a metabolic alkalosis.
Sodium bicarbonate by infusion rather than bolus • Seizures and respiratory depression may occur
injection induces less hypercarbia and may be safer. when arterial pH is more than 7.6.
Non-bicarbonate buffers such as tris-hydroxy methyl • Serious cardiac arrhythmias may be precipitated
aminomethane (TRIS or THAM) have occasionally been by the alkalosis itself or by electrolyte disturbanc-
used for severe metabolic acidosis. Tris-hydroxymethyl es.
aminomethane (THAM) is a commercially available • When severe alterations in mental status or re-
weak alkali rarely used as a clinical therapy because of spiratory function occur, control of the patient’s
concerns about side-effects that include hyperkalemia, airway is likely to be advisable.
hypoglycemia, extravasation-related necrosis and
neonatal hepatic necrosis. Metabolic alkalosis can be sub-divided into two broad
categories
In acute lung injury, THAM has been demonstrated to
be an effective buffer in ventilated patients as it is not • Chloride-responsive
associated with an increased CO2 load and is capable • Chloride-unresponsive
of ameliorating some of the haemodynamic effects
of hypercapnia but it is unclear whether buffering of Diagnosis
hypercapnic acidosis in acute lung injury patients is A history and physical exam will reveal most causes
of any benefit. As THAM did not increase PaCO2 , it of metabolic alkalosis. Chronic metabolic alkalosis is
was recommended in patients with high level mixed unusual and is usually the result of mineralocorticoid
acidosis. However there is no evidence to show that excess or chronic diuretic use. Most cases of acute
administration of THAM in patients with lactic acidosis metabolic alkalosis are due to loss of acid from the
improves outcome. Severe metabolic acidosis may GI tract (vomiting, or gastric drainage), to volume
require treatment with renal replacement therapy.

DISTAL RTA PROXIMAL RTA TYPE 4 RTA

Etiology Sjogren syndrome, lupus, sickle Fanconi syndrome, Diabetes, NSAID,
cell anemia, hyperthyroidism, hereditary fructose ACE inhibitors,
hyperparathyroidism, intolerance, Wilson tubulointerstitial
s disease, MM , nephritis, obstructive
chronic active hepatitis, primary acetazolamide, uropathy , k+ sparing
biliary cirrhosis, diuretics, adrenal
Amyloidosis , hypocalcemia insufficiency, heparin,
analgesic nephropathy, hereditary
aldosterone deficiency ,
form of deafness, vitamin D deficiency,
resistance
ifosfamide,
rejection of transplanted kidney,
obstructive uropathy, medullary outdated tetracyclines
cystic renal disease,
chronic urinary tract infection,
idiopathic
Pathogenesis Systemic disease by abnormal Impaired proximal tubular Aldosterone resistance,
calcium deposition at distal tubule or bicarbonate absorption or deficiency
as a part of autoimmune process DT
affected, impaired distal tubule H+
secretion
Urine pH >5.3-5.5 variable <5.3-5.5
Plasma <10 meq/l 11-20 meq/l >15 meq/l

HCO3-
Plasma K+ Hypokalemia, gets corrected with Hypokalemia, worsened in Hyperkalemia
alkali therapy alkali therapy associated
with bicarbonaturia
UAG positive variable positive
Associated Nephrocalcinosis Fanconi syndrome, rickets, CKD

conditions osteomalacia
Growth Present Autosomal recessive form No
retardation of Fanconi syndrome
associated with growth
retardation
Treatment Sodium bicarbonate, potassium Higher doses of bicarbonate treat the underlying
citrate, sodium citrate therapy required(associated cause for
bicarbonaturia) hypoaldosteronism,
diuretics, sodium
bicarbonate,
fludrocortisones, sodium
polystyrene sulfonate
Table 3. Types of Renal Tubular Acidosis

contraction or to the administration of non-chloride • There is a severe deficiency of intracellular cations
containing sodium salts (e.g. acetate, citrate, lactate). such as magnesium or potassium. This decreases
intracellular Cl- and secondarily total body Cl-.
Often metabolic alkalosis patients have underlying post-
hypercarbic states and the alkalaemia is aggravated Causes are:
by salt-depleted hypovolemia. Except when part of • Diuretic use (or abuse) is one of the most common
a complex (mixed) disorder, metabolic alkalosis is cause of metabolic alkalosis.
manifest by alkalaemia (arterial pH >7.45), a high
bicarbonate (HCO3- >26 mmol/L), hypercarbia (PaCO2 • Gastrointestinal losses of Cl- may be due to
>5.3 kPa (40 mm Hg)) and an increased SBE (>3 mmol/L). vomiting, gastric drainage, and rarely, chloride
wasting diarrhoea (villous adenoma).
The urine Cl- concentration can be used to help narrow
• Administration of non-chloride sodium salts can
the differential diagnosis.
occur with massive blood transfusions (sodium
Chloride-responsive metabolic alkalosis, Cl- losses citrate), parenteral nutrition (sodium acetate),
in excess of Na+ increase the SID. The urine Cl - plasma volume expanders (acetate or citrate),
concentration is usually <10 mmol/L. GI loss, post- Ringer’s solution (sodium lactate) or overzealous
use of sodium bicarbonate.
diuretic use and post-hypercarbic states are chloride-
responsive. • For several hours (or longer) following recovery
from chronic, renal compensated hypercarbia,
Chloride-unresponsive alkalosis results in a urine metabolic alkalosis (chloride-responsive) will
Cl - concentration >20 mmol/L and is caused by persist.
mineralocorticoid excess or active diuretic use.
• Mineralocorticoid excess: primary
Determine if a respiratory disorder is also present. The hyperaldosteronism (Conn’s syndrome),
expected arterial PaCO2 in response to a metabolic secondary hyperaldosteronism, Cushing’s
alkalosis can be determined either using the bicarbonate syndrome, Liddle’s syndrome, Bartter’s syndrome,
concentration or the SBE. Measured PaCO2 >2 mmHg exogenous corticosteroids, and excessive
more than expected indicates a concomitant respiratory liquorice intake.
acidosis while measured PaCO2 <2 mmHg less than Clinical management
expected indicates a respiratory alkalosis.
Treat the underlying disorder. This is especially true
PaCO2 = (0.7 × HCO3-) + 21 for the large number of chronic conditions associated
PaCO2 = 40 + (0.6 × SBE) with metabolic alkalosis. When it’s due to volume
contraction related, iv fluids are to be used. Parenteral
The normal response of the kidney to alkalosis is nutrition formulae should be adjusted to maximize
to retain chloride, thereby narrowing the SID and chloride and minimize citrate and acetate.
increasing water dissociation leading to more hydrogen
ion generation to counteract the alkalosis. Chloride-responsive alkalosis
There are four mechanisms causing metabolic alkalosis: • For patients with diuretic-induced metabolic
alkalosis, 0.45% saline is effective for reversing
• Severe depletion of free water inducing a parallel free water deficit and treating alkalosis. Also
increase in Na+ and Cl-. Since the concentration of consider expanding the circulating volume and
Na+ > Cl-, the difference between them increases. stopping diuretics.
• Cl- is lost from the GI tract or urine (diuretic use or • For patients with volume overload and metabolic
abuse) in excess of Na+. alkalosis, KCl can be administered along with
loop diuretics. Alternatively, K+ sparing diuretics
• Na+ is administered in excess of Cl-. (which will also spare Cl-) can be used.

• Acetazolamide (250–500 mg bid), inhibits In general, each acute 10 mm Hg change in the PaCO2
carbonic anhydrase and can induce excretion of causes a 0.08 change in the arterial pH.
Na+ in excess of Cl- and thus reduce the SID.
In respiratory acid–base disorders, the kidneys
• For patients with renal failure and at risk of compensate for changes in the PaCO2 by increasing the
volume overload, dilute (0.1N) HCl acid can be plasma bicarbonate (HCO3−) in respiratory acidosis, or
administered through a central venous line. Each decreasing the plasma HCO3− in respiratory alkalosis.
litre of this solution contains 100 mmol of Cl-, and
Acute respiratory acid–base disorders result in small
it is advisable to recheck the acid-base status after
each litre. However, it is important to remember changes in the HCO 3− concentration, and cellular
this treatment has potential risks and may not be buffering predominates. Chronic renal compensation
licensed in many jurisdictions. occurs during days to weeks, and results in a larger
change in plasma HCO3−
• Due attention should be paid towards
correcting electrolyte changes occurring along Compensatory change in HCO3− is associated with a
with or secondary to alkalosis (hypokalemia, shift in the pH back toward normal. A normal pH is not
hypomagnesaemia). achieved by compensation alone and overcompensation
• In patients with ongoing gastric losses, does not occur. Therefore, a mixed respiratory and
H2- blockers or proton pump inhibitors may prove metabolic disorder is present if the pH is normal and the
a useful adjunct to therapy. PaCO2 is altered. For example, a pH of 7.4 with a PaCO2
of 60 mm Hg means that, in addition to the respiratory
Chloride–unresponsive alkalosis acidosis, a metabolic alkalosis is present that has moved
These are often more difficult to treat. For neoplastic the pH back to normal. Mixed acid–base disorders do
diseases such hyperaldosteronism, or Cushing’s not include the renal HCO3− compensation that occurs
syndrome, spironolactone may be helpful but surgery for acute and chronic respiratory acid–base disorder.
is usually required. ACE inhibitors such as captopril Evaluation of respiratory acid–base disorders can be
are often effective for secondary hyperaldosteronism. relatively straightforward in patients with an isolated
Triamterene may be tried in cases of Bartter or Liddle acute primary respiratory acidosis or alkalosis, such as
syndromes though with varying success. occurs in a patient with an acute asthma exacerbation
Outcome or in an otherwise healthy patient with anxiety-induced
hyperventilation, or more difficult when superimposed
Metabolic alkalosis is usually mild and not life- metabolic acid–base disorders are present in a critically
threatening. However, when it is severe or develops ill patient. Further complicating evaluation is the change
quickly, the condition can produce seizures and that occurs in the serum HCO3− in acute and chronic
respiratory depression. Although case-reports of respiratory acidosis and alkalosis
mortality from acute severe metabolic alkalosis exist,
no large studies have explored the relationship between Respiratory acidosis results from hypercapnia induced
metabolic alkalosis and outcome in critically ill patients. by alveolar hypoventilation and includes disorders in any
component of the ventilator mechanism, such as the
Respiratory acid-base disorder central or peripheral nervous system, neuromuscular
junction, respiratory muscles, chest wall, pleura, upper
Respiratory acid–base disorders are commonly seen
airway, or lungs.
in the critically ill pts, and can occur independently or
coexist with metabolic acid–base disorders .Respiratory Causes for respiratory acidosis
acidosis is characterized by an elevated PaCO2 and
decreased pH, and respiratory alkalosis by a decreased CNS
PaCO2 and elevated pH. The PaCO2 in healthy adults • Metabolic alkalosis
is 35 to 45 mm Hg and the normal pH is 7.35 to 7.45. • Central apnoea , hypopnoea e.g sedatives
Fig 1 : Evaluation of metabolic alkalosis

• Medullary stroke • Upper airway obstruction
• Hypothyroidism • Abdominal compartment syndrome
• Central hypoventilation syndrome • Metabolic acidosis
Anterior Horn Cell • Sepsis
• Polio Treatment is aimed at improving alveolar ventilation

• ALS, motor neuron disease and includes bronchodilators for patients with
• Cervical spinal cord injury asthma and chronic obstructive pulmonary disease
(COPD), bi-level positive airway pressure, mechanical
Motor neuron disease ventilation (used with caution in patients with chronic
• GBS respiratory acidosis with an elevated serum HCO3− as
• Tick paralysis, rapid correction can cause a life-threatening metabolic
• Diphtheria alkalosis), reversal of drug effects, treatment of
• Fish toxin pulmonary edema and addressing neuromuscular
diseases. NaHCO3− is not recommended in respiratory
• CIPN
acidosis as it may worsen hypercapnia and pulmonary
NM Junction edema, or cause a metabolic alkalosis. Small doses
• Myasthenia gravis of sodium bicarbonate can be considered in cases of
severe acidosis (pH<7.1) with intractable hypercapnia.
• Eaton lambert myasthenic syndrome
• Botulism Respiratory alkalosis can be associated with a normal
• OP poisoning or elevated alveolar-arterial oxygen gradient (P[A-a]
O2) gradient, abbreviated A-a gradient. In mechanically
Muscle
ventilated patients, minute ventilation should be
• Myopathy decreased by decreasing the respiratory rate and/
• Drug, steroids or tidal volume. In psychogenic hyperventilation,
• Hypothyroidism reassurance and anxiolytics can be used. In patients at
• Polymyositis high altitudes, acetazolamide can be used to induce a
• Dermatomyositis metabolic acidosis to compensate for the respiratory
• Muscle dystrophy alkalosis
• Diaphragmatic dysfunction Causes for respiratory alkalosis
Alveoli and airways • Central Hyperventilation-psychogenic,fever, pain,
• Pulmonary oedema encephalitis/meningitis, raised ICP
• Pulmonary fibrosis • Mechanical ventilator
• COPD, asthma, cystic fibrosis • Pregnancy
• Hyperthyroidism
Excessive work of breathing
• Drugs-salicylate, progesterone, catecholamines
• Scoliosis
• Hypoxia induced-severe anemia, high altitude
• Obesity

MCQ
1. Organs involved in acid-base homeostasis are 4. Henderson Equation is H+ = _____ *PaCO2 /
all except HCO3
a. Lungs a. 12
b. Liver b. 24
c. Kidneys c. 6
d. GI tract d. 20
2. Compensation for metabolic acidosis is 5. Serum Osmolarity is calculated using
following variables except
a. Decreased HCO3
b. Increased Paco2 a. BUN
c. Decreased Paco2 b. Chloride
d. Increased HCO3 c. Glucose
3. Causes of high anion gap acidosis are all d. Sodium
except
a. Methanol
b. Diarrhea
c. Lactates
d. Diabetic ketoacidosis
5. (b) 4. (b) 3. (b) 2. (c) 1.(b)

Answers

33
34 ANESTHESIA MACHINE
ANESTHESIA MACHINE
Professor (Sr. Scale)

Professor Pankaj Kundra
Pankaj Kundra
JIPMER
Jipmer,
Puducherry
Puducherry.
Key points
¾ Modern anesthesia machines are still based on the design characteristics of the olden days Boyle machine,
except for incorporation of electrical and monitoring components along with the data collecting system.
¾ The pressures zones within the anesthesia workstation: A high-pressure, an intermediate-pressure and a
low-pressure circuit.
¾ Safety measures are incorporated in to all the three pressure system of the machine.
¾ The newer work station is more compact and all the connections are internalized with less likelihood of
misconnections, disconnections or kinking.
Over the years, the anesthesia delivery system box.

has evolved from a simple pneumatic device to a
(ii) Pressure gauges on oxygen cylinders and fine-
complex workstation with pneumatics and electronics
adjustment reducing valves. These produce a
incorporated. The transition from ether inhalers and
manageable breathing system pressure. It had a
chloroform soaked handkerchiefs to more sophisticated
spirit flame to warm these and prevent obstruction
anesthesia delivery equipment occurred gradually, with
of gas flow from ice.
incremental advances supplanting older methods. The
efforts of those developing anesthetic apparatus have (iii) Flowmeters to control gas flow rate and adjust
been directed towards increasing safety, improving proportions of gas delivered.
accuracy and improving the ergonomic aspects of
machine design and adding to sophistication but the (iv) A metal and glass vaporizer bottle for ether.
result has also been an increase in the complexity of (v) A breathing system comprising a Cattlin bag, three
the apparatus. The most common type of anesthetic way stopcock and facemask.
machine in use in the developed world is the continuous-
flow anesthetic machine, which is designed to provide Modifications (e.g. dry bobbin flowmeters in 1933, pin-
an accurate and continuous supply of medical gases, index system in 1952) were driven by a consideration
mixed with an accurate concentration of anesthetic for greater safety.
vapor and deliver this to the patient at a safe pressure The older machines had only pneumatic components.
and flow. Modern machines incorporate a ventilator,
suction unit and patient-monitoring devices. The modern anesthetic machine has pneumatic and
electrical components with electronics incorporated.
Basic design of an anesthetic machine The basic component systems of the new anesthesia
Pressurised gases are supplied by cylinders or workstations include what was formerly referred to as
pipelines to the anesthetic machine which controls the anesthesia machine proper (the pressure regulating
flow of gases before passing them through a vaporiser and gas mixing components), the vaporizers, the
and delivering the resulting mixture to the patient via anesthesia breathing circuit, the ventilator, the
the breathing circuit. scavenging system, and respiratory and physiologic
monitoring systems.
The early Boyle’s machine had five elements which are
still present in all modern machines. The pressures within the anesthesia workstation can
be divided into three circuits: a high-pressure, an
(i) A high-pressure supply of gases. It housed two intermediate-pressure, and a low-pressure circuit. The
oxygen and two nitrous oxide cylinders in a wooden
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high pressure circuit includes the cylinders and the (Schrader) sockets at the wall, which are gas specific.
cylinder primary pressure regulators. For oxygen, the Flexible pipelines, which are color coded connect the
pressure range of the high-pressure circuit extends terminal outlet to the anesthetic machine. The pipeline
from a high of 2200 psig to 45 psig, which is the inlet fittings are gas specific Diameter Index Safety
regulated cylinder pressure. For nitrous oxide in the system threaded body fittings. This is a threaded, non
high-pressure circuit, pressures range from a high interchangeable connection specific for each gas, and
of 750 psig in the cylinder to a low of 45 psig. The minimizes the risk of misconnection. A check valve
intermediate-pressure circuit begins at the regulated prevents reverse flow of gases from the machine to
cylinder supply sources at a pressure of 45 psig and the pipeline or the atmosphere.
also includes the pipeline sources at 50 to 55 psig
and extends from here to the flow control valves. Cylinder supply
Some machines incorporate a second stage pressure Cylinders usually serve as a backup, should the central
regulator to decrease the pipeline supply pressures to gas supply fail. They are mounted on yokes attached
even lower levels such as 14 psig or 26 psig. Finally, to the machine. A valve block screws into the open
the low pressure circuit extends from the flow control end of the cylinder. It is marked with the gas chemical
valves to the common gas outlet and includes the flow symbol, tare weight, pressure at the last hydraulic test
tubes, vaporizer manifold, vaporizers and the one way and a serial number. Turning a longitudinal spindle,
check valve between the vaporizer and the common set within a gland screwed into the block, opens the
gas outlet in some machines (some Datex-Ohmeda valve. Leaks are prevented by the compression of a
machines). nylon ring around the spindle. A safety outlet is fitted
Parts between the valve block and cylinder neck. This melts
at relatively low temperatures to allow gas to escape in
Anesthetic machines have six basic subsystems case of fire and minimize the risk of explosion.
(i) Gas supplies: pipelines and cylinders; Additional safety features of cylinders include:
(ii) Gas flow measurement and control (flowmeters); (i) Molybdenum steel alloy construction. This
is stronger and lighter than its carbon steel
(iii) Vaporizers;
predecessor.
(iv) Gas delivery: breathing system and ventilator;
(ii) Color-coding for each gas or vapor.
(v) Scavenging;
(iii) Pin-index system. This prevents the accidental
(vi) Monitoring. connection of a cylinder to the wrong machine yoke.
The cylinder valve block bears an arrangement of
Box shaped sections of welded steel or aluminum holes, into which fit pins protruding from the yoke.
provide a rigid metal framework mounted on wheels
with antistatic tyres and brakes. Antistatic measures (iv) Bodok seals (bonded disk). These are non-
improve flowmeter performance and, where flammable combustible neoprene washers with aluminium
vapors are used, reduce the risk of ignition. edges, interposed between the cylinder head and
yoke to provide a gas-tight seal.
A typical modern workstation has open architecture with
easily cleaned work-surfaces, and drawers, shelves Each gas entering the machine from a cylinder flows
and rails to accommodate customized accessories. through a filter, one-way check valve and primary
Machines are mains powered and a rechargeable regulator. Bourdon gauges are fitted adjacent to each
battery provides up to 60 min of backup. yoke and pipeline connection. These are calibrated,
labelled and color-coded for each gas service.
Gas supplies
Pressure regulators
Piped gas supply
Modern machines have several primary and secondary
This is the primary gas source for the anesthesia regulators. Primary regulators reduce potentially
machine. Gases are drawn from a cylinder manifold, dangerous high cylinder pressures to the machine
vacuum insulated evaporator or oxygen concentrator. working pressure of 45 psig. Secondary regulators
They are fed into a labelled and color coded level out gas delivery. Machine working pressures
distribution network, which terminates in self closing may vary by up to 20%, for example during periods
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of peak hospital demand. Pressure fluctuations can may have an illuminated flowmeter bank. Some have
cause parallel changes in (and damage to) flowmeter the ability for ultra-low flow anesthesia at rates of <
performance. Secondary regulators set below the 1 litre/min. Auxiliary oxygen flowmeters are featured
anticipated decrease in pressure will make the on larger units; they are separate from the back bar
emergent pressure more uniform. In order to minimize flowmeters and common gas outlet.
connections and potential leaks, the NIST connection,
cylinder yoke, primary regulator and pressure gauges
Hypoxic mixture prevention devices
are housed in a single cast brass block. Oxygen and nitrous oxide supply sources existed as
independent entities in older models of anesthesia
Gas flow measurement and control
machines, and they were not pneumatically or
Flow control valves govern the transition from the mechanically interfaced. Therefore, any oxygen
high to the low-pressure system. These reduce the pressure failure had the potential to lead to the
pressure of 45 – 55 psig to just above atmospheric as delivery of a hypoxic mixture. The 2000 ASTM F 1850-
gas enters the flowmeter block. Flow rate is indicated 00 standard states that, “The anesthesia gas supply
by a flowmeter. Conventional flowmeters (rotameters) service shall be designed so that whenever oxygen
consist of a needle valve, valve seat and a conically supply pressure is reduced to below the manufacturer
tapered and calibrated gas sight tube containing a specified minimum, the delivered oxygen concentration
bobbin. Flowmeters may be mechanical or electronic. shall not decrease below 19% at the common gas
In a mechanical system, gas entering the sight tube lifts outlet.
the bobbin in proportion to flow. The bobbin floats and
Contemporary anesthesia machines have a number of
rotates without touching the sides, giving an accurate
safety devices that act together in a cascade manner
indication of gas flow. Flow is read from the top of the
to minimize the risk of delivery of a hypoxic gas mixture
bobbin. Features reducing inaccuracy to within 2%
as oxygen pressure decreases.
include:
They have interlocked oxygen and nitrous oxide flow
(i) Sight tubes for each gas are individually calibrated
controls. This prevents inadvertent delivery of a hypoxic
at 20°C and 1 atm; they are non-interchangeable.
inspired gas mixture, as the ratio of oxygen to nitrous
(ii) Tubes have different lengths and diameters, and oxide concentrations never decreases below 0.25.
may have a pin-index system at each end. This can be achieved by a mechanical, pneumatic or
electronic mechanisms.
(iii) Tubes are leak-proof because of neoprene washers
(O-rings) at both ends of the flowmeter block. 1. Pneumatic and electronic alarm devices: Many older
anesthesia machines have a pneumatic alarm device
(iv) The tubes have an antistatic coating on their inner
that sounds a warning when the oxygen supply
and outer surfaces. This prevents the bobbin from
pressure decreases to a predetermined threshold
sticking to the tube wall.
value such as 30 psig. Electronic alarm devices are
(v) The bobbin is visible throughout the length of the now used in the newer machines.
tube and has vanes to improve its rotation in the
2. Oxygen failure cut off (Fail safe) valves: A fail-safe valve
gas flow.
is present in the gas line supplying each of the flow
Modern oxygen flowmeters are arranged to feed meters except oxygen. Controlled by oxygen supply
downstream of other gases in the event of a proximal pressure, the valve shuts off or proportionally decreases
leak. The oxygen control knob is larger, more the supply pressure of all other gases (nitrous oxide,
protruding and differently shaped compared with those air, carbon dioxide, helium, nitrogen) as the oxygen
of air or nitrous oxide. Some modern units may use supply pressure decreases. Unfortunately, the term
microprocessors to control gas flow; flow is indicated “fail safe” is a misnomer. Machines that either is not
electronically by a numerical display or ‘virtual flow equipped with a flow proportioning system or whose
tubes’ (e.g. Drager Fabius GS; Datex-Ohmeda S/5 system which may be disabled by the user can deliver
Anesthesia Delivery Unit). These allow easy identifica- a hypoxic mixture under normal working conditions.
tion of gas flows in a darkened theatre and the export On such a system, the oxygen flow control valve can
of electronic data to an information system. In the event be closed intentionally or accidentally. Normal oxygen
of an electrical failure, there is a pneumatic backup, pressure will keep the other gas lines open so that a
which continues the delivery of fresh gas. Other units hypoxic mixture can result.
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Many Datex-Ohmeda machines are equipped with valve opens. Nitrous oxide flows freely to the nitrous
a fail-safe valve known as the pressure sensor shut- oxide flow control valve. In Fig.1B, the oxygen supply
off valve (Fig. 1). This valve operates in a threshold pressure is less than 20 psig, and the force of the valve
manner and is either open or closed. Oxygen supply return spring completely closes the valve. Nitrous oxide
pressure opens the valve, and the valve return spring flow stops at the closed fail-safe valve, and it does not
closes the valve. Fig. 1 shows a nitrous oxide pres- advance to the nitrous oxide flow control valve.
sure sensor shut-off valve with a threshold pressure of
20 psig. In Fig. 1A, an oxygen supply pressure greater
than 20 psig is exerted on the mobile diaphragm. This
pressure moves the piston and pin upward and the
Figure 1. Pressure sensor shut-off valve. The valve is open in A because the oxygen supply pressure is greater than the
threshold value of 20 psig. The valve is closed in B because of inadequate oxygen pressure.
North American Dräger uses a different fail-safe valve right panel is 0 psig. The spring is expanded and forces
known as the oxygen failure protection device (OFPD) the nozzle against the seat, thereby preventing flow
to interface the oxygen pressure with that of other through the device. Finally, the center panel shows an
gases, such as nitrous oxide or other inert gases. In intermediate oxygen pressure of 25 psig. The force of
contrast to Datex-Ohmeda’s oxygen pressure sensor the spring partially closes the valve. The nitrous oxide
shut-off valve, the OFPD is based on a proportioning pressure delivered to the flow control valve is 25 psig.
principle rather than a threshold principle. The There is a continuum of intermediate configurations
pressure of all gases controlled by the OFPD will between the extremes (0 to 50 psig) of oxygen supply
decrease proportionally with the oxygen pressure. The pressure. These intermediate valve configurations are
OFPD consists of a seat nozzle assembly connected responsible for the proportional nature of the OFPD.
to a spring-loaded piston ( Fig.2). The oxygen supply An important concept to be understood with these
pressure in the left panel of Fig.2 is 50 psig. This particular fail-safe devices is that the Datex-Ohmeda
pressure pushes the piston upward, which forces the pressure sensor shut-off valve is threshold in nature
nozzle away from the valve seat. Nitrous oxide alone or (all or nothing) whereas the Dräger OFPD is a variable-
combined with other gases advances toward the flow flow type proportioning system.
control valve at 50 psig. The oxygen pressure in the
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Anesthesia Machine
Machine 339
271 Pankaj
Pankaj Kundra
Kundra
Figure 2. An oxygen failure protection device that responds proportionally to changes in oxygen supply pressure.
concentration at the common gas outlet is between

