class general anaesthesia
DESCRIPTION
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.TRANSCRIPT
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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