Part 6 Anesthesiology

Chapter 1 Introduction

Anesthesiology and its development

Basic concept
Anesthesia: Make the whole or part of the body lose its sensation
temporarily by drug or other ways.
Analgesia: Make the body lose its pain feeling sensibility reversibly.
Anesthesiology: A science that research in abolishing surgical pain,
ensure perioperative safety and provide good surgical condition.
Brief history:
Ancient anesthesia: In China and other country, some herbs used to
be used as anesthetics. Acupuncture was also used in anesthesia and
resuscitation.
Modern anesthesia: The marker of modern anesthesia is the public
demonstration of ester anesthesia by Morton in MGH in 1846. Other
volatile agent was synthesized successively. The first intravenous
anesthetics barbitoue was developed in 1903. The first muscle relaxant d
tubercurarine was developed in 1936. The discovery of local anesthetic
cocaine in 1860 started the local anesthesia(1884), nerve block(1885),
spinal anesthesia (1896) and epidural anesthesia. (1884). Other invention
including anesthetic machine, tracheal intubation hypothermia et al ,
promoted the development of anesthesiology.
The range of anesthesiology
Clinic anesthetic work
Preanesthesia
Intra anesthesia
Postanesthesia
Post anesthetic room and intensive care unit (ICU)
Resuscitantion
Pain therapy
Classification of anesthesia methods
General anesthesia: Make the whole body painless by using the drug
which acting on central nervous system. It concludes inhalation
anesthesia and intravenous anesthesia.
Local anesthesia: Use the drug on peripheral nerve, which causes part
of body painlessness. It concludes superficial anesthesia, infiltration
anesthesia, regional anesthesia and nerve block.
Intrathecal block: It concludes spinal block, epidural block and
caudal block.
Combined anesthesia (Balanced anesthesia): Combining different
drugs and methods together.
Basal anesthesia: Cause a sleep like state before continuous anesthesia.

Chapter 2 Preanesthesia And Premedication

Preoperative assessment
Reasons
Perioperative risk factors Operation (stress stimulation), anesthetic
agents and anesthetic manipulation, accompanied illness.
Contents
Preoperative visit
Purposes
1 Establish rapport with the patient.
2 Obtain a history and perform a physical examination.
3 Order special investigation.
4 Assess the risk of anesthesia and surgery and if necessary postpone or
cancel the date of surgery.
5 Institute preoperative management.
6 Prescribe premedication and plan the anesthetic management.
ASA grading system
ASA grading system and perioperative mortality rate
ASA rating Physical status scale Morality rate
1 A normally healthy individual 0.06 – 0.08
2 A patient with mild systemic disease 0.27 – 0.40
3 A patient with severe systemic disease that is not incapacitating
1.82 – 4.30
4 A patient with incapacitating systemic disease that is a constant threat
to life
7.80 – 23.0
5 A moribund patient who is not expected to survive 24h or without
operation
9.40 – 50.7
Add “E” as a suffix for emergency operation
Preparation before anesthesia
Correct pathophysiological status.
Improve nourishment status.
Transfusion of blood when necessary.
Correct imbalance of homeostasis.
Diagnose and treat complications such as Heart Failure, Atrial
Fibrillation, Enlarged heart.
Psychological preparation
Too much preoperative anxiety can cause hypertension, tachycardia, and
even myocardial or brain infarction, stress ulcer bleeding.
Visit and communicate with patient, explain anesthetic methods to the
nervous patient or corporate with drug therapy.
Gastrointestinal Preparation
Purpose: To avoid regurgitation, vomiting and aspiration.
Normal adult’s gastric emptying time is 4 – 6 h.
Fasting time of adult is 12 h; child is 4 – 8 h.
Water deprivation time of adult is 4 h; child is 2 – 3 h.
Preparation of epuipments, apparatus and drugs
Equipment: Anesthetic machine, oxygen source, aspirator.
Apparatus: Monitors, laryngoscope, tracheal tube and its connector.
Drug: Must recheck before used.
Premedication
Purpose
Remove the nervous, anxious and fear mood of patient; strengthen the
effect of anesthetics.
Increase pain threshold, facilitate the patient’s corporation with
preanesthetic procedures.
Inhibit secretion in air way, keep dry in mouth, decrease the probability of
aspiration.
Abolish the mal reflex during anesthesia and operation-vagal reflect,
sympathetic reflection caused by pain and excitation.
Selection of drugs
Principle: The selection of drug, dosage, administrative path and time are
according to the anesthesia and patient’s condition.
1 General anesthesia: Sedatives and anticholinergics.
2 Spinal anesthesia: Sedatives.
3 Epidural anesthesia: Sedatives, and sometime analgesics.
4 Anticholinergics: Atropine is the primary choice for bradycardia,
upper abdominal or pelvic operation(Except forbidden);
Scopolamine for Valvulopathy, heart failure and severe patients.
5 Dosage: a Dosage decrease in older age, bad condition, cachexia, and
hypothyroidism patients.
b Dosage increase in young, hyperthyroidism patients.
6 Time and pathway: 30 – 60 minutes before operation, intramuscular
injection.
Drugs in common use
1 Sedatives: Sedation, hypnogenesis, antianxiety and anticonvulsion that

prevents toxic reaction of local anesthetic agents. Diazepam

(Valium): Adult dose2.5 – 5 mg for oral administration; 5 – 10 mg for
 intravenous or intramuscular injection. Midazolam: Adult dose 10 –
15 mg orally; 5 – 10 mg intramuscularly. Phenergen: Adult dose 12.5
– 25 mg intramuscularly.
2 Hypnotics: Sedation, hypnogenesis and anticonvulsant.
Phenobarbital: 30 – 60mg orally, 0.1 – 0.2g intramuscularly;
Secobabital: 0.1 – 0.2g orally, 0.1 – 0.2g intramuscularly.
3 Analgesics: Analgesia and sedation, synergism with general
anesthetics, alleviation of visceral reaction. Morphine: 5 – 10mg,
hypodermal; Pethedine: 25 – 100mg, hypodermal.
4 Anticholinergics: Block M-cholinergic receptor, inhibit glandular
secretion in trachea and mouth, relive smooth muscle spasm and
cardiac inhibition by vagal excitation.
Atropine: 0.5mg, hypodermal; Scopolamine: 0.3mg,hypodermal.