3. Second-stage oxygen pressure regulator
23% and 25%, depending on the manufacturer.
Most contemporary Datex-Ohmeda workstations have
a second-stage oxygen pressure regulator set at a
Datex-Ohmeda Link-25 Proportion-Limiting Control
specific value ranging from 12 to 19 psig. Output from
System
the oxygen flow meter is constant when the oxygen Conventional Datex-Ohmeda machines use the Link
supply pressure exceeds the threshold (minimal) value. 25 system. The heart of the system is mechanical
The pressure sensor shut-off valve of Datex-Ohmeda integration of the nitrous oxide and oxygen flow
is set at a higher threshold value (20 to 30 psig) to control valves. It allows independent adjustment of
ensure that oxygen is the last gas flowing if oxygen either valve, yet automatically intercedes to maintain a
pressure failure occurs. minimum 25% oxygen concentration with a maximum
nitrous oxide–oxygen flow ratio of 3 : 1. The Link-25
4. Safety features in flowmeters
automatically increases oxygen flow to prevent delivery
Contemporary flow control valve assemblies have of a hypoxic mixture.
numerous safety features. The oxygen flow control knob
Fig. 3 illustrates the Datex-Ohmeda Link-25 system.
is physically distinguishable from other gas knobs. It is
The nitrous oxide and oxygen flow control valves are
distinctively fluted, projects beyond the control knobs of
identical. A 14-tooth sprocket is attached to the nitrous
the other gases, and is larger in diameter than the flow
oxide flow control valve and a 28-tooth sprocket to the
control knobs of other gases. All knobs are color-coded
oxygen flow control valve. A chain physically links the
for the appropriate gas, and the chemical formula or
sprockets. When the nitrous oxide flow control valve is
name of the gas is permanently marked on each. Flow
turned through two revolutions, or 28 teeth, the oxygen
control knobs are recessed or protected with a shield
flow control valve will revolve once because of the 2 : 1
or barrier to minimize inadvertent change from a preset
gear ratio. The final 3 : 1 flow ratio results because
position. If a single gas has two flow tubes, the tubes
the nitrous oxide flow control valve is supplied by
are arranged in series and controlled by a single flow
approximately 26 psig whereas the oxygen flow control
control valve.
valve is supplied by 14 psig. Thus, the combination of
5. Proportioning systems the mechanical and pneumatic aspects of the system
yields the final oxygen concentration. The Datex-
Manufacturers equip anesthesia workstations with
Ohmeda Link-25 proportioning system can be thought
proportioning systems in an attempt to prevent the
of as a system that increases oxygen flow when
creation and delivery of a hypoxic mixture. Nitrous
necessary to prevent delivery of a fresh gas mixture
oxide and oxygen are interfaced mechanically or pneu-
with an oxygen concentration of less than 25%.
matically (or both ways) so that the minimum oxygen
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Anesthesia Machine 340 Pankaj Kundra
Dräger Fabius GS and Narkomed 6000 series. The
ORMC and the S-ORC are pneumatic oxygen–nitrous
oxide interlock systems designed to maintain a fresh
gas oxygen concentration of at least 25% ± 3%. The
ORMC and S-ORC limit nitrous oxide flow to prevent
delivery of a hypoxic mixture. This is unlike the Datex-
Ohmeda Link-25, which actively increases oxygen
flow.
A schematic of the ORMC is shown in Fig. 4. It is
composed of an oxygen chamber, a nitrous oxide
chamber, and a nitrous oxide slave control valve. All are
interconnected by a mobile horizontal shaft. Pneumatic
input into the device is from the oxygen and nitrous
oxide flow meters. These flow meters are unique in
that they have specific resistors located downstream
from the flow control valves. These resistors create
Figure 3. Ohmeda Link-25 Proportion-Limiting Control
backpressure directed to the oxygen and nitrous oxide
system.
chambers. The value of the oxygen flow tube resistor
North American Drager oxygen ratio monitor con-troller/ is three to four times that of the nitrous oxide flow
sensitive oxygen ratio controller system tube resistor, and the relative value of these resistors
determines the value of the controlled fresh gas oxygen
North American Dräger’s proportioning system, the
concentration. Backpressure in the oxygen and nitrous
Oxygen Ratio Monitor Controller (ORMC), is used on
oxide chambers pushes against rubber diaphragms
the North American Dräger Narkomed 2A, 2B, 3, and
attached to the mobile horizontal shaft. Movement
4 series. An equivalent system known as the Sensitive
of the shaft regulates the nitrous oxide slave control
Oxygen Ratio Controller (S-ORC) is used on some
valve, which feeds the nitrous oxide flow control valve.
newer Dräger anesthesia workstations such as the
Figure 4. North American Dräger Oxygen Ratio Monitor Controller.
RACE 2019
If the oxygen pressure is proportionally higher than the Most modern anesthesia workstations are equipped
nitrous oxide pressure, the nitrous oxide slave control with an auxiliary O2 flow meter. This is used for
valve opens wider to allow more nitrous oxide to flow. connection to supplemental oxygen tubing to a nasal
As the nitrous oxide flow is increased manually, the cannula or facemask. It must be recognized that there
nitrous oxide pressure forces the shaft toward the is no O2 analyzer in use with such an arrangement and
oxygen chamber. The valve opening becomes more that the user is assuming that the auxiliary flow meter
restrictive and limits flow of nitrous oxide to the flow is delivering O2. However, a misconnection of gas sup-
meter. ply lines to the machine could result in the delivery of
hypoxic gas from this flow meter.
Fig. 4 illustrates the action of a single ORMC/
SORC under different sets of circumstances. The Vaporizers
backpressure exerted on the oxygen diaphragm, in
the upper configuration, is greater than that exerted Modern vaporizers have several safety advantages
on the nitrous oxide diaphragm. This causes the over their predecessors: (i) an interlock to isolate
horizontal shaft to move to the left, thereby opening vaporizers not in use; (ii) a clear indication of liquid level;
the nitrous oxide slave control valve. Nitrous oxide is (iii) a non-spill reservoir with up to 180°of allowable tilt;
then able to proceed to its flow control valve and out (iv) a keyed-filler or pour-fill systems prevent filling with
through the flow meter. In the bottom configuration, the an incorrect volatile agent and minimize leaks; and (v)
nitrous oxide slave control valve is closed because of an increased wick capacity.
inadequate oxygen backpressure. Continuous flow machines use variable bypass
To summarize, in contrast to the Datex-Ohmeda Link- vaporizers, which may be mechanically or electronically
25 system, which actively increases oxygen flow to controlled. Each is designed and calibrated for a specific
maintain a fresh gas oxygen concentration greater anesthetic vapor. The heated blended vaporizer was
than 25%, the Dräger ORMC and S-ORC are systems designed for desflurane. Recent innovations have
that limit nitrous oxide flow to prevent delivery of a included injection of volatile agent into the fresh
fresh gas mixture with an oxygen concentration of less gas stream, at a rate calculated (by computer) to
than 25%. produce the desired concentration. Datex-Ohmeda
has replaced conventional vaporizers with Aladin
Proportioning systems are not foolproof. Workstations vaporizer cassettes in their S/5 Anesthesia Delivery
equipped with proportioning systems can still deliver Unit. The cassettes are more lightweight (2–3 kg), are
a hypoxic mixture under certain conditions: Wrong virtually service-free and have no restrictions for tilting.
supply gas, defective pneumatics or mechanics, leaks Integrated electronic fresh gas flow measurement of
downstream, inert gas administration and by dilution varying gas mixtures enable the unit to dispense more
of inspired oxygen concentration by volatile inhaled accurately a dialed concentration, compared with
anesthetics (especially high concentration of less traditional vaporizers.
potent volatile agents).
Safety features on or downstream of the back bar
Oxygen analyzer include
Many anesthesia delivery systems (e.g., Drager (i) Oxygen failure warning device. This alarm should
Fabius GS; Drager Medical, Telsford, PA; Datascope be powered solely by the oxygen supply pres-
Anestar) incorporate a galvanic fuel cell oxygen sensor sure in machine piping and activated when that
located near the inspiratory unidirectional valve. Other pressure decreases below 30 psig. In case of
workstations (e.g., GE Aisys, GE ADU, Drager Apollo) complete oxygen failure, ventilation with room air
use a multigas analyzer (sampling gas from the vicinity is facilitated.
of the Y-piece) that incorporates a paramagnetic
oxygen analyzer. These analyzers actually measure (ii) Spring-loaded non-return valve. This prevents
the oxygen tension (PO2), although the readout is in surges in back pressure from damaging vaporizers
volumes percent.They are calibrated to read 21% O2 and flowmeters.
(ideally at 1 atmosphere pressure) and are not deceived (iii) Pressure relief valve. This is set at 30–40 kPa to
by the presence of other gases. On contemporary prevent back pressure from damaging vaporizers
workstations, the oxygen analyzer is automatically and flowmeters.
enabled whenever the machine is capable of delivering
an anesthetic gas mixture. (iv) Emergency oxygen flush, which is supplied from
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Ramachandra AnesthesiaContinuing
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the high pressure circuit upstream of the flowme- fresh gas flow, small leaks or patient compliance. They
ters and back bar, and provides flow between 35 are marketed as being suitable for a broader range of
and 75 litre/min. patients from neonates receiving 20 ml tidal volumes
to patients with ARDS.
All gas mixtures (from back bar or oxygen flush) exit the
machine through a 22 mm male OD/15 mm female ID Scavenging
conically tapered outlet. Modern machines have mini
Modern scavenging has four components for collecting,
Schrader gas sockets for air and oxygen. These may
transferring, receiving and disposal of waste gases
be used to power Venturi systems for a bronchoscope
from the breathing circuit:
or Sanders injector.
(i) The collecting system comprises a gas-tight shroud
Gas delivery—breathing systems and ventilators enclosing the APL valve of the breathing circuit (or
Breathing systems: expiratory port of the ventilator) utilizing 30 mm
conical connections. Some systems (Ohmeda
Either circle systems or T piece configurations are AGS) have an over-pressure relief valve which
used. In modern workstations, circle systems come blows at 1 kPa.
readily assembled and are, in all but the most compact
versions, integrated into the unit. A single housing (ii) The transfer system comprises wide bore tubing
comprises the carbon dioxide absorber, adjustable leading from the collecting systems to the receiving
pressure limiting (APL) valve, reservoir bag, circuit system.
pressure gauge and switch to select manual or (iii) The receiving system comprises a reservoir, air
mechanical ventilation mode. A switch may allow the brake, flow indicator and filter. A closed system
absorber to be removed from the circle. The Anmedic requires a dumping valve to prevent excessive
Q-mix (Anmedic) circle system uses a shunt valve negative pressure developing (0.5 cm water at 30
to adjust the proportion of exhaled gas that passes litre/min gas flow) and a pressure relief valve to
through the absorber canister. In this way, end-tidal prevent excessive positive pressure (5 cm H2O at
carbon dioxide concentration may be manipu-lated. 30 litre/min gas flow).
Some systems use a circulating pump or fans, in
(iv) Disposal systems are active and high flow. The sub-
place of unidirectional valves, to reduce resistance to
atmospheric pressure required is generated by an
gas flow. Modern breathing systems strive to have a
exhauster unit, which uses a fan to generate a low
minimal number of connections in order to reduce the
pressure, high volume system capable of removing
potential for leaks. Parts in contact with patient gas are
75 litre/ min at a peak flow of 130 litre/min.
autoclavable (except the fuel cell oxygen analyser) and
latex-free. Newer machines may have an electronically Monitoring
adjustable and calibrated APL valve.
Some anesthetic machines conduct an automatic self-
Ventilators: test on start-up, e.g. Primus (Drager). The test results
are recorded and displayed. This is not intended to
Ventilators may be integrated with the anaes-
replace the pre-use check by an anesthetist.
thetic machine or configured later. These are often
electronically controlled and pneumatically powered. Anesthesia units must incorporate certain minimum
The autoclavable bellows are often suitable for adult equipment-related monitors. North American
and pediatric use. Traditionally, anesthetic machine standards specify airway pressure, volume of expired
ventilators have had a minimal number of controls. gas and inspired oxygen concentration. Monitors for
The anesthetist could vary minute volume by setting other anesthetic gas concentrations and physiological
tidal volume and ventilatory frequency directly or by parameters may be incorporated into the machine.
adjusting inspiratory time, inspiratory flow rate and
Machines are configured with respect to their monitors
the ratio of inspiratory to expiratory time. The newest
in one of two ways. Modular systems require stand-
models resemble critical care ventilators in their
alone physiological monitors to be added separately.
capabilities. These may perform self-test upon start-up
Preconfigured systems are manufacturer-assembled,
(using dual processor technology), volume or pressure
with an integrated display and prioritized alarms.
controlled ventilation modes, assisted spontaneous
These may have automated anesthetic record keeping
ventilation and electronically adjustable PEEP.
(AARK) for anesthesia delivery and physiological
Sophisticated spirometry compensates for changes in
parameters.
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Limitations of conventional anesthesia machines and keyed filling ports and a new mechanism to prevent
the solutions to these in modern machines the escape of liquid through the vent hole or into
the bypass chamber when the vaporizer is tilted
a) Refers to conventional machines and b) is the (Drager Vapor 2000). The mechanism is active
solution in the modern machines. when the vaporizer is placed in the “T” position for
removal or transport.
1. a) Presence of many external connections: This
leads to disconnection or misconnection, kinking or 4. a) Medical gas consumption: Many facilities do
obstruction. not have piped medical gases and must rely on
cylinders. Others leave their backup cylinders open
b) Systems internalize connections and reduce
(incorrectly), and these can be drained when wall
the likelihood of misconnections, disconenctions or
supplies dip below the cylinder regulator pressure.
kinking. This is accomplished with internal modular
Conventional ventilators are designed to consume
(Aestiva/5) or manifold (Julian) components.
an amount of drive gas roughly equivalent to the
2. a) Limited protection against barotraumas minute volume. Or they partially entrain room air
and absence of advanced ventilation features: through a Venturi.
Conventional machines incorporate pressure
b) Incorporating a piston instead of a bellow (Fabius
limiters in the mechanical breathing circuit, but
GS and 6400) reduces medical gas consumption.
some require a manual preset to maintain pressures
below clinical extremes. Others will only generate 5. a) Inaccurate delivery of tidal volume and system
an alarm when the preset value is exceeded. resistance: It is possible for the user to improperly
Patients could be at risk from activating the oxygen set the inspiratory flow or time such that the
flush during inspiration, adding 500-800 ml/sec to standing bellows of the ventilator fails to descent
the tidal volume. Pressure sensors are not located completely. A potentially large percentage of the
close to the patient’s trachea in many machines. bellows volume is lost into the breathing circuit,
Ventilators of some conventional machines do not secondary to compliance (e.g., 5ml/cm H2O) and
offer PCV, SIMV etc, so there could be stacking of compression (around 3%). Leaks and sampled
a breath on a patient breathing spontaneously. gas flow further reduce desired tidal volume (Vt).
Alternatively, the contribution of fresh gas to the
b) Newer machines offer better protection against
inspiratory phase might significantly increase
barotrauma by isolating FGF from the Vt (Fresh
tidal volume and airway pressure, similar to, but
gas decoupling) and ventilators provide several
of less magnitude than the actuation of oxygen
modes.
flush. Com-bined, these discrepancies significantly
3. a) Vaporizer risks: Variable bypass vaporizers are alter Vt. Furthermore, the spirometer will falsely
either fixed-mounted or removable. If tilted, agent report Vt, because it includes the breathing hose
could enter the bypass chamber, vaporize and compliance. During volume controlled ventilation
thus deliver an overdose of agent to the circuit. in neonates or children, these discrepancies may
Inadequate volatile agent could be delivered if constitute an overwhelming percentage of the
there is a leak around the mounting O rings. desired Vt. Conventional ventilators require a
two-step, mechanical/electrical conversion from
b) The ADU uniquely features electronic control
manual ventilation; human error can leave the
and measurement of vaporization and eliminates
patient apneic.
the need for multiple vaporizers. Color coded,
magnetically labelled cassettes store each agent. b) Newer machines have several methods for accurate
Volatile agent delivery is reported to the information delivery of Vt: i) Fresh gas decoupling implies that
management system. Furthermore, the ADU uses fresh gas is not delivered to the patient during
these data to make compensatory adjustments in inspiration. Practically, it means that FGF does
N2O to maintain the desired FIO2 and to reduce not contribute to Vt. It is accomplished in a variety
the ventilator’s drive gas to maintain desired tidal of ways, depending on the machine. ii) A second
volume. The cassettes have overfill protection, are method of accurate delivery of Vt is compliance
automatically leak tested during checkout and have compensation, to replace volume lost to the
a check valve to prevent liquid from entering the breathing hoses and/or circuit. The ADU, Fabius,
bypass circuit. New “conventional” vaporizers offer Julian and 6400 all measure the total compliance
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20192016
Education
(with attached hoses) during checkout and use 2. Information management system (IMS): The newer
this data to incrementally adjust piston or bellows workstations integrate physiological and respiratory
excursion, according to generated airway pressure monitoring data with the digital fresh gas and
(Paw). iii) Leaks are measured and reported iv) volatile agent flow data and all are sent to an IMS.
Electronic settings of the new ventilators should
reduce previous user errors with incorrect settings 3. Dependence on electricity: All new systems have
and v) one step activation of CMV in the Aestiva/5 battery backup and some warn of impending power
or ADU might prevent previous failures to initiate loss, suggesting a switch to manual ventilation. In
CMV; others require an additional confirmatory the event of dead battery, all can deliver oxygen,
step. iv) The ADU incorporates a specialized “D-lite” but not measure it electronically. ADU cannot
flow and pressure transducer into the circle system deliver volatile agent; Julian terminates all FGF,
at the level of the Y-connector. This is a better requiring the user to open a needle valve for
location for measuring exhaled tidal volume, and oxygen, which could still flow through the vaporizer,
allows monitoring of airway gas composition and ADU terminates delivery of N2O but allows air
pressure with a single adapter and provides the substitution; Fabius GS and ADU provide a single
ability to assess both inspiratory and expiratory gas flow meter to estimate combined FGF; all will lose
flow and therefore the generation of complete flow- PEEP.
volume spirometry. v) The inspiratory and expiratory New workstation designs: new problems
unidirectional valves have been relocated from a
horizontal to a vertical position to reduce breathing Some anesthesia workstations (e.g., Drager Narkomed
system resistance. 6400, Apollo, Fabius GS; Datascope Anestar) use
fresh gas decoupling (FGD) to ensure that changes
6. a) Automated checkout: Conventional machines in fresh gas flow (FGF) do not affect the desired (set)
are manually inspected, often inaccurately tidal volume delivered to the patient’s airway. With
according to the FDA recommended checkout FGD, during the inspiratory phase of IPPV, only gas
procedures. Clinicians often fail to check their from the piston chamber (Drager) or bellows (Anestar)
equipment thoroughly, or often not successful is delivered to the inspiratory limb of the circle system
in detecting machine faults, or don’t check their because the decoupling valve closes to divert fresh
machines at all. gas into the reservoir bag. The FGD circuits differ from
b) A multitude of surveillance alarms and automated the traditional circle system in function and therefore
checkout procedures are present in newer machines may be associated with different problems, including
but are associated with increasing complexity, detection of an air entraining leak in the breathing
since the user cannot determine a problem by system and failure of the FGD valve resulting in failure
conventional checkout methods. Despite these to ventilate.
automated checkout procedures, not every fault The new workstations incorporate many more
may be detected. Most important is the immediate electronic systems than their predecessors. Not sur-
availability of back up ventilation equipment prisingly, these systems sometimes fail and render the
1. Monitoring: Perhaps the greatest advance in the workstation nonfunctional. The user must understand
design of modern anesthesia gas delivery systems how to proceed in the event of a power loss. In addition,
has been the incorporation of integrated monitoring the electrical systems are sometimes the cause of a
and prioritized alarm systems such that certain basic fire or smoke condition.
monitors and alarms are automatically enabled Anesthesia machine obsolescence
whenever the system is capable of delivering an
anesthetic gas mixture or is performing mechanical Concerned that older anesthesia delivery systems may
ventilation. Aspects of the patient’s breathing be more likely to be associated with critical incidents,
system that can be monitored routinely include the American Society of Anesthesiologists Committee
pressure, volume, capnography, respiratory gas on Equipment and Facilities developed guidelines for
composition, and gas flows. When applied correctly determining anesthesia machine obso-lescence. The
(i.e., with appropriate monitors, alarm threshold following is a summary of the guidelines that were
limits, and alarms enabled and functioning), such published in June 2004.
monitoring should detect most, but not all, delivery
system problems
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Absolute criteria for a machine to be considered 2. Problems with maintenance.

