class general anaesthesia

GENERAL ANAESTHETICS

Dr. RAGHU PRASADA M SMBBS,MDASSISTANT PROFESSOR DEPT. OF PHARMACOLOGYSSIMS & RC.

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History

1776- priestly- nitrous oxide 1845-Horrace wells –dentist-Nitrous oxide 1846-William Mortan –ether dome

Definition

General anaesthetics are the drugs which produce reversible loss of sensation and consciousness.

Ideal anaesthetic gas-should induce unconciousness smoothly, rapidly, and prompt recovery

Balanced anaesthesia- various combinationsMonitored anaesthesia- local Ana’s +Gen Ana’s

Stages of Anaesthesia

Guedel described stages of ether anaesthesia 1. Stage of analgesia -starts from beginning of anaesthetic inhalation and

lasts upto loss of conciousness2. Stage of delirium from loss of conciousness to beginning of respiration -apparent excitement is seen.

patient may struggle, shout, hold his breath -micturition or defecation may occur

Stages of Anaesthesia

Surgical anaesthesia Extends from onset of regular respiration to

cessation of spontaneous breathing Plane1- Rolling eye balls-till eyes become fixed Plane2- Loss of corneal and laryngeal reflexes- Plane3- Loss of light reflex-dilation of pupils Plane4- Intercostal paralysis-shallow abdominal

respiration Medullary paralysis-cessation of breathing to failure

of circulation and death

Potency Of Inhaled AnaesthesiaPotency α 1/MACMinimal Alveolar Concentration :- Is the alveolar

concentration of an inhaled anesthetic that prevents movement in 50 % of patients in response to standardized stimulus (surgical incision ).

Mechanism of action Anaesthetic gases interact with hydrophobic regions

of neuronal membrane proteins that interface with membrane lipids

Inhaled Ana’s barbiturates, benzodiazepines, etomidate and propofol facilitates GABA- mediated inhibition at GABAA receptor sites and thereby increase cl flux through its channel.

Ketamine blocks the action of glutamate (an excitatory neurotransmitter) on NMDA receptor.

Mechanism of action

Inhalational anaesthetics like enflurane and isoflurane decrease the duration of opening of nicotinic receptors activated Na channels decreases the effects of Ach at cholinergic synapses

By affecting neuronal membrane proteins, general anaesthetics disrupt neuronal firing and sensory processing in the thalamus, thereby causing loss of conciousness and analgesic effects.

The motar activity is reduced because they also inhibit neuronal output from the internal pyramidal layer of cerebral cortex

Classification

INHALATIONAL ANAESTHETICS Nitrous oxide, cyclopropane,xenonVOLATILE LIQUIDS Isoflurane, Sevoflurane Desflurane, Halothane (Ether), EnfluraneINTRAVENOUS ANAESTHETICS

INDUCING AGENTS Thiopentone sod.

Methohexitone sod., Propofol, Etomidate

Intravenous anaesthetics

SLOWER ACTING DRUGSBenzodiazepines

DiazepamLorazepamMidazolam

Dissociative anaesthesiaKetamine

Neurolept analgesiaFentanyl

Pharmacokinetics of inhalational anaesthesia

Aim is to attain rapid pp in brain-pleasant, adequate sedation, analgesia

Eqlbrium of par pr- alveoli, blood and tissues Anesthetic uptake from the alveoli to the blood is

dependant on three factors: the solubility of the anesthetic (S), the cardiac output (Q) and the alveolar to venous partial pressure (Pa-Pv):

Anaesthetic Uptake = (S) x (Q) x (Pa-Pv)

--pulmonary ventilation(A/v) --pulmonary ventilation/perfusion ratio --second gas and conc effect

Nitrous Oxide

•widely used

•Potent analgesic

•Produce a light anesthesia

•Do not depress the respiration/vasomotor center

•Used as adjunct to supplement other inhalationals

•Least hepatotoxic

Second gas effect

It can concentrate halogenated anaesthetics in the alveoli after concomitant administration faster uptake from alveolar gas

Diffusion hypoxia-the solubility of nitrous oxide in blood is more than oxygen the speed of movement of nitrous oxide retards the oxygen uptake during recovery cause diffusion hypoxia use of 100% oxygen helps in recovery

Nitrous oxide- demerits and adverse effects

Within close compartmentit can increase volumepneumothorax, sinuses pressure

No muscle relaxation Post anaesthetic nausea and vomiting >4hrs megaloblastic anaemia Abortion, birth defects

Ether –historical importance Highly volatile liquid, produces irritating vapours

which are inflammable and explosive Ether is a potent anaesthetic produces good

analgesia and marked muscle relaxation Highly soluble in blood, induction is prolonged and

unpleasant with struggling Recovery is slow, post anaesthetic nausea, vomiting,

and retching Disadvantages- less used now –because of

unpleasant and inflammable properties.