Chapter3 General Anesthesia

General Anesthesia: It is the kind of anesthesia in which the drugs are

absorbed by tracheal inhalation or intravenous or intramuscular injection,
produces depression of central nervous system and present
unconsciousness, painlessness, oblivion, depression of nervous reflex and
to some extent of muscle relaxation.
Characteristics: The depth of inhibition on central nervous system is
correlated with drug blood concentration, which we can control and is
reversible.
General anesthetics
Inhalation anesthetics: The anesthesia which produce general anesthetic
action by inhalation.
Physiochemical and Pharmacological properties
MAC-Minimum Alveolar Concentration
It is defined as the index of inhalation anesthetics potency. It is the
minimum alveolar concentration of an anesthesia at 1 atmosphere
absolute that prevent movement of 50% of the population to a standard
stimulus.
The depth of anesthesia is related to the partial pressure of an inhalation
agent in brain. When the equilibrium of inhalation agent is reached
among alveoli, blood and brain tissue, the concentration in alveoli
represents the concentration in brain. Thus it can be used as an index of
anesthetic depth.
The relation of oil/gas, blood/gas partition coefficient with
anesthetic properties.
Oil/gas is positively proportioned to inhalation anesthetic potency.
The controllability of inhalation agent is correlated with blood/gas
coefficient. The smaller the latter, the easier the agent is controlled,
because the quick equilibrium of anesthetic among alveoli, blood and
central nervous system may reach.
The factors which influence the alveolar concentration of
anesthetics
FA Drug concentration in alveoli FI Drug concentration in circuit and
airway.
FA / FI is a common index of rate of rising of drug concentration in
alveoli. It is determined by following factors.
Ventilation effect: The increased ventilation accelerates the increase
of FA and FA / FI especially to the anesthetics with bigger blood/gas
partition coefficient.
Concentration effect: FI can affect not only FA but also the rate of FA
rising, that a higher F1 improve FA rising.
cardiac output (CO): If ventilation is kept fixed, the increase of CO
can slow down the rising of anesthetics. The increase of CO can also
decrease FA of an anesthetic with higher blood/gas partition coefficient.
Blood/gas partition coefficient: It is referred to the volume of a gas
dissolving in unit volume of blood when the gas and blood reach
equilibrium. An anesthetic with higher blood/gas slows down its rising of
alveolar concentration that prolongs induction and recovery of anesthesia.
The controllability of an anesthetic is inverse to its blood/gas partition
coefficient.
The concentration gradient between alveoli and venous blood(FA-V):
The higher FA-V, the more anesthetics is taken by pulmonary circulation,
and also the concentration in the alveoli and venous blood reach
equilibrium.
Metabolism and Toxicity
The most inhalation anesthetics are discharged from the airway; a
fraction goes out with urine after metabolized.
The main metabolic site is in liver and the predominant metabolic
enzyme is cytochrome P450 a kind of important oxidase. Some drugs can
improve autometabolic rate by inducing metabolic enzyme.
The toxicity of anesthetics is involved with their metabolic rate,
intermediate product and terminal product, so it is said low rate
producing low toxicity.
Reasons: Toxicity of intermediate metabolite.
Inorganic fluorine in plasma: Producing renal toxicity predominately.
Concentration Criteria: <50μmol/L,no toxicity; 50-100μmolly/L,possible
toxicity; >100μmol/L ,Affirmative toxicity.
Inhalation Anesthetics in Commmon Use.
The Physiochemical Properties of inhalation Anesthetics
Anesthetics Molecular weight oil/gas blood/gas metabolic rate(%) MAC
Diethyl ether 74 65 12 2.1 - 3.6 1.9
Nitrous Oxide 44 1.4 0.47 0.004 105
Halothane 197 224 2.4 15 – 20 0.75
Enflurance 184 98 1.9 2–5 1.7
Isoflurance 184 98 1.4 0.2 1.15
Sevoflurance 200 53.4 0.65 2–3 2.0
Desflurance 168 18.7 0.42 0.02 6.0
Nitrous Oxide(N2O)
Properties:Gas anesthetics with weak potency, Its MAC is 105%,
stored in compressed form as a liquid in cylinder at a pressure of
5000kPa.
Cardiovascular system: A direct depressant to myocardium but this
effect is antagonized by indirectly sympathetic stimulation. So there is
little change in CO, HR and BP in healthy individuals. But it can decrease
CO and BP in patients with coronary heart diseases and hypovolemia.
The vasoconstriction of pulmonary vessels results in increased right atrial
pressure. Respiratory system: Depressed slightly. Decrease tidal volume
and rise breathing rate. Central nerve system: Increase cerebral blood
flow thus slightly increases intracranial pressure. Clinical application:
FI:50% - 70%, FI O 2: >30%(to avoid hypoxemia).When the anesthesia is
stopped, continue to inhale pure oxygen for another 5-10 mins to prevent
hypoxemia. Patients with intestinal obstruction are forbidden to use.
Enflurane
Properties: Powerful anesthetic potency, MAC 1.7%
CNS: Depression, but increase CBF and ICP. At a moderate high
concentrations( >3% ) it produces epileptiform spike activity and burst
suppression in EEG.
Cardiovascular system: Inhibit contractibility of myocardium that
cause BP, CO and O2 consumption decrease. Dilate peripheral vessels
which decreases BP and increases HR.
Respiratory system: No irritative to airway, so do not increase oral
and tracheal secretions. Respiration is depressed obviously, presented by
decreasing tidal volume and fasting frequency.
Strengthen the effect of non depolarizing muscular relaxants.
Metabolism: 2% - 5% metabolize in body . The predominant
metabolite F- is renal toxic but its blood concentration in clinical
anesthesia is far low than threshold value.
Clinical application: Used in induction and maintenance. FI in
induction is 4%, in maintenance is 0.5% - 2%. Epileptic patients should
be avoided.
 Isoflurane
Properties : Powerful anesthetic potency, MAC is 1.15%.
CNS: At high concentrations(>1 MAC), it dilates cerebral blood
vessels that increases CBF and ICP, but the effect is mild than that of
halothane and enflurane.
Cardiovascular system : Mild inhibition to myocardium and CO.
Decrease BP by reducing peripheral resistance. Dilate coronary arteries
can produce coronary stolen blood possibly.
Respiratory system: Mildly inhibit and dilate tracheal smooth
muscle. Irritative to airway.
Strengthen the effect of non depolarizing muscular relaxants.
Metabolism: Low metabolic rate (0.2%),blood concentration of F- is
lower than 10μnol/L. No toxicity to liver and kidney.
Clinical application: Used in induction and maintenance. Because of
its odor, it is seldom used in children’s induction. Concentration in
maintenance is 0.5% - 2%.
Sevoflurane
Powerful potency, MAC is 2%.
CNS: Depression , dilate cerebral vessels, decrease ICP.
Cardiovascular system : Slightly inhibits myocardium, reduces
peripheral resistance thus depresses BP and CO . Induces “stolen blood”
in coronary arteries at the concentration higher than 1.5MAC.
Respiratory system: NO irritability to airway , no oversecretion in
airway. Strong inhibition in respiration and dilatation of tracheal smooth
muscle.
Potentates and prolongs the effect of non depolarizing muscular
relaxants.
Metabolism: Main metabolites are F- is 20 – 30μmol/L, lower than
renal toxicity threshold value.
Clinical application: Used in induction and maintenance. When it
used in induction, FI 4% plus 40% N 2 O, the mean induction time 10 min.
FI used maintenance is 1.5% - 2.5%. The average recovery time in adult
is 10 min, in child is 8.6 min.
Desflurane
Properties: Weak potency, adult MAC is 6.0% - 7.25%.
CNS: Inhibits cortical electric activity and reduces CMRO2; Low FI
does not inhibit central nervous response to CO2, also not decreasing ICP
when over ventilated. High FI can dilate cerebral vessels, and impair auto
regulatory function.
Cardiovascular system : Inhibits myocardium slightly. It can
decrease peripheral resistance at high concentration.
Respiratory system :Slight inhibition. Inhibits response to increased
PaCO2 and is slight irritative to airway.
Potentiates the effect of muscle relaxants by inhibiting the
neuromuscular junction.
Metabolism: It has a very low metabolic rate; most are discharged
from lung by prototype.
Clinical application: Used in induction and maintenance. When FI in
induction is higher than 7%, it can cause cough, breath holding and
secretion in airway, and even laryngeal spasm. When FI ≥ 12% - 15%,
intubations can be done without muscular relaxants. It is easy to be
controlled when used in maintenance alone or combined with N2O and
benefits to patients with heart disease receiving cardio surgery and
noncardiosurgery. Induction and recovery are quick, which is suit for day
case anesthesia.
Shortcoming：special evaporator is needed.
Halothane
Properties: Powerful potency, adult MAC is 0.75%.
Cardiovascular system: It has a relative strong inhibition to
myocardium ,and reduces O2 consumption ； it dilates peripheral vessels
that decrease circulatory resistance ;Inhibits sympathetic nerve that
decreases HR, so atropine should be used as premedication; Increases
sensitivity of myocardium to exogenous catecholamine, which is easy to
produce arrhythmia.So adrenaline is cautious to be used in this
anesthesia.
Respiratory system : Non irritative to airway. Reduces tidal volume
and increases PaCO2 by inhibiting respiration. Dilates tracheal smooth
muscle and decreases airway resistance.
Metabolism: 20% metabolized in liver, the major metabolites are
bromine, chlorine, trifluoroacetic acid and trifluoroacetylethanol amid .
Trifluoroacetic acid is hepatotoxic especially when hypoxemia is present.
Enzyme inducing agents, such as phenobarbitone can activate the
formation of F-.
Clinical application: Induction concentration:1%;Maintenance
concentration: 0.5% - 2%,combined with N2O often. It is forbidden in
patients with hepatic malfunction, latest using halothane in 3 – 6 months,
jaundice and fever after halothane anesthesia. Adrenaline and
noradrenaline is forbidden during halothane anesthesia.
Intravenous Anesthetics
The anesthetics which depresses CNS through intravenous pathway.
Its merits are rapid induction, non irritant to airway, non pollutant and no
need of special equipment.
Comparison of intravenous anesthetics in common use
Thipentone Ketamin Propofol Etomidate
CNS hypnosis Hypnosis(Slight), hypnosis hypnosis
 analgesia
Circulation Myocardial Depression(+),BP Depression(++ Depression(+)sl
Depression(+ ↑HR↑ vessal +),BP↓ ight dilatation
+),vessal resistance ↑ HR↓vasodilata
tion
dilatation

