Beruflich Dokumente
Kultur Dokumente
Shalini Garg
NORMAL MECHANICS OF SPONTANEOUS
VENTILATION
VENTILATION AND RESPIRATION
Spontaneous breathing or spontaneous ventilation, is
simply the movement of air into and out of the lungs.The
main purpose of ventilation is to bring in fresh air for gas
exchange into the lungs and to allow the exhalation of air
that contains CO2.
RESPIRATION is defined as movement of gas molecules
across a membrane
EXTERNAL RESPIRATION is movement of O2 from the
lungs into bloodstream and of CO2 from bloodstream into
alveoli.
INTERNAL RESPIRATION is movement of CO2 from the
cells into the blood and movement of O2 from the blood
into cells.
Normal inspiration is accomplished by the expansion
of thorax or chest cavity. It occurs when the muscles of
inspiration contract.During contraction, the diaphragm
descends and enlarges the vertical size of thoracic cavity.
The external intercostal muscles contract and raise the
ribs slightly, increasing the circumference of thorax. The
activities of these muscles represent the “work” required
to inspire.
Normal exhalation is passive and does not require any
work. During normal exhalation, the muscles relax, the
diaphragm moves upward to its resting position, and the
ribs return to their normal position. The volume of
thoracic cavity decreases, and air is forced out of alveoli.
GAS FLOW AND PRESSURE GRADIENTS
DURING VENTILATION
Basic concept of Air flow is that, for air to flow
through a tube or airway, pressure at one end must be
higher than the pressure at the other end. Air always
flows from the high pressure point to the low pressure
point (pressure gradient).
The conductive airway begins at the mouth and nose
and ends at the small airways near the alveoli. Therefore
gas flows into the lungs when the pressure in the alveoli
is lower than the pressure at the mouth and nose.
Conversely, gas flows out of lungs when the pressure in
the alveoli is greater than the pressure at the mouth and
nose. When the pressure at the mouth and alveoli are
same, as occurs at the end of inspiration or the end of
expiration, no gas flow occurs as no pressure gradient
exists.
DEFINITION OF PRESSURES AND GRADIENTS IN
THE LUNGS
Airway opening pressure (Pawo), or Mouth
pressure(PM) is often called airway pressure (Paw).
Unless pressure is applied to mouth or nose, Paw is
Zero (atmospheric).
Body surface pressure (Pbs) is the pressure at body
surface. This is equal to Zero unless the person is using
a pressurized chamber (e.g., hyperbaric chamber) or a
negative pressure ventilator (e.g., iron lung).
Intrapleural pressure (Ppl) is the pressure in the
potential space between the parietal and visceral
pleurae. Normal Ppl is about -5cm H2O at the end of
exhalation during spontaneous breathing and -10 cm
H2O at the end of inspiration.
Alveolar pressure(PA or Palv): This pressure is also
called intra-pulmonary pressure or lung pressure.
Alveolar pressure normally changes as the intra-pleural
pressure changes. During inspiration alveolar pressure
is about -1cm H2O and during exhalation it is about
+1cm H2O.
Four basic pressure gradients are used to describe
normal ventilation:
1. Trans-Airway pressure (PTA): It is the pressure gradient
between the air opening and the alveolus.
PTA = Pawo – PA
PTA produces air way movement in the conductive
airways. It represents the pressure caused by
resistance to gas flow in the airways (i.e. airflow
resistance).
2. Trans-Thoracic pressure(Pw or Ptt) It is the pressure
difference between the alveolar space(lung) and the
Body surface.
Pw = PA - Pbs
Raw = PTA/flow
Timing failure
Heater/humidifier malfunction
VOLUME VENTILATION
The operator sets a volume for delivery to the patient. Volume
ventilation is also called
Volume-targeted ventilation
Volume-limited ventilation
Volume-controlled ventilation
PRESSURE VENTILATION
The operator sets a pressure for delivery to the patient. Pressure
ventilation is also called
Pressure-targeted ventilation
Pressure-limited ventilation
Pressure-controlled ventilation
The primary variable the ventilator adjusts to
achieve inspiration is called the control variable. As the
equation of motion shows, the ventilator can control
four variables: pressure, volume, flow, and time.
However, the ventilator can control only one variable
at a time. Therefore it must operate as a pressure
controller, a volume controller, a flow controller, or a
time controller.
Ventilator Control Functions during Inspiration
Cardiac arrest
Relative contraindications
Cardiovascular instability (hypotension, dysrhythmias, acute
myocardial infarction)
Uncooperative patient (impaired mental status, somnolence)
Copious or viscous secretions
Fixed nasopharyngeal abnormalities
Extreme obesity
Disorders Sometimes Managed with Noninvasive Positive Pressure
Ventilation
Chronic respiratory failure
Neuromuscular disorders
Cystic fibrosis
Bronchiectasis
Pneumonia
Postoperative complications
Asthma
Heart failure
ADVANTAGES
Avoids complications associated with artificial airways
Provides flexibility in initiating and removing mechanical
ventilation
Reduces requirements for heavy sedation
Preserves airway defense, speech, and swallowing mechanisms
Reduces need for invasive monitoring
DISADVANTAGES
Can cause gastric distention, skin pressure lesions, facial pain,
dry nose, eye irritation (conjunctivitis), discomfort,
claustrophobia, and poor sleep, and mask leaks can occur
Circumstances in Which Noninvasive Positive Pressure Ventilation
Should Be Changed to Invasive Ventilation
Respiratory arrest
Respiratory rate >35 breaths/min
Severe dyspnea with use of accessory muscles and possibly
paradoxical breathing
Life-threatening hypoxemia: Pa02 <40 mm Hg or Pa02/FI02
<200
Severe acidosis (pH <7.25) and hypercapnia (PaC02 >60 mm
Hg)
Somnolence, impaired mental status
Cardiovascular complications (hypotension, shock, heart failure)
Failure of noninvasive positive pressure ventilation
Other circumstances (e.g., metabolic abnormalities, sepsis,
pneumonia, pulmonary embolism, barotrauma, massive pleural
effusion)
INVASIVE POSITIVE PRESSURE VENTILATION
FULL AND PARTIAL VENTILATORY SUPPORT
The terms full ventilatory support (FVS) and partial
ventilatory support (PVS) describe the extent of mechanical
ventilation provided.