obsolete include: 3. Potential for human error
1. Lack of essential safety features such as an oxygen/ 4. Inability to meet practice needs such as accepting
nitrous oxide proportioning system; oxygen failure vaporizers for newer agents; ability to deliver low,
safety device; oxygen supply failure alarm; vaporizer fresh gas flows (FGFs); and a ventilator that is not
interlock device; and non interchangeable, gas- capable of safely ventilating the lungs of the target
specific pin indexed and diameter-indexed safety patient population.
systems for gas supplies. Preuse machine check
2. Presence of unacceptable features such as The ASA Committee on Equipment and Facilities,
measured flow vaporizers (e.g., Copper Kettle); in conjunction with the major delivery system
more than one flow control knob for a single gas manufacturers and other interested groups, has
delivered to the common gas outlet; vaporizer with developed ‘‘Recommendations for Pre-Anesthesia
a dial such that the concentration increases when Checkout Procedures (2008)’’ that would have
the dial is turned clockwise; and connections in the applicability to all anesthesia workstations and
scavenging system that are the same (15 or 22mm that would be reliably performed. The 2008
diameter) as in the breathing system. recommendations comprise 15 separate items to be
3. Adequate maintenance no longer possible such checked at the beginning of each day or whenever a
that the machine cannot be serviced with ac- machine is moved or serviced or the vaporizers are
ceptable replacement parts so that it performs as changed (Table 1). Eight of these items should be
originally designed. checked before each procedure. Some of these steps
Relative criteria for a machine to be considered may be included in the automated checkout process on
obsolete include: many workstations. It is believed that these checklists
would require less than 5 minutes at the beginning of
1. Lack of certain safety features such as a manual/ the day and less than 2 minutes between cases. The
automatic bag/ventilator selector switch; a fluted 2008 ASA guidelines have been endorsed by the Food
oxygen flow-control knob that is larger than the other and Drug Administration as educational information. It
gas flow-control knobs; an oxygen flush control that is essential that all anesthesia caregivers be trained to
is protected from unintentional activation; an anti perform the appropriate checkout procedures correctly.
disconnection device at the common gas outlet;
and an airway pressure alarm.
Steps Item to be completed Responsible party
Verify auxiliary oxygen cylinder and manual ventilation device (Ambu Bag) are available and
Item 1 Provider and technician
functioning
Item 2 Verify patient suction is adequate to clear the airway Provider and technician
Item 3 Turn on anesthesia delivery system and confirm that AC power is available. Provider or technician
Item 4 Verify availability of required monitors, including alarms Provider or technician
Verify that pressure is adequate on the spare oxygen cylinder mounted on the anesthesia
Item 5 Provider and technician
machine
Item 6 Verify that the piped gas pressures are ≥50 psig Provider and technician
Item 7 Verify that vaporizers are adequately filled and, if applicable, that the filler ports are tightly closed Provider or technician
Verify that there are no leaks in the gas supply lines between the flow meters and the common
Item 8 Provider or technician
gas outlet
Item 9 Test scavenging system function Provider or technician
Item 10 Calibrate, or verify calibration of, the oxygen monitor and check the low-oxygen alarm Provider or technician
Item 11 Verify carbon dioxide absorbent is fresh and not exhausted Provider or technician
Item 12 Perform breathing system pressure and leak testing Provider and technician
Item 13 Verify that gas flows properly through the breathing circuit dur-ing both inspiration and exhalation Provider and technician
Item 14 Document completion of checkout procedures Provider and technician
Confirm ventilator settings and evaluate readiness to deliver anesthesia care (Anesthesia Time
Item 15 Provider
Out)
Table 1. Recommended essential steps in a preanesthesia checkout procedure
To be completed daily, or after a machine is moved or vaporizers changed
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PankajKundra
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Eight of these Items (2,4,7,11,12,13,14 and 15) should
References
again be checked between cases.
1. Miller’s Anesthesia by Ronald D Miller. 7th edition.
The future Churchill Livingstone.
The future development of anesthesia machines would
2. Understanding anesthesia equipment. Jerry A
involve closed loop control using feedback from the
Dorsch and Susan E Dorsch. 5th edition. Lippincott
depth of anesthesia monitoring and respiratory gas
Williams & Wilkins.
monitoring to automatically adjust the gas flows and
anesthetic vapor concentration. Further development 3. Ward’s anesthetic equipment by Andrew J Davey
could involve making machines more compact like the and Ali. 5th edition. Elsevier Sauders.
size of a laptop or notebook using cable less monitors.
4. Sinclair CM, Thadsad MK, Barker I. Modern
Already, researchers have developed several closed
anesthetic machines CEACCP 2006;6(2):75-78.
loop systems, but they are used for intrave¬nous
anesthesia (“McSleepy”). Similar developments could 5. Micahel A Olympio. Modern anesthesia ma-chines
come for inhalational anesthesia as well. offer new safety features. www.apsf.org/resource_
center/newsletter/2003/summer/machines.htm
Conclusion
6. Guidelines for determining anesthesia
The evolution of the modern anesthetic machine has
machine obsolescence: American Society of
been driven by safety standards. Even as computer-
Anesthesiologists. 2004. www.asahq.org/
controlled systems have become more common,
publicationsand-services/machineobsolescence.
anesthetists should be familiar with the basic concepts
pdf.
that underlie the subsystems of the modern anesthetic
machine. A thorough knowledge combined with pre 7. Eisenkraft JB. Hazards of the anesthesia
use check of this important piece of equipment is workstation. ASA 2009 refresher course lectures.
essential. Adverse outcomes resulting from anesthesia Volume 37, Chapter 4, Pg 37-55.
delivery systems are usually complex in origin and
involve specific errors, failures, and sequences of 8. ASA Committee on Equipment and Facilities Work
events. An educated and vigilant anesthesia caregiver Product. Recommendations for Pre-Anesthesia
is the ultimate patient monitor; his or her timely and Checkout Procedures, 2008. www.asahq.org/
appropriate intervention can often prevent an adverse clinical/finalcheckoutdesignguidelines.
outcome. Ultimately, the anesthesia machine is only as 9. Hemmerling TM. Automated anesthesia. Curr Opin
safe as the anesthesiologist using it. in Anaesthesiology 2009;22:757-763.
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Education
MCQ
1. Safety features of cylinders does not include 4. Safety features on or downstream of the back
bar does not include
a. Color-coding
b. It has a Pin-index system a. ORMC
c. Made up of carbon steel b. Spring-loaded non-return valve
d. It also has bonded disk made up of c. Pressure relief valve
neoprene d. Oxygen flush
2. What are the features responsible for 5. False about Aladin vaporizer
maintaining accuracy in flowmeters?
a. Seen in Datex-Ohmeda machines
a. Rotameters for each gas are
individually calibrated b. Cassettes are more light weight
b. Tubes may have a pin-index system at c. It has restrictions for tilting

each end d. Integrated with electronic fresh gas
c. Tubes are leak-proof because of flow to dispense more accurately than
neoprene washers(O-rings) at both traditional vaporizers.
ends
d. All of the above
3. False about Oxygen failure protection device
(OFPD)
a. Used in North American

Drägermachines
b. It is a fail-safe valve
c. It works based on threshold principle
d. Thepressure of other gases
willdecrease proportionally with the
oxygen pressure.
5.(c) 4.(a) 3.(c) 2.(d) 1.(c)

Answers

SNAP SESSIONS
35 GASTRIC ULTRASOUND
Professor, Ekta Rai

Christian Medical College,
Vellore
Introduction Indications
Aspiration of gastric contents can lead to serious • Lack of adherence to fasting instructions
perioperative complications associated with significant • Emergency/urgent procedure
morbidity and mortality. In particular, aspiration of
• Miscommunication
solid particulate matter, large volumes or fluid with
low pH carries high morbidity. To minimize aspiration • Unreliable / unclear fasting history:
risk, various anaesthesia related interventions are • Altered sensorium
recommended. Current preventive strategies rely • Language barrier
mainly on recommended fasting periods for elective • Cognitive dysfunction
surgery, i.e., NPO protocol. However, underlying medical
• Potential delay in gastric emptying
conditions that slow gastric emptying can predispose
patients to greater amount of gastric content at the • Pregnancy/labour
time of anesthetic induction despite appropriate fasting • Diabetes
intervals. Even fasting status assessment depends on • Severe liver or kidney dysfunction
accurate history alone. • Neuromuscular disorders
Gastric ultrasound is a recently described non-invasive • Trauma patients
bedside point-of-care tool that quantifies gastric
Acquisition (How to Scan?)
contents, and gives an estimation of aspiration risk. It
can help determine the nature of the content (empty, • Abdominal settings
clear fluid, thick fluid/solid) and when clear fluid is • Transducer:
present, its volume can be estimated.
• Adults: curved array low-frequency (2-5 mHz)
Frame to follow for Gastric USG • Small children(<40 kg): linear high-frequency
(5-12 mHz)
I-Indication
• Scan the epigastrium in a sagittal plane
A-Acquisition
• Sweep the transducer from the left to the right
I –Interpretation
subcostal margins
M-Medical decision making
• Identify the gastric antrum
Indications • Patient position:
Main objective of gastric ultrasound (POCUS) is • First Supine (An examination performed solely in
• To assess gastric contents when NPO status is the supine position is considered incomplete as
unknown or uncertain in the immediate pre- it underestimates the amount of gastric
anesthetic or sedation period. content. Failure to visualize gastric content
in the supine position does not guarantee an
• A&E-airway management. empty stomach (Fig1)

Gastric Ultrasound 352 Ekta Rai
followed by The gastric antrum

• Right Lateral Decubitus (RLD)- gastric content • Is the most amenable to sonographic examination
is expected to gravitate to the antrum (Fig 2) • Consistent shape and consistently located in
epigastric region
• Occasionally, a semi-sitting position is used
• Accurately reflects the content of the entire
should the patient not able to turn to right
stomach. It lies superficially
lateral decubitus
• Least amount of air that can block ultrasound
• Interpret only after scanning both positions beams
• Hollow viscus with a prominent multi-layer wall
• Between the liver (anteriorly) and the pancreas
(posteriorly)
• Important landmarks (Fig 3 & Fig 4)
• Left lobe of the liver
• Pancreas
• Aorta
• Inferior vena cava
• Superior mesenteric artery and vein
Fig 1: Sagital scan in supine position
Fig 2: Sagittal scan in RLD position
Applied Anatomy
Stomach has 3 anatomical parts-
• Fundus Fig 3: Landmarks- Gross anatomy
• Body
• Antrum & pylorus

Fig 4: Landmarks- USG anatomy

Sonoanatomy
Stomach has five layers (outside to inside) Fig 5 & Fig 6
• Serosa (thin, hyperechoic)
• Muscularis propria (hypoechoic, usually the thickest
gastric wall layer)
• Submucosa (hyperechoic)
• Muscularis mucosae (hypoechoic)
• Mucosal/lumen interface (thin hyperechoic line) Fig 6: Relation to other structures
Ao-Aorta; R-Rectus Muscle; A-Antrum;Sma-Superior
mesenteric artery;D-deudonum;L-liver;P-pancreas
Interpretation
Based on
• Content, Stomach wall thickness
• CSA-Cross sectional area
Empty Stomach
• Antral Wall-Thick with muscularis propriae
• Content- None/Small amount of hyopechoiec
substance
• Antral Stage-Flat and collapsed(Bull’s Eye)
Clear Fluid Intake (Fig 7)
• Antral Wall-Thin
Fig 5: Axial Scan Showing Antrum and Pylorus • Content- Hypoechoic
RM-Rectus Muscle; Py-Pylorus; A-Antrum; • Antral Stage-Round and distended
P-Pancreas; A-Aorta

Fig 7: Clear fluid intake

Fig 8: Solid intake
Milk/Suspension Intake
Grading and Association with aspiration of gastric
• Antral Wall-Thin content
• Content- Hyperechoic
• Antral Stage-Round and distended
Solid Intake (Fig 8) Grade Volume anticipated Aspiration
Risk
• Antral Wall-Thin 0 Minimal Low
• Content- Hyperechoic; Heterogenous; particulate
mixed with air 1 < 1.5 ml/kg; including the Low
• Antral Stage-Round and distended gastric secretions
2 Clear Fluid visible in both High Risk
position >1/5 ml/kg ; excluding
the gastric secretions

Based on Cross sectional area Limitations of gastric ultrasound

The cross-sectional area of the antrum (CSA) has a linear • Gastric ultrasound findings may be inaccurate in
correlation with the gastric volume. subjects with abnormal underlying gastric anatomy.
For example,
To measure the CSA:
• previous gastric resection or bypass
• Position-RLD • gastric band in situ
• Identify the antrum at the level of the aorta • previous fundoplication
• Freeze the antrum image in between the peristaltic • large hiatus hernia
contractions. Trace the full thickness of gastric wall.
(Fig 9) Special scenerios should need special consideration
• Use a predictive model to assess the gastric volume • Pregnancy
• Morbid Obesity
Further Reading
• An de Putte P, Perlas A. Ultrasound assessment of

gastric content and volume. Br.J. Anaesth. 2014
Jul. 113(1): 12-22. http://www.ncbi.nlm.nih.gov/
pubmed/24893784
• Benhamou D. Ultrasound assessment of gastric
contents in the perioperative period: why is this
not part of our daily practice? Br. J. Anaesth. 2015
Apr;114(4):545-8. http://www.ncbi.nlm.nih.gov/
pubmed/25354945
• Perlas A, Van de Putte P, Van Houwe P, Chan VW. I-AIM
framework for point-of-care gastric ultrasound. Br.J
Fig 9: Determining CSA of stomach Anaesth. 2016 Jan;116(1):7 11. http://www.ncbi.
nlm.nih.gov/pubmed/25951832

MCQ
1. Interpretation of gastric ultrasound is based 4. A patient with following characteristics on
on all of the following except gastric ultrasound qualitative examination-
clear fluid, volume <1.5ml/kg - is risk
a. Content
stratified as ____ to aspiration risk
b. Stomach wall thickness
a. Low risk
c. Cross sectional area
b. High risk
d. Position of Gastric tube
c. Additional information necessary to
2. Following are characteristics of clear fluid risk stratify
intake in gastric ultrasound except
d. No risk of aspiration
a. Antral Wall-Thin
5. Which of the following is the thickest gastric
b. Hypoechoic contents wall layer in the sonographic assessment of
c. Antral Stage-Round and distended the stomach
d. Hyperechoic contents a. serosa
3. Following are points to differentiate between b. Muscularispropria
stomach and colon in an USG except c. Submucosa
a. Colon is usually located caudad to d. Muscularis mucosae
the stomach and its wall is thinner and
not-so-well defined
b. In an empty or low content state, the
internal folds of the gastric wall can be
appreciated, but not with the colon
c. The colon and other bowel
consistently have a “hazy” appearance
which represents the air content
most of the time , the antrum has air
content mostly after a recent solid
meal.
d. Persistalisis is clearly visible in colon
than stomach
5.(b) 4.(a) 3.(d) 2.(d) 1.(d)

Answers

36 DIAPHRAGM SPARING BLOCKS IN SHOULDER SURGERY
Professor, Venkatesh S
SRIHER,
Chennai
Among orthopedic procedures, shoulder surgery results are innervated by the suprascapular, upper and lower
in the most intense postoperative pain. Interscalene subscapular (C5–C6), and axillary nerves. The clinical
brachial plexus blocks (ISBs) is the current standard aim of regional anesthesia or analgesia is to deliver
of postoperative analgesia after shoulder procedures. local anesthetic to some or all of these key nerves that
But the most common adverse effect after ISB remains contribute to pain after shoulder surgery. The specific
the occurrence of ipsilateral phrenic nerve block. nerves to be targeted will depend in part on the surgical
ISB results in a 100% incidence of ipsilateral phrenic approach that is used. This traditionally has been
nerve block, which can result in about 27% decrease achieved by performing an interscalene block, which
in forced vital capacity (FVC) and forced expiratory targets the C5 and C6 roots of the brachial plexus in the
volume at 1 second. Although well tolerated by healthy interscalene region. However, conventional interscalene
subjects, hemidiaphragmatic paresis (HDP) becomes a block is associated with several complications, the most
prohibitive risk for patients with pulmonary pathology, common of which is phrenic nerve palsy with ensuing
who may be unable to withstand the 30% reduction hemidiaphragmatic paresis, and this has driven the
in FVC. Paradoxically, these are the very patients who development of modifications to the interscalene
would benefit most from peripheral nerve blocks, as block as well as alternative techniques that target the
systemic opioids will further compromise oxygenation peripheral sensory supply to the shoulder at sites distal
and ventilation. In this article, we will review the to the C5 and C6 roots.
reason for hemidiaphragmatic paresis due to phrenic
nerve palsy following ISB and the regional nerve block
options available for postoperative analgesia in patients
following shoulder surgery.
Anatomy of nerve supply to shoulder joint
Shoulder joint has a complex innervation. Cutaneous
innervation is provided by the axillary, suprascapular
nerve, and supraclavicular nerves (of the cervical
plexus). Bony and capsular components are innervated
by the suprascapular, axillary, lateral pectoral,
musculocutaneous, and long thoracic nerves. The
Fig 1: Nerve supply to shoulder
suprascapular nerve provides up to 70% of the
innervation to the glenohumeral joint, with the axillary Relavant anatomy of the Phrenic Nerve
nerve supplying the majority of the remaining joint
The anatomy of the phrenic nerve is the key for
capsule as shown in the figure 1. Sensory contributions
understanding the basis of phrenic nerve palsy. The
to the muscles of the shoulder comprise the following:
phrenic nerve originates primarily from the fourth
the ventral rami of the third and fourth cervical nerves
cervical ventral ramus but also receives contributions
to the trapezius muscle, the pectoral nerves to the
from third and fifth ventral rami, as well as the cervical
pectoral muscles, the dorsal scapular nerve to the
sympathetic ganglia or thoracic sympathetic plexus.
levator scapulae and rhomboid muscles, and the axillary
This small nerve forms at the upper lateral border of
nerve to the deltoid muscle. The rotator cuff muscles
Diaphragm Sparing Blocks in Shoulder Surgery 358 Venkatesh S
the anterior scalene muscle and descends obliquely anesthetic blockade of the accessory nerve also may
across the anterior surface of the muscle toward its lead to diaphragmatic paresis.
medial border. The phrenic nerve lies deep to the
Clinical implications of phrenic nerve palsy
prevertebral fascia here and remains posterior to the
sternocleidomastoid muscle, the inferior belly of the Phrenic nerve palsy leading to hemidiaphragmatic
omohyoid, the internal jugular vein, the dorsal scapular paresis can be a temporary or persistent phenomenon
and transverse cervical arteries, and the thoracic duct after interscalene block. Transient phrenic nerve palsy
on the left. The phrenic nerve courses in close proximity is caused by local anesthetic spreading directly to the
to the brachial plexus, initially lying 18 to 20 mm medial phrenic nerve and its contributing nerves (including
to the C5 nerve root at the level of the cricoid cartilage the accessory phrenic nerve) or proximally to the roots
but diverging an additional 3 mm further away for every of the phrenic nerve. The duration of phrenic nerve
centimeter that it descends over the anterior scalene palsy is determined by the duration of local anesthetic
muscle as shown in the figure 2. effect, which in turn is related primarily to the type and
mass of local anesthetic administered. The incidence
of transient phrenic nerve palsy is virtually 100% after
landmark and paresthesia-guided interscalene block
techniques that use a large-volume injection of 20 ml
or greater. Despite this, the vast majority of patients in
clinical trials of interscalene block exhibit few symptoms
and require no specific treatment. Thus, transient
phrenic nerve palsy appears to have little clinical
significance in terms of both objective (respiratory
support) and subjective (dyspnea) features in otherwise
healthy patients. But it may be clinically significant in
patients with pulmonary impairment in whom this
regional technique as a sole anesthetic technique will
avoid the complications of endotracheal anesthesia.
There is also a lack of studies formally examining
clinical predictors of symptomatic phrenic nerve palsy
Fig 2: Cadaveric image showing the proximity of after interscalene block, and thus it remains difficult to
phrenic nerve to brachial plexus determine which patients, healthy or otherwise, will
benefit most from avoidance of phrenic nerve palsy.
As it approaches the root of the neck, the phrenic It therefore falls to the individual anesthesiologist to
nerve usually lies between the subclavian artery assess the likely impact of phrenic nerve palsy in any
and vein, before coursing medially in front of the given patient undergoing shoulder surgery and to
internal thoracic artery. An accessory phrenic nerve select the appropriate regional anesthetic technique
is present in 60 to 75% of individuals and provides an accordingly.
independent contribution to the phrenic nerve. The
fibers of the accessory phrenic nerve arise primarily The phrenic nerve palsy can also be a permanent
from C5 and run within the nerve to subclavius, the complication. The possible causes explained are
ansa cervicalis, or the nerve to sternohyoid. These fibers • Nerve damage can be due to direct needle
then emerge from any one of these nerves to form the trauma or intraneural injection of the local
accessory phrenic nerve, which then joins the phrenic anesthetic
nerve at a variable location along its course. Isolated
damage to the accessory phrenic nerve is associated • Inflammatory scarring due to local anesthetic
with diaphragmatic dysfunction, and similarly, local toxicity

