SEMINAR TOPIC

General Anesthesia

DEPARTMENT OF ORAL AND

MAXILLOFACIAL SURGERY

SEMINAR MODERATOR
Dr. Suhas S. Godhi
Dr. Rajesh Kalra

PRESENTER
Dr. ASHOK KUMAR
M.D.S (FIRST YEAR)
CONTENTS

1- Introduction and History of General anesthesia

2- Properties of ideal General anesthetic
3- Classification of General anesthetic agents
4- Mechanism of Anesthesia
5- Stages of Anesthesia
6- Inhalation anesthetic agents
7- Intravenous anesthetic agents
8- Techniques of inhalation of anesthetics
9- Induction, Maintenance and Extubation
10- Anaesthetic Machine (Boyle’s equipment)
11- Complications of General anesthesia
12- Preanesthetic medication
13- General anesthesia- facts and fiction
GENERAL ANESTHETICS

• General anaesthetics (GAs) are drugs which produce

reversible loss of all senations and consciousness. Or,

• General anaesthetics (GAs) are a class of drugs used to

depress the CNS to a sufficient degree to permit the
performance of surgery and other noxious or unpleasant
procedures.

• Triad of General Anesthesia”

– need for unconsciousness
– need for analgesia
– need for muscle relaxation
History of Anesthesia
• Ether synthesized in 1540 by Cordus
• Ether used as anesthetic in 1842 by Dr. Crawford W.
Long
• Ether publicized as anesthetic in 1846 by Dr. William
Morton

• Chloroform used as anesthetic in 1853 by Dr. John

Snow
• Endotracheal tube discovered in 1878
• Thiopental first used in 1934
• Curare first used in 1942 - opened the “Age of
Anesthesia”
Properties of an ideal anaesthetic

A. For the patient - It should be pleasant, nonirritating,

should not cause nausea or vomiting.
Induction and recovery should be fast with no after
effects.

B. For the surgeon - It should provide adequate

analgesia, immobility and muscle relaxation.
It should be noninflammable and nonexplosive so that
cautery may be used.

C. For the anaesthetist - Its administration should be

easy, controllable and versatile.
• Margin of safety should be wide - no fall in BP. Heart,
liver and other organs should not be affected.
• It should be potent so that low concentrations are
needed and oxygenation of the patient does not suffer.
• Rapid adjustments in depth of anaesthesia should be
possible.
• It should be cheap, stable and easily stored.
• It should not react with rubber tubing or soda lime.
CLASSIFICATION

Inhalational Intravenous
Gas Inducing agents Slower acting
Nitrous oxide Thiopentone sod. Benzodiazepines
Liquids Methohexitone sod. Diazepam
Ether Propofol Lorazepam
Halothane Etomidate
Midazolam
Enflurane Dissociative
anaesthesia
Isoflurane Ketamine
Desflurane Neurolept analgesia
Sevoflurane Fentanyl + droperidol

MECHANISM OF ACTION OF ANAESTHESIA

The mechanism of action of GAs is not precisely known.

A wide variety of chemical agents produce general
anaesthesia. Therefore, GA action had been related to
some common physicochemical property of the drugs.

• Minimal alveolar concentration (MAC) is the lowest

concentration of the anaesthetic in pulmonary alveoli
needed to produce immobility in response to a painful
stimulus (surgical incision) in 50% individuals.
 It is accepted as a valid measure of potency of inhalational
GAs because it remains fairly constant for a given species
even under varying conditions.
MAC reflects capacity of the anaesthetic to enter into CNS
and attain sufficient concentration in neuronal membrane.
Mayer and Overton (1901) proposed that the anaesthetic
by dissolving in the membrane lipids increases the degree of
disorder in their structure favouring a gel-liquid transition
(fluidization) which secondarily affects the state of
membrane bound functional proteins, or expands the
membrane disproportionately (about 10 times their
molecular volume) closing the ion channels.
Different anaesthetics may be acting through different
molecular mechanisms.
Many inhalational anaesthetics, barbiturates,
benzodiazepines and propofol potentiate the action of the
inhibitory transmitter GABA at the GABAA receptor.
Certain fluorinated anaesthetics and barbiturates in
addition inhibit the neuronal cation channel gated by
nicotinic cholinergic receptor. As such, the receptor operated
ion channels appear to be a major site of GA action.
Unlike local anaesthetics which act primarily by blocking
axonal conduction, the GAs appear to act by depressing
synaptic transmission
 SIGNS & STAGES OF ANAESTHESIA (GUEDEL’S
Signs)