With FVS the ventilator provides all the energy necessary
to maintain effective alveolar ventilation. FVS ensures that
the patient is not required to assume any of the work of
breathing (WOB).
FVS is commonly provided by using a ventilator mode
that gives a set volume or pressure whenever a breath is
delivered. The mode must be set so that the patient receives
adequate alveolar ventilation regardless of whether the
person can breathe spontaneously. For example, FVS might
include fully controlled, and assist- control positive pressure
ventilation.
PVS is any degree of mechanical ventilation in which set
machine rates are lower than 6 breaths/min and the patient
participates in WOB to help maintain effective alveolar
ventilation. Any of a variety of ventilator modes can be used
for PVS; however, by definition the patient actively
participates in ventilation to maintain adequate levels of
PaCO2.
PVS strategies are appropriate when attempts are made
to discontinue ventilator support. PVS should be avoided in
patients with ventilatory muscle fatigue and when a patient
has a high WOB.
MODE OF VENTILATION AND BREATH DELIVERY
The breath type and pattern of breath delivery during
mechanical ventilation constitute the mode of ventilation.
The mode is determined by the following factors:
Type of breath (mandatory, spontaneous, assisted)
Targeted control variable (volume or pressure)
Timing of breath delivery (continuous mandatory ventilation
[CMV], SIMV, or spontaneous).
TYPE OF BREATH DELIVERY
Mandatory breaths are breaths for which the ventilator
controls the timing or tidal volume (or both). For example, a
patient-triggered, volume-targeted, volume-cycled breath is a
mandatory breath. The machine controls tidal volume
delivery.
For spontaneous breaths, the patient controls the timing
and the tidal volume. The volume or pressure (or both)
delivered is based on patient demand, and the patient's lung
characteristics, not on a set value.
Assisted breaths have characteristics of both mandatory
and spontaneous breaths. In an assisted breath, all or part of
the breath is generated by the ventilator, which does part of
the WOB for the patient. If the airway pressure rises above
baseline during inspiration, the breath is assisted. For
example, in the pressure support mode, the patient starts the
breath (patient triggered). A target pressure is set by the
clinician. The ventilator delivers the set pressure above
baseline pressure to assist the patient's breathing effort. The
patient cycles the breath.
TARGETING VOLUME AS THE CONTROL VARIABLE
By choosing either volume or pressure ventilation, the
clinician determines the control variable that will be used to
establish gas flow to the patient . Control variables are
independent variables; in volumetargeted ventilation, for
example, the volume provided is constant and independent
of what happen to pressure when the patient's lung
characteristics (CL and Raw) change or when the patient's
effort changes. The selection of using volume or pressure
ventilation is based on whether consistency of tidal volume
delivery is important or the limiting of pressure is
important.
The main advantage of volume ventilation (VV) is that it
guarantees a specific volume delivery and VE, regardless of
changes in lung compliance and resistance or patient effort.
Volume ventilation is used when the goal is to maintain a
certain level of PaCO2
The main disadvantage of VV becomes evident when the
lung condition worsens. This can cause the peak and alveolar
pressures to rise, leading to alveolar over distention.
However, this type of problem is reversible. When the lung
condition improves, less pressure is required, and ventilating
pressures decline.
Volume ventilation is commonly chosen as the initial
form of ventilation in adults. The controls for setting volume
ventilation usually are tidal volume, respiratory rate,
inspiratory flow, and a flow pattern
TARGETING PRESSURE AS THE CONTROL
VARIABLE
Pressure ventilation (PV) allows the clinician to set
pressure as the independent variable; that is, the pressure
remains constant whereas volume delivery (the dependent
variable) changes as lung characteristics change, With PV,
the pressure is set and volume delivery must be monitored.
PV has several advantages. First, it allows the clinician to set
a maximum pressure, which reduces the risk of
overdistention of the lungs by limiting the pressure put on
the lung. Second, the ventilator delivers a descending flow
pattern during PV. The proposed advantage of PV is that
limiting the pressure spares more normal areas of the lungs
from overinflation ; this is considered a component of lung
protective strategies. It also may be more comfortable for
patients who can breathe spontaneously.
Disadvantages of PV include the following:
Volume delivery varies.
Clinicians are less familiar with PV (although this is
changing).
VT and VE decrease when lung characteristics
deteriorate.
PV and VV are equally beneficial in patients who are not
spontaneously breathing when a descending flow pattern is
used. On the other hand, in spontaneously breathing
patients, PV may lower the WOB and improve patient
comfort to a greater extent than VV, thereby reducing the
need for sedatives and neuromuscular blocking agents.
BREATH DELIVERY AND MODES OF VENTILATION
The term mode describes a breath type and the timing of
breath delivery. Modes of ventilation are shorthand terms or
acronyms used to describe the way a ventilator performs in a
particular situation. The front panel of a ventilator has a dial
or control pad that allows the practitioner to select the mode.
Basically there are three breath delivery techniques:
CMV, SIMV, and spontaneous modes.
Continuous Mandatory Ventilation (CMV)
In continuous mandatory ventilation. all breaths are
mandatory and can be volume or pressure targeted. Breaths
also can be patient triggered or time triggered. When they are
patient triggered, the CMV mode sometimes is called
assist/control (A/C). When they are time triggered, the CMV
mode is called controlled ventilation or the control mode . In
the control mode, the patient usually makes no spontaneous
effort.
The only difference between control and assist/control is
the trigger; the control mode is time triggered, whereas the
A/C mode can be either patient triggered or time triggered.