Propofol-2,6 di iso propyl phenol

Short-acting agent used for the induction, maintenance of GA and sedation in adult patients and pediatric patients older than 3 years of age. It is highly protein bound in vivo and is metabolised by conjugation in the liver.T1/2-30-60 minTIVA- P:K-4:1Side-effects is pain on injection hypotension and transient apnea following induction

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Halothane• Non-flammable•Relaxes both skeletal and uterine muscles used in obstetrics•Not hepatotoxic in pediatrics

• 20% metabolism by P450induction ofhepatic microsomal Enzymes• Myocardial depressant (SA node), • sensitization of myocardium to catecholamines -

arrhythmia • Relaxes both skeletal and uterine muscles used in

obstetrics• Has vagomimetic action

Halothane-ADVERSE EFFECTS

Transient hepatic damage Liver necrosis In repeated exposureImmunosensititation Malignant hyperthermia (MH) is a pharmacogenetic

hypermetabolic state of skeletal muscle induced in susceptible individuals by inhalational anesthetics and/or succinylcholine (and maybe by stress or exercise).Dantrolene sodium

hypotension, hypercapnia

Rapid, smooth induction and maintenance• 2-10% metabolized in liver release fluride ions

nephrotoxic• Introduced as replacement for halothane• Curare like effectADR-CNS excitation at twice MACISOFLURANEsmooth and rapid induction and recovery very little metabolism (0.2%)Does not sensitize heart to catecholaminesno reports of hepatotoxicity or renotoxicitymost widely employed

Enflurane

Sevoflurane

Rapid uptake with out irritation Low solubility Faster recovery Metabolismliver release fluride ions nephrotoxic

DESFLURANE low volatility, needs special vapouriserAirway irritant, less tissue toxicity

Thiopental sodium

rapid onset (20 sec), short-acting Effect terminated not by metabolism but by

redistribution repeated administration or prolonged infusion

approached equilibrium at redistribution sites Build-up in adipose tissue = very long emergence

from anesthesiaSide effects Hypotension apnoea airway obstruction

Etomidate

Smooth induction Shorter acting than thiopental Lesser chances of hypotension side effects pain at site of injection poor analgesic, adrenocortical suppression

Ketamine- Dissociative anesthesia

NMDA Receptor Antagonist Dissociative anesthesia- feeling of dissociation from

once own body and surroundings primary site of action in cortex and subcortical areas

usually stimulate rather than depress the circulatory system.

Analgesic Cataleptic appearance, eyes open, reflexes intact,

purposeless but coordinated movements

Neurolept analgesia

drugs which induce state of apathy and mental detachment

Method of combination of neuroleptic drug with opiod analgesic drug

Droperidol+ fentanyl Droperidol-butyrophenone derivative Fentanyl-morphine like opiod analgesic

What is Balanced Anesthesia? Use specific drugs for each component

1. Sensory▪ N20, opioids, ketamine for analgesia

2. Cognitive▪ Produce amnesia, and preferably

unconsciousness▪ inhaled agent▪ IV hypnotic (propofol, midazolam, diazepam,

thiopental)3. Motor▪ Muscle relaxants

Pre-anaesthetic Medication

Sedatives / Anxiolytics

▪ Benzodiazepines,Barbiturates

▪ Butyrophenones,Phenothiazines

▪ Chloral hydrate & Paraldehyde Opioid Analgesics

▪ Morphine▪ Pethidine ▪ Buprenorphine

Pre-anaesthetic Medication

Anticholinergic DrugsAtropine SO4 Scopolamine (Hyoscine)Synthetic Anticholinergics – GlycopyrrolateAntiemeticsPhenothiazines (Promethazine and Trimeprazine) Cyclizine Trimethobenzamide Benzquinamide Metoclopramide

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