GAs cause an irregularly descending depression of CNS,

i.e. the higher functions are lost first and progressively lower
areas of the brain are involved, but in the spinal cord lower
segments are affected somewhat earlier than the higher
segments.
The vital centres located in the medulla are paralysed
the last as the depth of anaesthesia increases. Guedel (1920)
described four stages with ether anaesthesia, dividing the III
stage into 4 planes.
• I. Stage of Analgesia Starts from beginning of
anaesthetic inhalation and lasts upto the loss of
consciousness. Pain is progressively abolished during
this stage. Patient remains conscious, can hear and see,
and feels a dream like state. Reflexes and respiration
remain normal.
• Though some minor and even major operations can be
carried out during this stage, it is rather difficult to
maintain - use is limited to short procedures.

• II. Stage of Delirium From loss of consciousness to

beginning of regular respiration. Apparent excitement is
seen - patient may shout, struggle and hold his breath;
muscle tone increases, jaws are tightly closed, breathing
is jerky; vomiting, involuntary micturition or defecation
may occur.
Heart rate and BP may rise and pupils dilate due to
sympathetic stimulation.
 No stimulus should be applied or operative procedure
carried out during this stage.
This stage can be cutshort by rapid induction,
premedication etc. and is inconspicuous in modern
anaesthesia.

• III. Surgical anaesthesia Extends from onset of regular

respiration to cessation of spontaneous breathing. This
has been divided into 4 planes which may be
distinguished as:
• Plane 1 Roving eye balls. This plane ends when eyes
become fixed.
• Plane 2 Loss of corneal and laryngeal reflexes.
• Plane 3 Pupil starts dilating and light reflex is lost.
• Plane 4 Intercostal paralysis, shallow abdominal
respiration, dilated pupil.

• IV. Medullary paralysis Cessation of breathing to

failure of circulation and death. Pupil is widely dilated,
muscles are totally flabby, pulse is thready or
imperceptible and BP is very low.
 Four stages of general Anesthesia

Inhalational Anesthetic Agents

Inhalational anesthesia refers to the delivery of gases or

vapors from the respiratory system to produce anesthesia.

Nitrous Oxide
It is prepared by Priestly in 1776
Anesthetic properties described by Davy in1799
Characterized by inert nature with minimal metabolism
Colorless, odorless, tasteless, and does not burn
Simple linear compound, not metabolized.
It is the only anesthetic agent that is inorganic
Major difference is low potency
MAC value is 105%
Weak anesthetic, powerful analgesic
Needs other agents for surgical anesthesia
Low blood solubility (quick recovery)
Nitrous oxide is generally used as a carrier and adjuvant
to other anaesthetics. A mixture of 70% N20 + 25-30% 02 +
0.2-2% another potent anaesthetic is employed for most
surgical procedures.
As the sole agent, N20 has been used with 02 for dental and
obstetric analgesia.
It is nontoxic to liver, kidney and brain. Metabolism of
N20 does not occur; it is quickly removed from body by
lungs. It is cheap and very commonly used

Nitrous Oxide Systemic Effects

Minimal effects on heart rate and blood pressure
May cause myocardial depression in sick patients
Little effect on respiration
Safe, efficacious agent
Nitrous Oxide Side Effects
Manufacturing impurities toxic
Hypoxic mixtures can be used
Large volumes of gases can be used
Beginning of case: second gas effect
End of case: diffusion hypoxia
Inhibits methionine synthetase (precursor to DNA synthesis)
Inhibits vitamin B-12 metabolism
Dentists, OR personnel, abusers at risk

Halothane

Synthesized in 1956 by Suckling

Halogen substituted ethane
Volatile liquid easily vaporized, stable, and nonflammable
Most potent inhalational anesthetic
MAC of 0.75%
Efficacious in depressing consciousness
Very soluble in blood and adipose
Prolonged emergence

It is currently one of the most popular anaesthetics

because of nonirritant, noninflammable, pleasant and rapid
action. Its deficiencies in terms of poor analgesia and muscle
relaxation are compensated by concomitant use of N20 or
opioids and neuromuscular blockers.
Inhibits sympathetic response to painful stimuli
Inhibits sympathetic driven baroreflex response
(hypovolemia)