In the A/C mode, the operator sets a minimum rate, and the
patient can trigger additional breaths if possible. If the
patient cannot trigger a breath because the sensitivity level is
set too high (i.e., less sensitive to patient effort), by definition
the mode is control.
Controlled Ventilation: Controlled (time-triggered)
ventilation is appropriate only when a patient can make no
effort to breathe or when ventilation must be completely
controlled. "Locking out" a patient by making the ventilator
totally insensitive to patient effort is rarely advisable.
Patients who are obtunded because of drugs, cerebral
malfunction, spinal cord or phrenic nerve injury, or motor
nerve paralysis may be unable to make voluntary efforts,
therefore controlled ventilation is appropriate for these
individuals.
In other types of patients, controlled ventilation is
difficult to use unless the patient is sedated or paralyzed with
medications or is deliberately hyperventilated to suppress
spontaneous breathing efforts. For example, sedation and
paralysis are used if seizure activity or tetanic contractions
cannot be prevented. Sedation and sometimes paralysis are
recommended during inverse ratio ventilation (IRV) and with
permissive hypercapnia because these conditions are
uncomfortable and not well tolerated by conscious patients.
Deliberate (iatrogenic) hyperventilation occasionally is
used to induce respiratory alkalosis and thereby reduce
intracranial pressure (ICP) in patients with a closed head
injury and severely elevated ICP. Iatrogenic hyperventilation
also has been used after neurosurgery when ICP is elevated.
Assist/Control Ventilation: A/C ventilation is a time-
triggered or patient-triggered CMV mode in which the
operator sets a minimum rate, sensitivity level, and type of
breath (volume or pressure). The patient can trigger breaths
at a faster rate than the set minimum, but only the set volume
or pressure is delivered with each breath.
With CMV every breath (patient triggered or time
triggered) is a mandatory breath. Patient triggering occurs
because the ventilator is sensitive to pressure or flow changes
that occur as the patient attempts to take a breath. When the
ventilator senses a slightly negative pressure (-1 cm H20) or a
drop in flow (2 to 3 L/min below the expiratory gas flow), the
inspiratory cycle begins. It must be keep in mind that with
CMV, a minimum breath rate is set on the ventilator to
guarantee a minimum VE. Patients can take additional
breaths if they are able.
Intermittent Mandatory Ventilation and Synchronized
Intermittent Mandatory Ventilation
In IMV, periodic volume or pressure-targeted breaths
occur at set intervals (time triggering). Between mandatory
breaths, the patient breathes spontaneously at any desired
baseline pressure without receiving a mandatory breath.
The spontaneous baseline pressure between mandatory
breaths can be set at ambient (zero gauge) pressures or
higher if a positive baseline pressure is desired (IMV with
PEEP/ CPAP). During this period the patient can breathe
either from a continuous flow of gas or from a demand
valve. Some ventilators can provide pressure support for
spontaneous breaths during the spontaneous period.
Successful use of IMV in the 1970s resulted in the
development of a similar mode of ventilation, SIMV. SIMV
operates in the same way as IMV except that mandatory
breaths normally are patient triggered rather than time
triggered. As in IMV, the patient can breathe spontaneously
through the ventilator circuit between mandatory breaths. At
a predetermined interval (respiratory rate), which is set by the
operator, the ventilator waits for the patient's next inspiratory
effort. When it senses the effort, the ventilator assists the
patient by synchronously delivering a mandatory breath. The
operator usually sets the volume target or pressure target, a
maximum mandatory breath rate, and the sensitivity level.
The machine then provides set volume or pressure breaths,
which are patient triggered. After delivering the mandatory
breath, the ventilator allows the patient to breathe
spontaneously without receiving another mandatory breath
until the next mandatory breath is due to occur.
As with IMV, SIMV spontaneous breaths can be pressure
supported. The pressure target for pressure support (PS)
breaths commonly is set lower than the peak pressure during
a mandatory breath. For example, the mandatory breath may
generate a peak pressure of 30 cm H2O, and the PS
spontaneous breath may be set at 15 cm H2O. For a
predetermined interval, the ventilator waits for a patient effort
to deliver another mandatory breath. If the patient fails to
initiate ventilation within that interval, the ventilator provides
a mandatory breath at the end of the time period.
SIMV originally was designed to eliminate the problem
of breath stacking, which occurs with IMV when a machine
timed breath accidentally is delivered at the same time the
patient spontaneously inhales. With breath stacking, the
patient's lungs receive huge volumes of air, which can cause
high pressure in the lungs and result in barotrauma or
ruptured lung tissue.
The IMV /SIMV mode is used when the goal is to have
the patient breathe spontaneously without receiving a
mandatory breath with every effort (partial ventilatory
support). The patient assumes part of the WOB by actively
breathing and not receiving complete support from the
ventilator, and this active participation in breath delivery
preserves a certain amount of respiratory muscle strength.
The work of breathing can increase with SIMV due to lack of
coordination between mandatory and spontaneous breaths.
The patient's efforts may not stop just because a mandatory
breath is delivered. Spontaneous breaths can be supported
with PSV if the WOB for spontaneous breathing is to be
reduced.
The IMV /SIMV mode potentially has fewer
cardiovascular side effects because parts of VE occur at lower
pressures. This mode also can be used to wean patients from
mechanical ventilation . As the mandatory rate is lowered; the
patient gradually assumes a greater part of the WOB.
Spontaneous Modes
The three basic means of providing support for continuous
spontaneous breathing (CSV) during mechanical ventilation
are :
Spontaneous breathing
CPAP
PSV
Increase this by
5% per ◦F above 99° F or 9% per ◦C above 37° C
20% for metabolic acidosis
5% per 2000 feet above sea level
50 % to 100% if resting energy expenditure is equally
increased
Decrease this by
9% per ◦C between 35° C and 37° C
TCT = TI + T E
TI = VT / Flow
If VT is 1.0 L and flow is 2 L/sec, then TI equals 1.0 L/2 L/ sec, or 0.5
sec. The flow control on adult ventilators is usually calibrated in
L/min, so the value for flow needs to be converted to L/sec.