Respiration Depression,spasm Depression Depression No depression

→apnoea,antis →apnoea
pasm
Clinical use induction Induction,maintenan Induction,m induction
ce basic anesthesia aintenance

Dosage(mg/kg) 4 – 6 (iv) 1 – 2(iv),5 – 10 (im) 1.5 – 2 (iv) 0.3 – 0.4 (iv)

Onset time 1 min 30 – 60 s ,5 – 8 min 30 – 40 s 30s

Maintenance time 15 – 20 min 10 – 15 min 4 – 5 min 5 – 5 min

Side effect Laryngeal ICP,Intraocular Circulatory Muscle tremor
spasm powerful pressure↑hallucin and depression of cortex
alkali ation,nightmare respiratory
depression,
local
irritation

Clearance 3.4 16 – 18 30 – 60 10 – 20
rate{ml/(Kg
min)}
Half time of 11.6 1–2 0.5 – 1.5 2–5
Clearance(h)

Thiopental sodium
Physical properties: It is a barbital with super short effect. It is
available in single dose ampoules of 1000mg, and is dissolved in distilled
water to produce a 2.5% solution with a PH of 10 -11, and may be kept
for 24h under normal temperature .
CNS:Thiopental sodium penetrates easily through blood brain barrier
and inhibits the activation of ascending reticular activating system by
enhancing the effect of inhibitive neurotransmitter γ-amino butyric acid
(GABA). It decreases cerebral metabolic rate and oxygen consumption,
and lowers CBF and ICP. Thus may produces protection to cerebral cell.
It produces anesthesia usually in less than 30s after i.v injection.
Cardiovascular system: BP decreases by depressing myocardiac
contractility being depressed and peripheral vasodilatation occurred.
The decreased extent is related to the dosage and rate of administration.
Respiratory system: Ventilation is reduced by relative strong central
respiratory depression, often presents as decreased tidal volume and
ventilatory frequency, even short period aponea. It increases the
 sensitivity of pharynx and bronchus by depressing sympathetic system
thus relatively activating parasympathetic system. So laryngeal and
bronchial spasm inclines to occur during this anesthesia.
Metabolism: It is metabolized mainly in liver, so the recovery time
may be postponed in patients with hepatic malfunction.
Clinical application: (1)Induction of general anesthesia. Usual dose is
4-6mg/kg and combined with muscular relaxant to do intubations.
Serious laryngeal spasm may occur when use it alone. (2) Short period
anesthesia: abscess incision and drainage, angiography. Dosage: i.v
injection of 2.5% solution 6-10ml ; (3) Control convulsion:2.5%
solution 2-3ml; (4) Pediatric basic anesthesia: i.m injection of 2%
solution 15-20mg/kg.
Caution: Hypodermal injection may cause tissue necrosis ; inadvertent
intra arterial injection may result arterial spasm, intense pain and distal
limb necrosis.
Ketamine
Physical properties: It is a phencyclidine derivative , water soluble .PH
value of solution is 3.5-5.5
CNS: It selectively depresses cerebral connective pathway and
thalamus neocortex system , excites limbic system, but influences little to
reticular formation. The somatic analgesia is remarkable even at sub
anesthetic blood concentration. CBF, ICP and cerebral metabolic rate may
increase.
Cardiovascular system: Increase HR , BP and pulmonary arterial
pressure by activating sympathetic system, but presents depression of
myocardium in hypovolemic shock and super sympathetic excitation.
Respiratory system: Overdose or quick injection or combination with
other analgesics may cause respiratory depression of apnoea . Saliva and
bronchial secretion may increase and bronchial muscle is dilated.
Metabolism: Metabolism is predominately occurred in liver. Among the
metabolites norketamine is pharmarcologically active. The terminal
metabolites is excreted from kidney.
Clinical 　 application: 　 ① Induction of anesthesia,1-2mg/kg,

