GENERAL ANAESTHETICs by siva

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General Anaesthetics :

General Anaesthetics By Dr.Siva

Anesthesiology :

Anesthesiology General anesthesia – for surgical procedure to render the patient unaware / unresponsive to the painful stimuli Anesthesia – is a reversible condition of comfort, quiescence and physiological stability in a patient before, during and after performance of a procedure.

History of Anesthesia:

History of Anesthesia Ether synthesized in 1540 by Cordus Ether used as anesthetic in 1842 by Dr. Crawford W. Long Ether publicized as anesthetic in 1846 by Dr. William Morton Chloroform used as anesthetic in 1853 by Dr. John Snow

History of Anesthesia:

History of Anesthesia

Basic Principles of Anesthesia:

Basic Principles of Anesthesia Anesthesia defined as the abolition of sensation Analgesia defined as the abolition of pain “Triad of General Anesthesia” need for unconsciousness need for analgesia need for muscle relaxation

What are General Anesthetics?:

What are General Anesthetics? A drug that brings about a reversible loss of consciousness. These drugs are generally administered by an anesthesiologist in order to induce or maintain general anesthesia to facilitate surgery.

Triad of General anaesthesia:

Triad of General anaesthesia Hypnosis Analgesia Muscle relaxation

General Anesthesia:

General Anesthesia Analgesia Amnesia Hypnosis/sedation Immobility

Analgesia:

Analgesia

Amnesia:

Amnesia

Hypnosis/Sedation:

Hypnosis/Sedation

Immobility:

Immobility

Anesthesiology:

Anesthesiology Stages of anesthesia Stage I : Analgesia Stage II : Excitement, Combative behavior – dangerous state Stage III : Surgical anesthesia Stage IV : Medullary Paralysis – respiratory and vasomotor control ceases

Anesthesiology:

Anesthesiology Anesthesia is associated with Decrease in systemic blood pressure – myocardial depression and direct vasodilation Blunting of baroreceptor control and decreased central sympathetic tone Muscle relaxation is valuable during the anesthesia – facilitates endotracheal intubation.

Anesthesiology:

Anesthesiology Preanesthetic medication : It is the use of drugs prior to anesthesia to make it more safe and pleasant. The aim is to relieve apprehension and facilitate smooth induction. To supplement analgesic, amnesic action of anesthetics Prevents bradycardia and secretion.

Anesthesiology:

Anesthesiology Preanesthetic medication : To relieve anxiety – benzodiazepines. To prevent allergic reactions – anti-histaminics To prevent nausea and vomiting – anti – emetics. To provide analgesia – opioids To prevent bradycardia and secretion - atropine

Phases of general anaesthesia:

Phases of general anaesthesia Induction Maintenance Recovery

Anesthesiology:

Anesthesiology Mechanism of action of anesthetics Lipid theory Protein theory

Anesthesiology:

Anesthesiology Molecular mechanism of the GA : GABA –A : ---- Cl channels ---- Halothane, Propofol Etomidate NMDA receptors : inhibited by Ketamine

Anesthesiology:

Anesthesiology The main target of inhalation anesthetics is the brain.

Anesthesiology:

Anesthesiology There are two types of anesthetics : Inhalational --- for maintenance Intravenous --- for induction

Anesthesiology:

Anesthesiology Inhalation anesthetics : Advantage of controlling the depth of anesthesia. Metabolism is very minimal Excreted by exhalation

Anesthesiology:

Anesthesiology The important characteristics of Inhalational anesthetics which govern the anesthesia are : Solubility in the blood (blood : gas partition) Solubility in fat (oil : gas partition)

Anesthesiology:

Anesthesiology Blood : gas partition co-efficient : is a measure of solubility in the blood It determines the rate of induction and recovery of Inhalational anesthetics Lower the blood : gas co-efficient – faster the induction and recovery – Nitrous oxide Higher the blood : gas co-efficient – Slower induction and recovery - Halothane

Anesthesiology:

Anesthesiology Oil: gas partition co-efficient : is a measure of lipid solubility. Lipid solubility - Correlates strongly with the potency of the anesthetic Higher the lipid solubility – potent anesthetic. E.g., Halothane

Anesthesiology:

Anesthesiology MAC value, a measure of inhalational anesthetic potency, is defined as the minimum alveolar anesthetic concentration ( % of the inspired air) at which 50% of patients do not respond to a surgical stimulus. MAC values are additive and lower in the presence of Opioids .