Conversely, VT can be determined when TI and flow are known and
flow is constant:
VT = flow X TI
Relative contraindications
Cardiovascular instability (hypotension, dysrhythmias, acute
myocardial infarction)
Uncooperative patient (impaired mental status, somnolence)
Copious or viscous secretions
Fixed nasopharyngeal abnormalities
Extreme obesity
Circumstances in Which Noninvasive Positive Pressure
Ventilation Should Be Changed to Invasive Ventilation
Respiratory arrest
Respiratory rate >35 breaths/min
Severe dyspnea with use of accessory muscles and possibly
paradoxical breathing
Life-threatening hypoxemia: Pa02 <40 mm Hg or PaO/FI02
<200
Severe acidosis (pH <7.25) and hypercapnia (PaC02 >60 mm
Hg)
Somnolence, Impaired mental status
Cardiovascular complications (hypotension, shock, heart
failure)
Failure of noninvasive positive pressure ventilation
Other circumstances (e.g., metabolic abnormalities, sepsis,
pneumonia, pulmonary embolism, barotrauma, massive
pleural effusion)
System for Analysing Ventilator Waveforms
Start with the airway pressure screen
Step 1: determine the CPAP level
This is the baseline position from which there is a
downward deflection on, at least, beginning of inspiration,
and to which the airway pressure returns at the end of
expiration.
Step 2: is the patient triggering?
There will be a negative deflection into the CPAP line just
before inspiration.
Step 3: what is the shape of the pressure wave?
If the curve has a flat top, then the breath is pressure
limited, if it has a triangular or shark’s fin top, then it is
not pressure limited and is a volume breath.
Look at the flow screen:
Step 4: what is the flow pattern?
If it is constant flow (square shaped) this must be volume
controlled, if decelerating, it can be any mode.
Is the patient gas trapping?
expiratory flow does not return to baseline before inspiration
commences (i.e. gas is trapped in the airways at end-
expiration).
Step 5: the patient is triggering – is this a pressure
supported or SIMV or VAC breath?
The pressure supported breath looks completely
differently than the volume control or synchronized
breath: the PS breath has a decelerating flow pattern, and
has a flat topped airway pressure wave. The synchronized
breath has a triangular shaped pressure wave.
Step 6: the patient is triggering – is this pressure support or
pressure control? The fundamental difference between
pressure support and pressure control is the length of the
breath – in PC, the ventilator determined this (the inspired
time) and all breaths have an equal “i” time. In PS, the
patient determined the duration of inspiration, and this
varies from breath to breath.
Step 6: is the patient synchronizing with the ventilator?
Each time the ventilator is triggered a breath should be
delivered. If the number of triggering episodes is greater
than the number of breaths, the patient is asynchronous
with the ventilator. Further, if the peak flow rate of the
ventilator is inadequate, then the inspiratory flow will be
"scooped" inwards, and the patient appears to be fighting
the ventilator. Both of these problems are illustrated below
At point A, the inspiratory valve opens and inspiratory gas
flow begins. This is also the point where expiration ends.
Flow rises quickly to point B, which is the flow control set
on the front panel of the ventilator. At point C, inspiratory
flow delivery stops.
Inspiratory flow = 60 L/min; inspiratory flow stops at 0.5
second. There is an inspiratory pause set. It is 0.25 second
long. TI is 0.75 second (0.5 + 0.25). The flow during the
inspiratory pause is zero.
As the expiratory valve opens at point D, gas leaves the
patient and the ventilator circuit and passes through the
ventilator's expiratory valve. Flow during exhalation is
graphed below the baseline. At point E, expiratory flow ends;
however, the total expiratory time (TE) lasts from point D to
point F, and the TE continues until the next inspiration
begins (point F).
TE = 1.5 seconds. 1.5 to 2.25 seconds (0.75 second total) is the
interval during exhalation when no more gas leaves the
patient.
PEFR is 80 L/min. (Even though the graph indicates minus
[-] 80 L/min, the value is read without the minus sign.)
Look first at the inspiratory portion of the pressure-time curve.
Note that the baseline pressure is about 5 cm H20, indicating that
the positive end-expiratory pressure (PEEP) is set at 5 cm H20. It
is important to remember that even though the baseline pressure is
positive, the flow and volume curves start from a zero baseline and
end at a zero baseline.
The peak inspiratory pressure PIP = 24 cm H20; Pplateau is
about 17 cm H20. VT ≈ 400 mL. Breaths are time-triggered.
There is no deflection below baseline pressure preceding a
mandatory breath in the pressure-time waveform. Inspiratory
pause is present.
On comparing the flow and volume curves at the same
moment in time, when no flow occurs, there is no volume
delivery. The volume curve also looks as if it has a pause, or
plateau.
The flow waveform looks like a modified sine wave. There is no
inspiratory pause as inspiratory flow never goes to zero. The peak
expiratory flow is approximately 30 L/min (absolute value). The
expiratory flow is very slow and rises to the zero baseline just before the
next breath starts. In expiratory volume curve , the gas takes a long time
to leave the patient's lungs. In fact, this patient has increased airway
resistance. Because of the resistance limitation on expiratory gas flow,
flow and volume take longer to leave the lungs. This kind of expiratory
pattern occurs in patients with chronic obstructive pulmonary disease
(COPD) and severe asthma.
The waveforms represent
flow, volume, and pressure
scalars. There is constant
flow during inspiration
(solid line). Flow suddenly
increases during inspiration
(dashed line and shaded
area). There is slight dip in
the pressure curve that
occurs simultaneously with
an increase in flow. The
dashed lines represent
actual flow, pressure, and
volume delivery. The solid
line represents the process
without active patient
inspiration.