i.v;②Maintenance :0.2mg/kg intravenous infusion of 1% solution. It can

couple with propofol or midazolam to do intravenous anesthesia.
③Pediatric basic anesthesia: 5-10mg/kg, i.m
Side effect: Short period apnoea, hallucination, nightmare, restlessness.
ICP and intraocular pressure increase .
Etomidate
Physical properties: soluble but unstable in water. The PH value of
solutin (0.2%) is 8.1
 CNS: CBF , ICP and metabolic rate decrease that may protect brain
from ischemic injury.
Cardiovascular system: Nondespression. Dilates coronary artery slightly
which may suit for coronary heart disease, cardiac malfuncrion and
senility.
Respiratory system: Influences slightly, but high dose or combined with
analgesics may cause lowering frequency, decreasing tidal volume and
short period apnoea.
Metabolism: Metabolism mainly occurs in liver, the metabolites are not
active. No influence to hepatorenal function.
Clinical application: ①Induction of anesthesia. 0.15-0.3mg/kg.It is
suitable for senility and severe patients.
Propofol
Physical properties: Extremely lipid soluble. The commercial available
one is a white, aqueous emulsion containing soybean oil and purified egg
phosphatide. Ampoule of drug contains 200mg of propofol in 20ml.
CNS:CBF,ICP and metabolic rate decrease.
Cardiovascular system: It results in BP,HR,CO and peripheral
resistance decreasing because of obvious cardiovascular depression. So it
is apt to cause hypotension in high dose, rapid injection and old or
hypovolemic patients.
Respiratory system: It depresses respiration remarkablely presented by
tidal volume and frequency decreasing even aponea .
Metabolism: Metabolizes in liver, its metabolites are activeless.
Accumulation may occur after repeat administration ,but no harm to
hepatorenal function.
Clinical application:①Induction of anesthesia:1.5-2.5mg/kg.
Cardiovascular response to endotracheal intubation is slight.
②Maintenance:6-10mg/kg intravenous infusion uniquely or combined

with other anesthetics. ③Outpatient anesthesia:2mg/(kg.h). Patients can

answer question 10min after administration stop , and can be discharged
131min (mean) later.④Supplementary drug of local anesthesia:1-2mg/
(kg.h).
Side effect: Irritation to vein; Respiratory depression; Postanesthetic
nausea and vomiting.
Muscular Relaxants
Mechanism and Classification
Structure of neuromuscular junction: Presynaptic membrane,
synaptic cleft and postsynaptic membrane.
Procedure of neuromuscular transmission: The neurotransmitter
acetylcholine is released into synaptic cleft when a nerve impulse reaches
the nerve end and induces the sac containing acetylcholine break at the
presynaptic membrane, then the neurotransmitter bind to the
acetylcholine receptors on the postsynaptic membrane thus produces
depolarization of muscularfibers and induces muscle contraction.
The muscular relaxants interfere the conduction of impulse at the
neuromuscular junction. So based on the interferential type, they are
divided into two classes : Depolarizing muscular relaxants and Non
depolarizing muscular relaxants.
Depolarizing muscular relaxants
The only Depolarizing muscular relaxants available is
succinylcholine (suxamethonium,Britain)
Mechanism: Its molecular structure and action to the postsynaptic
receptor are similar with those of acetylcholine but has a long period, so
the postsynaptic membrane persists in depolarization and can not be
repolarized. The further potentials can not pass down and muscle
becomes flaccid. When the concentration of acetylcholine at the junction
decrease, and the postsynaptic membrane becomes repolarized, the
conductivity of the junction gradually resumes. Repeat administration
results desensitisitonal blockade that is caused by decreasing the
sensitivity of acetylcholinergic receptors which prolongs the muscular
relaxing time.
Characteristics: 1Keep the postsynaptic membrane in persisting
depolarization;2At the first bolus, fasciculation occurs before muscular
flaccid.3Muscular flaccid can not be antagonized by anticholinesterases
(neostigmine) but can be enhanced.
Non depolarizing muscular relaxants
The representative is tubocurarine.
Mechanism: These drugs can bind to acetylcholine receptors but fail
to depolarize the postsynaptic membrane. When 70%-80% receptors are
occupied by non depolarizing muscle relaxant, though the nerve impulse
can release acetylcholine, there are no sufficient receptors left to bind
them, the muscular cell can not be depolarized then the neuromuscular
transmission is blocked. The non depolarizing muscular relaxants show a
dose dependent character because of the competitive binding to the
acetylcholine receptors. Anticholinesterase can slow down the catabolism
of acetylcholine, which makes the latter compete the receptors with non
depolarizing muscle relaxant repeatedly. As the quantity of the binding
receptors reaches the threshold value, muscle constriction is resulted.
.Characteristics: 1The block site is at neuromuscular junction, to
occupy acetylcholine receptors on postsynaptic membrane.2The amount
of releasing acetylcholine does not reduce but can act;3No fasciculation
before muscle relaxes;4 It can be antagonized by anticholinerases.
Comparison of muscular relaxants in common use
Relaxant ED95 intubation Maintenance Onset time Maintenance clearance
(mg/kg) dose(mg/kg) (mg/kg) (min) time(min) halftime(min)