Halothane Systemic Effects

Decreases respiratory drive
Depresses myocardium-- lowers BP and slows conduction
Mild peripheral vasodilation

Halothane Side Effects

“Halothane Hepatitis” -- 1/10,000 cases
fever, jaundice, hepatic necrosis, death
metabolic breakdown products are hapten-protein conjugates
-Malignant Hyperthermia-- 1/60,000 with succinylcholine to
1/260,000 without halothane in 60%, succinylcholine in
77%.
Rapid rise in body temperature, muscle rigidity,
tachycardia, rhabdomyolysis, acidosis, hyperkalemia.
most common masseter rigidity
Ether (Diethyl ether)
It is a highly volatile liquid, produces irritating vapours
which are inflammable and explosive.
Ether is a potent anaesthetic, produces good analgesia and
marked muscle relaxation by reducing ACh output from
motor nerve endings.

It is highly soluble in blood - induction is prolonged and

unpleasant with struggling, breath holding, salivation and
marked respiratory secretions.
Recovery is slow; post-anaesthetic nausea, vomiting and
retching are marked.
It does not sensitize the heart to Adr and is not
hepatotoxic.
Ether was very popular in the past, but not used now
because of its unpleasant and inflammable properties.

Enflurane
Developed in 1963 by Terrell, released for use in 1972
Stable, nonflammable liquid
Pungent odor
MAC 1.68%

Enflurane Systemic Effects

Potent inotropic and chronotropic depressant and decreases
systemic vascular resistance-- lowers blood pressure and
conduction dramatically
Inhibits sympathetic baroreflex response

Enflurane Side Effects

Metabolism one-tenth that of halothane-- does not release
quantity of hepatotoxic metabolites
Metabolism releases fluoride ion-- renal toxicity

Isoflurane

Synthesized in 1965 by Terrell, introduced into practice in

1984
Not carcinogenic
Nonflammable,pungent
Less soluble than halothane or enflurane
MAC of 1.30 %

Isoflurane Systemic Effects

Depresses respiratory drive and ventilatory responses-- less
than enflurane
Myocardial depressant-- less than enflurane
Inhibits sympathetic baroreflex response-- less than
enflurane
Sensitizes myocardium to catecholamines -- less than
halothane or enflurane
Produces most significant reduction in systemic vascular
resistance.
Excellent muscle relaxant-- potentiates effects of
neuromuscular blockers

Isoflurane Side Effects

Little metabolism (0.2%) -- low potential of organotoxic
metabolites
No EEG activity like enflurane
Bronchoirritating, laryngospasm

Sevoflurane and Desflurane

Low solubility in blood-- produces rapid induction and
emergence
Minimal systemic effects-- mild respiratory and cardiac
suppression
Few side effects
Expensive
Intravenous Anesthetic Agents
First attempt at intravenous anesthesia by Wren in 1656--
opium into his dog
Use in anesthesia in 1934 with thiopental

INDUCING AGENTS
These are drugs which on i.v. injection produce loss of
consciousness in one arm-brain circulation time (-11 sec);
are generally used for induction because of rapidity of onset
of action.
Anaesthesia is then usually maintained by an inhalational
agent. They also serve to reduce the amount of maintenance
anaesthetic. Supplemented with analgesics and muscle
relaxants, they can also be used as the sole anaesthetic.

1. Thiopentone sod.
It is an ultrashort acting thiobarbiturate, highly soluble in
water yielding a very alkaline solution, which must be
prepared freshly before injection.
 Extravasation of the solution or inadvertent intraarterial
injection produces intense painnecrosis and gangrene may
occur.
Injected i.v. (3-5 mg/kg) as a 2.5% solution, it produces
unconsciousness in 15-20 sec.
Its undissociated form has high lipid solubility - enters brain
almost instantaneously. Initial distribution depends on organ
blood flow - brain gets large amounts.

Thiopentone is a poor analgesic. Painful procedures

should not be carried out under its influence unless an opioid
or N20 has been given, otherwise the patient may struggle,
shout and show reflex changes in BP and respiration.
It is a weak muscle relaxant
BP falls immediately after injection, but recovers rapidly.
Cardiovascular collapse may occur if hypovolemia, shock or
sepsis are present.
Thiopentone is the commonest inducing agent used. It can be
employed as the sole anaesthetic for short operations that are
not painful.