Newer ICU ventilators are different from earlier models. With
the newer machines, during inspiration and depending on
the ventilator, a patient who actively inspires during volume
ventilation can receive additional flow. This feature allows a
patient who wants additional flow to receive it. It also
increases volume delivery above the set value. The increased
flow and VT do not increase the pressure delivery. Pawo
decreases slightly with active patient inspiration. Pleural
pressures and alveolar pressures also decrease as a result of
respiratory muscle activity. This type of flexibility in flow
delivery would seem to be more comfortable for and
accommodating to the patient.
A. Patient triggered breath with
an appropriately set
sensitivity and adequate flow
during inspiration.
B. Inadequate sensitivity and
inadequate flow with a
pressure-time curve showing
a concave or downward scoop
during inspiration
These are examples of breath delivery by a ventilator that holds
flow constant at the set value regardless of the amount of flow the
patient tries to receive. The flow the operator sets during volume
ventilation is the maximum flow the patient can receive.
Increasing the set flow may provide for the flow demand of the
patient.
An inappropriate sensitivity setting and an inadequate flow setting
are two causes of dyssynchrony between the patient and the
ventilator.
Chronic obstructive pulmonary disease
Patients with COPD have increased Raw and may also have
increased CL, which, when combined, cause significant
expiratory obstruction, lengthen the time constant, and lead
to air trapping. When patients with COPD require
mechanical ventilation, it is often because their chronic
disease has been coupled with another problem, such as a
respiratory infection, leading to an acute-on-chronic
respiratory failure.
Basic guidelines for mechanically ventilating patients with
COPD have been established. They include :
If possible use noninvasive ventilation to help avoid problems
associated with artificial airway use. Bilevel positive airway
pressure (Bilevel PAP), is ideal for patients with chronic
pulmonary disorders. If intubation is necessary, an
orotracheal intubation is recommended.
The clinician can select a ventilator mode. It has been noted
that VC- or PC-CMV may unload the work of the respiratory
muscles more than SIMV. Using patient-triggered CMV in an
alert patient with COPD may increase the risk of hyperinflation
and elevated lung pressures, and this mode should be
monitored carefully.
In patients with COPD and asthma, where airway obstruction
and resistance are high, an initial VT of 8 to 10 mL/kg with a
rate of 8 to 12 breaths/min, and TI 0.6 to 1.2 sec is acceptable.
PEEP ≤5 cm H2O or about 50% of auto- PEEP should be used
initially.
Provide the longest expiratory time (TE) possible. This might
include decreasing TI, increasing TE, reducing f and/or VT, and
accepting hypercapnia (PaCO2 higher than the patient's
normal). Patients with COPD are usually ventilated in their
normal PaCO2 range (e.g., PaCO2 = 50 to 60 mm Hg; pH 7.30
to 7.40).
Pplateau should be monitored and maintained at <30 cm
H20 to avoid alveolar overdistention and, consequently, lung
injury. Accurate measurement of Pplateau may require
sedation and paralysis.
Maintain PaO2 at 55 to 75 mm Hg or near the patient's
normal rate, with FIO2 <0.5, unless the patient's condition
worsens and he or she requires more oxygen.
Pressure control ventilation (PCV) may be ideal for this
patient group for several reasons. PCV provides flow on
demand to meet the patient's needs, and TI can be set, along
with a back-up rate, but patient triggering is still permitted.
PCV has an advantage over PSV for this patient population
because inspiration during PSV can be too long or too short,
depending on patient active breathing patterns. This can
result in increased WOB and poor patient-ventilator
synchrony. Auto-PEEP can be a lethal complication.
Case Study of a Patient with COPD
A 73-year-old man with a history of chronic bronchitis is
brought to the emergency department by his wife. He is
complaining of severe shortness of breath. Infiltrates in the
lower lung fields and thick yellow sputum suggest the presence
of a respiratory infection. The SpO2 was 71 % taken on room
air. An ABG was obtained. A 28% air-entrainment mask is
placed on the patient.
The patient was given an aerosol treatment with albuterol by
small-volume nebulizer followed by an aerosolized mucolytic.
His dyspnea persists. ABGs on an FIO2 of 0.28 are pH = 7.24 ;
PaCO2 = 97 mm Hg; PaO2 = 38 mm Hg; and HC03- = 41
mEq/L. What would you recommend at this time?
The ABGs indicate a chronic CO2 retention (elevated HC03-)
that has now progressed into an acute-on-chronic phase
(elevated PaCO2 and low pH). Hypoxemia is also present and
severe. Based on the assessment, a decision is made to begin
ventilatory support. The patient is 5'10" tall and weighs 148 lbs.
Initial Ventilator Settings
BSA=1.85m2 ; IBW = 106 + 6(10) = 166 lbs (75.5 kg)
Initial VE = 4 x 1.85 = 7.4 L/min
Because of concern for air trapping, consider a lower set VE
Attempt to synchronize the ventilator with the patient
Noninvasive ventilation is appropriate. A BiPAP ventilator is
selected.
Rate is set at 8 breaths/min; TCT = 60/8 = 7.5 sec; and TI = 13%
of TCT; I:E ratio = 1 :6.5; TI= 1.0 sec; and TE = 6.5 sec
IPAP = 10 cm H20 initially and is titrated to obtain an exhaled VT
of 600 mL (0.6 L). Final IPAP is 14 cm H20; EPAP = set at 4 cm
H20
Spontaneous/timed setting is selected, providing a back-up rate,
at which point time triggered breaths are modified pressure-
controlled (PC) breaths; spontaneous breaths are pressure-
supported (PS) breaths.