Succinylcholine 0.2 1-2 1 0.5-1 3-8 --

Turbocurarine 0.5 0.6 0.15 4-6 30-40 231
Pancuronium 0.06-0.07 0.1 0.02 3-6 30-60 120
Atracurium 0.2-0.25 0.6 0.1 3-5 15-35 20
Vecuronium 0.05 0.1 0.01-0.02 2-3 25-35 62-80
Succinylcholine
It is one unique depolarizing muscular relaxant. Fasciculation occurs
15-20s after intravenous injection and can be prevented by small dose
non depolarizing muscular relaxant administered short before injection.
Recovery time is 10-12min. Hemodynamic change is little, but transient
hyperkalemia may occur, even arrhythmia may occur. No histamine
release, so bronchial spasm is rare. It is hydrolyzed soon by
cholinesterase and the metabolites are excreted in urine.
Predominate clinic use is in endotracheal intubation. Maintenance is
used by infusion and may result desensitize block thus prolonging the
recovery time .
Side effect: Bradycardia or other arrhythmia; hyperkalemia; intraocular
and intracranial and intragastric pressure increasing; postanethetic muscle
ache.
Tubocurarine
It is earliest non depolarizing muscular relaxant. Its onset is slow but
remains long. It seldom metabolizes in body and most discharge from
kidney and bile in prototype.
In clinic it is mainly used for maintenance.
Side effect: Hypotension and tachycardia, even bronchial spasm may
occur because of histamine release. So contraindication to asthma and
myasthenia gravis.
Pancuronium
It is long acting, non depolarizing muscular relaxant. In clinical dose, it
can increase HR by weak anti vagal effect. It does not block ganglions
and release histamine. Its metabolites are pharmacologically active, so
repeated administration may result residual muscular flaccid
postanesthetically. 40% of pancuronium is discharged from kidney
prototypically, the rest is from bile tract.
Clinical application: Induction and Maintenance. Intubation time is 2-
4min. Anticholinesterse can be used when anesthesia finishes.
Contraindication to myasthenia gravis.
Vecuronim
It is short acting non depolarizing muscular relaxant. No histaminic
and anti vagal effect, so it suits for ischemic patients. Its metabolites also
have relaxant effect. 30% is discharged by kidney prototypically and the
rest by bile. In clinical, it is used in intubation and maintenance.
Intravenous injection intermittently or continuous infusion can be used in
maintenance.
Atracurium
It is short acting non depolarizing muscular relaxant. It can cause a
dose dependent histamine releasing that induces rash, tachycardia and
hypotension and bronchial spasm. It is often used in intubation and
maintenance. Asthmatic and supersensitive patients are forbidden.
Cautions in application of muscular relaxants
1 To keep the airway, endotracheal intubation and control respiration
should be done; 2 It must no be used uniquely and must combine with
sufficient other sedatives and analgesics. 3 Succinylcholine increases
serum potassium, intraocular and intracranial pressure , so it is forbidden
for severe traumatic, burn, paraplegic glaucomatous and high ICP
patients. 4 Hypothermia prolongs the relaxant effect ; Inhalation
anesthetics , some antibiotics ( streptomycin, gentamycin ) and
magnesium sulfate enhance the effect of the non depolarizing relaxants. 5
In patients with neuromuscular junction disease (myasthenia gravis), the
application of non depolarizing relaxants is forbidden.6 Some relaxants is
histamine releasing, so they should be carefully used in asthmatic and
anaphylactic patients.
Supplementary drugs to anesthesia
Diazepam: effects: sedation, anticonvulsant, hypnosis, amnesia and
antianxiety. Application: premedication, adjuvant and induction (0.2-
0.3mg/kg). The anticonvulsive effect is used to prevent and treat the toxic
reaction of local anesthetics.
Midazolam: Effect : sedation, anticonvulsant, hypnosis, amnesia,
antianxiety and decreasing muscular tension. Application: premedication ,
adjuvant and induction (0.15-0.2mg/kg). Its anterograde amnesia is dose
dependent, 5mg i.v can produce 20-32 min amnesia. Respiratory
depression is related to dose and rate of injection. 0.5mg/kg i.v can cause
obvious depression
Promethazine (phenergan) : Effects: sedation and antihistamine. In
clinic,the combination of promethazine and pethidine (promethazine
25mg, pethidine 50mg) is usually used as adjuvant and premedication.
Droperidol: Central sedatives, has neuroleptic and antiemetic effect.
It decreases BP and peripheral vassal resistance by slight &-adrenergic
block. In clinic , a mixture, which commercial name is Innovar is made of
droperidol and fentanyl under proportion 50:1(1uinnovar cotains 2.5mg
droperidol and 0.05mg fentanyl). Innovar is used in neuroleptic
anesthesia or adjuvant or premedication or in inhibition of intubation
response.
 Morphine : Narcotic analgesic .It acts on cerebral limbic system that
can eliminate nervous and anxiety, also produce euphoria and addiction .
It abates pain by increasing pain threshold. It depresses respriratory
center that causes respiratory frequency slow and tidel volume decresase
and even aponea. Sometime it induces bronchial spasm by the reason of
histamine releasing . Morphine dilates aterioles and veins which
decreases peripheral resistance and returned blood volume and produce
hypotension, but it dose depress myocardium remarkably. Its predominant
use in clinic is in analgesia (ttrauma, operation and angina pectoris ) and
treatment of pulmonary edema resulted by left heart failure. In anesthesia
it is used as asjuvant an premedication, sometime as a component in
intravenous anesthesia. Dosage: adult 5-10mg hypodermal or i.m.
Pethidine :Effects: analgesia, hypnosis,anti smooth muscular spasm.
Depression of myocardiac contractility produces hypotension and CO
decreasing. Respiratory depression is slight . It can produce addiction and
euphoria. Application : Usually used as premedication. Dose: adult 50mg
i.m; child 1mg/kg i.m but unsuitable for who under 2 years old. It also
corporates with droperidol or promethazine as premedication. (Pethidine
50mg and droperidol 5mg or promethazine 25mg ). When used in
postanalgesia,the dose is 50mg i.m 4-6h intermittently.
Fentanyl : Effect is similar with other opioid. It analgetic effect is
75-125 time stronger than that of morphine. The respiratory depression is
remarkable when combines with midazolam. Its analgesia persists for
only 20-30min, but respiratory depression lasts for 1h. Assisted
ventilation is necessary after large dose is administrated (50 – 100 g/kg).
Analgesic dose (2 – 10 g/kg) and anesthetic dose (30 – 100 g/kg) are
hemodynamic stable. Adjuvant dose is 0.05 – 0.1mg.
Fundamental Structure and Appication of Anesthesia Machine
①Gas Suppies
The equipment which reserves oxygen or nitric oxide contains cylinder
and gas storage center. Through pressure regulator, the high pressure is
reduced to 343 – 392kPa which fits for anesthetic machine use.
②Vaporizer
The apparatus that facilitates volatile anesthetics vaporizing and adjusts
the outlet gas concentration accurately.
③Breathing circle system
A circuit that suppies oxygen and the gas anesthetics from the machine to
the patient and discharge the expiratory gas out from patient. The
common used circuit systems are “opened”, “semi opened ” and “closed”
system.
④Ventilator
There are two type of ventilator, one is volume cycled and the other is
pressure cycled. Tide\al volume or minute volume, or airway pressure,
breathing frequency, Inspiration Expiration ratio ,et al can be preset.
Endotracheal Intubation
Endotracheal Intubation :Insert a tracheal tube into patient’s windpipe
through oral or nasal cavity.
Purposes :① To keep the airway during anesthesia, and prevent foreign
body falling down and facilitate suction of secretion and blood in time.
②To facilitate effective artificial or mechanical ventilation, prevent
patient from hypoxemia and hypercapnia. To facilitate the application of
inhalational anesthetics.
Indication:①Patients accept general anesthesia which is difficult to keep
the airway. ②Salvage, respiratory failure which mechanical ventilation is
necessary ,cardiopulmonary resuscitation, some drug toxicities and
newborn choke.
Methods :Bright sighted intubation through oral or nasal cavity; blinded
intubation through nasal cavity.
Bright sighted intubation through oral cavity
①Flex the neck and extend the head with a thin pillow, then open the
mouth by tilting mandible upward and forward using both hands.
②Laryngoscope in left hand, place the blade into mouth from right side
while the right hand open the mouth. Push the tongue to left side and
advancing. When uvula is in sight, lift the laryngoscope vertically while
advancing until see the epiglottis.
③Expose vocal gate by lifting epiglottis. If a curved blade is used, insert