Thiopental Side Effects

Laryngospasm- Can be prevented by atropine premedication
and administration of succinylcholine immediately.
Succinylcholine and thiopentone react chemically - should
not be mixed in the same syringe.
Shivering and delirium may occur during recovery.
Post-anesthetic nausea and vomiting are uncommon.
Propofol
Rapid onset and short duration of action
Myocardial depression and peripheral vasodilation may
occur-- baroreflex not suppressed
Not water soluble-- painful (50%)
Minimal nausea and vomiting

Unconsciousness after propofol injection occurs in 15-

45 sec and lasts -15 min. It distributes rapidly (distribution
t1/2 2-4 min) and elimination is much shorter than
thiopentone due to rapid metabolism.
It is particularly suited for out patient surgery because
residual impairment is less marked and incidence of post
operative nausea and vomiting is low.
Dose:2mg/kg bolus i.v. for induction; 9 mg/kg/hr for
maintenance.

Etomidate
Structure similar to ketoconozole
Direct CNS depressant (thiopental) and GABA agonist.
Etomidate Systemic Effects
Little change in cardiac function in healthy and cardiac
patients
Mild dose-related respiratory depression
Decreased cerebral metabolism

Etomidate Side Effects

Pain on injection (propylene glycol)
Myoclonic activity
Nausea and vomiting (50%)
Cortisol suppression

Slower Acting Drugs

Benzodiazepines
Produce sedation and amnesia
Potentiate GABA receptors
Slower onset and emergence
Diazepam
Often used as premedication or seizure activity, rarely for
induction
Minimal systemic effects-- respirations decreased with
narcotic usage
Not water soluble-- venous irritation
Metabolized by liver-- not redistributed

Lorazepam
Slower onset of action (10-20 minutes)-- not used for
induction
Used as adjunct for anxiolytic and sedative properties
Not water soluble-- venous irritation

Midazolam
More potent than diazepam or lorazepam
Induction slow, recovery prolonged
May depress respirations when used with narcotics
Minimal cardiac effects
Water soluble

Ketamine
Interrupts cerebral association pathways -- “dissociative
anesthesia”
Stimulates central sympathetic pathways
Ketamine Systemic and Side Effects
Characteristic of sympathetic nervous system stimulation--
increase HR, BP.
Maintains laryngeal reflexes and skeletal muscle tone
Emergence can produce hallucinations and unpleasant
dreams (15%)

TECHNIQUES OF INHALATION OF
ANAESTHETICS

Different techniques are used according to facility available,

agent used, condition of the patient, type and duration of
operation.

1. Open drop method -Liquid anaesthetic is poured over a

mask with gause and its vapour is inhaled with air. A lot of
anaesthetic vapour escapes in the surroundings and the
concentration of anesthetic breathed by the patient cannot be
determined.

It is wasteful - can be used only for cheap anaesthetics.

Some rebreathing does occur in this method. However, it is
simple and requires no special apparatus. Ether is the only
agent used by this method, specially in children.

2. Through anaesthetic machines - Use is made of gas

cylinders, specialized graduated vaporisers, flow meters,
unidirectional.valves, corrugated rubber tubing and reservoir
bag.
The gases are delivered to the patient through a tightly fitting
face mask or endotracheal tube.
Admmlstralton of the anaesthetic can be more precisely
controlled and in many situations its concentration
determmed. Respiration can be controlled and assisted by
the anaesthetist

(a) Open system - The exhaled gases are allowed to escape

through a valve and fresh anaesthetic mixture is drawn in
each time.
No rebreathing is allowed - flow rates are high - more drug
is consumed. However, inhaled 02 and anaesthetic
concentration can be accurately measured.

(b) Closed system The patient rebreaths the exhaled gas

mixture after it has circulated through sodalime which
absorbs C02. Only as much 02 and anaesthetic as have been
taken up by the patient are added to the circuit.

The flow rates are low; specially useful for expensive and
explosive agents (little anaesthetic escapes in the
surrounding air) e.g. halothane, enflurane, isoflurane.

However, determination of inhaled anaesthetic concentration

is difficult.

It should not be used for trichloroethylene which forms a

toxic compound with sodalime.
(c) Semiclosed system - Partial rebreathing is allowed
through a partially closed valve. Conditions ·are intermediate
with moderate flow rates

Induction, Maintenance and Extubation

Patients are premedicated with oral diazepam 10mg on night
before surgery.