• Co-existing cervical spine stenosis or pressure Strategies to Reduce Phrenic Nerve Palsy in Regional
ischemia resulting from high volumes of local Anesthesia of the Shoulder
anesthetic injected within the tight confines of
The incidence of transient phrenic nerve palsy can be
the interscalene sheath
decreased by reducing the dose of local anesthetic
It must be noted that these causes of persistent phrenic reaching these neural structures. This can be achieved
nerve palsy differ from those implicated in transient by modifying the local anesthetic dose (volume
phrenic nerve palsy. and concentration), injection site and technique in
interscalene block, or by modifying the location of local
Physiologic Effects of Phrenic Nerve Palsy
anesthetic injection, and by using a different regional
The diaphragm is the most important inspiratory anesthetic technique altogether. Ultrasound has been
muscle, accounting for 75% of the increase in lung instrumental in the development of these modifications:
volume during quiet inspiration; intercostal, scalene, the increased accuracy of local anesthetic deposition
and sternocleidomastoid muscles contribute the allows the use of lower doses, and direct visualization
remaining 25%. There is little crossover innervation increases the range of available sites for injection.
of the right and left hemidiaphragms, and each can
Modifications of Interscalene Block
contract independently of the other in the event of
unilateral phrenic nerve palsy. In the presence of • Local Anesthetic Volume: There is a clear
diaphragmatic paresis, inspiration is achieved largely by relationship between the volume of local
contraction of intercostal and accessory muscles and anesthetic injected during interscalene block
expansion of the rib cage. Pleural pressure is reduced, and the occurrence of phrenic nerve palsy.
which leads to air intake and expansion of intrathoracic This is likely to be related to the greater extent
volume. However, this reduction in pleural pressure of spread that occurs with larger volumes.
during inspiration also causes the paralyzed diaphragm An injection around the C5–C6 nerve roots
to move cephalad and the abdominal muscles inward. with volumes of 20 ml or greater inevitably
Consequently, there is reduced lung ventilation on the produces phrenic nerve palsy, regardless of
affected side, particularly of the lower lobe. In healthy localization technique. When an ultrasound-
individuals, however, tidal volumes remain unchanged guided technique is used, a volume of 10 ml
due to a greater contribution from the rib cage. In reduces the incidence of phrenic nerve palsy
higher-risk patient groups, hypoxia and dyspnea may to as low as 60%, whereas a volume of 5 ml
ensue and require treatment by sitting the patient
reduces it still further to between 27 and 45%,
upright and administering supplemental oxygen
without compromising analgesic efficacy up to
therapy or, in severe cases, instituting noninvasive or
24 hours postoperatively.
invasive ventilatory support to augment tidal volumes.
Subjectively, dyspnea is the cardinal symptom of • Local Anesthetic Concentration: Several studies
phrenic nerve palsy after interscalene block. However, have shown that reducing local anesthetic
just as phrenic nerve palsy does not always result in concentration independent of volume, thus
dyspnea, dyspnea may also be experienced in the reducing the dose of drug delivered, also
absence of phrenic nerve palsy. Although up to 40% of produces a significant decrease in the incidence
patients complain of dyspnea after interscalene block or of phrenic nerve palsy and an improvement in
supraclavicular block, only one third to three quarters pulmonary function. Halving the concentration
of these patients have objective evidence of phrenic of bupivacaine from 0.5% to 0.25% reduced
nerve palsy. Patients who are obese are more likely to the incidence of phrenic nerve palsy from
experience dyspnea in association with phrenic nerve 100% to 17% when 10 ml was administered
palsy. Thus, although dyspnea clearly is more prevalent via a landmark approach. Unfortunately, this
in the presence of phrenic nerve palsy, it is neither reduction in phrenic nerve palsy generally
sensitive nor specific for phrenic nerve palsy.
appears to come at the expense of reduced • Injection Method: Interestingly, injection
analgesic efficacy. The reduction in local of local anesthesia through a catheter
anesthetic concentration and dose decreased appears to produce a less dramatic change
duration of sensory blockade by 34% and in diaphragmatic sonographic excursion than
increased postoperative opioid requirements if the same large-volume bolus was injected
by up to 50%. Thus, decreasing the dose and directly through a needle, possibly supporting
concentration can be reduce the incidence to a benefit of titrated injection. This suggests that
about 20% with a risk of reducing the duration injection dynamics may play an important role
of analgesia. in development of diaphragmatic dysfunction
• Site of Injection: Ultrasound-guided extrafascial and should be investigated further.
(periplexus) injection of 20 ml bupivacaine Alternative blocks to Interscalene Block
0.5%, performed 4 mm lateral to the brachial
plexus sheath not only provided similar The conventional ultrasound-guided interscalene
analgesia compared with an intraplexus block is a direct carryover from the landmark-guided
injection between the C5 and C6 roots but also approach, which relied on the interscalene groove and
reduced the incidence of diaphragmatic paresis the anterior tubercle of the C6 transverse process as key
from 90% to 21%. In addition, FEV1, forced landmarks, and thus necessitated a needle approach
vital capacity, and peak expiratory flow rates to the brachial plexus at the root level. This restriction
were less affected in the extrafascial group no longer exists; ultrasound allows visualization of the
compared with an intraplexus injection. entire brachial plexus and its individual branches, and
thus similar analgesic effects can be achieved with more
• Intrafascial Injection: Another strategy to avoid
selective injection further away from the phrenic nerve
phrenic nerve palsy involves injecting local
and the C5 and C6 roots.
anesthetic further away from the C5 and C6
roots and phrenic nerve. It has been shown • Superior Trunk Block
that ultrasound-guided injection of 10 ml
The superior trunk is formed by the union of C5 and
ropivacaine 0.75%, around the C7 nerve root
C6 roots and is an appealing alternative target for local
resulted in similar analgesia, but only a 13%
anesthetic injection, given that the phrenic nerve has
incidence of phrenic nerve palsy compared
diverged a considerable distance away from the brachial
with 93% with a neurostimulation guided
interscalene block using the same dose of plexus in the interscalene groove. All the terminal
local anesthetic. Recovery of diaphragmatic nerves supplying the shoulder arise distal to the origin
function also was faster in the patients who of the superior trunk and hence analgesic efficacy is not
received the C7 root injection. In a subsequent compromised. The superior trunk also can be targeted
study, the same authors reported that the at the supraclavicular brachial plexus level.
minimum effective anesthetic volume to • C7 nerve root block
achieve complete sensory block of C5 and
C6 dermatomes within 30 minutes in 50% A similar ultrasound guided ISB at the level of the C7
of patients using this technique was 2.9 transverse process can be done which is quite away
ml ropivacaine 0.75%. They noted that from the phrenic nerve at this level.
none of the 20 patients who received 6 ml
• Suprascapular and Axillary Nerve Block
ropivacaine 0.75%, or less had any evidence
of diaphragmatic paresis up to 2 hours after The risk of phrenic nerve palsy might be eliminated
injection. by avoiding injection around the brachial plexus and

performing a suprascapular nerve and axillary nerve the supraspinous fossa. At the notch, the nerve is next
block instead. The suprascapular nerve provides to the suprascapular artery and vein but the vessels
sensory fibers to approximately 70% of the shoulder pass above the ligament. After traveling through the
joint capsule, and blocking this peripheral nerve supraspinous fossa, the SSN reaches the spinoglenoid
can be performed with either a landmark-guided or notch laterally and exits into the infraspinous fossa.
ultrasound-guided technique. The suprascapular nerve Between the two notches, it is in direct contact with
can be blocked in the suprascapular fossa. The axillary bone, covered by the inferior fascia of the supraspinatus
nerve is a terminal branch of the posterior cord of muscle and accompanied by the suprascapular artery.
the brachial plexus. It may be blocked in the anterior The course of the SSN within the fossa is considerably
chest where it arises from the posterior cord of the oblique which has important impact on correct
brachial plexus in the infraclavicular and proximal transducer positioning as shown in the figure 3.
axillary area or posterior to the humerus as it emerges
Scanning technique
from the quadrangular space. This latter approach may
occasionally miss the articular branches of the axillary Ask the patient to place the hand over to the contralateral
nerve and may be responsible for inferior analgesic shoulder. This will move the scapula laterally to provide
outcomes. more space for SSN scanning. Also, this will move the
target SSN injection site more laterally away from the
Suprascapular nerve (SSN) block
thorax. Position the transducer oblique (not parallel)
Relevant anatomy to the spine of the scapula in the supraspinous fossa
because the SSN runs an oblique course between the
The SSN passes underneath the omohyoid muscle
suprascapular notch and the spinoglenoid notch. Place
in the posterior triangle of the neck. Then, it passes
one end of the transducer over the scapular spine and
posteriorly towards the scapula together with the
the other end directing towards the coracoid process as
omohyoid muscle towards the suprascapular notch.
shown in the figure 4. The transducer aims to capture
The nerve passes deep to the superior transverse
a transverse view of the nerve.
scapular ligament through the scapular foramen into
Fig 3: shows the course of suprascapular nerve in the Fig 4: Transducer position for suprascapular nerve
suprascapular and spinoglenoid notch block

Technique Catheter Techniques
The goal is to block the SSN approximately halfway Continuous catheter infusions, if limited to less than
in between the suprascapular and the spinoglenoid 2ml/hour, reduces the risk of transient phrenic nerve
notches. There is no need to visualize the notches at the palsy after interscalene nerve block.
time of injection. We recommend an in-plane needle
approach aiming from posteromedial to anterolateral Subscapularis plane block and sub omohyoid plane
as shown in figure 5. Needle insertion from the lateral block
side, on the other hand, is more challenging because
the acromion is in the path of the needle making The innervation to the shoulder joint usually travels
it necessary to insert the needle at a steep angle through various intermuscular planes before reaching
thus reduces needle visibility. Accidental anterior the shoulder, and these intermuscular planes are easily
advancement of the needle can possibly puncture the identified by musculoskeletal ultrasonography as shown
pleura causing pneumothorax. in the figure 6 and 7. The suprascapular nerve leaves the
superior trunk close to the supraclavicular fossa and travels
In arthroscopic shoulder surgery, suprascapular nerve
in the posterior triangle of the neck deep and parallel
block alone or combined with an axillary nerve block
to the inferior belly of the omohyoid muscle to enter
has been shown to provide superior analgesia compared
with placebo or subacromial local anesthetic infiltration the suprascapular notch. The axillary nerve leaves the
but is less effective compared with interscalene block. posterior cord in the infraclavicular fossa and bifurcates
Because this peripheral nerve block technique primarily into anterior and posterior branches while traversing the
targets the capsular innervation of the shoulder, it subscapularis muscle before winding around the humerus
also may be less useful in open or extensive shoulder to enter the quadrangular space. The subscapular nerves
surgery. arising from the posterior cord are also present on the
ventral surface of the subscapularis muscle. In addition to
In view of the trade-off in analgesic efficacy, suprascapular
and axillary nerve blocks are probably best reserved for this, PECS-1 block (depositing local anaesthetic between
patients with preexisting respiratory dysfunction or who pectoralis major and minor) can be combined to block
have other comorbidities that are likely to lead to clinically the lateral pectoral nerve in the same probe position
significant dyspnea and hypoxemia in the presence of if the acromioclavicular joint is being operated upon
unilateral phrenic nerve palsy. concomitantly.
Fig 5: Needle direction and the ultrasound image

Current status
Out of the possible diaphragm-sparing strategies, three
techniques have been investigated with RCTs, and can
be inferred that ISB with low volume, dilute LA, and
injection 4 mm lateral to the brachial plexus shows
promising results as surgical anesthetic technique.
While the other studied modalities like combined AXB-
SSB (Axillary nerve block-Suprascapular nerve block),
C7 root block, and SCB (Supraclavicular nerve block)
with LA injection posterolateral to the brachial plexus,
none has convincingly been shown to provide effective
surgical anesthesia. In terms of postoperative analgesia,
C7 root block appear equivalent to the current analgesic
Fig 6: Site of scanning for Subscapularis plane block
criterion-standard ISB. Combined AXB-SSB may provide
(B) and Sub-omohyoid plane block(C)
adequate postoperative analgesia for minor shoulder
surgery but does not compare favorably to ISB for major
surgical procedures. In terms of HDP occurrence, AXB-
SSB and SCB (with LA injection posterolateral to the
brachial plexus) appear to sidestep the issue (HDP risk
= 0%). At 13%, the incidence of phrenic block following
C7 root blocks may still be prohibitively high.
Conclusions
Regional anesthesia continues to be of value in
providing analgesia for shoulder surgery, but its benefits
must be weighed against the risks, including phrenic
nerve palsy. The high incidence of phrenic nerve
palsy associated with the conventional technique of A
interscalene block shows that it should be avoided
in the respiratory wise crippled high risk patients.
However, the evidence indicates that temporary phrenic
nerve palsy is inconsequential in the vast majority of
healthy patients and, second, that relatively simple
modifications such as minimizing local anesthetic
doses and injection volumes, as well as performing
injection further distal to the C5–C6 nerve roots will
significantly reduce the incidence of phrenic nerve
palsy. Combined suprascapular and axillary nerve blocks
are another alternative to consider in scenarios in which
avoiding phrenic nerve palsy is critical, particularly in
arthroscopic shoulder surgery.
B
References
Fig 7: USG image of Subscapularis plane block (A) and
1. De Q.H. Tran, Maria Francisca Elgueta, Julian Aliste,
Sub-omohyoid plane block (B)
Roderick J. Finlayson, Diaphragm-Sparing Nerve

Blocks for Shoulder Surgery. Reg Anesth Pain Med 4. S. Riazi, N. Carmichael, I. Awad, R. M. Holtby, C. J. L.
2017; 42: 32–38 McCartney Effect of local anaesthetic volume (20 vs
5 ml) on the efficacy and respiratory consequences
2. Kariem El-Boghdadly, Ki Jinn Chin, Vincent W. S.
of ultrasound-guided interscalene brachial plexus
Chan, Phrenic Nerve Palsy and Regional Anesthesia
block Br J Anesth 2008;101 (4): 549–56
for Shoulder Surgery Anesthesiology 2017;
127:173–91 5. M. J. Fredrickson, S. Krishnan and C. Y. Chen
Postoperative analgesia for shoulder surgery: a
3. R. V. Sondekoppam, L-M. Lopera-Velasquez,
critical appraisal and review of current techniques
L. Naik, S. Ganapathy. Subscapularis and sub-
Anaesthesia, 2010; 65: 608–624
omohyoid plane blocks: an alternative to peripheral
nerve blocks for shoulder analgesia Br J Anesth. 6. Figures reproduced from www.nysora.com and
2016;117(6):831-832 www.usra.com

MCQ
1. Cape region of the shoulder is supplied by 4. Out of the following diaphragm sparing
strategies which can be used as surgical
a. axillary nerve
anesthetic technique
b. suprascapular nerve
a. injection 4 mm lateral to the brachial
c. dorsal scapular nerve
plexus
d. lateral pectoral nerve
b. Combined individual nerve block for
2. In subscapularis plane block, apart from suprascapular and axillary nerve
subscapular nerve which nerve is blocked c. SCB with LA injection posterolateral to
a. axillary nerve the brachial plexus
b. suprascapular nerve d. C7 root block
c. dorsal scapular nerve 5. Accessory phrenic nerve is present in

d. lateral pectoral nerve a. 10% of the population
3. What is the distance between brachial plexus b. 20%of the population
and the phrenic nerve at the C6 vertebra level c. 60%of the population
a. 3cm d. 100% of the population
b. 1.8cm
c. 3.6cm
d. 0.8cm
5. (c) 4. (a) 3. (d) 2. (a) 1.(b)

Answers

37 TRANSNASAL HUMIDIFIED
RAPID-INSUFFLATION VENTILATORY EXCHANGE (THRIVE)
Director, Professor Anesthesiology, Rakesh Kumar

Maulana Azad Medical College & Lok Nayak Hospital,
New Delhi.
President, Airway Management Foundation (AMF)
Transnasal humidified rapid-insufflation ventilatory i) Using a Venturi system driven by high oxygen
exchange (THRIVE) is a method of delivering high flow pressure.
of oxygen enriched air into the nostrils (transnasal)
ii) Using two high-pressure sources, high-pressure
of patients through specific high-flow cannula. The air and oxygen.
mixture is fully humidified with water vapor at 37°C
(relative humidity of 100% carrying nearly 6% or 44 mg iii) Using a turbine system.
H2O/L). The gas flow or insufflation is rapid and usually iv) Using a conventional compressed air or turbine-
varies from 30-70 liters per minute (lpm) in adults and driven mechanical ventilator with a dedicated
the FIO2 varies from 0.21-1.0. The other names for HFNT system.
THRIVE are high-flow nasal therapy (HFNT), high-flow
nasal cannula (HFNC), high-flow oxygen therapy (HFOT), Different systems are available like Vapotherm’s
high-flow nasal oxygen therapy (HFNOT) etc. 2000i High Flow Therapy system, Teleflex Comfort
Flo Humidification System, AirVO2 High Flow delivery
A heated humidifier connected to a heated insulated system with Optiflow Nasal High Flow cannula (Fisher
single-limb circuit provides active humidification. High & Paykel) (Fig 1). Airway patency can be maintained
flow may be generated in different ways: during its use by application of jaw thrust.
Fig 1: AirVO2 High flow delivery system with Optiflow Nasal High Flow Cannula (Fisher & Paykel)

Transnasal Humidified 368
Rapid-Insufflation Ventilatory Exchange (Thrive) Rakesh Kumar
Physiological effects of THRIVE Indications in ICU

1) Warmed humidified gas keeps airway surface a. It has been shown that THRIVE can reduce
moist and does not produce warming-humidifying intubation requirements in patients with
load on the airways. This improves secretion non-cardiogenic ARF with a PaO2/FIO2 ratio
clearance and decreases chances of atelectasis. of <200. It also significantly reduces mortality
2) The oxygen consumption of a healthy adult rate both during ICU admission and within
is 250 ml/min and the CO2 production is 200 90 days. It is particularly useful in acute
ml/minute. With ‘apneic oxygenation’, the respiratory failure patients with increased work
alveolar uptake of oxygen continues even in the of breathing who do not tolerate facemask
absence of respiratory movements because of therapy or those who have a high secretion
the concentration gradient created between load. In addition, patient acceptability, comfort
the alveolus and pulmonary capillaries. On the and tolerability are its biggest assets.
other hand, the rate of CO2 elimination is only
8-20 ml/minute. This is because there is hardly b. THRIVE improves dyspnea and arterial oxygen
any gradient for CO2 to flow from blood into tension in patients with hypoxemia due to
the alveoli. This differential movement of gases cardiogenic pulmonary edema.
across the alveolus is responsible for a resultant
pressure in the alveolus that is sub-atmospheric c. Weaning from ventilator: THRIVE facilitates
(-20 cm H2O) which draws in a mass flow of gas and smoothens the weaning process by tiding
from the airway above. On the other hand, high over the immediate post-extubation time. In
gas flow during THRIVE causes CO2 washout that is our experience, it is better tolerated than the
not available during standard apneic oxygenation
classical non-invasive ventilation (NIV) and
or even conventional oxygen therapy. While the
is more effective than conventional oxygen
rate of rise of carbon dioxide levels with the usual
apneic oxygenation is reported between 0.35-0.45 therapy with venturi-mask or low-flow nasal
kPa/min (2.63-3.38mmHg/min), THRIVE reduces prongs for this purpose.
this rate of rise to 0.15 kPa/min (1.13mmHg/
d. Paraoxygenation (term coined by AMF) or
min), thus providing indirect evidence of flow-
dependent, non-rhythmic ventilatory exchange Oxygenation while airway is being secured
exists during THRIVE. This high gas flow also – As described above, under Physiologic
reduces the anatomical dead space and provides Effects of THRIVE, it can be used to decrease
an oxygen reservoir that is replenished rapidly the severity of the desaturation in patients
thereby allowing delivery of FIO2 close to 1.0. needing emergency intubation or endotracheal
tube (ETT) change in ICU who are rapidly
3) Continuous insufflation achieves a continuous
positive airway pressure of approximately 3-7cm desaturating.
H2O [41] that splints the upper airways and reduces e. Non-intubated patients with mild hypoxemia
shunting [42, 43]. This leads to increased end- undergoing bronchoscopy in ICU may benefit
expiratory lung volume and alveolar recruitment.
from THRIVE.
Indications
f. Its use in chronic obstructive pulmonary
The initial rationale for the use of THRIVE in neonates disease (COPD) patients is still evolving.
was to provide a distending pressure to counteract a However, high-flow nasal cannula oxygen
lack of surfactant. In adults, THRIVE is gaining popularity therapy reduces respiratory rate and increases
in the ICU, operation theaters and post anesthesia care minute volume in COPD patients both at rest
units (PACU). Its clinical indications at present are: and during exercise.

Indications in the OT Other prospective uses

g. Preoxygenation - Preoxygenation with THRIVE l. THRIVE could be suitable for use in some
may be beneficial in those patients who have patients deemed not suitable for intubation,
a reduced functional residual capacity, or or patients requiring palliative care. It can
increased metabolic demand for oxygen such alleviate respiratory distress symptoms in
as the obstetric, bariatric, and septic patients. cancer patients by reducing respiratory rate
In anticipated difficult airway cases that need in respiratory failure.
the airway to be secured under anesthesia, m. It may be useful in COPD patients to reduce
THRIVE may be a better option than the the duration (but not the frequency) of
classical methods of preoxygenation. It can exacerbations of COPD.
then be persisted with during attempts to
secure the airway as well, as described below. n. The triad of humidity, compliance and high
FIO2 offered by THRIVE is likely to be of use
h. P a r a o x y g e n a ti o n – T H R I V E i s b e i n g in a wide variety of clinical situations. Thus
recommended to increase the time to it may be of use in pre-hospital care, and
desaturation, decrease the severity of the inter-hospital transfers, primarily for its ability
desaturation and reduce the rate of rise of to deliver an FIO2 of close to 1.0. Within
CO2 in apneic anesthetized patients, allowing the hospitals also, it is likely to become a
for unhurried attempts at intubation. It has replacement for conventional nasal cannula
been used successfully in awake fiberoptic and facemask delivering cold, dry gases to the
intubation, where a major advantage appears patients.
to be its ability to provide an FIO2 of nearing
Contraindications of THRIVE
1.0 via soft nasal cannula that allow the
passage of a fiberoptic scope. 1. Any contraindication to the application of PEEP.
i. During surgery – THRIVE has been used as the 2. Patients with reduced levels of consciousness
sole method of maintaining oxygenation and or uncooperative patients.
eliminating CO2 during some laryngo-tracheal
3. Patients with epistaxis, facial injury, or airway
surgeries.
obstruction.
Postoperative use 4. As mentioned above, THRIVE should not
j. THRIVE has the potential of replacing delay mechanical ventilation in those with
conventional oxygen therapy (of using high severe respiratory failure, particularly in type
FIO2) to prevent postoperative hypoxemia in II respiratory failure.
the susceptible patient population (patients Advantages of THRIVE
undergoing major abdominal or thoracic
surgery) as it not only increases FIO2 but also 1. THRIVE provides effective humidification and
treats the de-recruitment by creating positive warming of gases, which allows more effective
airway pressures. clearance of secretions, decreases atelectasis
and prevents airway surface dehydration.
k. In post-cardiac surgery population, it has been
shown to reduce respiratory rate, increase 2. Compared with humidified oxygen via a
end-expiratory lung volume, reduce the facemask, and traditional non-invasive
ventilation masks, THRIVE is better tolerated
requirement for CPAP via a facemask interface
by the patients.
and re-intubation rates.