the tip into the vallecula and pressure on the hypoepiglottic ligament
move the epiglottis to expose the vocalgate.If a straight blade is used,pass
the tip posterior to the epiglottis which is lift anteriorly and vocal gate is
visuliazed.
④Take the tracheal tube between thumb,index finger and middle finger
(like taking a pen ),then place the tube into mouth from right side,observe
the advancing direction from the space between bade and tube, insert the
tip into the vocal gate. Some time a semirigid stiletto is needed keep
correct curve of the tube. The depth of tube in adult is 4—5cm,the
distance from the tip to central incisor is 18-22cm.
⑤Affirm the position and fix the tube. Methods :a. Airflow can be felt
when the chest is pressed; b. Symmetrical thorax undulation and clear
alveolar breathing sound can be heard when artificial ventilation is
suppied. C. The wall is clear when inspiring and “mist like” when
expiring and tube is transparent. d. Monitor end expiratory CO2 partial
pressure (ETCO2). If ETCO2 is showed,the position can be certained.
Blind intubation through nasal cavity
①Keep autonomous respiration during intubation. Judge the direction
according to the force of airflow.
②Anesthetize the nasal mucosa by 1% tetracaine, and drop 3%
ephedrine to reduce bleeding and increase nasal cavity volume.
③Select appropriate tube and take it in right hand .Listen the airflow
while advancing the tube and adjust the position of patient’s head to find
the point of the strongest airflow.
④Push the tube rapidly when expiring. If the tube enters the trachea,the
advancing resistance reduces and expiring airflow is obvious. Patients
often cough. When anesthetic machine is connected with patient,repeated
inflation of reservoir bag can be seen.
⑤If airflow disappears after the tube is pushed, it shows the tube is
misled into oesophagus. Retreat the tube to nasopharyngeal region,flex
the head posteriorly slightly and try again.
Compications of Intubation
①Trauma may be occurred to teeth, mucosa of oral cavity,pharynx and
nasal cavity. Jaw dislocation even occurs when the force of lifting
laryngoscope is too hard.
②Intubational responses may be severe under light anesthesia. It may
induce cough breathing hold,laryngeal of bronchial spasm,tachycardia
and dramatic undulation of blood pressure which may induce myocardial
ischemia. The severe vagal reflex may results arrhythmia, bradycardia
and even sudden arrest of heart. Preventions are deepening anesthesia
suitably, superficial anesthesia on larynx and trachea or administration of
narcotics or short effect depressant before intubation.
③Unappropriate tracheal tube. Too thin tube may increase respiratory
resistance, but too large diameter or too hard may damage tracheal
mucosa, and even induce acute laryngeal edema. The soft tube can be
misshaped easily, thus airway obstruction may be occurred under press
and kink.
④Too deep intubation may mislead tube into lateral bronchus that may
result in insufficient ventilation, hypoxia and postoperative
atelectasis.Too shallow intubation may result in accidental dislodgement
of tube when changing the patient’s posture. So check the depth of tube
carefully after intubation and changing the patient’s posture.Regularly
auscultate the breathing sound on both sides of the lungs.
Practice of General Anesthesia
Induction of anesthesia
It refer the period that patient lose his consciousness after being
administrated anesthetics and receive tracheal intubation. The methods
conclude inhalational induction and intuavenous induction
①Inhalational induction
Open dripped induction :Put a round metal net wrapped by gauze over
patient’s mouth and nose,then drip liquid anesthetics on the gauze. The
patient is anesthetized by inhaling vaporized anesthetics. It was once used
in diethyl ether induction.
Mask induction: Put a mask around patient’s mouth and nose, and then
increase the inhaled concentration of anesthetics gradually. When patient
becomes unconciousness and falls in third stage of anesthesia ,a bolus of
muscular relaxant is injected intravenously and the tracheal intubation is
given.
②Intravenous induction:
Induction which is produced by intravenously injected anesthetics and
muscular relaxant consequently and then intubates tracheal tube. Before
induction, inhale pure oxygen for 2-3min for increasing oxygen reserve
and exhaling nitrogen. Comparing with inhalational induction,its
advantages are quick,comfortable and non pollutant. Disadvantages are
obscure stage and hemodynamic disturbing.
Maintenance of anesthesia
Purpose : To keep appropriate anesthetic depth to satisfy operational
request and keep the stability of physiological function of patient during
operation.
①Maintenance by inhalational anesthetics
At present the gaseous anesthetics is nitrous oxide, and volatile
anesthetics are fluorides anesthetic agents which include enflurane,
isoflurane et al.Nitrous oxide is difficult to maintain anesthesia alone
because of its weak potency and risk to result hypoxia. Most volatile
anesthetics can maintain anesthesia alone. But when inhaling them with
high concentration,they may influence physical function remarkablely. So
in clinic,N2O,O2 and volatile anesthetics are often combined.The
concentration of N2O is controlled between 50%-70% to avoid hypoxia,
volatile anesthetic is regulated based on anesthetic depth. Neuromuscular
relaxant can be given if necessary. F1O2 or SpO2 monitoring is necessary
under N2 O anesthesia.
②Maintenance by intravenous anesthetics
Administrative methods conclude single, intermittent and continuous
injection. Selection of these is based on operation and drugs. Except
ketamine, most intravenous anesthetics in present use are hypnotice,
which is poor in analgesic effect. So single intravenous anesthetic alone is
fit for induction and short period operation.
③Combined anesthesia
It refers to the use two or more kinds of aesthetics together to achieve
optimal anesthesia. Based on administrative pathway, it is divided into
total intravenous anesthesia (TIVA) and combined intravenous
inhalational anesthesia.
TIVA:It refers to anesthesia which is inducted by intravenous anesthesia
and maintained by combining several kinds short effect intravenous
anesthetics through intermittent or continuous injection.
To receive a stable anesthetic effect under pure intravenous anesthetic
agents, it must combine with intravenous anesthetic agent, narcotics and
neuromuscular relaxant together to exert their advantages and conquer
their side effects. Because of the weak analgesic effect of most
intravenous anesthetics, narcotics are often added to enhance the
anesthetic effect. Muscular relaxant is necessary to facilitate ventilation
an operation. The advantages of TIVA are inducing quickly, manipulating
simply and no air pollution, The duration of anesthesia should be stable
and the recovery should be quick if the drugs were given in right time and
dose. The disadvantages of TIVA are difficulties in selecting anesthetics
and administrating dime, difficulty in differentiation anesthesia stages and
signs. The delayed recovery and residual muscular relaxation may cause
severe complication. So anesthetists should be familiar with the
pharmacological characters of different anesthetics. During the anesthesia
there should be monitoring of respiratory and circulatory function and the
signs of stress reaction should also be carefully observed. Did it permit
monitor of blood concentration of anesthetics and administration under
computer control should be practiced to avoid “knowing” during
anesthesia. Propofol and Midazolam are the common intravenous agents
used in practice. Narcotics includes Morphine are Fentany. Long effect
muscular relaxants could be administered intermittently but the short
effect cones should be kept on continuous infusion, especially under
minimal pump control at the best. The common dispensing are : (1)
Rentany13-2mg/kg+propofol 4-8mg/(kg.h) + muscular relaxant; (2)
Fentany150-100mg/kg+Midazolam +muscular relaxant; (3) Propofol
(Midazolam)
+ ketamine + muscular relaxant .
Intravenous inhalation combined anesthesia: Because of the lack of remarkable
sign of anesthetic depth in TIVA. It is difficult to control the time of giving drug.
Sometime anesthesia may become light suddenly. Thus further inhaling volatile
agent can keep anesthetic stability. The agents in use are Enflurane, Isoflurane,
Sevoflurane and Desflurane. Inhalation agents are intermittently used when
intravenous anesthesia becomes light which can reduces the dose of inhalation
agents and be propitious to early recovery. It also can inhale low concentration of
volatile agents continuously or 50% - 60% N2O. Its merits are wide indication, easy
manipulation and management. But postponed recovery may occur if no well
control.

