Make your own free website on

General Anaesthetics

Home My Personal Site Medical Notes BM-13 Site Guest Book Contact Me
Pharmacology Notes Medicine Notes Surgery Notes




Definition of general anaesthesia—

It may be defined as a condition of temporary and reversible disintegration of cerebral function which will allow surgical operation. Anaesthetic patient cannot be aroused unless the condition of anaesthesia is over.



o  For surgical operation

o  In case of Epilepsy


Objectives or states of General Anaesthetics—

o  Analgesia—acts on Substantia Gelatinosa of the spinal cord.

o  Amnesia—acts on the Hippocampus of the cerebral cortex.

o  Loss of consciousness—acts on the reticular activating system.

o  Inhibition of sensory and autonomic reflexes (by inhibiting the effects on polysynaptic reflexes)

o  Muscle relaxation (by inhibiting the effects on polysynaptic reflexes)


Criteria of ideal anaesthetic drugs—

o  Induce anaesthesia smoothly and rapidly

o  Permit rapid recovery as soon as administration is ceased

o  Wide margin of safety

o  Devoid of adverse effects

*** no single agent is capable of achieving all those desirable effects without some disadvantages when used alone.


Drugs used in GA—


Gases like N2O

Volatile liquid like Ether, Chloroform, Halothane, Enflurane, Isoflurane etc


Barbiturates—Thiopentone Sodium, Methohexital

Benzodiazepines—Diazepam, Midazolam

Aryl Cyclohexamine / Dissociative—Ketamine

Neuroleptic analgesics—Droperidol, Fentary

Miscellaneous—Disoproform, Etomidate


Stages of anaesthesia—there are 4 stages which are best seen in anaesthesia done by ether.


Stage-I or stage of analgesia—

There is analgesia. Amnesia develops at the later part of the stage-I just before beginning of the stage-II. Consciousness is retained.


Stage-II or stage of excitement—

The patient is excited, struggling, shouting and delirious. But he is amnesic and unconscious. Breathing becomes irregular, pupil is dilated. These are due to sympathetic stimulation (↑ adrenaline secretion).


Stage-III or stage of surgical anaesthesia—

This stage is subdivided into 4 planes—


Breathing full, regular, automatic and equally abdomino-thoracic

Roving movement of the eyeball

Pupil becomes constricted

Muscle tone begins to ↓



Respiration becomes more abdominal than thoracic

Eyeball is fixed

Pupil begins to dilate

Muscle tone decreases further



Respiration is mainly abdominal, thoracic component is decreased

Beginning of the paralysis of the intercostal muscle

Pupil dilates further

Further fall of muscle tone



Almost cessation of the thoracic component of respiration, becomes fully abdominal

Full dilatation of the pupil

Loss of light reflex

Atonia of muscle


 *** Transition from the plane-3 to plane-4 is marked by complete paralysis of the intercostal muscle


Stage-IV or stage of medullary depression—

There is stoppage of the spontaneous respiration (patient cannot survive without artificial respiration). Vasomotor and respiratory center of the medulla are severely depressed. There is severe fall of BP.


The pupil changes in the 2nd and 4th stages after administration of ether—

2nd stage—pupil is dilated and light reflex is present

4th stage—pupil is widely dilated and light reflex is absent

Causes of pupil changes—

2nd stage—reflex secretion of adrenaline

4th stage—medullary paralysis


How can you identify that the patient is in the 3rd stage of anaesthesia after ether administration?—

It can be identified by—

Respiration—full, regular, automatic and equally abdomino-thoracic

Eyelid reflexes and conjunctival reflexes—absent

Eyeball—Roving movement of the eyeball

Arm—if it is elevated and then released it will fall fail like

Head—can be rotated easily, side to side

*** if more anaesthetics is given suddenly then respiratory and swallowing reflex is no longer present


Respiration in the 3rd stage of anaesthesia—

1st plane—full, regular, automatic and equally abdomino-thoracic

2nd plane—regular but less excursive (respiration will be reduced). More abdominal than thoracic.

