General anaesthetics Miss Rani Dhole

1. GENERALANESTHETICS
MISS.R.S.DHOLE
ASST.PROFESSOR
ANNASAHEBDANGECOLLEGEOFD.PHARMACY,ASHTA

2. GENERAL ANESTHESIA
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General anesthesia (GA) is the state produced
when a patient receives medications for amnesia,
analgesia, muscle relaxation, and sedation. An
anesthetized patient can be thought of as being
in a controlled, reversible state of
unconsciousness.
General anaesthetics
These pharmacological agent which are used to
produce reversible loss of consciousness is called
as general anaesthetics

3. CLASSIFICATION OF GENERAL
ANAESTHETICS
General
anaesthetics
Inhalational
Gas:
Nitrous oxide
Volatile
liquids:
Halothane
Ether
Chloroform
Intravenous
•Barbiturate
-
Thiopentone
sod.
•Non
Barbiturte-
Ketamine

4. PROPERTIES OF GENERAL
ANAESTHETICS
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It should be non toxic
It should be non irritaant
It should be non inflammable
It should be stable
It should be easy to administer
It should have proper muscle relaxant property
Should have adequate analgesic property

5. PREANESTHETIC MEDICATIONS
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Preanesthetic medications are defined as the use of
drugs or medications before or concurrent to the
administration of anesthetics to make anaesthesia safe
& pleasant
They are used to achieve following objectives like:
 To reduce anxiety in patient occuring before & during surgery
 To produce sedation, calm the patient & relieve pain
 Counteract certain adverse effects of anaesthetics such as
salivation, vomitting etc.to reduce secretions
 To reduce pre & post operative pain
 To produce synergistic effect along with anaesthetics
 facilitate smooth induction of anesthesia,
 lowered the required dose ofanesthetic
There is no single drug which can achieve the above objective & hence
usually combination of drugs are useful

6. PREANESTHETIC MEDICATIONS:
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Analgesics eg. Paracetamol
Anxiolytics/ Tranquilizer eg. Diazepam, phenobarbitone
Anticholinergics: eg. Atropine, scopolamine
(Reduces bronchial and salivary secretion)
Skeletal muscle relaxants: eg. D- tubocurarine
Antiemetics: eg. Promethazine
Prevents aspiration of stomach contents and post surgical vomiting

7. DEPTH OF ANESTHESIA (GUEDEL’SSIGNS)
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Guedel (1920) described four sequential stages with anaesthesia, dividing the
stage into 4 planes.
Stage of
Analgesia
• analgesia and amnesia, the patient is conscious and
conversational. Starts from beginning of anaesthetic inhalation
and lasts upto the loss of consciousness
• Pain is progressively abolished
• Reflexes and respiration remain normal
• Use is limited to short procedures
Stage of
Delirium
• From loss of consciousness to beginning of regular respiration
• 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 operative procedure carried out
• Can be cut short by rapid induction, premedication

8. DEPTH OF ANESTHESIA (GUEDEL’SSIGNS)
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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 moving 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.
Medullary
paralysis • Cessation of breathing to failure of circulation and death.

10. MECHANISMOFACTIONOFANAESTHESIA
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No specific receptor has been identified. The fact that
chemically unrelated compounds produce anesthesia argues
against the existence of a single receptor.
The focus is NOW on proteins comprising ion channels:
GABAAreceptors, Glycine receptors,
NMDAglutamate receptors (nitrous oxide and ketamine ):
Nicotinic receptors: Blocks the excitatory postsynaptic current
of the nicotinic receptors.

11. MECHANISM OF ACTION OF
GENERAL ANAESTHETICS
 GABA –A receptor : Potentiated by
Halothane,
 Propofol, Etomidate ,Enflurane,
 isoflurane, Desflurane,
sevoflurane
 NMDA receptors:
 Glycine receptors :
Inhibited by Ketamine,
nitrous oxide and xenon
Potentiated by Halothane,
Propofol, ,Enflurane,
isoflurane, Desflurane,
sevoflurane
Also has effect on neuronal nicotinic receptorsand
5-HT3 receptors

12. INHALATIONAL
ANAESTHETICS
Inhalational anaesthesia refers to the delivery of gases or
vapours to the respiratory system to produce anaesthesia
Ether
 It is explosive
 Irritant to respiratory tract
 High incidence of nausea and vomiting during
 induction and post-surgical emergence

13. Colourless, odourless gas at room temperature.
Very insoluble in blood and other tissues (quick recovery)
Rapid induction of anaesthesia and rapid emergence
following discontinuation of administration.
Completely eliminated by the lungs.
It is weak anaesthetic and powerful analgesic.
The mac value is 105%.
Causes megaloblastic anaemia.
Used as adjunct to supplement other inhalationals.
NITROUS OXIDE

14. Volatile liquid at room temperature.
Light sensitive
High fat solubility => slow induction & recovery
Eliminated unchange via lungs
Commonly used in children, where preoperative
placement of an iv catheter can be difficult
It is marketed in amber bottles with thymol added as a
preservative
Metabolised in liver by Cyt-P450
HALOTHANE

15.  Side effects of halothane :
CVS : Cardiac arrhythmia, depression of myocardial contraction.
Respiratory system : Depression of respiration
Muscles : Malignant hyperthermia
Kidney : Decrease renal blood flow and g.f.r
Liver and GIT: Cause halothane induced hepatitis & nausia and
vomitting
 DRUG INTERACTION : Halothane + adrenaline, theophylline => arrhythmia
may be precipitated.
 CONTRAINDICATION : Hepatic dysfunction and/or jaundice.

16. INTRAVENOUS ANAESTHETICS
THIOPENTAL
 Ultrashort acting barbiturate
 High lipid solubility rapid entry into the brain
 Rapid onset (20 sec) , short duration
 Effect terminated not by metabolism but by redistribution
 Risk of sever vasospasm if accidently injected intoartery
 Depress cerebral blood flow
 Decrease intracranial pressure
 Tissue necrosis—gangrene, Tissue stores, hypotension, apnea
 Build-up in adipose tissue = very long emergence fromanaesthesia

17.  Rapid onset and have a short duration of action
 Highly protein bound in vivo and is metabolised by conjugation
in the liver
 Very good anesthetic for induction and maintaince of anesthesia
with no accumulation effect
 Side-effects are pain on injection, hypotension and transient
apnea following induction
 Used for the induction, maintenance of GA andsedation
 Useful for day-case surgery
PROPOFOL

18.  Dissociative anaesthetic
 NMDA ReceptorAntagonist
 Cardiovascular stimulant
 Catatonia, analgesia, and amnesia without loss of consciousness
 Useful for anesthetizing patients at risk for hypotension and
bronchospasm and for certain paediatric procedures
KETAMINE

19.  Rapid induction
 Minimal change in cardiac function and respiratory rate
 Not analgesic
 Cause pain on injection and nausea postoperatively
 Prolonged administration may cause adrenal suppression
ETOMIDATE