Judgement of general anesthesia depth

Guedel’s classic signs of anesthesia are those seen in patients premedicated
with morphine and atropine and breathing ether in air. The clinical signs associated
with anesthesia produced by other inhalational agents follow a similar course, but
the division between the stages and planes are less precise.
Stage 1: The stage of analgesia, which start from induction to disappearance of
conciousness. The cortex is inhibited lightly. Analgesia becomes blunt but most relax
still exists. This stage is unfit for surgeny.
Stage 2: Stage of excitement. This is seen with inhalation induction, but rapidly
passed during i. v. induction.The subcortical center is lost of control because the
inhibition of cortex. The clinical manifestation is excitement such as respiratory
turbulence, BP and HR fluctuation. Deep and rhythmic respiration spears at last.
Surgery is forbidden in this stage.
Stage 4: Surgical anesthesia. Subcortical center is depressed which presents
consciousness and analgesia lost. This deepens through 4 planes which increasing
concentration of anesthetic drug. Plane 1: Respiration is still regular but frequency is
little faster; Eyelid reflex disappears and movement of eyeball slower; Muscle is not
relax. Superficial operation can be done under this plane. Plane 2 :Eyeball fixes but
pupils are not enlarged. Respiratory frequency becomes slower but still keeps its
magnitude. Muscular tension becomes weaker. Abdominal operation can be done
under this plane. Plane 3: Pupils start enlarging . Thoracic respiration is depressed by
the paralysis of intercostal muscle; however abdominal respiration becomes stronger
for compensation. BP becomes lower and muscle relaxes. Some operation with
intensive stimulation can be done under this plane. Plane 4: Muscle becomes
completely relaxed and respiration and circulation are circulation are depressed
remarkably in this plane. Anesthesia should be lighten inmdiatly.
Stage 4: Stage of medulla oblongata anesthesia. In this stage patient has no
respiration and measures BP. The pupils are enlarged and unreactive. Cardiac arrest
may occur if no salvage in time.
The judgment of anesthetic depth under combined anesthesia is more
complicated. Under combine anesthesia, several kinds of drugs are used to reach the
aim of unconsciousness, painlessness and inhibition of reflex and muscle relaxation,
but no inhibition to hemodynamic, But under the administration of narcotics and
relaxants. The patients could know what happened during the operation but could
feel no pain and could not move. This is called “knowing in operation ”. It indicates
consciousness still existed during the operation. Thus the judgment of the anesthetic
depth should be based on the complex influence of individual drugs to
consciousness, movement . nerve reflex and homeostasis. In the clinic the depth
under combined anesthesia is often divided in three stages: light,surgical and deep
stage.
The criterion of anesthetic depth under combined anesthesia
Stage Respiration Circulation Ocular sign Others
irregular, cough ciliary reflex(-) swallowing reflex
Light airway resistance↑ BP↑ HR↑ eyeball movement(+) sweating
laryngeal spasm (+) eyelid reflex secretion ↑
(+)lacrimation movement