3rd plane—↑ abdominal respiration, delayed thoracic respiration, beginning of the intercostal paralysis

4th plane—less abdominal respiration, complete paralysis of the intercostal muscles


Mechanism (at gross level)—

o  At low concentration the anaesthetics acts on the SGR (Substantia Gelatinosa Ronaldi) present on the tip of the dorsal horn of the spinal cord and produces a block in the synaptic transmission of pain carriage at the SGR, so there is analgesia.

o  At slight higher concentration anaesthetics act on the hippocampus of the brain and non-functioning hippocampus produces loss of memory resulting in amnesia.

o  When the concentration rises further in the brain there is inhibition of the golgy type-II neurons and there is inhibition of the inhibitory neurons. So, there is excitation.

o  Then the concentration of anaesthetics rises further in the brain, there is block of transmission of the RAS fibers in the midbrain resulting in drowsiness, loss of alertness and ultimately unconsciousness.

o  Further increase of concentration affects medulla, when vital center of the medulla like VMC (vasomotor center) and respiratory center depresses resulting in stoppage of respiration and severe fall of BP.


Mechanism (at molecular level)—

According to the Mayer Overton principle—any substance can behave as narcotic-anaesthetic provided, it attained a sufficient molar concentration in the CNS neuronal membrane. Because cell membrane are made up of mostly by phospholipids is oily in nature. So substances which are lipid soluble therefore can enter the oily cell membrane from the ECF and attain sufficient molar concentration to produce anaesthesia. More a substance is lipid soluble; more is its potency and anaesthetic irrespective of its chemical structure.

When the molecules of anaesthetic have appeared within the cell membrane, they exert a pressure which tends to obliterate the sodium channels of the cell membrane. Therefore the sodium channels fail to open properly, there is insufficient flow of Na+ from ECF to ICF. So there is no development of action potential resulting in non-responsiveness of the cell and this will block the normal transmission.



Inhaled anaesthetics are primarily removed from body via lungs, though 20% of the Halothane and 2% of the Enflurane are metabolized in the liver.



1. Nitrous oxide is a gas at ordinary room temperature under 760mm of Hg pressure

2. The other modern anaesthetics like Enflurane, Buflurane, Methoxyflurane, Helotane etc all have Halogen atom in their molecules and thus called halogenetic anaesthetics.

3. Ether is not halogenated

*** Ether is highly inflammable and there is tendency of catching fir, so should be handled carefully.


Pharmacological effects of inhaled anaesthetics—


Myocardial depression

Reduced myocardial O2 consumption

On respiratory system—

Increase respiratory rate

Decrease ventilatory response to hypoxia

Decrease mucociliary function of the airways



Increase cerebral blood flow



On kidney—

Decrease GFR

Increase renal vascular resistance

On liver—

Decrease hepatic blood flow



Highly potent drugs have less MAC (minimum alveolar concentration) value.

If there is high blood/gas partition co-efficient then more soluble in blood and induction is delayed.


Individual agents—

Nitrous Oxide (N2O)—

o  It is a gas with slightly sweet smell.

o  Neither inflammable nor explosive.

o  It produces light anaesthesia without marked depression in respiratory and vasomotor center provided the normal O2 tension is maintained.

o  Induction and recovery is rapid but potency is poor, so it is not used alone. N2O-Halothane-O2 mixture is popular.

o  N2O is more or less a safe drug and when given with other modern anaesthetics it reduces the dose of others.

o  N2O (50%)-O2 combination is used to relieve pain in obstetrics.

o  N2O has low blood-gas coefficient, less soluble in the blood and so induction time is less.

o  Recovery time rarely exceeds 4min after administration.


*** {N2O→ pain relief, Halothane→ sleep production, O2→ life saving}

*** after anaesthesia N2O again comes into the lungs and its concentration in the lung increases. As there was already high concentration of N2O in the alveoli (↑ MAC value) hypoxia occurs. During recovery O2 is given.