3. There is a reduced subjective feeling of 6. Schwabbauer N, Berg B, Blumenstock G,

dyspnea. Haap M, Hetzel J, Reissen R. Nasal high-flow
4. In most cases, it causes decrease in respiratory oxygen therapy in patients with hypoxic
rates and airway dryness. respiratory failure: effect on functional and
subjective respiratory parameters compared
Disadvantages of THRIVE to conventional oxygen therapy and non-
1. As this technique needs less monitoring, it has invasive ventilation (NIV). BMC Anaesthesiol
the potential of delaying institution of invasive 2014; 14: 66
ventilation thereby leading to avoidable 7. Rea H, McAuley S, Jayaram L et al. The clinical
morbidity. utility of long- term humidification therapy in
2. Sensations of neck discomfort and gas flow chronic airway disease. Resp Med 2010; 104:
being too warm have been reported on rare 525–33
occasions. We have not encountered it in any
of our cases yet. 8. Peters SG, Holets SR, Gay PC. Nasal high flow
oxygen therapy in do-not-intubate patients
Suggested technique of using THRIVE with hypoxaemic respiratory distress. Respir
Care 2013; 58: 597–600
Some users suggest that THRIVE should be commenced
at lower flows and temperatures and then gradually 9. Ward JJ. High-flow oxygen administration by
increased the flow and temperature within the initial nasal cannulae for adult and perinatal patients.
30 min of therapy. However, our experience and that Respir Care 2013; 58: 98–122
of many other investigators shows that THRIVE is
well accepted even when it is started at high flows of 10. Frat JP, Ragot S, Thille AW. High-flow oxygen
70 lpm at 37°C. through nasal cannula in acute hypoxaemic
respiratory failure. N Engl J Med 2015; 372:
References for Further Reading 2185–96
1. Patel A, Nouraei SAR. Transnasal Humidified 11. Ni Y, Luo J et al. Can high-flow nasal cannula
Rapid-Insufflation Ventilatory Exchange
reduce the rate of reintubation in adult
(THRIVE): a physiological method of increasing
patients after extubation? A meta-analysis.
apnoea time in patients with difficult airways.
BMC Pulmonary Medicine. 2017; 17:142
Anaesthesia 2015; 70(3):323-29.
12. Bartlett RG Jr, Brubach HF, Specht H.
2. Ashraf-Kashani N and Kumar R. High-flow nasal
oxygen therapy. BJA Education, 2017;17 (2): Demonstration of aventi- latory mass flow
63–67 during ventilation and apnea in man. Journal
of Applied Physiolology 1959; 14: 97–101
3. Cortegiani A, Accurso G, et al. High flow
nasal therapy in perioperative medicine: 13. Frumin MJ, Epstein RM, Cohen G. Apneic
from operating room to general ward. BMC oxygenation in man. Anesthesiology 1959;
Anesthesiology 2018;18:166 20: 789–98.
4. Xu Z, Li Y et al. High-flow nasal cannula in 14. Eger EI, Severinghaus JW. The rate of rise of
adults with acute respiratory failure and after PaCO2 in the apneic anesthetized patient.
extubation: a systematic review and meta- Anesthesiology 1961; 22: 419–25
analysis. Respiratory Research (2018) 19:202
15. Meltzer SJ, Auer J. Continuous respiration
5. Roca O, Riera J, Torres F, Masclans JR. High-flow without respiratory movements. Journal of
oxygen therapy in acute respiratory failure. Experimental Medicine 1909; 11:622–5.
Respir Care 2010; 55:408–13
MCQ
1. In apneic preoxygenation the rate of rise of 4. High flow oxygen can be delivered by all of
pc02 levels when THRIVE is used is around the following ways except
a. 1-1.3 mmhg/min a. Using a Venturi system
b. 2- 3 mmhg/min b. Using two high-pressure sources
c. 6- 7mmhg/min c. Using a turbine system.
d. 4- 6mmhg/min d. Nasopharyngeal catheter
2. All are indications for the use of THRIVE 5. Physiological effects of Transnasal Humidified
except Rapid Insufflation Ventilatory Exchange are all
except
a. Non-intubated patients with mild
hypoxemia undergoing bronchoscopy a. Decrease epistaxis from splinting of
b. Upper airway obstruction blood vessels in upper airway
c. In Preoxygenation of patients with b. Increased end-expiratory lung volume
reduced functional residual capacity and alveolar recruitment
d. Paraoxygenation c. Continuous insufflation of air mixture
leading to splinting of upper airways
3. THRIVE is shown to be beneficial in all of the and reduces shunting
following ways except
d. Continuous positive airway pressure of
a. provides effective humidification and approximately 3-7cm H2O
warming of gases
b. clearance of secretions
c. decreases atelectasis
d. Acutely Reverses smoking related
pathological changes
5.(a) 4.(d) 3.(d) 2.(b) 1.(a)

Answers

38 BLOOD PRODUCTS
Associate Professor, Vishnu Mahesh Babu

Rangaraya Medical College,
Kakinada.
The whole blood, which is a mixture of cells, colloids efficiency of each component is dependent on
and crystalloids can be separated into different blood appropriate processing and proper storage. To utilise
components. Any therapeutic substance prepared from one blood unit appropriately and rationally, component
human blood is a blood product. This includes whole therapy is to be adapted universally.2
blood, blood components and plasma derivatives.
Blood components are prepared by PRP (Platelet
Blood components include : red blood cell concentrates
Rich Plasma)method or Buffy coat method. In
or suspensions, platelets produced from whole blood
the PRP method, an initial centrifugation to separate
or via apheresis, plasma and cryoprecipitate, Plasma
red blood cells (RBC) is followed by a second
derivatives- Albumin, Coagulation factor concentrates
centrifugation to concentrate platelets, which are
& Immunoglobulins.1
suspended in the smallest final plasma volume (Fig 1).
Each blood product is used for a different indication;
Buffy coat method: Whole blood samples can be
thus the component separation has maximized the
fractionated as a pre-treatment to separate buffy coat,
utility of one whole blood unit. Different components
comprising white blood cells and platelets ( < 1% of total
need different storage conditions and temperature
blood), from erythrocytes and plasma (Fig 2).
requirements for therapeutic efficacy.
Components can be collected by Apheresis. Apheresis
In increasing order, the specific gravity of blood
is a procedure where required single or more than
components is plasma, platelets, leucocytes (Buffy Coat
one component is collected, and the rest of blood
[BC]) and packed red blood cells (PRBCs). Functional
components are returned back to the donor.
PRP method
Fig 1 : Preparation of blood components - PRP method

Blood Products 374 Vishnu Mahesh Babu
Fig 2 : Preparation of blood components - Buffy coat method
Blood Products Red Cell Suspension

Red Cell Concentrate (‘Packed red cells’, ‘plasma- • 150–200 ml red cells with minimal residual
reduced blood’) plasma to which ±100 ml normal saline,
adenine, glucose,mannitol solution (SAG-M)
• 150–200 ml red cells from which most of the
or an equivalent red cell nutrient solution has
plasma has been removed
been added
• Haemoglobin approximately 20 g/100 ml (not
less than 45 g per unit) • Haemoglobin approximately 15 g/100 ml (not
less than 45 g per unit)
• Haematocrit 55%–75%
• Haematocrit: 50%–70%
• Infection risk : Same as whole blood
• Storage : Same as whole blood • Indications: Same as red cell concentrate
• Indications : Replacement of red cells in • Administration : Same as whole blood

anaemic patients • Better flow rates are achieved than with red
• Use with crystalloid replacement fluids or cell Concentrate or whole blood.3
colloid solution in acute blood loss
Leucocyte-Depleted Red Cells
• Administration - Same as whole blood
• A red cell suspension or concentrate
• To improve transfusion flow, normal saline containing <5 x 10 6 white cells per pack,
(50–100 ml) may be added using a Y-pattern prepared by filtration through a leucocyte-
infusion set. depleting filter

• Haemoglobin concentration and haematocrit • Longer storage increases the risk of bacterial
depend on whether the product is whole blood, proliferation and septicaemia in the recipient
red cell concentrate or red cell suspension.
• Indications: Treatment of bleeding due to
• Leucocyte depletion significantly reduces the
risk of transmission of cytomegalovirus (CMV) • Thrombocytopenia
• Platelet function defect
• Indications: Minimizes white cell immunization • P r e v e n ti o n o f b l e e d i n g d u e t o
in patients receiving repeated transfusions but, thrombocytopenia, such as in bone marrow
to achieve this, all blood components given to failure
the patient must be leucocyte-depleted
• Contraindications
• Reduces risk of CMV transmission
• Not generally indicated for prophylaxis of
• Patients who have experienced two or more bleeding in surgical patients, unless known
previous febrile reactions to red cell transfusion to have significant pre-operative platelet
• Contraindications: Will not prevent graft- deficiency
vs-host disease: for this purpose, blood • Not indicated in
components should be irradiated where
facilities are available (radiation dose: 25–30 • Idiopathic autoimmune thrombocytopenic
Gy)4 purpura (ITP)
• Thrombotic thrombocytopenic purpura
Platelet Concentrates5 (TTP)
• Single donor unit in a volume of 50–60 ml of • Untreated disseminated intravascular
plasma should contain: coagulation (DIC)
• Thrombocytopenia associated with
• At least 55 x 109 platelets s e p ti c a e m i a , u n ti l t re a t m e n t h a s
• <1.2 x 109 red cells commenced or in cases of hypersplenism
• <0.12 x 109 leucocytes
• Dosage: 1 unit of platelet concentrate/10
• Unit of issue: May be supplied as either kg body weight: in a 60 or 70 kg adult, 4–6
• Single donor unit: platelets prepared from single donor units containing at least 240 x
one donation 109 platelets should raise the platelet count
• Pooled unit: platelets prepared from 4 to by 20–40 x 109/L
6 donor units ‘pooled’ into one pack to
• Increment will be less if there is
contain an adult dose of at least 240 x 109
platelets • Splenomegaly
• Disseminated intravascular coagulation
• Infection risk : Same as whole blood, but a
• Septicaemia
normal adult dose involves between 4 and 6
donor exposures • Administration
• Bacterial contamination affects about 1% of • After pooling, platelet concentrates
pooled units should be infused as soon as possible,
generally within 4 hours, because of the
• Storage : Up to 72 hours at 20°C to 24°C (with
risk of bacterial proliferation. Must not be
agitation) unless collected in specialized
platelet packs validated for longer storage refrigerated before infusion as this reduces
periods; do not store at 2°C to 6°C platelet function

• 4–6 units of platelet concentrates (which • Administration: Same as recovered donor
may be supplied pooled) should be platelets, but ABO compatibility is more
infused through a fresh standard blood important: high titre anti-A or anti-B in the
administration set donor plasma used to suspend the platelets
• Special platelet infusion sets are not may cause haemolysis of the recipient’s red
required cells.
• Should be infused over a period of about Fresh Frozen Plasma (FFP)6
30 minutes
• Do not give platelet concentrates prepared • Pack containing the plasma separated from
from RhD positive donors to an RhD one whole blood donation within 6 hours of
negative female with childbearing potential collection and then rapidly frozen to –25°C or
• Give platelet concentrates that are ABO colder. (Plasma frozen within 24 hours - PF24:
compatible, whenever possible Frozen ≥ 8 hours, but ≤ 24 hours of collection).
• Complications: Febrile non-haemolytic • It contains normal plasma levels of stable
and allergic urticarial reactions are not clotting factors, albumin and immunoglobulin
uncommon, especially in patients receiving
multiple transfusions. • Factor VIII level at least 70% of normal fresh
plasma level
Platelet Concentrates (collected by Plateletpheresis)
• Unit of issue : Usual volume of pack is 200–300
• Volume : 150–300 ml ml. Smaller volume packs may be available for
children
• Platelet content 150–500 x 109, equivalent to
3–10 single donations • Infection risk: If untreated, same as whole
blood
• Platelet content, volume of plasma and
leucocyte contamination depend on the • Very low risk if treated with methylene blue/
collection procedure ultraviolet light inactivation
• Unit of issue 1 pack containing platelet • Storage: At –25°C or colder for up to 1 year
concentrates collected by a cell separator • Before use, should be thawed in the blood
device from a single donor bank in water which is between 30°C to 37°C.
• Infection risk: Same as whole blood Higher temperatures will destroy clotting
factors and proteins. Once thawed, should be
• Storage : Up to 72 hours at 20°C to 24°C
stored in a refrigerator at +2°C to +6°C
(with agitation) unless collected in specialized
platelet packs validated for longer storage • Indications :
periods; do not store at 2°C to 6°C • Replacement of multiple coagulation factor
• Indications : Generally equivalent to the same deficiencies: e.g Liver disease
dose of platelet concentrates prepared from • Warfarin (anticoagulant) overdose
whole blood • Depletion of coagulation factors in patients
• Receiving large volume transfusions
• If a specially typed, compatible donor is
Disseminated intravascular coagulation (DIC)
required for the patient, several doses may be
Thrombotic thrombocytopenic purpura
obtained from the selected donor
(TTP)
• Dosage: 1 pack of platelet concentrate • Precautions :
collected from a single donor by apheresis is
• Acute allergic reactions are not uncommon,
usually equivalent to 1 therapeutic dose
especially with rapid infusions

• Severe life-threatening anaphylactic Cryoprecipitate7
reactions occasionally occur. Hypovolaemia
• Prepared from fresh frozen plasma by collecting
alone is not an indication for use
the precipitate formed during controlled
• Dosage : Initial dose of 15 ml/kg
thawing at +4°C and resuspending it in 10–20
• Administration : ml plasma
• Must normally be ABO compatible to avoid • Contains about half of the Factor VIII , Factor
risk of haemolysis in recipient III & fibrinogen in the donated whole blood:
• No compatibility testing required e.g. Factor VIII: 80–100 iu/ pack; fibrinogen:
• Infuse using a standard blood administration 150–300 mg/pack
set as soon as possible after thawing
• Unit of issue : Usually supplied as a single
• Labile coagulation factors rapidly degrade;
donor pack or a pack of 6 or more single donor
use within 6 hours of thawing.
units that have been pooled
Liquid Plasma • Infection risk - As for plasma, but a normal
• Plasma separated from a whole blood unit and adult dose involves at least 6 donor exposures
stored at +4°C • Storage: At –25°C or colder for up to 1 year
• No labile coagulation factors (Factors V and • Indications: As an alternative to Factor VIII
VIII) concentrate in the treatment of inherited
Freeze-Dried Pooled Plasma deficiencies of
• Von Willebrand Factor (von Willebrand’s
• Plasma from many donors pooled before
disease)
freeze-drying
• Factor VIII (haemophilia A)
• Infection risk: No virus inactivation step so • Factor XIII
the risk of transmitting infection is therefore
multiplied many times • As a source of fibrinogen in acquired
coagulopathies: e.g. disseminated intravascular
• This is an obsolete product that should not coagulation (DIC)
be used.
• Administration: If possible, use ABO-compatible
Cryoprecipitate-Depleted Plasma product
• Plasma from which approximately half the • No compatibility testing required
fibrinogen and Factor VIII has been removed • After thawing, infuse as soon as possible
as cryoprecipitate, but which contains all the through a standard blood administration set
other plasma constituents.
• Must be infused within 6 hours of thawing.
Virus ‘Inactivated’ Plasma
The blood components of red blood cells (RBC),
• Plasma treated with methylene blue/ultraviolet plasma (FFP), and platelets are found to have the most
light inactivation to reduce the risk of HIV, benefit to the patient and to reduce mortality when
hepatitis B and hepatitis C. administered together in ratios of 1:1:1. The focus of
• The cost of this product is considerably higher the Massive Transfusion Protocol should be to maintain
than conventional fresh frozen plasma. the 1:1 or 1:2 ratio of RBC and FFP.
Prophylactic plasma transfusion does not result in fewer Cryoprecipitate should be given as part of the massive
bleeding events.6 transfusion when laboratory values indicate fibrinogen
levels < 100 mg/dl.
Plasma derivative8 • Factor VIII ranges from 0.5–20 iu/mg of protein.
Preparations with a higher activity are available
Human Albumin Solutions
• Products that are licensed in certain countries
• Prepared by fractionation of large pools of (e.g.USA and European Union) are all heated
donated plasma and/or chemically treated to reduce the risk
• Preparations of transmission of viruses
• Unit of issue: Vials of freeze-dried protein
• Albumin 5%: contains 50 mg/ml of albumin
labelled with content, usually about 250 iu of
• Albumin 20%: contains 200 mg/ml of
Factor VIII
albumin
• Albumin 25%: contains 250 mg/ml of • Infection risk: Current virus ‘inactivated’
albumin products do not appear to transmit HIV, HTLV,
• Stable plasma protein solution (SPPS) hepatitis C and other viruses that have lipid
and plasma protein fraction (PPF): similar envelopes: the inactivation of non-enveloped
albumin content to albumin 5% viruses such as hepatitis A and parvovirus is
• Infection risk: No risk of transmission of viral less effective
infections if correctly manufactured • Storage: +2°C to +6°C up to stated expiry date
• Indications: • Indications
• Replacement fluid in therapeutic plasma • Treatment of haemophilia A
exchange: use albumin 5% • Treatment of von Willebrand’s disease:
• Treatment of diuretic-resistant oedema in use only preparations that contain von
hypoproteinaemic patients: e.g. nephrotic Willebrand Factor
syndrome or ascites. Use albumin 20% with • Alternatives: Cryoprecipitate, fresh frozen
a diuretic plasma, Factor VIII prepared in vitro using
• Although 5% human albumin is currently recombinant DNA methods is commercially
licensed for a wide range of indications available. It is clinically equivalent to Factor VIII
(e.g. volume replacement, burns and derived from plasma and does not have the
hypoalbuminaemia), there is no evidence risk of transmitting pathogens derived from
that it is superior to saline solution or other plasma donors.
crystalloid replacement fluids for acute
plasma volume replacement Plasma Derivatives containing Factor IX
• Precautions: Administration of 20% albumin • Prothrombin complex concentrate (PCC) and

may cause acute expansion of intravascular Factor IX concentrate
volume with risk of pulmonary oedema • PCC contains Factor II, IX & X, Factors IX
• Contraindications : Do not use for IV nutrition: concentrate contains Factor IX only
it is an expensive and inefficient source of • PCC also contains Factor VII
essential amino acids
• Both are indicated in the treatment of
• Administration : No compatibility testing haemophilia B (Christmas disease)
required. No filter needed.
• PCC is also used for Immediate correction of
COAGULATION FACTORS prolonged prothrombin time.
Factor VIII concentrate9 Immunoglobulins
• Partially purified Factor VIII prepared from • Immunoglobulins are commonly given by
large pools of donor plasma intramuscular route

• Concentrated solution of the IgG antibody 3) Guidelines for the clinical use of red cell transfu-
component of plasma. sions. BCSH web page or BJHaem2001, 113: 24
–31.
• Indications: Hyperimmune or specific
immunoglobulin: from patients with high levels 4) British Committee for Standards in Hematology,
of specific antibodies to infectious agents: e.g. Blood Transfusion task Force. Guidelines on
hepatitis B, rabies, tetanus gamma irradiation of blood components for
prevention of Transfusion-associated graft-
• Prevention of specific infections versus-host disease. Transfus Med. –6:261;1996
71
• Treatment of immune deficiency states
5) Guidelines for the use of Platelet transfusions.
The appropriate use of blood and blood products means BCSH web page or BJHaem 2003: 122, 10-23
the transfusion of safe blood products only to treat a
condition leading to significant morbidity or mortality 6) Guidelines for the use of FFP, cryoprecipitate &
that cannot be prevented or managed effectively by cryosupernatant. BCSH web page or BJHaem
2004: 126: 11-8
other means.
7) J Segal, W Dzik, et al., Transfusion 2005;45 (9):
References
1413-25 .
1) Blood Safety and Clinical Technology, World
8) Handbook of Transfusion Medicine. The Statio-
Health Organization, 20 Avenue Appia, 1211 Ge-
nery Office, 4th Edition 2007.
neva 27. www.who.int/bct , bct@who.int
9) Simon TL, Snyder EL, Solheim BG, Stowell CP,
2) Hardwick J. Blood processing: Introduction
Strauss RG, Petrides M, editors. 4th ed. West
to blood transfusion technology. ISBT Sci
Sussex, UK: AABB Press-Blackwell Publishing Ltd;
Ser. 76–3:148;2008.
2009. Rossi’s Principles of Transfusion Medicine.

MCQ
1. Each of the following treatments might be 4. A 42-year-old woman is anesthetized
useful in restoring a prolonged prothrombin for resection of a large (22-kg), highly
time (PT) to the normal range EXCEPT vascular sarcoma in the abdomen. During
the resection, 20 units of RBCs, 6 units of
a. Recombinant factor VIII
platelets, 10 units of cryoprecipitate and
b. Vitamin K 5 units of FFPare administered. At the
c. Fresh frozen plasma (FFP) conclusion of the operation, the patient’s
vital signs are stable, and she is transported
d. Cryoprecipitate
to the intensive care unit. Three and a half
2. All of the following characterize packed RBCs hours later, a diagnosis of sepsis is made, and
that have been stored for 35 days at 4° C in antibiotic therapy is started. Which of the
citrate phosphate dextrose adenine-1 (CPDA- items below would be the most likely cause of
1) anticoagulant preservative EXCEPT. sepsis in this patient?
a. Serum potassium greater than 70 a. Packed RBCs

mEq/L
b. Cryoprecipitate
b. pH less than 7.0
c. Platelets
c. Blood glucose less than 100 mg/dl
d. FFP
d. P50 of 28 mmHg
5. Which of the following is false?
3. Which of the measures below does NOT
reduce the incidence of transfusion-related a. Leucocyte depletion in red cell
acute lung injury (TRALI)? suspension significantly reduces the
risk of cytomegalovirus.
a. Exclusion of female donors
b. Blood is routinely screened for Human
b. Use of autologous blood T – Cell Lymphotrophic Virus
c. Leukocyte reduction c. The significance of immunoglobulin
d. Use of blood less than 14 days old A (IgA) antibodies in transfusion
medicine is related to allergic reaction
d. The process aimed at reducing
graft-versus- host disease (GVHD) in
transfusion recipients is the washing
of erythrocytes.
5. (d) 4. (c) 3. (c) 2. (d) 1.(a)

Answers

39 Polytrauma coming for STAT surgery: Assessment
Professor, Anju Grewal

Dayanand Medical College & Hospital,
Ludhiana
Introduction The ‘polytrauma’ definition of Butcher and colleagues

using the Abbreviated Injury Scale (AIS) ≥ 3 for at
Trauma continues to be the leading cause of death least two different body regions has been found to be
worldwide in young individuals younger than 40 years, feasible for identifying polytrauma patients. However,
associated with the highest socioeconomic impact on the definition of polytrauma based on the number of
society. Severe trauma has been found to be associated injured body regions does not reflect the physiological
with trimodal death distribution, wherein the first peak course after injury, which can be very dynamic in
of death occurs within minutes of trauma and is usually a nature and may profoundly influence outcomes. Hence
pre-hospital occurrence. The second peak occurs within the Berlin definition was introduced in 2014 as an
minutes to several hours following injury. Deaths that international consensus which proposes two injuries
occur during this period are usually due to subdural and that are greater or equal to 3 on the AIS and one or
epidural hematomas, hemopneumothorax, ruptured more additional diagnoses (pathologic condition), that
spleen, lacerations of the liver, pelvic fractures and/ is, hypotension (systolic blood pressure ≤ 90 mm Hg,),
or multiple other injuries associated with significant unconsciousness (GCS score ≤ 8), acidosis (base deficit
blood loss. The golden hour of care after injury is ≤6.0), coagulopathy (PTT ≥ 40 seconds or INR ≥1.4) and
characterized by the need for rapid assessment and age (≥70 years) for defining polytrauma.2-7
resuscitation, which are the fundamental principles of Pathophysiological changes in Trauma8-14
Advanced Trauma Life Support.1 We shall be delving
with optimising outcomes and prevention of death Trauma leads to an interplay of tissue damage,
that occurs during the second peak mainly by rapid haemorrhagic shock, pro-inflammatory responses,
with patient co-morbidities, age and secondary
assessment and management for polytrauma patients
hits or interventions. This results in a cascade of
who are scheduled for either Early Total Care (ETC) or
hypothermia, hypotension, poor global perfusion,
Damage Control urgent lifesaving Surgery (DCS).
acidosis and coagulopathy. Hence as anaesthesiologist
Definition of Polytrauma2-7 our initial assessment should be aimed to determine
the injury pattern, physiological effects, patient
Polytrauma is generally used to describe trauma factors and response to resuscitation, which would
patients whose injuries involve multiple body regions, assist in decision making for either an ETC or DCS
compromise the patients’ physiology and potentially and an optimal anaesthetic management plan. One
cause dysfunction of uninjured organs, leading to ARDS must remember that when deciding amongst various
& multiple organ failure (MOF). multiple injuries, severe abdominal, pelvic, thoracic
injuries take priority over skeletal or other injuries.
The Injury Severity Score (ISS) of ≥16 points, which is Presence of traumatic brain injury adds an additional
based on Abbreviated Injury Scale (AIS) has been used responsibility of maintaining a fine balance between
for defining major trauma and evaluating the severity hypotensive resuscitation and adequate perfusion
of injury for the multiple injured victim. pressure to prevent secondary brain injury. Thus,
assessment of polytrauma patient in this complex
Another way to define polytrauma has been based on
scenario requires knowledge and skills ably supported
injury to at least two anatomical areas.
with good communication and teamwork.
Polytrauma coming for Stat surgery: 382 Anju Grewal
Assessment
What is Stat Surgery in the context of Polytrauma?1,8-14 extremely important to communicate with the surgical
and trauma team to maintain continuity of care and
Exsanguinating penetrating injuries requiring immediate ensure optimal management strategies at all times.
surgical control of bleeding, major whole limb traumatic
amputations, decompressive craniotomy, vascular The following concerns need evaluation during this
injuries of extremities with unstable long bone fractures assessment[1,8-14]
are some of the conditions which need the patient to
Airway maintenance with restriction of cervical spine
be taken up immediately for DCS. motion
Assessment 1,8-14 Examination should assist decision for definitive airway
The anaesthetic management of multiple trauma control, best intubation strategy which ensures a safe
patients is very complex, requiring a good collaboration smooth control of airway without any further secondary
with trauma surgeon and other members of trauma hits like hypoxia, especially in cases of concomitant
team. The goals of assessment are to plan optimal brain injury. The decision-making, planning, preparation
anaesthetic care, prevent secondary hits and the vicious and backup plans should be communicated with the
rest of the trauma team.
cycle of acute coagulopathy of trauma (ACOT) and the
triad of hypothermia, acidosis and coagulopathy. If the patient is able to communicate verbally, the
airway is not likely to be in immediate jeopardy;
Hence the aim of pre-anaesthetic assessment are to
however, repeated assessment of airway patency is
ascertain the following:
prudent. However, it is safer to secure a definitive
1) Nature, extent and severity of all injuries and plan airway in a polytrauma patient whenever there is doubt
of surgical intervention on the ability of patient to maintain airway integrity, for
2) Hemodynamic stability example a GCS score of 8 or lower or exsanguinating
3) Response to initial resuscitation injuries necessitating prolonged volume resuscitation,
etc.
4) Co-existing pre-morbidities of the patient
5) Presence of risks of aspiration Airway assessment should always include a quick
but thorough evaluation of anticipated difficulties in
These shall help to formulate plan of anaesthesia airway management inflicted many a times by the
which supports the ongoing resuscitation and avoid need for manual in-line stabilisation of the cervical
any infliction of secondary hit to the compromised spine. It is imperative that an expert help should be
physiology of the patient. Hence, physiological available easily and a double set-up prepared for all
assessment is fundamental to assist in optimising airway management plans in such patients. Double
modifiable factors within the limited window of set-up refers to preparing and planning the best
opportunity. This assessment can indeed help possible attempt at intubation along with a fully-
anaesthesiologist to classify patients into four groups: ready backup for surgical airway intervention if need
Stable, Borderline, Unstable and In extremis and arises. Thus, the cricothyroid membrane is marked and
guides optimisation measures including haemostatic surgical/ ENT team is ready with standard equipment
resuscitation and Damage control resuscitation. for a fast definitive surgical cricothyrotomy in case of
failure to secure airway with plan A. Successful airway
Initial Assessment includes an ABCDE approach to management hinges on the combination of expertise,
delineate all multiple injuries, vital signs and based equipment and human factors.
on these, a logical sequence for treatment priorities
should be agreed upon collectively as a team. This Breathing and ventilation
ABCDE assessment can be performed simultaneously
Includes a careful clinical examination, SpO2 and serial
collectively along with the trauma team in ED. Thus, it is blood gas analysis. If indicated, chest drainage should
Assessment
be placed prior to anesthesia and ventilation. Clinical Exposure/Environmental control