Oxygen is titrated to ≥90% oxygen saturation measured by pulse
oximeter (Sp02)
Neuromuscular disorders
Disorders such as myasthenia gravis, amyotrophic lateral
sclerosis, muscular dystrophy, poliomyelitis or post-polio
syndrome, Guillain-Barre, tetanus, cervical spinal cord injury,
botulism etc. may cause ventilatory failure. These usually
have a normal ventilatory drive and normal or near-normal
lung function. Most of these disorders cause respiratory
muscle weakness, so these patients have trouble coughing
and clearing secretions. As a result they tend to develop
atelectasis and pneumonia. If the glottic response is weak,
they may also have a risk of aspiration. Ventilation is most
often needed because of progressive respiratory muscle
weakness that eventually leads to respiratory failure (e.g.,
Guillain-Barre and myasthenia gravis).
Because these patients often have normal lung function, they
are at low risk for barotrauma and are most comfortable when
ventilated with higher VT values (12 to 15 mL/kg) and high
inspiratory flow rates of >60 L/min using a constant flow or
descending ramp when VV is used. Patients with spinal cord
injuries such as high quadriplegia require full ventilatory support.
Other patients only require partial support until their own
breathing capacity returns, such as with myasthenia gravis.
Guidelines for Neuromuscular Disorders are :
Full or partial support
Negative or positive pressure ventilation
Noninvasive or invasive ventilation
Assist/Control mode (CMV)
Volume ventilation
High VT (12 to 15 mL/kg)
f = 8 to 12 breaths/min
Inspiratory flow rates ≥ 60 L/min to meet patient need ; (TI about 1 sec to start)
Flow waveform: constant or descending ramp
PEEP = 5 cm H2O may be needed to relieve dyspnea
FIO2 = 0.21
A 5'2", 115 lb, 68-year-old woman with a history of myasthenia gravis
was brought to her doctor's office. She complained of progressive
weakness and that she was extremely weak. Physical examination
revealed that she demonstrated drooping eyelids and difficulty talking
and swallowing. She was unable to walk more than a step or two. She
was transferred to the hospital, where she was given edrophonium
(Tensilon), which improved her muscle function for 10 to 15 minutes.
On admission, her vital signs were unremarkable. Her maximum
inspiratory pressure (MIP) was -35 cm H2O, and her vital capacity (VC)
was 1.8 L (predicted was 3.3 L). Her SpO2 on room air was 96%.
Anticholinesterase therapy was administered, and MIP and VC were
monitored every 8 hours. The nursing staff reported that the patient was
having trouble swallowing when she ate and they feared that she would
aspirate. MIP and VC values progressively declined. After being
hospitalized for 24 hours, her MIP was -25 cm H2O and VC was 1.0 L.
ABGs on room air were as follows: pH = 7.36; PaCO2= 48 mm Hg;
PaO2 = 62 mm Hg; HC03= 27 mEq/L. Since the patient was having
difficulty managing secretions, NPPV would not be recommended in
this case.
Initial Ventilator Settings with Neuromuscular Disorder
(Myasthenia Gravis)
Intubate patient because of increased risk of aspiration. Use
mechanical ventilation because patient's ability to swallow is
worsening and she is tending toward acute respiratory failure
despite anticholinesterase therapy.
Patient is 5'2" and weighs 115 lbs, so:
IBW = 105 + 5(2) = 115 lbs (52 kg).
BSA is 1.5 m2.
Estimated VE is 3.5 x 1.5 = 5.25 L.
VT = 625 mL (12 mL/kg); A/C mode (VC-CMV).
Rate = 8 breaths/min.
Flow = 60 L/min using a constant waveform.
PEEP = 2 cm H20 and FI02 = 0.21.
Calculate TI and TE.
TI = VT/flow (L/sec) = 0.625 L/(1 L/sec) = 0.625 sec.
TCT = 60 sec/8 = 7.5 sec.
TE = 7.5 - 0.625 = 6.9 sec.
PIP = 20 cm H20.
Pplateau = 12 cm H20.
Transairway pressure= 20 - 12 = 8 cm H20.
CL = VT/(Pplateau - PEEP) = 0.625/(12 - 3) = 0.069 L/cm
H20 or 69 mL/cm H20. I
The patient received ventilatory support for a total of 21
days with one occurrence of a respiratory infection that
responded to antibiotic therapy. She was successfully weaned
and extubated on the 22nd day.
ASTHMA
Patients with acute severe asthma (status asthmaticus) requiring
mechanical ventilation are among the most difficult to manage.
Increased Raw from bronchospasm, increased secretions, and
mucosal edema make air trapping inevitable. Trapped air can cause
uneven hyperexpansion of various lung units, which can cause
rupture or compress other areas of the lungs, leading to
pneumothorax, pneumomediastinum, subcutaneous emphysema, and
other forms of barotrauma. Tight airways make gas movement into
and out of the lung impossible in some areas. Aggressive treatment
with bronchodilators and steroids may not be enough to reverse the
course of an acute asthma episode.
During the episode the patient struggles to breathe, trying to
move air against increasing loads. The result is dramatic changes in
intrapleural pressures (Ppl) during inspiration and expiration that not
only affect gas distribution, but also alter blood flow through the
heart, resulting in pulsus paradoxus. Progressive hypoxemia further
enhances the patient's drive to breathe and compounds anxiety.
Guidelines for Asthma
VC- or PC-CMV are acceptable modes immediately
following intubation. With PC-CMV it is easier to keep the
pressures controlled.
Keep peak and Pplateau minimized. PIP may be high due
to the high Raw and the use of high inspiratory gas flows.
Alveolar (plateau) pressures must still be kept low (<30 cm
H2O) despite the high PIP.
Maintain oxygenation by using an FIO2 as needed to keep
the PaO2 from 60 to 100 mm Hg, usually ≥0.5. Monitor
hemodynamic status to be sure cardiac output is stable.
The use of permissive hypercapnia (PaCO2 45 to 80 mm
Hg) is acceptable as long as pH range is acceptable (i.e.,
7.10 to ≥7.20).
If the ventilator cannot be matched to accommodate patient
needs, the use of sedatives and paralytics may be necessary.