Advantages of N2O—

o  Powerful analgesic effect

o  Rapid induction and recovery because of low blood-gas coefficient

o  Very low concentration is needed to produce unconsciousness as well as analgesia

o  Safe and non-irritating


Disadvantages of N2O—

o  Low potent inhalation anaesthetic with no muscle relaxation activity.

o  Produce incomplete anaesthesia

o  Must be used in conjunction with other more potent anaesthetics and muscle relaxants to produce a state of full surgical anaesthesia.

o  Transient post-anaesthetic hypoxia may also occur if large volume of N2O is exhaled.



o  For emergency management of injury.

o  Post operative physiotherapy.

o  For refractory pain in the terminal illness.



Closed gas field chambers in the body tend to expand under N2O. So it should be avoided in intestinal obstruction, pneumothorax, COPD etc. it an also produce diffusional hypoxia.


Limitation of N2O as general anaesthetics—

o  Not effective for anaesthesia as a single agent

o  High concentration (75-80%) is needed for maintaining the anaesthesia so hypoxia may result

o  No property of muscle relaxation

o To achieve complete anaesthesia; opioids (analgesic), thiopental sodium (narcotic), and n-m blocking agent (muscle relaxation) is needed with it



o  Induction requires time

o  Stage-II is prolong

o  Ultimately deep anaesthesia is produced

o  Recovery is also delayed

o  But it is a largely safe drug

o  Cardiac depression and fall of BP does not occur in ether, rather there is ↑ of BP as it acts as a sympathomimetic and there is tachycardia and ↑CO

o  It is given by open drop method (through nose)

o  It is very cheap



The great disadvantage of ether is inflammable and also it causes severe bronchial secretion.




o  Colorless, volatile liquid, sweet in taste. Not irritant and non-explosive.

o  In anaesthetic dose depresses both cerebral function and sympathetic autonomic activity.



o  Induction and recovery are smooth and rapid, efficacy is high. Surgical anaesthesia reaches in 2-5 min.

o  The stage-II is virtually absent, so induction is smooth

o  Surgical stage can be reached quickly

o  There is no bronchial secretion

o  Medullary paralysis, depression of VMC and respiratory center appear easily. To reduce the dose of Halothane N2O is concurrently used

o  It is nor inflammable neither explosive.

o  Diffusion hypoxia is insignificant (MAC value is 0.8%)

o  Post operative nausea, vomiting is less.



o  Cardiac depressant, so there is ↓BP. For this it is combined with N2O

o  Respiratory depression

o  Poor analgesic action and muscle relaxation—should be used with N2O, opioids and muscle relaxants

o It suppresses endogenous sympathetic activity but sensitizes heart to dysrrhythmic effects of catecholamines, both endogenous and exogenous

o  Sensitization of the heart muscles in presence of epinephrine and also various types of arrhythmia (AV dissociation, Nodal rhythm, Ventricular extrasystole) may occur

o  May cause acute hepatotoxicity

o  Can cause uterine relaxation

o  Can cause malignant hyperthermia (particularly when used with muscle relaxant Succamethonium)

o  Shivering—early post-operative period (may occur)

o  Halothane hepatitis


Drug interaction—

o  Potentate the response of antihypertensives.

o  Premedication with Atropine reduces the risk of hypotension and bradycardia.



Thiopentone Sodium—

Ultra short acting barbiturate, pleasant and without excitement

Highly lipid soluble, so very quickly cross BBB and reaches neuron within 30sec

Concentration in CNS rises very quickly, as a result there is rapid induction

Rapid recovery due to high lipid solubility. So comes out quickly and redistributed in adipose tissue, muscles and peripheral tissue.

Blood flow per min in brain is very high but poor in adipose tissue, so more number of Thiopentone is deposited in brain and less in adipose tissue.