factors (Injuries and physiology) and arterial blood gas
After completing the assessment, initiation of active pre-
analysis guide decision to continued ventilatory support
warming using convective forced air warming blankets
utilising lung protective strategies in perioperative
period. can pre-empt hypothermia. In addition, temperature
should be assessed for further optimisation.
Circulation with haemorrhage control
In addition to a thorough evaluation of ABCDE, one
Blood volume, cardiac output and bleeding are major must obtain a quick focussed history from patient,
circulatory issues to consider. It is imperative to evaluate family, observers, ED staff and trauma team. The AMPLE
the response of the patient to initial resuscitation. mnemonic maybe be used1:
Anesthesiologist must combine assessment and
management simultaneously within the limited time A – allergies;
frame available whilst transporting polytrauma patient M – medications;
to operating room or to radiology suites for urgent P – past medical history;
interventions. L – last meal;
The elements of clinical observation that yield important E – event leading to injury and environment.
information for adequacy of blood volume within
seconds are level of consciousness, skin perfusion and Physiologic parameters such as pulse rate or heart
pulse. The source of bleeding is usually identified by rate (HR), blood pressure (BP), respiratory rate (RR),
physical examination and imaging (e.g., chest x-ray, pulse pressure, ventilatory rate, peripheral oxygen
pelvic x-ray, focused assessment with sonography for saturation (SpO2), ABG levels, body temperature and
trauma [FAST], or diagnostic peritoneal lavage [DPL]). urinary output are assessable measures that reflect
FAST has indeed overtaken DPL or other imaging the adequacy of resuscitation. Values for these
modalities as it provides comprehensive information parameters should be obtained as soon as possible
in a safer environment. and re-evaluated periodically. Point of care blood gas
analysis for assessment of lactate and base excess
Though definitive bleeding control is essential, insertion helps in prediction of outcome in polytrauma patients,
of two large bore peripheral IV access is essential. in assessment of global perfusion in patients with
Hence, assessment for feasibility and availability of haemorrhagic shock, and identifying end point of
peripheral, intraosseous access should be included. resuscitation. A threshold base deficit (BD) of ≥6 mmol/L
Blood samples for baseline hematology, pregnancy test is used as an indicator of haemorrhagic shock and a BD
for women of child bearing age and blood typing and of <5 mmol/L predicts survival. In addition, point of
cross matching should be performed, along with a point care assessment of coagulopathy like International
of care arterial blood gas analysis to assess the presence normalised ratio (INR), Prothrombin time (PT), ROTEM /
and degree of shock, blood gases and/or lactate level. Thromboelastography (TEG), Platelet count, Fibrinogen
Disability (assessment of neurologic status) levels is indicated in the window period available to
assessment and preparation prior to stat surgery. [10, 11]
A rapid neurologic evaluation establishes the patient’s
level of consciousness and pupillary size and reaction; It is imperative that this rapid systematic clinical
identifies the presence of lateralizing signs; and assessment, focussed assessment with sonography
determines spinal cord injury level, if present. Drug in trauma and CT be documented in an organised
or alcohol intoxication may be present concomitant checklist so that handovers ensure a clear forward
to traumatic brain injury and should be repeated at communication, especially during patient transfers
regular time intervals. from ED to Radiology and then to operating rooms
and forward to intensive care. MIST structure [1]
Assessment
(M-Mechanism of injury; I- Injuries sustained or (ATLS) student course manual Chicago, IL: American
suspected; S- Vital Signs prior, during and after College of Surgeons, 2018
transport; T- Treatment and response) is an example
2. Boyd, C.R.; Tolson, M.A.; Copes,W.S. Evaluating
of a structured tool for handover and forward clear
trauma care: The TRISS method. Trauma Score
specific communication.
and the Injury Severity Score. J. Trauma 1987, 27,
This structured documentation is vital in stat surgery, for 370–378.
example surgical control of an exsanguinating external
3. Butcher, N.; Balogh, Z.J. The definition of polytrauma:
haemorrhage which poses immediate threat to life,
The need for international consensus. Injury 2009,
where time is of great essence.
40 (Suppl. 4), S12–S22.
In addition to patient evaluation,
4. Paffrath, T.; Lefering, R.; Flohe, S. How to define
• Assess preparedness for stat surgery severely injured patients?—An Injury Severity Score
(ISS) based approach alone is not sufficient. Injury
• Verify blood products availability before Incision
2014, 45 (Suppl. 3), S64–S69.
with rapid transfusers
5. Butcher, N.; Balogh, Z.J. AIS > 2 in at least two body
• Operating rooms, fluids are pre-warmed, forced air
regions: A potential new anatomical definition of
convective warming continues
polytrauma. Injury 2012, 43, 196–199.
• Monitoring, especially invasive monitoring can be
6. Pape, H.C.; Lefering, R.; Butcher, N.; Peitzman, A.;
instituted without delay
Leenen, L.; Marzi, I.; Lichte, P.; Josten, C.; Bouillon,
• Difficult airway cart, experienced senior help, B.; Schmucker, U.; et al. The definition of polytrauma
additional personnel including nursing, technical revisited: An international consensus process and
and other staff should be available proposal of the new ‘Berlin definition’. J. Trauma
Acute Care Surg. 2014, 77, 780–786
• The role of non-technical skills like team work and
clear communication is vital to good outcomes. 7. Cheng-Shyuan Rau, Shao-Chun Wu, Pao-Jen Kuo,
Yi-Chun Chen, Peng-Chen Chien, Hsiao-Yun Hsieh
In conclusion, the anaesthesiologist should clinically and Ching-Hua Hsieh. Polytrauma Defined by the
assess anatomical injury pattern, severity extent and New Berlin Definition: A Validation Test Based on
mechanism of injury, it’s effect on patient physiology, Propensity-Score Matching Approach Int. J. Environ.
and the patient’s response to initial resuscitation. Res. Public Health 2017, 14, 1045; doi:10.3390/
One must remember that anaesthetic agents often ijerph1409104
worsen the “functional” volume status by increasing
intravascular capacity, hence response to initial 8. Philip F. Stahel*, Christoph E. Heyde*, Wolfgang
resuscitation and volume status should be continually Ertel. Current Concepts of Polytrauma Management.
monitored. Combining ABCDE approach of assessment Eur J Trau ma 2005;31:200–11
with assessment of physiologic parameters provides the
9. C. M. Lamb, P. MacGoey, A. P. Navarro and A.
anesthesiologist with the challenges to be combated
J. Brooks. Damage control surgery in the era of
during the perioperative period, thereby guiding in
damage control Resuscitation. British Journal of
planning optimal anaesthetic management.
Anaesthesia 113 (2): 242–9 (2014) doi:10.1093/
References bja/aeu233
1. American College of Surgeons Committee on 10. N. Enninghorst, R. Peralta, O. Yoshino,R. Pfeifer,

Trauma: Advanced trauma life support for doctors H. C. Pape, B. M. Hardy, D. C. Dewar, Z. J. Balogh

Assessment
Physiological assessment of the polytrauma patient: Polytrauma Patients. Hindawi Publishing Corporation
initial and secondary surgeries. Eur J Trauma Emerg ISRN Orthopedics Volume 2013, Article ID 329452,
Surg (2011) 37:559–566 DOI 10.1007/s00068-011- 9 pages http://dx.doi.org/10.1155/2013/329452
0161-y
13. Grinţescu Ioana Marina, Ungureanu Raluca, Mirea
11. A. L. McCullough*, J. C. Haycock, D. P. Forward and Liliana. Emergency Anaesthesia for Multiple
C. G. Moran. Early management of the severely Trauma. Anaesthesia and Intensive Care Clinic,
injured major trauma patient. British Journal of Clinical Emergency Hospital, Bucharest, Romania
Anaesthesia 113 (2): 234–41 (2014) doi:10.1093/
14. CW Kam, CH Lai, SK Lam, FL So, CL Lau, KH Cheung.
bja/aeu235
What are the ten new commandments in severe
12. Ratto Nicola. Early Total Care versus Damage polytrauma management? World J Emerg Med,
Control: Current Concepts in the Orthopedic Care of Vol 1, No 2, 2010

Assessment
MCQ
1. Berlin definition of Polytrauma includes the 3. What values of base deficit predict
following: haemorrhagic shock and poor survival?
a. Two injuries that are greater or a. ≥6 mmol/L
equal to 3 on the AIS (abbreviated
Injury Scale) and one or more b. =4 mmol/L
additional diagnoses (pathologic c. ≤ 4 mmol/L
condition), that is, hypotension d. =5 mmol/L
(systolic blood pressure ≤ 90 mm
Hg,), unconsciousness (GCS score 4. What is full form MIST structure for adequate
≤ 8), acidosis (base deficit ≤6.0), complete handovers
coagulopathy (PTT ≥ 40 seconds or INR
a. M- Management of airway; I- Injuries
≥1.4), and age (≥70 years)
on limbs; S – Symptoms; T- Treatment
b. Three injuries that are greater or equal
b. M-Mechanism of injury; I- Injuries
to 3 on the AIS (abbreviated Injury
sustained or suspected; S- Vital Signs
Scale) and two additional diagnoses
prior, during and after transport; T-
(pathologic condition), that is,
Treatment and response
hypotension (systolic blood pressure
≤ 70 mm Hg,), unconsciousness (GCS c. M- Multiple injuries; I- Injuries; S-
score ≤ 8), acidosis (base deficit ≤6.0), Signs on arrival; T- Treatment
coagulopathy (PTT ≥ 40 seconds or INR d. M- Mechanism of injury; I- Initiation
≥1.6), and age (≥50 years) of blood transfusion; S- Symptoms on
c. The Injury Severity Score (ISS) of ≥16 arrival; T- Treatment
points
5. Peroperative assessment for Damage Control
d. Abbreviated Injury Scale (AIS) ≥ 3 for Surgery and Hemostatic Resuscitation
at least two different body regions includes the following approaches:
2. Which of the following are examples of Stat a. ABCDE approach
surgery for polytrauma?
b. CABD approach
a. Stable long bone fractures c. ABCDE and Physiological parameters
b. Decompressive craniotomy assessment
c. Facio-maxillary fixation d. Assessment using, ABCDE,
Physiological parameters, and AMPLE
d. Debridement of wound
history approach
5. (d) 4. (b) 3. (a) 2. (b) 1.(a)

Answers

TEG, ROTEM & Platelet Function Assay 388 Ramkumar D
ROTEM is a modern modification of the TEG is transmitted to the torsion wire and is detected by an
technology originally described by Hartert in1948. electromagnetic transducer.
These technologies provide a visual assessment of
In the ROTEM system, a cylindrical cup containing a
clot formation and subsequent lysis under low shear
0.34 ml whole blood sample remains fixed while a
conditions (0.1/sec) similar to those present in the vena
pin suspended on a ball bearing mechanism initially
cava and well below those seen in venules, large veins,
oscillates through 40 75’ every 6 sec through application
and the arterial system.
of a constant force. As the viscoelastic strength of the
Technology (Fig 2) clot increases, the rotation of the pin is impeded and
is detected optically using a charge coupled device
Both ROTEM and TEG assess clot formation/dissolution
image sensor system. It should be noted that a standard
kinetics and strength by measuring and displaying the
ROTEM device is capable of analyzing 4 samples
amount of a continuously applied rotational force that
simultaneously while a standard TEG device is capable
is transmitted to an electromechanical transduction
of analyzing 2 samples. In addition, the TEG device is
system by developing clot. In the TEG system, a
very sensitive to vibration and must be maintained level
cylindrical cup containing a 0.34 ml whole blood
on a stable bench. While ROTEM provides automated
sample oscillates through 40 45’ every 5 sec and a pin
pipetting, the TEG requires manual pipetting of blood
on a torsion wire is suspended in the blood. As the
samples into the cups.
viscoelastic strength of the clot increases, more rotation
Fig 2: TEG and ROTEM devices

Characteristic TEG ROTEM

Pipetting Manual Automated
Cup motion Moving Fixed
Pin motion Fixed Moving
Angle of rotation 4045’/5 sec 4075’/6 sec
Detection Pin transduction Impedance of
Rotation
Temperature control (0C) 24–40 30–40
Temperature regulation Heated cup Heated metal block
Cup interior Smooth Ridged (thickness
0.6–0.9 mm)
Cup material Cryolite (acrylic polymer) Polymethyl methacrylate
Table 1: TEG and ROTEM Operating Characteristics
ROTEM and TEG provide essentially the same results are not interchangeable. Furthermore, the two
information on clot formation kinetics and strength. tests use different nomenclature to describe the same
Because of differences in operating characteristics, the parameters (Fig 3).
Fig 3: Typical TEG and ROTEM tracings. TEG, thromboelastography; ROTEM, rotational thromboelastometry;
R, reaction time; K, kinetics; a angle, slope between R and K (TEG) or slope of the tangent at 2 mm amplitude
(ROTEM); MA, maximum amplitude; CL30, clot lysis at 30 min; CL60, clot lysis at 60 min; CT, clotting time; CFT,
clot formation time; MCF, maximum clot firmness; LY30, lysis at 30 min; LY60, lysis at 60 min

Derived TEG & ROTEM Parameters
TEG ROTEM Definition Significance

R (reaction time): WB CT (clotting time) Time until initiation s Indicates concentration of soluble
4–8 min INTEM 137–246 s of fibrin formation, clotting factors in the plasma.
taken as a period to 2 s Prolonged by anticoagulants,
EXTEM 42–74 s mm amplitude on the factor deficiencies, and severe
tracing hypofibrinogenemia
s Reduced by hypercoagulable
conditions.
K time: WB 1–4 min CFT (clot formation Time period for the s Measurement of clot kinetics.
time) amplitude of the s Prolonged by anticoagulants,
INTEM 40–100 s tracing to increase hypofibrinogenemia, and
from 2 to 20 mm thrombocytopenia
EXTEM 46–148 s s Shortened by increased
fibrinogen level, increased platelet
function.
Alpha angle: WB alpha angle Angle between a s Rapidity of fibrin build up
47–74o INTEM 71–82 o tangent to the tracing and cross-linking. Increased
at 2 mm amplitude by increased fibrinogen level,
EXTEM 63–81 o and the horizontal increased platelet function.
midline s Decreased by anticoagulants,
hypofibrinogenaemia,
thrombocytopenia.
MA (maximum MCF (maximum clot Greatest vertical width s Number and function of platelets
amplitude): WB firmness) achieved by the tracing and fibrinogen concentration.
55–73 mm INTEM 52–72mm Reflecting maximum s Increased by hypercoagulable
clot strength states, thrombocytosis
EXTEM 49–71mm s Decreased by thrombocytopenia,
platelet blockers, fibrinolysis, factor
deficiencies
CL30 LY30 Per cent reduction in s Clot stability and fibrinolysis.
amplitude 30 min after s Prolonged by anticoagulants,
MA hypofibrinogenemia, and
thrombocytopenia
s Shortened by increased
fibrinogen level, increased platelet
function.
CL60 LY60 Per cent reduction of Clot stability and fibrinolysis
clot firmness 1 h after
MCF
WB : Whole blood
Table 2: TEG and ROTEM parameters

TEG output in various coagulopathic states
TEG
Platelet deficiency

Factor deficiency
Hypercoagulable state

Flowchart for diagnosis of clotting abnormalities using TEG
Strengths and limitations of TEG/ROTEM
Strengths Limitations
Viscoelastic point-of-care tests such as TEG and The tracing cannot reflect the contribution of the
ROTEM provide a rapid assessment of the overall endothelium to coagulation, therefore is very poor at
coagulation status of the patient and the derived detecting conditions affecting platelet adhesion, e.g.
parameters can be used to guide the administration von Willebrand’s disease
of specific blood components
TEG and ROTEM analyze all three phases of Preoperative baseline TEG/ROTEM are poor
coagulation, initiation, amplification, and predictors of postoperative bleeding
propagation, reflecting the interactions of the cellular
and plasma components of coagulation and the
activity of the fibrinolytic system
TEG and ROTEM-based transfusion algorithms Will not reflect the effects of hypothermia as the
have been shown to reduce rates of transfusion of measurement is undertaken at 370C
blood components and reduce rates of surgical re-
exploration
Viscoelastic testing has also been shown to be of TEG/ROTEM tracings are insensitive to aspirin and
benefit in detecting a hypercoagulable state in clopidogrel
postoperative patients; the best predictive parameter
being an increased maximum amplitude (MA or MCF)

The TEG kaolin and ROTEM INTEM cartridges are TEG and ROTEM methodology is yet to be
exquisitely sensitive to residual heparin (0.005 standardized in terms of sample collection and
IU / ml) which may be useful in the detection of processing (native or citrated, time delay), activators
inadequate heparin reversal or heparin rebound used and other modifications, making it difficult to
compare results between institutions
There may also be concerns about adequate
maintenance, quality control, and supervision of
personnel running the tests away from the controlled
environment of the laboratory
Although the tracings appear similar, they are not
interchangeable and agreement between ROTEM and
TEG is only moderate
TEG & ROTEM modification assays

TEG Assays
TEG test Description and interpretation

Kaolin Contact activation. Reagent contains kaolin as activator and
provides information similar to that of the PTT.
Rapid TEG Tissue factor and contact activation. Reagent contains
tissue factor and kaolin as activators. Roughly analogous
to an activated clotting time (ACT). Information about
coagulation kinetics initiated via contact activation alone is
lost.
HTEG Reagent contains lyophilized heparinase for neutralizing
unfractionated heparin; used in conjunction with kaolin
reagent and compared to Kaolin analysis to assess heparin
effect.
Functional Fibrinogen Reagent contains tissue factor and abciximab, a GPIIb/
IIIa platelet receptor inhibitor that blocks the platelet
contribution to clot formation. When compared to Kaolin
analysis allows qualitative analysis of the fibrinogen
contribution to clot strength independent of platelets.
Platelet Assay utilizes heparinized blood mixed with Activator F
(reptilase and factor XIIIa). Sufficient heparin is present to
Mapping entirely suppress thrombin generation while fibrinogen is
converted to fibrin and cross-linked due to the presence of
reptilase and factor XIIIa.
Subsequent addition of either ADP or arachadonic acid (AA)
allows determination of the platelet activation response to
these agonists in the absence of thrombin. These results
are compared to Kaolin analysis to determine platelet
response to ADP and AA. This assay requires use of 4
simultaneous TEG channels (2 devices).

ROTEM Assays
ROTEM test Description and interpretation

INTEM Contact activation. Reagent contains
phospholipid and ellagic acid as activators and
provides information similar to that of the APTT.
EXTEM Tissue factor activation. Reagent contains tissue
factor as an activator and provides information
similar to that of the PT.
HEPTEM Contains lyophilized heparinase for neutralizing
unfractionated heparin; used in conjunction with
INTEM reagent and compared to INTEM analysis
to assess heparin effect
APTEM Contains aprotinin for inhibiting fibrinolysis;
used in conjunction with EXTEM reagent
and compared to EXTEM analysis to assess
fibrinolysis.
FIBTEM Utilizes cytochalasin D, an actin polymerization
inhibitor to block the platelet contribution to
clot formation. Used in conjunction with EXTEM
reagent and when compared to EXTEM analysis,
allows qualitative analysis of the fibrinogen
contribution to clot strength independent of
platelets.