The use of sedation and paralysis may permit resting of
fatigued respiratory muscles, particularly during the first 24
hours.
Avoid or reduce air trapping (auto-PEEP) by providing long
expiratory times:
f = <8 breaths/min; VT = 4 to 8 mL/kg; TI= ≤1 sec ;
inspiratory gas flow = 80 to 100 L/min descending flow
waveform.
The occurrence of barotrauma in the form of pneumothorax
is not uncommon in these patients.Regular evaluations of
breath sounds and diagnostic chest percussion, along with
chest radiographs, help to monitor for this potential problem.
Case Study of a Patient with Asthma
A 13-year-old girl with a history of severe persistent asthma
was brought to the emergency room. Wheezing was heard
without the use of a stethoscope. Auscultation of the chest
confirmed that the wheezing was bilateral. The patient had
used her albuterol MDI 10 times (20 puffs) in the past 4
hours. Peak expiratory flow rate (PEFR) was 150 L/min.
A chest radiograph showed increased radiolucency and
depressed hemidiaphragms. ABGs on a 2 L/min nasal
cannula were: pH = 7.43; PaCO2 = 25 mm Hg, PaO2 = 43
mm Hg; HCO3= 17 mEq/L. Her SpO2 was 73%. She is
started on bronchodilators (albuterol and Atrovent) by
continuous aerosol and intravenous corticosteroids (Solu-
Medrol).
The patient did not improve in the past 5 hours, in spite of
therapy. Her breath sounds are more distant and there is
hyperresonance to percussion of the chest wall. She becomes
cyanotic and anxious and her breaths are labored. On a 4
L/min nasal cannula, ABGs are: pH = 7.25; PaCO2 = 59 mm
Hg; PaO2 = 53 mm Hg; HCO3 = 25 mEq/L. SpO2 is 79%.
PEFR is 120 L/min and f is 16 breaths/min (down from 30
breaths/min on admission). Blood pressure (BP) is 160/100
and heart rate (HR) is 175 beats/min. She is transferred to
the ICU, and the decision is made to intubate her and begin
ventilatory support.
Based on this patient's history and size (5'3", 108 lbs), the
initial ventilator settings are :
IBW = 105 + 5(3) = 120 lbs (54.5 kg)
BSA= 1.5 m2
Initial VE = 1.50 x 3.5 = 5.25 L/min
Targeted VT in the low range (4 to 8 mL/kg); 220 to 435 mL
f = VE/VT = (5.25 L/min)/0.435 L =12 breaths/min.
ADULT RESPIRATORY DISTRESS SYNDROME
ARDS has been recognized as one of the most difficult
pulmonary disorders to manage. Mortality rates are high
(ranging from 40% to 90%).
Diagnostic Criteria for ARDS are :
History of precipitating condition
Refractory hypoxemia (Pa02/FI02 ≤200)
Severe pulmonary shunting (>20%)
Reduced CL (total compliance <30 mL/cm H20)
Diffuse bilateral alveolar infiltrates on chest radiograph
Pulmonary capillary wedge pressure <15 to 18 mm Hg (with
normal colloidal osmotic pressures)
This disease has two phases: the early phase (first 7 to 10
days), which is characterized by increased vascular
permeability, lung water, and lung protein; and the later
phase (after 10 days), which is accompanied by extensive
lung fibrosis. Management of ARDS inevitably includes
mechanical ventilatory support.
Guidelines in Restrictive Disease and ARDS
In patients with chronic or acute restrictive disease, such as
pulmonary fibrosis or ARDS, an initial VT of 4 to 8 mL/kg
with a rate of 15 to 25 breaths/min is indicated.
Choose a mode capable of supporting oxygenation and
ventilation, such as PC or VC CMV.
Maintain Sa02 ≥ 88% to 90%. Start at 100% oxygen. To
support oxygenation, use PEEP at a level that prevents
alveolar collapse and over distention to prevent lung damage.
PEEP may allow reduction of FI02 to safe levels. High PEEP
levels of > 15 cm H20 may be required in ARDS.
Keep Pplateau <30 cm H20 by lowering VT to 4 to 6 mL/kg.
Allow PaC02 to rise above normal (permissive hypercapnia) if
necessary, unless there is a risk of increased ICP or
contraindications exist that demand a more normal PaC02 or
pH. Rapid rises in PaC02 should be avoided.
Use flow in VV (>60 L/min) and TI in PV to keep inspiration
long enough to enhance oxygenation, but short enough to
allow adequate TE to avoid auto-PEEP; e.g., TI <1 sec.
PEEP is needed in the management of ARDS to prevent the
opening and closing of alveoli during a breath. This opening
and closing can cause lung injury from the shear stress
(frictional forces) between the alveoli.
In management of ARDS, acceptable end points based on
ABGs are PaC02 = 40 to 80 mm Hg; pH = 7.20 to 7.40; Pa02
= 60 to 100 mm Hg
Case Study of a Patient with ARDS
A 60-year old man sustained multiple lacerations after hitting
a tree with his car. Admission to the emergency department for
evaluation revealed a fractured left femur, a deep laceration of
the right arm, an open pneumothorax on the right side of the
chest, abdominal bruising, but no injury to the head or neck.
The patient was taken to surgery for repair of internal injuries; a
chest tube with pleural drainage was inserted for the
pneumothorax.
The patient developed a fever of 39.5 ◦C and severe refractory
hypoxemia 4 days after surgery. A chest radiograph showed
resolution of the pneumothorax and the presence of bilateral
fluffy infiltrates. ABGs on a nonrebreathing mask at the time
were pH =7.29; PaC02 =51 mm Hg: PaO2 =76 mm Hg; HCO3
= 24.8 mEq/L. Vital signs were BP= 148/90 mm Hg, HR =152
beats/min; f =40 to 42 breaths/min and labored. The patient
was restless and anxious. The patient, who was 6'2" and
weighed 258 lbs, was sedated, paralyzed, orally intubated, and
placed on ventilatory support.