Advantages of Thiopentone—

o  Rapid, pleasant induction

o  Rapid recovery and little or no post-operative excitement or vomiting

o  Useful to promote light sleep during regional anaesthesia for quietening excitement

o  To control convulsion

o  May also be used to provide anaesthesia for short surgical procedure

o  May be given prior to GA for induction



o  Insignificant analgesic action

o  Muscle relaxation is too brief

o  Cannot be used individually because repetitive doses accumulate in the fatty tissue which is then slowly released and causes prolong anaesthesia

o  Therapeutic index is less

o  Can cause cardiac depression

o  Overdose causes HTN, respiratory depression, bronchospasm and laryngospasm


Adverse effects—

o  Coughing

o  Sneezing

o  Laryngeal spasm

o  Severe hypotension


Uses of Thiopentone—

o  To induce general anaesthesia prior to maintenance of anaesthetic stages by other agents

o  To produce anaesthesia for short surgical procedure

o  To provide light anaesthesia to cover spinal anaesthesia or other local anaesthesia

o  As an anti-convulsant in tetanus or epilepsy

o  To produce basal anaesthesia in children (rectally)


Contraindication—hepatic insufficiency




It may cause respiratory depression and can produce hypercapnia if not supplemented by O2.

2% is metabolized in the liver, so it can be safely given in liver disease

It does not sensitize heart to adrenaline

Diffusional hypoxia is negligible as MAC value is 1.7%

Prolong use causes deposition of fluoride ion and may cause renal failure



Low blood/gas partition coefficient

Rapid induction

Has tendency to produce bronchial secretion

0.2% is metabolized in the liver

Less depression of myocardium

Dilates the coronary artery

Releases free inorganic chloride which may be toxic to kidney


Effects of Halothane, Enflurane and Isoflurane—







Usually does not occur

Does not occur

Cardiac output

Depresses myocardial performance and produces vasodilatation of the vessels of the skin and skeletal muscle. ↓PVR, ↓CO, ↓BP

Does not ↓CO as much as Halothane

May ↑CO


↓ blood flow

↓ but reversible

Not such

Heart muscles in presence of adrenaline

Sensitizes and there is ventricular arrhythmia

Less sensitization

No sensitization

Muscle relaxation


Better relaxation than Halothane

Better than both


May be delayed

Excitement during induction

Smooth and rapid

(used in emergency)


Depression and bronchodilatation

There may be respiratory depression (dose related)


Significant respiratory depression


Post operative shivering

Halothane hepatitis

Malignant hyperthermia

Circulatory failure


Respiratory failure

Not significant



It produces dissociated anaesthesia


Pre-anaesthetic medication—

Administration of medication 1-2 hours prior to surgery for production of sedation analgesia is termed as pre-anaesthetic medication.



1. to relieve anxiety

2. to provide amnesia for the pre-operative period

3. to provide analgesia if there is existing pain

4. to potentate the effects of anaesthetics

5. to combat unwanted effects (excess salivation, cough, nausea, reflex bradycardia etc)

6. to reduce stress responses during per-operative period


Drugs used in pre-anaesthetic medication—

§    To reduce anxiety and tension and for sedation and amnesia—Benzodiazepines (Diazepam, Midazolam) or Promethazine in children.

§    To prevent bronchial and salivary secretions, hence to make the airway passage remain clear—Atropine Sulphate.

§    For analgesia—Morphine Sulphate, Pethidine (opioid analgesics)

§    To prevent vomiting—Promethazine Hydrochloride (Avomine), Prochlorperazine.

§    To reduce reflex bradycardia and hypotension—Atropine Sulphate.

§    To reduce gastric acid secretion—H2 blocker.


Hazards of GA—

§    Prolongation of the post-operative period

§    Cardio respiratory depression


Balanced anaesthesia—

The sequential use of a combination of the anaesthetic agents to obtain full loss of both consciousness and pain induced reflexes, along with muscle relaxation to produce general anaesthesia is termed as balanced anaesthesia.


It provides—

§    Most effective and comfortable and the least hazardous anaesthetic experience for the patient.

§    The best operating condition for the surgeon



Pre-anaesthetic medication with—

Diazepam IV (basal anaesthetic)

Pethidine IV (narcotic analgesic)

Atropine IV (anti-muscarinic agent)


Induction by—

Thiopentone Sodium (ultra-short acting Barbiturate)


Maintenance of unconsciousness, analgesia and reflex inhibition by—

N2O + O2 (gas)

Halothane (volatile)

Pethidine IV (narcotic analgesic)


Maintenance of muscle relaxation—

Suxamethonium (neuromuscular blocker)

Atracurium (neuromuscular blocker)

Tubocurarine (neuromuscular blocker)