Injection glycopyrrolate 0.2mg I/V should be given before

induction.

Patients are induced with thiopentone sodium 4-7 mg/kg

body weight after adequate preoxygenation.

Succinylcholine 1-2 mg/kg body weight should be given to

facilitate laryngoscopy and intubation.

Anaesthesia is maintained with N2O + O2 mixture. 0.5%

halothane along with nondepolarizing muscle relaxant like
vecuronium bromide are also used in maintenance.

Neostigmine (0.05-.08 mg/kg body weight) and

glycopyrrolate are used for extubation.
Anaesthetic Machine (Boyle’s equipment)
The anaesthetic machine
• Gas source- either piped gas or supplied in cylinders
• Flow meter
• Vaporisers
• Delivery System or circuit

A continuous flow (Boyle’s) anaesthetic machine

THE GAS SOURCE
Piped gas
Piped gases are stored in a “bank”, remote from the
operating room. The gases are piped into the operating room
and connected to the anaesthetic machine via hoses with
special connections to ensure that the nitrous oxide cannot
be connected to the oxygen inlet and vice versa.

Cylinders are fitted directly on to the anaesthetic machine by

means of yokes.

The cylinders contain gases under a very high pressure.

Oxygen is compressed at a pressure of about 147 bar (2000
psi). Nitrous oxide is compressed at a pressure of about 44
bar (600 psi).

They are made entirely out of steel that meets certain

chemical and physical requirements or out of a chrome
molybdenum mixture that is 20% lighter than steel.

Colour code for cylinders: There is an international

standard for colour coding gas cylinders but not all countries
follow it. In India nitrous oxide cylinder is of blue colour
and oxygen cylinder is of black colour with white shoulder.

Pin index system: An ever-present hazard in anaesthesia is

the danger of attaching a cylinder to the yoke meant for a
different gas. This is eliminated by the pin index system
The system consists of two pins projecting from the yoke in
the anaesthetic machine, designed to fit into matching holes
in the body of the cylinder valve.

For any one gas there is only one combination of pins and
holes. Unless the correct cylinder valve is attached to the
correct yoke these pins and holes will not match and the
cylinder will not fit.

Therefore it is not possible with this system to fit a nitrous

oxide cylinder to an oxygen yoke or vice versa.

THE FLOWMETER

The gases pass from the reducing valve, via pressure tubing,
to the flowmeter calibrated for each gas.
The flowmeters record the volume of gas flowing to the
patient per minute. There are various designs for the
flowmeters. We will describe those used in the Boyle's
machine.

The flowmeter in the Boyle’s machine is referred to as a

"Rotameter". It consists of a vertical glass tube tapered at the
lower end.

Rotating a knob at the base of the machine permits the entry

of gases into the flowmeter. In the glass tube is an indicator
or a bobbin.

The height of the float in the tube indicates the flow of gases
through the flowmeter. The flow should be read at the top of
the bobbin.

THE VAPORISER
From the flowmeters the gases pass in the direction of the
vaporisers. The vaporiser enables volatile agents to be
introduced into the gaseous mixture.
These volatile agents are liquids at room temperature and do
not need to be stored under pressure. The function of the
vaporiser is to vaporise this liquid.

OTHER FEATURES OF ANAESTHETIC MACHINE

Alarm devices are designed to initiate a signal when the
oxygen pressure is low.
The alarm should be triggered by a low oxygen pressure
and not by nitrous oxide flow. Alarm devices triggered by
nitrous oxide flow will not function if the nitrous oxide and
oxygen fail simultaneously or if there is prior failure of the
nitrous oxide supply.

Oxygen flush valves

The valve directs a very high flow of oxygen (at least
30L/min) to the outlet of the machine.
The valve is useful if it is necessary to fill the reservoir bag
quickly with 100% oxygen.
 COMPLICATIONS OF GENERAL
ANAESTHESIA

A. During anaesthesia
1. Respiratory depression and hypercarbia.
2. Salivation, respiratory secretions -less now as non-irritant
anaesthetics are mostly used.
3. Cardiac arrhythmias, asystole.
4. Fall in BP
5. Aspiration of gastric contents: acid pneumonitis.
6. Laryngospasm and asphyxia.
7. Delirium, convulsions. Excitatory effects are generally
seen with i.v. anaestheticsspecially if phenothiazines or
hyoscine have been given in premedication. These are
suppressed by opioids.
8. Fire and explosion - rare now due to use of non-
inflammable agents.