Surgical regular BP mild lower eyelid reflex(-) no secretion

But stable fixed eyeball

diaphragtic
Deep respiration BP↓ light reflex(-)
Respiration↑ enlarged pupil
 Complications of General Anesthesia and Treatment
(1)Regurgitation and Aspiration
Etiogogy: General induction ( unconsciousness, laryngopharyngeal
reflex lost), delayed gastric empting ( gastric liquid and air accumulation
in stomach) and recovery period after anesthesia.
Clinical manifestation: Airway obstruction, choke and hypoxia may
occur when airway is obstructed completely. Aspiration may cause
pulmonary injury, bronchospasm and increasing permeability of
pulmonary capillaries, thus may acidity of gastric contents. To reduce
gastric pressure and protect the airway by cricoid pressure and rapid
tracheal intubation are essential especially in emergency. Strict fasting
and administration H2 receptor blocker may reduce the risk of aspiration.
Gastric catheter may necessary when general anesthesia needed in full
stomach patients.
(2)Airway Obstrction
Airway obstruction can be divided into upper and lower airway
obstruction at vocal gate.
(a) Upper airway obstruction
Etiology: Mechanical obstructions as apposition of the tongue and
pharyngeal soft tissue, oral secretion , foreign body and pharyngeal edema.
Clinical feature: Partial obstruction present as noisy breathing or stridor,
whereas complete obstruction is silent. Tracheal tug, paradoxical chest and
abdominal movement (see saw’ respiration) and inadequate reservoir bag
movement are other signs.
Management: Apposition of the tongue can be easily overcome by jaw
lift and use of an oral or nasopharyngeal airway. Suction will remove
accumulate secretions, but care is required as laryngospasm may be
precipitated during light anesthesia. The mild laryngospasm can be
overcome by positive mask ventilation; however severe one should do
tracheal intubation after using muscular relaxant . Pharyhgeal edema
mostly occurred in pediatric patients or after difficult intubation. The mild
patient can be remitted by injection of steroid hormone or aerosol
inhalation of epinephrine. The server patients must be done tracheotomy.
(b) Lower airway obstruction
Etiology: Tracheal tube torsion. adhesion of slope end of tube to tracheal
wall, secretion and aspiration.
Clinical feature: Mild patients have o symptom but rales on chest;
severe ones could have difficult breathing, VT decreasing, high sirway
resistance, hypoxemia and cyanosis, tachycardia and hypotestion.
Managemnet: Select tracheal tube carefully, too soft ineligible tube
should be abandoned . Chectk the position of tube after patient’s position
changes. Auscultate the lungs during the anesthesia and aspirate the
secreation in time. Maintain adequate anesthetic depth to avoid
brochospasm in asthmatic and chronic bronchitic patients. Intravenous
injection of aminophylline 0.25mg or hydrocortisone 100mg is necessary
when bronchospasm persists.
(3)Hypoventilation
Clinical feature: CO2 retention. Hypoxemia can be occurred when
hypoventilation appears in recovery period. Blood gas analysis shows
PaCO2 being higher than 50mmHg and PH smaller than 7.30.
Management: Keep mechanical ventilation until respiratory function
recovers when central respiratory depression is resulted by cerebral injury
and residual effect of anesthetic agents, nacortics and analgesics or the
residual effect of muscular relaxant which induces by renal malfunction,
electrolyte disturbance and the use of some antibiotics. Antagonist such
as neostimine can be given to promote recovery of muscular strengthen.
Postoperative pain, abdominal distension and over obesity which restrict
the movement of thorax may induce hypoventilation. Postoperative
analgesia and deep breath and cough should be incented in these patients.
(4)Hypoxemia
SpO2<90%, PaO2<8kPa(60mmHg) when inhaling air or
PaO2<12Kpa(90mmHg) when inhaling pure oxygen can be diagnosed as
hypoxemia.
Clinical feature: Tachypnea, cyanosis, restlessness , tachycardia,
arrhythmia and hypertension.
Reasons and management:(1) Falure of anesthetic machine, too law
F1O2 or tracheal tube dislocation and misleading into one side bronchus
and airway obstruction. Correct them immediately. (2) Diffuse hypoxia:
Mostly occur after N2O anesthesia, Inhale pure oxygen fo 5-10 min after
stopping inhalation of N2O. (2) Pulmonary atelectasis: It is always the
result of too much secretion or hypoventilation which decrease
pulmonary capacity. Obstinate hypoxemia could occur when the
atelectatic area lager. The treatment is exsuction of secretion through
Fiberobrochoscope or by PEEP in severe patients . (4) Aspiration of
gastric contents : The danger is determined by the PH value and volume
the aspiratory contents. When PH<2.5 and volume >0.4ml/kg the death
risk increase lagely, Mild case can be treated by pure oxygen. The severe
one should be treated under mechanical ventilation. (5) Pulmonary
edema: It occur when acute left heart failure or byperpermeability of
pulmonary capillary vessels. The treatment conclude cardiac stimulation,
diuresis, vassal dilatation, oxygen inhalation and mechanical ventilation.
(5)Hypotension
Hypotension during anesthesia may be defined as a systolic arterial
pressure less than 80mmHg or 30% less than the patient’s preoperative
level.
Clinical feature: Oliguria (urine output less than 0.5ml/(kh.h) or
metabolic acidosis. The severe ones can present symptoms of insufficient
perfusion of organ, as myocardial ischemia and disturbance of central
function.
Etiology and treatment: Lighten the anesthesia and increase blood
volume at the same time . Too much hemorrhage can induce hypovolemic
shock, so urinal volume, hemoglobin and HCT (hematocrit), even CVP
and PVPW should be monitored to guide infusion. The treatments
conclude complement blood volume, vassal restriction and aetiological
trerapy.
(6) Hypertension
Hypertension during anesthesia may be defined as a diastolic arterial
pressure higher than 100mmHg or systolic pressure 30% higher than
preoperative level.
Etiology:(1)Caused by companied diseases, as essential hypertension,
hyperthyroidism, pheochromocytoma and high incranial pressure;
(2)Caused by manipulation in operation, as probing is abdominal cavity,
pressing abdominal aorta and tracheal intubation; (3)CO2 retention cause
by hypoventilation; (4) Caused by drugs , as pancuronium, ketamine.
Treatment: To essential hypertension, fentany 3-5µ
g /kg. min i.v . before induction may reduce intubation reaction , During
the operation, regulate the anesthetic depth according to the stimulation.
To obstinate hypertension, controlled hypotension may keep the
circulation stable the common hypotensors are urapidil 12.5 - 25mg i.v. or
2-4µg.kg, min i.v i.v. infusion; phentolamine 0.5-lmg i.v. infusion;

nitoglycerine 10 – 100µg/min i.v. infusion; phentolamine 0.5-1 mg i.v. or

0.3-0.5mg/min.
(7) Arrhythmias
Tachycardia: Inadequate anesthesia, anemia, low blood volume and
hypoxia are all factors which increase heart rate.
Bradycardia: Some reflexes, as cholecardiac and oculocariac reflex can
increase vagal tone which produces bradycardia and some time sinus
arrest. At this time . operation must be stopped and anticholinergic agent
is necessary.
Premature systole: Occasional atrial premature beat most happen under
inadequate anesthesia and need no special treatment. Frequent atrial
premature beat is possible to induce atrial fibrillation, so it should be treat
with cedilanid. Occasional ventricular premature beat usually appear in
light anesthesia or CO2 retention and need no special treatment or CO2
expiration. But frequent ventricular premature systole or companying
multiorigion or R on T which indicate inadequate myocardiac perfusion
should be treated actively. First lodocaine 1-1.5mg/kg i.v. followed by
14mg/min i.v. infusion.
Ventricular fibrillation: Electrical defibrillation must be done
immediately and follow resuscitation procedure.
(8) Hyperthermia, twitch and convulsion
Thest mostly occur in pediatric anesthesia because immature of
regulatory center of body temperature. If high temperature is not treated
in time, twitch even convulsion may occur. Physical cooling especially on
head is necessary to prevent cerebral edema. Malignant fever is a
dangerous complication which present persistent muscle constriction,
PaCO2 increase and rapid increasing body temperature
(1℃/5min,temperature may higher than 42℃). The ansthetics that easily
induce malignant fever are succinylcholine and halothane.