BSA=2.42m2; IBW=106+6(14)=190 lb(86.4kg)
initial VE =4 X BSA=9.68L/min;
VT=5 to 8 mL/kg ; 430 to 690 mL. The value 600 mL is
used to establish an initial f.
f =VE/VT= 9.68/0.6=16 breaths/ min
Flow should be set at 100 L/min to keep TI short and a
descending ramp waveform used.
Initial PEEP of 5 cm H2O and an FIO2 of 1 set
Any mode i.e. VC-SIMV+PSV or VC-CMV or PC-SIMV+PSV
or PC-CMV can be used
ACUTE CARDIOGENIC PULMONARY EDEMA AND
CONGESTIVE HEART FAILURE
Much of the treatment of acute heart failure is based on
medical management. For example, diuretics are given to
reduce vascular fluid load, positive inotropic agents are given
to improve cardiac contractility, and vasodilators can improve
myocardial oxygenation and reduce preload and afterload.
Many patients can successfully be managed with drug
therapy and do not require mechanical ventilatory support.
However, mechanical ventilation may be indicated when
severe heart failure leads to increased myocardial work,
increased WOB, and hypoxemia. In patients with left
ventricular failure the use of positive pressure, particularly
PEEP can effectively reduce the size of the heart. Bringing
an over distended left ventricle back to a more functional size
can improve stroke volume.
Potential Effects of PEEP in Left Ventricular Dysfunction
Increased Paw and intrathoracic pressure lead to reduced
venous return, which can reduce preload to a failing heart,
improving its function.
Increased functional residual capacity from PEEP leads to
increased pulmonary vascular resistance and increased afterload
to the right heart, and decreased left heart filling.
Increased right heart pressures with the increased afterload may
shift the intraventricular septum to the left. With the left shift of
the intraventricular septum, the left ventricular volume is
reduced. This may reduce the load it must pump. However, it
may also affect the compliance of the left ventricle and either
increase or decrease left heart function (the response varies).
The mechanical compression of the heart and aorta by the
pleural pressure surrounding them can also alter ventricular
function. The vascular pressure in the heart and thoracic aorta
is transiently increased relative to the extrathoracic aorta (i.e.,
left ventricular afterload decreases). This response is not always
consistent, and cardiac tamponade from PEEP can negatively
alter myocardial compliance as well.
Guidelines for mechanically ventilating patients with acute
cardiogenic pulmonary edema and congestive heart failure
(CHF) are :
Select a mode of ventilation that reduces WOB. This may be
as simple as noninvasive mask CPAP. NPPV by mask CPAP
may improve oxygenation, reduce PaCO2, reduce the WOB,
and reduce myocardial work. NPPV in patients with CHF
may allow sufficient time for pharmacological treatment to
become effective.
When life-threatening hypoxemia occurs with severe CHF,
PEEP and/or PPV may have beneficial effects on myocardial
function and improve oxygenation.
Careful evaluation of the effects of PPV on hemodynamics is
essential. This may include the use of a pulmonary artery
catheter in severe cases, particularly if PEEP > 10 to 15 cm
H20 is used.
The use of VC- or PC-CMV is recommended to avoid
spontaneous breathing, which may divert increased blood
flow and oxygen consumption to the respiratory muscles.
VT range is moderate from 8 to 10 mL/kg ; set f from ≥10
breaths/min and peak flows ≥ 60 L/min using either
descending or constant waveforms. TI range is 1 to 1.5 sec.
Set a PEEP of 5 to 10 cm H2O to support the cardiac function.
Start FI02 at 1.0 and titrate quickly with Sp02 to maintain SpO2
>90% to 92%.
Case Study in CHF
A 63-year-old man who is complaining of severe shortness
of breath is brought by ambulance to the emergency
department. He is 5'11" and weighs 175 lbs. His vital signs are
BP = 175/115 mm Hg; HR = 140 beats/min and the rhythm is
irregular; f = 22 to 24 breaths/min; and normal temperature.
His lips are cyanotic, his neck veins are distended, and both of
his ankles have pitting edema. Breath sounds reveal bilateral
basilar crackles and wheezes. He has a productive cough with
small amounts of pink, frothy secretions.
A chest radiograph shows cardiomegaly and dense, fluffy
opacities in the lower lung fields. The ECG reveals atrial
fibrillation with a ventricular rate of 138 to 140 beats/min and
occasional premature ventricular contractions (PVCs).
The patient is started on a nasal cannula at 2 L/min and
given intravenous furosemide, dobutamine, and digitalis.
ABGs 1 hour later read pH = 7.16; PaC02 = 79 mm Hg;
Pa02= 33 mm Hg; HC03 = 28 mEq/L on 2 L/min by nasal
cannula. The patient's urine output was 580 mL in the past
hour and he remained cyanotic. The 2 L/min nasal cannula
was not adequate. He is slow to respond to verbal
commands.
Noninvasive ventilation is started on this patient using a
full face mask and bilevel PAP with IPAP at 9 cm H20, EPAP
at 3 cm H20, and FI02 at approximately 0.5. The patient's
spontaneous respiratory rate on these settings is 25
breaths/min, and the Sp02 is now 88%.
To reduce f and increase Sp02, the IPAP and EPAP are
increased. After several adjustments, the final values for
adequate ventilation are IPAP = 15 cm H20; EPAP = 5 cm
H20; approximate FI02 = 0.6 ; f = 16 breaths/min; and VT =
760 mL Sp02=95%.
Although NPPV was successful in this individual, it is
important to recognize that it is not always successful. Some
patients with decompensated heart failure will temporarily
improve with NPPV, but then worsen and may even go into
cardiac arrest. Some clinicians prefer to intubate and provide
invasive rather than NPPV in this patient population, feeling
that invasive ventilation provides more controlled conditions.
Initial Ventilator Settings Based on Pulmonary Disorder