B. After anaesthesia
1. Nausea and vomiting.
2. Persisting sedation: impaired psychomotor function.
3. Penumonia, atelectasis.
4. Organ toxicities: liver, kidney damage.
5. Nerve palsies - due to faulty positioning.
6. Emergence delirium.
 PREANAESTHETIC MEDICATION
Preanaesthetic medication refers to the use of drugs before
anaesthesia to make it more pleasant and safe.
1. Opioids Morphine (10 mg) or pethidine (50-100 mg),
i.m. allay anxiety and apprehension of the operation,
produce pre and postoperative analgesia, smoothen
induction, reduce the dose of anaesthetic required and
supplement poor analgesic (thiopentone, halothane) or weak
(N20) anaesthetics. Postoperative restlessness is also
reduced.

2. Antianxiety drugs Benzodiazepines like diazepam (5-10

mg oral) or lorazepam (2 mg i.m.) have become popular
drugs for preanaesthetic medication because they produce
tranquility and smoothen induction; there is loss of recall of
intaoperative events (specially with lorazepam) with little
respiratory depression or postoperative vomiting.
They counteract CNS toxicity of local anaesthetics and
are being used along with pethidine/fentanyl for a variety of
minor surgical and endoscopic procedures.
Midazolam is a good amnesic with potent and shorter action;
it is also better suited for injection

3. Sedative-hypnotics Barbiturates like pentobarbitone,

secobarbitone or butabarbitone (100 mg oral) have been used
night before (to ensure sleep) and in the morning to calm the
patient.
However, their popularity has decreased in the recent years
because they tend to depress respiration and circulation;
emergence delirium is more common and they lack analgesic
or antiemetic property.

4. Anticholinergics Atropine or hyoscine (0.6 mg i.mJi.v.)

have been used, primarily to reduce salivary and bronchial
secretions.
The main aim of their use now is to prevent vagal
bradycardia and hypotension (which occur reflexly due to
certain surgical procedures), and prophylaxis of
laryngospasm which is precipitated by respiratory secretions.
They should not be used in febrile patients. Dryness of
mouth in the pre and postoperative period may be
distressing.
Glycopyrrolate (0.1-0.3 mg i.m.) is a longer acting
atropine substitute. It is a potent anti secretory and
antibradycardiac drug; acts rapidly and is less likely to
produce central effects

5. H2 blockers Patients undergoing prolonged operations,

caesarian section, obese patients are at increased risk of
gastric regurgitation and aspiration pneumonia. Ranitidine
(150 mg) or famotidine (20 mg) given night before and in
the morning benefit by raising pH of gastric juice.
Prevention of stress ulcers is another advantage.
Now routinely used before prolonged surgery.

6. Antiemetics Metoclopramide 10-20 mg i.m.

preoperatively is effective in reducing post operative
vomiting. By enhancing gastric emptying it reduces the
chances of reflux and its aspiration. Extrapyramidal effects
and motor restlessness can occur. Combined use of
metoclopramide and H2 blockers is more effective.

Ondansetron (4-8 mg i.v.) and Granisetron (0.1 mg) has

been found to be highly effective in reducing the incidence
of post anaesthetic nausea and vomiting.
 General Anesthesia:
Facts and Fiction

“Anesthetic awareness”?

Only occurs under general anesthesia

Medication given to render patient unconscious fails
May recall some or all events during surgery
May or may not feel pain or pressure
Occurs infrequently: 1 in 1,000 cases
Duration and severity vary
Extreme awareness experiences are very uncommon.
Patients Need Not be Afraid!
Anesthesia today nearly 50 times safer than it was just 20
years ago.
Causes of awareness
--Inadequate anesthesia
--Equipment failure or misuse

Awareness might not be completely avoidable in the

following types of surgery:
Cardiac
Emergency C-section
Trauma

“Awake” movie
Released in November 2007
Exploits anesthesia awareness as plot device

“Awake” movie
Irresponsible: Movie ads claim 1 in 700 patients under
general anesthesia are awake for entire surgery
 REFERENCES
• The Pharmacological basis of therapeutics- Goodman &
Gilman

• Clinical Pharmacology- Bennett & Brown

• Essentials of medical pharmacology- Tripathi KD

• Basic & Clinical Pharmacology- Katzung G

• Peterson‘s Principles of oral and maxillofacial surgery