Clinical Applications a sequence of interventions based on ROTEM and TEG
analysis and clinical observations that address the
Use of ROTEM and TEG in transfusion algorithms, either multifactorial nature of perioperative coagulopathies.
alone or in combination with other rapid POC tests such
as whole blood platelet multiple electrode aggregometry Cardiac surgery
(MEA) allows goal directed hemostatic therapy to take
Bleeding following pediatric and adult cardiac and aortic
place with administration of nonerythrocyte blood surgery is a common and difficult clinical problem.
products administered to address specific deficiencies. Heparinase assays are very useful in patients on
Ideally, this strategy would be expected to reduce total cardiopulmonary bypass for early assessment of clot
allogenic blood product administration as compared kinetics and strength in the presence of unfractionated
to an empiric transfusion strategy or one based on heparin. The concentrations of UFH present during
laboratory tests with long turnaround times. The cardiopulmonary bypass will yield a flat line ROTEM
turnaround time for standard laboratory tests (PT, and TEG trace without the addition of heparinase to
aPTT, fibrinogen concentration, and platelet count) the sample. The goal directed nature of comprehensive
is generally considered to be too long (45–60 min in ROTEM and TEG analysis based algorithms is apparent
some instances) to guide hemostatic therapy in severely and they appear to reduce the overall transfusion of
bleeding patients whereas meaningful ROTEM and erythrocyte and nonerythrocyte blood products as
MEA measurements are available within 15–20 min. compared to empiric therapy or transfusion algorithms
Currently, algorithms are vertically organized and define based on standard laboratory coagulation tests.
TEG-based transfusion algorithm (Br J Anaesth 2009; 103 (Suppl. 1): i14–i22)
TEG variable Implication Therapy

R>14 and <21 mm ↓ clotting factors One fresh frozen plasma
R>21 and <28 mm ↓↓clotting factors Two fresh frozen plasma
R>28 mm ↓↓↓clotting factors Four fresh frozen plasma
MA <48 mm ↓↓platelet number/function One pooled platelets
MA <40 mm ↓↓↓ platelet number/function Two pooled platelets
Lys30>7.5% Increased lysis Antifibrinolytics (Aprotinin)
Trauma presence of hyperfibrinolysis on initial presentation is

associated with increased mortality and recently, the
Acute Trauma Coagulopathy (ATC) characterized by
ability of comprehensive ROTEM analysis to quickly
systemic anticoagulation and hyperfibrinolysis believed
and accurately detect low grade hyperfibrinolysis as
secondary to endothelial injury and activation of protein
compared to more sensitive assays such as plasmin
C may progress to Trauma Induced Coagulopathy (TIC)
antiplasmin complexes has been questioned.
following on-going blood loss, fluid replacement, and
the development of hypothermia and tissue acidosis Liver transplantation
from hypoperfusion. ROTEM and TEG analysis is proving
The presence of intraoperative bleeding remains a
to be useful in identifying the coagulation profile of
major challenge in orthotopic liver transplantation.
ATC and TIC and is being incorporated in diagnosis
The underlying coagulopathies of cirrhosis, the
and treatment algorithms. In trauma patients, the

intraoperative replacement of large blood losses, and and improve clinical outcome in this high-risk patient
the changing metabolism of coagulant factors during population.
the prehepatic, anhepatic, and neohepatic phases of
Obstetrics
liver transplantation create a complicated, dynamic
hemostatic profile. Interestingly, preoperative ROTEM Standard laboratory coagulation tests correlate
MCF in cirrhotic patients correlates well with the poorly with blood loss in postpartum hemorrhage
model of end stage liver disease (MELD) and Child- (PPH) and a role for comprehensive ROTEM and
Pugh severity of illness scores. ROTEM algorithms TEG based algorithms for diagnosis and treatment
designed to differentiate hypofibrinogenemia of specific coagulation deficiencies in patients with
from thrombocytopenia have been reported but a PPH has been suggested. These technologies would
be particularly useful given the common occurrence
comprehensive algorithm needs to be formulated
of hypofibrinogenemia and hyperfibrinolysis in these
and formally tested. Based on TEG analysis, there
patients. It is important to point out however that
was a reduction in erythrocyte and fresh frozen the coagulopathy of PPH is multifactorial (dilutional,
plasma transfusion in conjunction with an increase in surgical, amniotic fluid embolus, and placental
cryoprecipitate and platelet transfusion, consistent with abruption), that normative ROTEM and TEG values for
a more goal oriented transfusion strategy. It remains patients need to be developed and that POC ROTEM
to be determined if more comprehensive ROTEM and and TEG testing in obstetrics requires the 24 hour
TEG analysis will impact transfusion requirements presence of trained personnel.
Monitoring of hemostasis during postpartum hemorrhage and implications for management (Anaesthesia
2015, 70 (Suppl. 1), 78–86)

Conclusion The normal vascular endothelium produces potent
platelet inhibitors such as nitric oxide, prostacyclin,
ROTEM and TEG technology provide real-time, analysis
and natural ADPase. Once subendothelial components
of the viscoelastic properties of clot formation and
including collagen, fibronectin, laminin or von
dissolution in whole blood. Both ROTEM and TEG,
Willebrand factor (vWF) become exposed upon vessel
using several samples run in parallel with a variety of
wall injury, platelets undergo a highly regulated series
activators and inhibitors, allow the processes of clot
of functional reactions like adhesion, spreading,
initiation, propagation, stabilization, and dissolution
release reaction, aggregation, procoagulant activity,
to be evaluated separately. In addition, it is possible
microparticle formation, and subsequently clot
to separate the effects of platelets and fibrinogen
retraction.
on overall clot strength. Diagnosis and treatment
algorithms incorporating ROTEM and TEG analysis for Adhesion is mediated by the interaction between the
bleeding patients in a variety of clinical situations have glycoprotein (GP) Ib/V/IX receptor complex on the
now been developed. There is some evidence that platelet surface to vWF and GP VI and GP Ia to collagen
these algorithms reduce transfusions and improve at the sites of vascular injury.
clinical outcome but more study is needed.
GP IIb/IIIa is the central platelet receptor mediating
Platelet Function Assay platelet aggregation. Only the activated GP IIb/IIIa
complex is able to bind soluble plasma fibrinogen
Introduction
leading to ultimate aggregation and further spreading
With the widespread use of antiplatelet drugs in of the stimulated platelets along the site of injury.
the management of cardiovascular, cerebrovascular Therefore, aggregation is critically dependent on
and peripheral vascular diseases, there is increasing G-protein coupled receptors and is mediated by
interest in the POCT of platelet function, both to bridges between fibrinogen/vWF (under high shear)
confirm the effectiveness of these drugs and to and the activated GP IIb/IIIa complexes on adjacent,
assess recovery of function when they are stopped. stimulated cells. After the clot has been formed,
Several whole blood point-of-care platelet function the activated platelets rearrange and contract their
tests have been developed with specific activators to intracellular actin/myosin cytoskeleton, which results
detect cyclooxygenase inhibitors (e.g. aspirin), P2Y12 in clot retraction.
antagonists like thienopyridines (e.g. clopidogrel,
Platelet Aggregometry
prasugrel, ticagrelor), and GPIIb/IIIa (glycoprotein IIb/
IIIa) antagonists (e.g. abciximab, tirofiban, eptifibatide) Light transmission aggregometry (LTA) is regarded as
the gold standard of platelet function testing and is still
Basic Physiology
the most used test for the identification and diagnosis
Platelets are small, anucleated cytoplasmic bodies of platelet function defects. Platelet rich plasma (PRP) is
circulating in blood stream. In steady state, stirred within a cuvette located between a light source
megakaryocytopoiesis supplies about 1011 platelets and a detector. After addition of a various panel of
per day with a new turnover every 8-9 days. This agonists, such as collagen, ADP, thrombin, ristocetin,
process is influenced by various environmental changes epinephrine, and arachidonic acid, the platelets
and platelets normally circulate at concentrations of aggregate and light transmission increases. Thrombin
150–400 × 109/L. is a potent platelet agonist. It can be masked if high
concentrations of agonists are added. Parameters
Resting platelets appear as small discoid cells (2–4 measured include the rate or slope of aggregation
𝜇m by 0.5 𝜇m), facilitating their margination toward (%/min) and the maximal amplitude (%) or percentage
the vessel wall, where they can constantly survey the of aggregation after a fixed period of time, usually 6–10
integrity of the vascular endothelium. minutes.

Platelet Function Assay prolonged in qualitative and quantitative abnormalities
of von Willebrand factor, which is the most common
A vacuum induces flow of citrated whole blood through
inherited coagulation disorders. The epinephrine
a collagen-coated membrane with a 150 mm aperture
to which the platelet activators epinephrine or ADP CT is prolonged in the presence of aspirin, while
are bonded. This results in activation of platelet and the ADP CT remains normal, making the PFA-100
aggregation. The time taken for a platelet plug to useful in assessing aspirin sensitivity. The CT for both
occlude flow through the aperture is defined as the cartridges is prolonged by GPIIb/IIIa antagonists. P2Y12
closure time (CT) (normally 5–8 min) and reflects cartridges had been introduced to evaluate the effects
platelet function. Both epinephrine and ADP CTs are of thienopyridines.
Major platelet function tests and their clinical applications
Name of test Principle Clinical applications
Platelet aggregometry Platelet aggregation to a panel of Diagnosis of inherited and acquired platelet
agonists defects
PFA-100/200 High shear platelet adhesion and Detection of inherited and acquired platelet
aggregation defects, monitoring antiplatelet drugs
Flow cytometry Measurement of platelet GP, secretion, Diagnosis of platelet GP defects, platelet
MP, and activation markers by release, PMP, platelet activation markers,
fluorescence monitoring antiplatelets drugs
Impact Measurement of platelet adhesion and Detection of inherited and acquired platelet
aggregation under high shear defects, monitoring antiplatelet drugs
Thrombelastography Monitoring rate and quality of clot Prediction of surgical bleeding, aid to blood
formation product usage, monitoring anti -platelets
(TEG/ROTEM) drugs
VerifyNow Platelet aggregation Monitoring antiplatelet drugs
Multiplate Platelet aggregation Monitoring antiplatelet drugs
VASP-P Flow cytometry with phosphoprotein- Monitoring P2Y12 receptor activity

phosphorylation
Microparticles Flow cytometry with calibrated beads Platelet activation markers, intercellular
communication
PFA: platelet function analyzer; GP: glycoprotein; MP: microparticles; PMP: platelet-derived microparticles;
TEG: thrombelastography; ROTEM: rotational thrombelastometry; VASP-P: phosphorylation of vasodilator-
stimulated phosphoprotein-phosphorylation.

Plateletworks Data from recent clinical trials (eg, EPIC, EPILOG) have
suggested that >80 percent of platelet receptors need
Plateletworks aggregation system uses an impedance
to be blocked in order to achieve significant clinical
cell counter to assess platelet count in a baseline
efficacy with antiplatelet agents. A modified platelet
whole blood EDTA sample. This was compared with
aggregometry device has been developed in order
the platelet count in a citrated sample plus agonist
to provide a simple and rapid functional means of
(arachidonic acid or ADP). The agonist causes platelet
monitoring anti-GPIIb/IIIa therapy (eg, abciximab). The
activation, leading to the formation of aggregates which
VerifyNow GPIIb/IIIa Assay is based upon the principle
exceed the threshold for platelet size and thereby not
that fibrinogen-coated beads will agglutinate in whole
counted. Thus, if platelet function is normal, the count
blood in proportion to the number of available platelet
decreases to zero. Any other ratio of the count between
GPIIb/IIIa receptors. A disposable cartridge employed
the baseline and test samples will be used to calculate
for this test contains fibrinogen-coated beads and a
the percentage of platelet aggregation or inhibition in
platelet activator (TRAP – Thrombin Receptor Activating
response to drugs such as aspirin (agonist arachidonic
Peptide) within reaction wells. There are two other
acid) and clopidogrel or GPIIb/IIIa antagonists (agonist
cartridges (VerifyNow Aspirin and VerifyNow P2Y)
ADP).
available for monitoring either aspirin or P2Y inhibition,
The VerifyNow system respectively.
The VerifyNow system measures the alteration in light Viscoelastic methods

transmission over time across an anticoagulated whole
Viscoelastic methods (TEG and ROTEM) alone appear
blood sample. The sample is agitated with fibrinogen
to have limited ability for prediction of blood loss and
- coated polystyrene beads and a platelet agonist
transfusion requirements after cardiac surgery.
designed to detect inhibition by aspirin (arachidonic
acid), clopidogrel (ADP), or glycoprotein IIb/IIIa receptor This limitation is particularly apparent in patients
antagonists (thrombin receptor-activating peptide). receiving antiplatelets medications. Modifications of
The activated platelets bind to the beads causing TEG, such as platelet mapping, attempt to overcome
aggregation. The greater the platelet activation and these limitations, demonstrating improved predictive
aggregation, the greater the light transmission through ability for blood loss and transfusion requirements
the sample, thus the degree of platelet inhibition. in patients on antiplatelet therapy. The quantitative
analysis of randomized control trials revealed that
Uses
the use of point-of-care platelet function tests as part
In patients undergoing different kinds of elective surgeries, of a blood transfusion algorithm is associated with a
the assessment of platelet dysfunction with PFA-100 reduction in our primary outcome of postoperative
may provide useful information for postoperative blood blood loss. The combination of viscoelastic and other
transfusion management. Especially in cardiothoracic platelet function testing methods (PFA-100, multiple
surgery, PFA methodology showed a high predictive electrode aggregometry, platelet mapping) achieved
value of platelet function for management of intra- and a larger effect size in terms of blood loss reduction
postoperative blood loss. In patients with biventricular compared with viscoelastic methods alone.
assist device implantation with clopidogrel, the use of
Conclusion
collagen (C) plus ADP – CADP cartridge diagnostics for
monitoring the degree of platelet inhibition allowed The variability in individual response to a fixed dose of
them to undergo transplantation without major blood antiplatelets medication is now well established and
loss. In addition, prolonged CADP CTs were found be near-patient platelet function analysis has the potential
independent risk factors for postpartum hemorrhage as a screening tool to identify patients who are either
(PPH) severity. hyper- or hypo-responsive to antiplatelets medication.
It also has a role in monitoring clotting during surgery.

In summary, evidence suggests that point-of-care duced coagulopathy in adult trauma patients
platelet function tests have not consistently been with bleeding (Review). The Cochrane Library
shown to predict the risk of bleeding in the surgical 2015, Issue 2.
patient. The incorporation of point-of-care platelet 6) TEG and ROTEM: Technology and clinical applica-
function tests into blood transfusion management tions, American Journal of Hematology, Vol. 89,
algorithms is associated with a reduction in blood loss No. 2, February 2014.
and transfusion requirements. The use of a combination
of viscoelastic methods and platelet agonist assays 7) Rotation thromboelastometry velocity curve pre-
dictsblood loss during liver transplantation. Brit-
achieved the greatest reduction in blood loss and blood
ish Journal of Anaesthesia, 117 (6): 741–8 (2016).
transfusion requirements.
8) Thrombelastography (TEG) or thromboelastom-
Further Reading etry (ROTEM) to monitor haemotherapy versus
1) Point-of-care coagulation testing. BJA ceaccp/ usual care in patients with massive transfusion
mks049. Advance Continuing Education in Anaes- (Review), Afshari A et al, Cochrane Database of
thesia, Critical Care & Pain | Volume 13 Number Systematic Reviews 2011, Issue 3.
1 2013. 9) Thromboelastometry (ROTEM) in children:
2) Point-of-care coagulation testing and transfusion age-related reference ranges and correlations
algorithms, British Journal of Anaesthesia 103 with standard coagulation tests, British Journal of
(BJA/PGA Supplement): i14–i22 (2009) Anaesthesia 105 (6): 827–35 (2010).
3) Haemostatic monitoring during postpartum hae- 10) The role of point-of-care platelet function testing
morrhage and implications for management, in predicting postoperative bleeding following
British Journal of Anaesthesia 109 (6): 851–63 cardiac surgery: a systematic review and me-
(2012). ta-analysis. Anaesthesia 2015, 70, 715–731
4) Thromboelastography (TEG) or rotational throm- 11) Antiplatelet agents and anaesthesia. Continuing
boelastometry (ROTEM) to monitor haemostatic Education in Anaesthesia, Critical Care & Pain |
treatment in bleeding patients: a systematic re- Volume 7 Number 5 2007
view with meta-analysis and trial sequential anal- 12) Clinical utility of closure times using the platelet
ysis. Anaesthesia 2017, 72, 519–531. function analyzer-100/200. Am J Hematol. 2017;
5) Thromboelastography (TEG) and rotational 92: 398–404
thromboelastometry (ROTEM) for trauma in-

MCQ
1. False about ‘R’ (reaction time) is 4. Which of the following viscoelastic
method used to assess the effectiveness of
a. Time until initiation of fibrin
antiplatelet drugs?
formation, taken as a period to 2 mm
amplitude on the tracing a. PFA-100/200
b. Prolonged by anticoagulants b. Flow cytometry
c. Corresponds to CT (clotting time) of c. Platelet aggregometry
ROTEM
d. Platelet Mapping
d. Indicates about fibrinolysis
5. Maximum Clot Firmness is all except
2. Hypercoagulation in TEG inferred by all
except a. Measured during Platelet Function
Assay
a. Decreased R
b. Indicates platelets and fibrinogen
b. Decreased K concentration
c. Decreased MA c. High value indicates hypercoagulabilty
d. Increased angle d. It is the greatest vertical width
3. False about FIBTEM achieved by the tracing reflecting
maximum clot strength
a. Utilizes cytochalasin D
b. Blocks the Fibrinogen
c. Allows qualitative analysis of the
fibrinogen contribution to clot
strength
d. Compared to EXTEM analysis for
analysis
5.(a) 4.(d) 3.(b) 2.(c) 1.(d)

Answers

41 DEFIBRILLATION
Professor (Sr. Scale), Pankaj Kundra

JIPMER,
Puducherry
Definition DC Defibrillation
D efi b r i l l ati o n i s n o n - sy n c h ro n i ze d ra n d o m In 1962, DC defibrillation was introduced by Lown B. The
administration of shock during a cardiac cycle. The DC shock requires charging of capacitors. The duration
process of defibrillation involves electrical current that and the strength of the DC shock are dependent on the
travels from the negative to the positive electrode by capacitor properties. The time for the repeated shock
traversing myocardium. It causes all of the heart cells may get prolonged because of the need for capacitor
to contract simultaneously. It interrupts and terminates recharging.
abnormal electrical rhythm and in turn allows the sinus A capacitor is charged with high DC voltage and then
node to resume normal pacemaker activity. rapidly discharged. The amount of energy that can be
discharged from the capacitor ranges from 2 – 400
AC Defibrillation Joules with peak value of current 20 Amps. A corrective
Zoll PM in 1956, first introduced alternating current (AC) shock of 750 – 800 volts is applied within 1/10th of
defibrillation to treat ventricular fibrillation in humans. second.
The first waveform used for ventricular defibrillation Principles of Defibrillation
was the 60 Hz AC similar to that used as standard
household current. AC can be used to induce ventricular • Energy storage of capacitor is charged from
AC line.
fibrillation and to defibrillate the heart. AC current after
defibrillating the heart can induce fibrillation again. In • Energy stored in the capacitor is then delivered
addition, because of myocardial damage and inability to at a rapid rate to the chest of the patient.
produce constant stable current from AC defibrillation, • Discharge of the capacitor energy occurs
direct current (DC) units were developed. through the patient’s resistance. The discharge
resistance which the patient generally presents
The effectiveness of this AC shock is dependent on the is roughly 50 – 100 ohms for a standard
amplitude and duration of the applied current. High- electrode size of 80 cm2.
amplitude current does not induce ﬁbrillation and low
Monophasic Defibrillation
amplitude current does not terminate the ﬁbrillation,
suggesting the lower and upper limit of vulnerability. In Type of shock that sent electrical current in a single
addition, the delivery of the current has to be sudden direction from an electrode on one side of the
and not a gradual increase from low amplitude to high patient’s chest to a 2nd electrode on the other side.
amplitude. This technology is known as monophasic waveform
defibrillation.
AC Defibrillation (Counter shock):
The waveform associated with monophasic
• Burst of 60 Hz for 0.25 to 1 sec at intensity of defibrillations contains a single peak. This peak current
6 Amps. is critical in determining successful defibrillation
because there must be enough current to reach the
• Burst can be repeated till the patient responds. heart to terminate the fibrillation, while at the same

Defibrillation 406 Pankaj Kundra
time avoiding too high of a peak current, which can defibrillator (AED). Current biphasic AEDs are small and
damage the heart. This peak current coupled with the portable, making it publicly-accessible devices.
body’s resistance to the current (impedance), comprise
the two components that make up defibrillation. In
a monophasic defibrillator, the delivered current is
typically very high (360 joules), thus requiring bulky
internal components to allow for the generation
and storage of the required amount of electrical
current. There are 2 types of monophasic waveform
defibrillators:
• Monophasic damped sinusoidal waveform
(MDS): Current returns to zero gradually
• Monophasic truncated exponential waveform
(MTE): Current is abruptly returned to baseline
to zero current flow.
Biphasic Defibrillation
Over time, these devices evolved to become more
efficient, more accurate, and easier to use, all while
delivering a less-powerful shock by using the same
type of current technology found in automatic
implantable cardioverter-defibrillators (ICD). This bi-
Advantages of Biphasic over Monophasic
directional current flow is known as biphasic waveform
defibrillation. 1) Lesser power required hence lesser trauma and
less battery consumption
Electric current is sent from one electrode (negative) to
the other (positive) in the first phase of this waveform, 2) Defibrillation is more effective at low energy lev-
followed by a return back to the originating electrode els
in the second phase. Reversing of polarity, depolarises 3) Fewer incidence of burns
all cells which is termed as “Burping response”. Biphasic
technology requires a much lower current to achieve 4) Lesser myocardial damage
successful termination of fibrillation (150 – 200 Joules). 5) First shock success rate in cardiac arrest due to
It is again of 2 types shockable rhythm is 90% when compared to 60%
with monophasic.
• Rectilinear biphasic waveform (RLB): 120
Joules Indications for Defibrillation (Shockable rhythms)
• Biphasic truncated exponential waveform • Pulseless ventricular tachycardia (VT)
(BTE): Requires 150 – 200 joules. RLB is better
than BTE. • Ventricular fibrillation
Biphasic current technology has shown a higher • Cardiac arrest due to or resulting in VF
efficacy with regards to successful defibrillations than Non-shockable rhythms
with monophasic technology. It comprises of lower
current, the components are reduced tremendously in Pulseless electrical activity and asystole. CPR should be
size, leading to the advent of the automated external continued till a shockable rhythm is noticed.

Contraindications Step 2: Power ON the defibrillator.
• Dysrhythmias due to enhanced automaticity Step 3: Apply electrode jelly to the paddles. Place the
(Digitalis toxicity and catecholamine-induced paddles on the anterolateral position (One on the
arrhythmia). A homogeneous depolarization right of sternum below the clavicle in the 2nd and 3rd
already exists. Cardioversion can lead to post intercostal space and the other in midaxillary line in
shock VT/VF. the left 4th – 5th intercostal space. Ensure paddles are
connected to the defibrillator.
• Multifocal atrial tachycardia
Step 4: Turn the defibrillator control knob to select
Efficacy of Defibrillation
paddle mode.
• Transthoracic impedance: It is a major
Step 5: Reidentify that there is a shockable rhythm.
factor and depends upon chest width and
configuration Step 6: Select the charge level of energy (120 joules) and
press charge and confirm the defibrillator has attained
• Duration of VF: Success rate decreases by
the selected energy level.
7-10% with every passing min.
Step 7: Instruct all personnel to stay clear.
• M y o c a r d i a l e n v i r o n m e n t : H y p o x i a ,
hypothermia, acidosis, electrolyte imbalance, Step 8: Deliver the shock by pressing the shock button.
drug toxicity impede success. However,
Step 9: After shock is delivered resume CPR for 2 min
defibrillation should not be delayed to correct
and assess rhythm.
them
Step 10: If second shock is indicated, select 200 joules
• Body size and type: Larger the body size, more
and deliver in similar fashion.
is the impedence
Cardioversion
• Previous counter shock: Repeated shock lower
resistance. Delivery of energy that is synchronized to the large
R wave or QRS complex. It uses lesser energy than used
• Paddles:
for defibrillation in shockable SCA.
• Paddle placement in pacemaker or AICD:
Indications for electrical cardioversion include the
Paddles should be placed at least 12 cm
following
from pacemaker generator and at 90
degrees to the AICD electrode. • Supraventricular tachycardia (atrioventricular
nodal re-entrant tachycardia [AVNRT] and
• Size of paddles: Use largest size paddles as
atrioventricular re-entrant tachycardia [AVRT])
they reduce current density. The paddles
should completely be in contact with chest • Atrial fibrillation
without touching each other
• Atrial flutter (type I and II)
• Paddle contact pressure: Firm pressure of
25 pounds should be applied on paddles • VT (monomorphic or polymorphic) with pulse
and lungs should be deflated. • Any patient with re-entrant tachycardia with
Steps of Defibrillation narrow or wide QRS complex (ventricular rate
>150 bpm) who is unstable (e.g., ischemic chest
Step 1: Shockable rhythm detected. Start and continue pain, acute pulmonary oedma, hypotension,
CPR till the defibrillator is arranged acute altered mental status, signs of shock)

Cardioversion should always be performed under • Wide regular QRS complexes: 100 joules
adequate sedation. Patients can be administered
• Wide irregular QRS complexes: Defibrillation
a small dose (midazolam 1 – 2 mg) of short acting
dose (unsynchronized)
sedative. Oxygen should be supplemented and airway
should be supported and maintained. Cardioversion Complications of cardioversion
can be done as an emergency or elective procedure.
NPO guidelines should be followed in an elective case. • Systemic embolization
Synchronized cardioversion: Initial recommended dose • Post shock arrhythmias: Asystole, heart
block, atrial/ventricular ectopics, ventricular
• Narrow regular QRS complexes: 50 – 100 joules tachyarrhythmias.
• Narrow irregular QRS complexes: 120 – 200 • Transient ST-T wave changes
biphasic, or 200 joules monophasic

MCQ
1. Indications of defibrillation are all, except? 4. AEDs use what kind of technology?
a. Pulseless VT a. Monophasic Damped Sinusoidal
b. VF waveform
c. Asystole b. Monophasic Truncated Exponential
waveform
d. Cardiac arrest due to VF
c. Biphasic waveform
2. Complications of cardioversion are all,
except? d. AC defibrillation
5. Advantages of biphasic waveform over
a. Ventricular tachyarrhythmias
monophasic waveform are all, except?
b. Atrial flutter
a. Less power requirement
c. Asystole
b. First shock success rate is more
d. Heart block
c. Effective at low energy levels
3. Minimum distance of defibrillating paddles to
be kept from the pacemaker is? d. More incidence of burns
a. 20cm
b. 5cm
c. 2cm
d. 12cm
5. (d) 4. (c) 3. (d) 2. (b) 1.(c)

Answers

42 VAP bundles
Professor and Head Jigi Divatia

Tata Memorial Hospital
Mumbai
Key points
Ø VAP is the commonest nosocomial infection in mechanically ventilated patients

