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THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.

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  2. 2.  1776- priestly- nitrous oxide  1845-Horrace wells –dentist-Nitrous oxide  1846-William Mortan –ether dome
  3. 3. 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 combinations Monitored anaesthesia- local Ana’s +Gen Ana’s
  4. 4. Guedel described stages of ether anaesthesia 1. Stage of analgesia  -starts from beginning of anaesthetic inhalation and lasts upto loss of conciousness 2. 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
  5. 5. 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
  6. 6. Potency α 1/MAC Minimal Alveolar Concentration :- Is the alveolar concentration of an inhaled anesthetic that prevents movement in 50 % of patients in response to standardized stimulus (surgical incision ).
  7. 7.  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.
  8. 8.  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
  9. 9. INHALATIONAL ANAESTHETICS  Nitrous oxide, cyclopropane,xenon VOLATILE LIQUIDS  Isoflurane, Sevoflurane  Desflurane, Halothane  (Ether), Enflurane INTRAVENOUS ANAESTHETICS INDUCING AGENTS Thiopentone sod. Methohexitone sod., Propofol, Etomidate
  10. 10. SLOWER ACTING DRUGS Benzodiazepines Diazepam Lorazepam Midazolam Dissociative anaesthesia Ketamine Neurolept analgesia Fentanyl
  11. 11.  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
  12. 12. •widely used •Potent analgesic •Produce a light anesthesia •Do not depress the respiration/vasomotor center •Used as adjunct to supplement other inhalationals •Least hepatotoxic
  13. 13.  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
  14. 14.  Within close compartmentit can increase volumepneumothorax, sinuses pressure  No muscle relaxation  Post anaesthetic nausea and vomiting  >4hrs megaloblastic anaemia  Abortion, birth defects
  15. 15.  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.
  16. 16.  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 min TIVA- P:K-4:1 Side-effects is pain on injection hypotension and transient apnea following induction 16
  17. 17. • Non-flammable •Relaxes both skeletal and uterine muscles used in obstetrics •Not hepatotoxic in pediatrics • 20% metabolism by P450induction of hepatic microsomal Enzymes • Myocardial depressant (SA node), • sensitization of myocardium to catecholamines - arrhythmia • Relaxes both skeletal and uterine muscles used in obstetrics • Has vagomimetic action
  18. 18.  Transient hepatic damage  Liver necrosis  In repeated exposureImmunosensititation  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
  19. 19. Rapid, smooth induction and maintenance • 2-10% metabolized in liver release fluride ions nephrotoxic • Introduced as replacement for halothane • Curare like effect ADR-CNS excitation at twice MAC ISOFLURANE smooth and rapid induction and recovery very little metabolism (0.2%) Does not sensitize heart to catecholamines no reports of hepatotoxicity or renotoxicity most widely employed
  20. 20.  Rapid uptake with out irritation  Low solubility  Faster recovery  Metabolismliver release fluride ions nephrotoxic DESFLURANE low volatility, needs special vapouriser Airway irritant, less tissue toxicity
  21. 21.  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 anesthesia Side effects  Hypotension  apnoea  airway obstruction
  22. 22.  Smooth induction  Shorter acting than thiopental  Lesser chances of hypotension side effects pain at site of injection poor analgesic, adrenocortical suppression
  23. 23.  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
  24. 24.  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
  25. 25.  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
  26. 26.  Sedatives / Anxiolytics ▪ Benzodiazepines,Barbiturates ▪ Butyrophenones,Phenothiazines ▪ Chloral hydrate & Paraldehyde  Opioid Analgesics ▪ Morphine ▪ Pethidine ▪ Buprenorphine
  27. 27. Anticholinergic Drugs Atropine SO4 Scopolamine (Hyoscine) Synthetic Anticholinergics – Glycopyrrolate Antiemetics Phenothiazines (Promethazine and Trimeprazine) Cyclizine Trimethobenzamide Benzquinamide Metoclopramide