Ø CDC introduced new surveillance definitions for monitoring mechanically ventilated patients which
consist of hierarchy of three tiers – VAC, IVAC and possible/probable pneumonia
Ø Microorganisms colonized in upper respiratory and upper GI tract gain access to the lower airways
through aspiration of small amounts of hypopharyngeal contents
Ø Preventive measures are routine oral hygiene, clearance of oral and subglottic secretions, nursing in
elevated head position, avoidance of H2 blockers and PPIs, hand hygiene, faster weaning from ventilator
and use of NIV
Ø Bundle care are group of therapies which give greater benefit in terms of outcome rather than the
individual therapeutic interventions.
Definition of ventilator associated pneumonia VAP is the second most common nosocomial infection
and is the commonest nosocomial infection in patients
Ventilator associated pneumonia (VAP) is defined
who are mechanically ventilated. The incidence
as an inflammation of the lung parenchyma caused
increases with duration of ventilation. The risk of VAP
by infectious agents not present or incubating when
is estimated to be 3%/day during the first 5 days of
mechanical ventilation (MV) was started and that
ventilation, 2%/day during Days 5 to 10 of ventilation,
occurs more than 48-72 hours after tracheal intubation.
Early VAP occurs within the first 4 days after intubation. and 1%/day after this. Because most mechanical
It may have a better prognosis and is more likely to ventilation is short term, approximately half of all
be caused by antibiotic sensitive bacteria. Late VAP, episodes of VAP occur within the first 4 days of
occurring 5 or more days after intubation is more likely mechanical ventilation.
to be caused by multi-drug resistant pathogens. In 2011, Centers for Disease Control (CDC) developed
Hospital Acquired Pneumonia (HAP) is defined as new surveillance definitions for patients receiving
pneumonia that occurs 48 hours or more after hospital mechanical ventilation based on objective criteria
admission, which was not incubating at the time of that would identify a broad range of conditions and
admission. Health Care Associated Pneumonia (HCAP) complications occurring in mechanically ventilated
includes any patient who was hospitalized in an acute adult patients. The new definitions consist of hierarchy
care hospital for two or more days within 90 days of of surveillance targets.
the infection; resided in a nursing home or long-term
The first target is Ventilator associated condition (VAC)
care facility; received recent intravenous antibiotic
therapy, chemotherapy, or wound care within the past and is an essentially a new respiratory deterioration.
30 days of the current infection; or attended a hospital It is defined as at least 2 days of stable or decreasing
or hemodialysis clinic. daily minimum positive end-expiratory pressure

VAP Bundles 412 Jigi Divatia
(PEEP) or daily minimum fraction of inspired oxygen • ETA with ≥105 colony-forming units per
(FiO2) followed by a rise in daily minimum PEEP of milliliter or BAL culture with ≥104 colony-
≥3 cm of water or a rise in the daily minimum FiO2 forming units per milliliter, or ETA or BAL
percentage by >20 points sustained for ≥2 calendar semiquantitative equivalent,
days. It is intentionally designed to be non-specific
and accommodate all types of pulmonary and non- within 2 calendar days before or after onset of a VAC,
pulmonary complications which can increase the excluding the first 2 days of mechanical ventilation
ventilator settings. Most of the VACs are due to The new definitions do not include radiographic criteria
pneumonia, pulmonary edema, atelectasis and acute as they increase complexity and subjectivity without
respiratory distress syndrome (ARDS). increasing accuracy. This exclusion does not mean
The remaining tiers of VACs are designed to identify that radiography is less important in diagnosing VAP
VACs that are infection related. and keeping in mind that these definitions are to aid
surveillance.
• Infection-related ventilator associated
complication (IVAC) is new respiratory The prevalence of VAP is often considered an important
deterioration with evidence of infection. IVAC quality indicator in intensive care. The rate of VAP
is VAC plus is expressed in terms of patients receiving MV via
endotracheal tube. VAP rate is defined as the number
• a temperature of <36°C or >38°C or a of VAPs per 1000 ventilator days. It is calculated as
leukocyte count of ≤4000 or ≥12,000 per
cubic millimeter, plus Number of patients with VAP
VAP rate = X 1000
• one or more new antibiotics continued for Number of days of MV
at least 4 days
where the total days of MV is the sum of the duration
within 2 calendar days before or after onset of a VAC, of MV of all patients receiving MV in the ICU in the
excluding the first 2 days of mechanical ventilation. given period.
• Possible pneumonia is new respiratory Etiopathogenesis
deterioration with possible evidence of
Microorganisms, usually gram-negative bacilli (GNB),
pulmonary infection. It is defined as IVAC plus
colonize the upper respiratory tract, the upper gastro
• Gram’s staining of endotracheal aspirate intestinal tract, or both, and act as sources of infection.
(ETA) or bronchoalveolar lavage (BAL) These organisms then gain access to the lower airways
showing ≥25 neutrophils and ≤10 epithelial through aspiration of small amounts of hypopharyngeal
cells per low-power field, or contents. Host factors and predisposing environment
further contribute to colonization and infection.
• positive culture for a potentially pathogenic
organism Sources of colonizing bacteria
within 2 calendar days before or after onset of a VAC, • Dentition: Dental plaque increases with ICU
excluding the first 2 days of mechanical ventilation. stay, and the bacterial flora frequently mirrors
that of tracheal aspirates
• Probable pneumonia is new respiratory
deterioration with probable evidence of • Oropharynx: In health, the oropharynx is
pulmonary infection. It is defined as IVAC plus colonized predominantly by non-pathogenic
bacteria, but in hospitalized patients this
• Gram’s staining of ETA or BAL showing ≥25 flora is replaced with pathogenic bacteria,
neutrophils and ≤10 epithelial cells per low- predominantly aerobic GNB and staphylococci,
power field, plus and this increases the risk of VAP
• Sinuses trauma, multi-organ involvement, severe illness (high
APACHE score), immunosuppressive therapy, previous
• Stomach: Reduction in gastric acidity increases
use of antibiotics, presence of nasogastric tubes,
the rate of gastric colonization. H2 antagonists
central venous lines and urinary catheters are sources
and antacids increase pH and gastric
of bloodstream infection and other host diseases like
colonization more than the cytoprotective
diabetes mellitus are also important contributory
agents such as sucralfate. Regurgitation of
factors for VAP.
gastric contents and pooling of these fluids in
the hypopharynx and above the tracheal tube Prevention of VAP
cuff is an important source of bacteria
General Measures
• Feco-oral or feco tracheal route: cross
1) Nursing care: strict infection control procedures
colonization or transfer of rectal bacilli by
should be in place, for example, hand washing
health care providers and the sterilization of equipment. Routine oral
Microbial entry mechanisms hygiene and the removal of secretions in the
mouth and subglottis are important. Nursing the
• Endotracheal tube is the most important patient in a 30-45o head-elevated position is a
risk factor as it bypasses the normal defense important method of reducing VAP.
mechanisms of cough reflex of glottis and 2) Avoidance of tracheal intubation and use of
larynx. noninvasive ventilation whenever possible.
• Pooling and trickling of subglottic secretions. 3) Oral vs nasal intubation: The use of oral rather
than nasal tracheal intubation has been associated
• Aspiration of oropharyngeal secretions past
with lower rates of VAP and is due to the reduced
the tracheal tube cuff. incidence of sinusitis with oral intubation.
• Impaired mucociliary clearance 4) Selective decontamination of the digestive
• Secretions are also pushed inside by the tract: involves infection control by general
hygiene, topical non-absorbable bactericidal
positive pressure exerted by ventilator
antimicrobials (chlorhexidine gel or mouth
• Contamination through the respiratory wash 1-2%) administered to the oropharynx.
apparatus Role of selective decontamination of the gut is
controversial.
• Biofilm laden with microorganisms (mostly
gram negative bacteria and fungal species) 5) Gastric alkalinisation: the gastric colonization
associated with H2 antagonists compared with
within the endotracheal tube.
sucralfate shows a trend towards an increase in
• Emergency intubations and especially VAP rates.
reintubation after extubation 6) Gastro-oesophageal reflux occurs in mechanically
• Ventilator circuit ventilated patients with nasogastric tubes.
7) Enteral feeding: Avoiding stomach overdistension
• H e at a n d m o i st u re exc h a n ge ( H M E )
by monitoring residual gastric volume during
humidification, as opposed to heated
feeding protocols, and the placing of jejunal
humidifiers may have a protective effect feeding tubes may be appropriate.
through minimizing tubing condensate and
colonization. 8) Ventilator circuit: should be actively managed so
that condensate fluid does not wash back into
Immunosuppression and other host factors like the patient but can be removed from water traps.
advanced age, underlying chronic lung disease, surgery,
9) HME filters should be considered. Tubing should 1) Identify a set of four to six evidence-based
be changed only if heavy soiling occurs. Closed interventions that apply to a cohort of patients
circuit suction may help. with a common disease or a common location.
Reduction in aspiration past the cuff 2) Develop the will in the providers to deliver the
1) Subglottic secretion drainage: is performed using interventions every time they are indicated.
a tracheal tube incorporating a separate dorsal 3) Measure compliance as “all” or “nothing.” The
lumen ending in the subglottic space just above
Institute for Healthcare Improvement and the
a HVLP cuff.
Centers for Medicare and Medicaid Services
2) Unplanned extubations: appropriate securing of proposed instituting “all or none” performance
tracheal tubes and the prevention of the need for measures.
reintubations may reduce the risk of VAP.
4) Redesign the delivery system to ensure the
3) Silver coated endotracheal tubes prevent interventions in the bundle are delivered.
bacterial colonization and biofilm formation.
One study showed significant reduction in the 5) Measure related outcomes to ascertain the
incidence of microbiologically proven VAP (4.8% effects of the changes in the delivery system.
Vs 7.5% with uncoated tubes) , however more
studies are required. Need for bundles
Enhancement of bacterial clearance from airways Bundle effectiveness comes from the excellence of the
and lung tissue as well as tracheal suctioning, three supporting evidence and its consistent comprehensive
mechanisms may help bacterial clearance. execution, with the impact being greater by performing
all elements together rather than any individual
1) Kinetic beds: possible advantages of rotational component. Invariably bundle elements are not new,
beds include intrathoracic postural drainage, have a strong clinical base, but because in normal
the limitation of pooled secretions in the upper
practice they are not uniformly performed, treatment
airway and improvements in gas exchange.
is unreliable and driven on occasion by idiosyncrasies.
2) Physiotherapy: chest physiotherapy, postural Bundles remove these variations by constructing the
drainage, occlusion and vibration in association elements into packages that must be followed for
with tracheal suctioning are used to promote every patient every single time. It is this simplicity and
secretion drainage and improve lung expansion. inherent strength that have increased the approach’s
Care Bundles attractiveness and applicability.
Bundles are a group of ‘therapies’ built around best Care bundles differ from standard care pathways in the
evidence based guidelines, which, when implemented way that compliance is measured; only if all elements
together give greater benefit in terms of outcome than of the bundle are applied, the team is compliant with
the individual therapeutic interventions. The Institute the bundle. The team fails if they fail to achieve even
for Healthcare Improvement and the Centers for one target or element. i.e., compliance is all or none.
Medicare and Medicaid Services proposed care bundles Ventilator Bundle or VAP Prevention bundle
to effectively deliver high quality, evidence-based care.
Care bundles are based on the principle that the whole The 5 element of VAP bundle introduced by Institute
is greater than the sum of its parts. of Healthcare improvement (IHI) are: Head of bed
elevation, oral care with chlorhexidine, stress ulcer
A bundle process that combines the best of medical prophylaxis, deep venous thrombosis prophylaxis, and
science and improvement science is developed in the daily sedation assessment and spontaneous breathing
following way : trials.

The INICC Bundle consists of: oral care, positioning in bed, striving to reduce
ventilator days, and discouraging scheduled changes of
1) Adherence to hand hygiene
ventilator circuits. “Highly recommended measures”
2) Maintenance of patients in a semi-recumbent were selective decontamination of the digestive tract,
position (30–45° elevation of the head of the bed) subglottic suctioning and short course antibiotics for
3) Performance of daily assessments of readiness to patients intubated with altered sensorium.
wean and use of weaning protocols Thus VAP bundles are easy to implement and effective
4) Performance of regular oral care with an in reducing the VAP rates significantly in developed as
antiseptic solution well as developing countries.
5) Use of non-invasive ventilation whenever possible Recommended Reading

and minimization of the duration of ventilation
1) American Thoracic Society, Infectious Diseases So-
6) Preferable use of orotracheal instead of ciety of America: Guidelines for the management
nasotracheal intubation of adults with hospital-acquired, ventilator-asso-
ciated, and healthcare-associated pneumonia.
7) Maintenance of an endotracheal cuff pressure of Am J RespirCrit Care Med 2005, 171:388-416
at least 20 cm H2O
2) CDC (2018a) ‘CDC/NHSN Surveillance Definitions
8) Removal of the condensate from ventilator for Specific Types of Infections’, January(17), pp.
circuits and keeping the ventilator circuit closed 1–30.
during condensate removal
3) Institute for Healthcare Improvement: Evi-
9) Change of the ventilator circuit only when visibly dence-Based Care Bundles (no date). Available
soiled or malfunctioning at: http://www.ihi.org/Topics/Bundles/Pages/
10) Avoidance of gastric overdistention default.aspx (Accessed: 17 July 2018).
11) Avoidance of histamine receptor 2 (H2) blocking 4) Institute For Healthcare Improvement, I. (2012)
agents and proton-pump inhibitors Institute for Healthcare Improvement: How-toGu-
ide: Prevent Ventilator-Associated Pneumonia.
12) Use of sterile water to rinse reusable respiratory Available at: http://www.ihi.org/resources/Pag-
equipment es/Tools/HowtoGuidePreventCatheterAssociat-
edUrinaryTractInfection.aspx (Accessed: 17 July
A landmark study demonstrated a 44.5% reduction 2018).
in VAP using bundle approach. In a study involving
Indian ICUs, the INICC approach including the above 5) Resar R, Pronovost P, Haraden C, et al. Using a
bundle of interventions, education, outcome and bundle approach to improve ventilator care pro-
process surveillance, and feedback of VAP rates and cess and reduce ventilator associated pneumo-
nia. JtComm J Qual Patient Saf 2005;31:243-8
performance, the VAP rate was reduced by 38%,
from a baseline rate of 17.4/1000 ventilator days to 6) Mehta Y, Jaggi N, Rosenthal VD, et al. Effective-
10.8/1000 ventilator days. In Spanish ICUs, there was ness of a multidimensional approach for preven-
a reduction of VAP rates by more than 50% with the tion of ventilator-associated pneumonia in 21
implementation of a VAP bundle among ICU’s across the adult intensive-care units from 10 cities in India:
country. The bundle they used is similar to other VAP findings of the International Nosocomial Infec-
bundles but notably avoided the DVT and peptic ulcer tion Control Consortium (INICC). Epidemiol In-
prophylaxis that was recommended by the IHI. They fect. 2013;141:2483-91
had seven mandatory recommendations including staff 7) Álvarez-Lerma, F. et al. (2018) ‘Prevention of
training in airway management, hand hygiene in airway Ventilator-Associated Pneumonia’, Critical Care
management, monitoring cuff pressure, chlorhexidine Medicine, 2(46), pp. 188–181.

8) Cook DJ, Walter SD, Cook RJ, Griffith LE, Guyatt 17) Klompas M: Complications of mechanical venti-
GH, Leasa D, et al. Incidence of and risk factors lation - the CDC’s new surveillance paradigm. N
for ventilator- associated pneumonia in criti- Engl J Med 2013, 368:1472-1475.
cally ill patients. Ann Intern Med. 1998 Sep 15.
129(6):433-40. 18) Chan EY, Ruest A, Meade MO, Cooke DJ. Oral de-
contamination for prevention of pneumonia in
9) Chastre J, Fagon JY: State of the art: ventilator-as- mechanically ventilated adults:systematic review
sociated pneumonia.Am J RespirCrit Care Med and meta-analysis. BMJ 2007;334:889
2002, 165:867-903.
19) George DL, Falk PS, Meduri GU, et al. Nosocomial
10) Dudeck MA, Horan TC, Peterson KD, et al. Na- sinusitis in patients in the medical intensive care
tional Healthcare Safety Network (NHSN) Report,
unit: a prospective epidemiological study. Clin In-
Data summary for 2011 available at http://www.
fect Dis 1998;27:463-70
cdc.gov/nhsn/PDFs/dataStat/2012NHSReport.
pdf. 20) Rocha LA, Marques Ribas R, da Costa Darini AL,
11) Mehta Y, Rosenthal VD, Chakravarthy M. Health- GontijoFilho PP: Relationship between nasal col-
care-associated infection rates, extra length of onization and ventilator-associated pneumonia
stay, mortality and microorganism profile in 12 and the role of the environment in transmission
adult ICUs of 7 cities in India. Findings of the the of Staphylococcus aureus in intensive care units.
International NosocomialInfection Control Con- Am J infect Control 2013, 41:1236-1240
sortium(INICC). Proceedings and Abstracts of the
21) Herzig SJ, Howell MD, Ngo LH, Marcantonio
8th Annual Meeting of the International Federa-
ER. Acid suppressive medication use and the
tion of Infection Control. Budapest, Hungary, Oct
18-21, 2007 risk for hospital acquired pneumonia. JAMA
2009;301:2120-8
12) Mehta A, Rosenthal VD, Mehta Y. Device-associ-
ated nosocomial infection rates in intensive care 22) Zolfaghari PS, Wyncoll DL: The tracheal tube:
units of seven Indian cities. Findings of the Inter- gateway to ventilator-associated pneumonia. Crit
national Nosocomial Infection Control Consor- Care 2011, 15:310-317
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23) Lacherade JC, De Jonghe B, Guezennec P, Debbat
13) Rosenthal VD, Bijie H, Maki DG, et al. International K, Hayon J, Monsel A, et al. Intermittent subglot-
Nosocomial Infection Control Consortium(INICC) tic secretion drainage and ventilator-associated
report, data summary of 36 countries, for 2004- pneumonia: a multicenter trial. Am J RespirCrit
2009. Am J Infect Control 2012;40:396-407 Care Med. 2010 Oct 1. 182(7):910-7.
14) Tablan OC, Anderson Lj, Besser R, et al; Health- 24) Gil-perotin S, Ramirez P, Marti V, et al. Implica-
care Infection Control Practices Advisory Commit- tions of endotracheal tube biofilm in ventila-
tee, Centers for Disease Control and Prevention. tor-associated pneumonia response: a state of
Guidelines for preventing healthcare associat- concept. Crit Care 2012;16:R93
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CDC and the Healthcare Infection Control Prac- 25) Torres A, Gatell JM, Aznar E, el-Ebiary M, Puig de
tices Advisory Committee. MMWR Recomm Rep la Bellacasa J, González J, et al. Re-intubation in-
2004;53(RR03):1-36 creases the risk of nosocomial pneumonia in pa-
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27) Wilkinson TS, Morris AC, Kefala K, et al. Ventilator risks of enteral nutrition in the critically ill:role
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Chest 2012;142:1425-32.
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Be the Answer? JAMA. 2008;300(7):842-844
30) Kollef MH. Prevention of ventilator associated
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tions: a worthy, yet challenging goal. Crit Care Rohwer M, Mallner F, et al. Continuous lateral
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pneumonia. Crit Care Med. 2010 Feb. 38(2):486-
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and meta-analysis. BMJ 2007;334:889 drid P, Ronning J, Susag A: Implementing a ven-
tilator bundle in a community hospital.JtComm J
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Bossuyt, M. B. Vroom, J. Dankert, Kesecioglu J.
2003. Effects of selective decontamination of di- 39) Resar R, Pronovost P, Haraden C, et al. Using a
gestive tract on mortality and acquisition of re- bundle approach to improve ventilator care pro-
sistant bacteria in intensive care: a randomised cess and reduce ventilator associated pneumo-
controlled trial. Lancet362:1011-1016 nia. JtComm J Qual Patient Saf 2005;31:243-8
33) Verwaest, C., J. Verhaegen, P. Ferdinande, M. 40) Mehta Y, Jaggi N, Rosenthal VD, et al. Effective-
Schetz, G. Van den Berghe, L. Verbist, and P. Lau- ness of a multidimensional approach for preven-
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tive digestive decontamination in 600 mechani- adult intensive-care units from 10 cities in India:
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fect. 2013;141:2483-91
34) Heyland DK, Drover JW, dhaliwal R, Greenwood
J. optimizing the benefits and minimizing the

MCQ
1. A pneumonia that was not incubating at the 3. patient position recommendation
time of admission is one that develops a
minimum of how many hours after hospital a. supine position is recommended
admission? b. prone position is recommended
a. 12 hrs c. semi-recumbent position
b. 24 hrs d. the position of patient doesn’t
c. 72 hrs influence the risk of VAP
d. 48 hrs 4. frequency of ventilator circuit changes
2. The type of organism that most often causes a. change every 48 hrs
VAP is which of the following? b. change only when soiled
a. Virus c. change every week
b. Bacteria d. change for every new patient
c. Fungi 5. ETT with extra lumen for drainage of
d. Protozoans subglottic secretions
a. These tubes reduce risk of VAP

b. Increase the risk of VAP
c. Does not influence VAP
5.(a) 4.(b) 3.(c) 2.(b) 1.(d)

Answers

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BASIC SCIENCE LECTURES

1 Gas Laws and its Applications in Anesthesia

Professor and Head, Gurudatt C L

Some of the practical applications of gas laws in anesthesia:

Anesthesiologist will be dealing with many of the gases Fluids

RACE 2019 Ramachandra Anesthesia Continuing Education

Gas laws 4) Avagadro’s hypothesis: States that equal volume of

Fig 2: Turbulent flow

Where P1-P2 is pressure gradient across the tube.

Fig 3: Bernoulli’s principle

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 4: Venturi effect

Fig 4: Coanda effect

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

a) Hagen – Poiseuille law

5. (a) 4. (a) 3. (b) 2. (d) 1. (c)

RACE 2019 Ramachandra Anesthesia Continuing Education

Chief Medical Officer : Mission Smile Ramkumar Venkateswaran

Ø Understanding respiratory mechanics during anesthesia helps to prevent postoperative pulmonary

Introduction Review of normal physiology of breathing

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

a. Assuming supine position from

5. (b) 4. (b) 3. (b) 2. (c) 1.(b)

RACE 2019 Ramachandra Anesthesia Continuing Education

Professor Anitha Shenoy

RACE 2019 Ramachandra Anesthesia Continuing Education

Implications of increase in dead space Rearranging and dividing both sides by VT

1) Carbon dioxide elimination is inversely propor- VD/VT x FACO2 = FACO2 – FeCO2

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 2: Fowler’s method of calculating anatomical dead space

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 4: Isoshunt diagram

RACE 2019 Ramachandra Anesthesia Continuing Education

4. true 5. true 3. (d) 2. (c) 1. (c)

RACE 2019 Ramachandra Anesthesia Continuing Education

Sathish K Ravi Shankar M

Introduction have the option of integrating, analyzing, displaying and

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 1: Schematic drawing of a Paramagnetic sensor;

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 4: An infrared rapidly identifying analyser (courtesy of Drager)

RACE 2019 Ramachandra Anesthesia Continuing Education

frequency in proportion to the concentration of are narrowband-filtered and detected by photo-voltatic

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

measurement could be affected by static electricity Ultrasonic Flowmeters

RACE 2019 Ramachandra Anesthesia Continuing Education

a. a. unpaired electron is attracted in a

5. (c) 4. (b) 3. (c) 1. (b) 2. (c)

RACE 2019 Ramachandra Anesthesia Continuing Education

Professor, Naheed Azhar

RACE 2019 Ramachandra Anesthesia Continuing Education

RACE 2019 Ramachandra Anesthesia Continuing Education

Fig 1: Bioavailability of oral and IV drugs LD = VD x C

Extraction ratio where LD is the loading dose and C is the required

Volume of distribution Rinf = C x Cl

Fig 2: Understanding Vd – One compartment model