Slide 33:

Inhalation Anesthetic MAC value % Oil: Gas partition Nitrous oxide >100 1.4 Desflurane 7.2 23 Sevoflurane 2.5 53 Isoflurane 1.3 91 Halothane 0.8 220

Anesthesiology:

Anesthesiology Inhalational anesthetics : Non-halogenated gas : Nitrous oxide Halogenated hydrocarbons : Halothane Enflurane Isoflurane Desflurane Sevoflurane Methoxyflurane - Nephrotoxicity

Inhalational anesthetics:

Inhalational anesthetics Nitrous oxide : Safest inhalational anesthetic. No effect on the respiration and heart. Non-toxic to liver, kidney and brain Metabolism does not occur and quickly removed from the body by lungs

Inhalational anesthetics:

Inhalational anesthetics Nitrous oxide : Weak anesthetic – surgical anesthesia cannot be produced on its own. It is a good analgesic and poor muscle relaxant Second gas effect and diffusional hypoxia seen Caution about pneumothorax and megaloblastic anemia

Inhalational anesthetics:

Inhalational anesthetics Halothane : It is a potent anesthetic but not a good analgesic. Induction is pleasant. Halothane is vagomimetic – bradycardia. It produce dose dependent hypotension

Inhalational anesthetics:

Inhalational anesthetics Halothane : It sensitizes the heart to catecholamines Bronchus dilate – preferred in asthmatics Inhibits uterine and intestinal contractions - obstetrics. Halothane Hepatitis Malignant hyperthermia occurs

Anesthesiology:

Anesthesiology Halothane : Halothane is the only inhalational anesthetics in current use which is metabolized significantly (30%) to bromide, trifluro-acetic acid – responsible for rare hepatotoxicity, leukemia, spontaneous abortion and congenital abnormalities

Inhalational anesthetics:

Inhalational anesthetics Enflurane : Non-irritating Does not sensitizes the heart to catecholamines Seizures occurs at deeper levels –contraindicated in epileptics Caution in renal failure – fluoride.

Inhalational anesthetics:

Inhalational anesthetics Isoflurane : Widely used. Coronary circulation is maintained and does not sensitize the heart to catecholamines Safe in myocardial ischemia Does not provoke seizures and preferred for neurosurgery

Inhalational anesthetics:

Inhalational anesthetics Desflurane : Delivered through special vaporizer Popular anesthetic for day care surgery Induction and recovery fast - cognitive and motor impairment is short lived Irritates the air passages – coughing, laryngospasm.

Inhalational anesthetics:

Inhalational anesthetics Sevoflurane : Induction and recovery is fast. Absence of pungency makes it pleasant and acceptability is good in pediatric patients Does not cause air way irritancy. Concerns about nephrotoxicity

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Anesth B:G PC O:G PC IRRIT INDUCT MUSCL RELAX Notes Haloth 2.3 220 PLEASANT INTER FAIR arrhyth M Hyp Enflur 1.9 98 PLEASANT INTER GOOD seizure M Hyp Isoflur 1.4 91 - - - - FAST GOOD Widely used Sevoflu 0.62 53 PLEASANT FAST GOOD Ideal Desflur 0.42 23 + + + FAST GOOD cough Nitrous 0.47 1.4 - - - - FAST POOR Anemia

Anesthesiology:

Anesthesiology Intravenous anesthetics : Used for induction Thiopental Methohexital Propofol Etomidate Ketamine

Anesthesiology:

Anesthesiology Parenteral anesthetics (IV) are used for induction of anesthesia High lipophilicity Rapid onset of action Recovery is mainly by redistribution Also reduce the amount of inhalation anesthetic for maintenance.

Anesthesiology:

Anesthesiology Thiopental : It is an ultra short acting barbiturates, highly soluble in lipid. Produces unconsciousness ~ 20 seconds Consciousness regained within 10-20 mins by redistribution to skeletal muscle. It is eliminated slowly from the body and produce hang over.

Anesthesiology:

Anesthesiology Thiopental : Not an analgesic and it is a weak muscle relaxant. Cerebral blood flow is not increased and thus no increase in ICT – preferred in cerebral swelling like head injury. Laryngospasm occurs commonly - can be prevented by atropine

Anesthesiology:

Anesthesiology Thiopental : It can be used for rapid control of seizures To facilitates the verbal communication with psychiatric patients

Intravenous anesthetics:

Intravenous anesthetics Methohexital : Three times more potent than the Thiopental Has quick and brief action like thiopental. Excitement and restless during the induction Pain on injection

Intravenous anesthetics:

Intravenous anesthetics Propofol : Most commonly used IV anesthetic Unconsciousness in ~ 45 seconds and lasts ~15 minutes Decreases the intracranial pressure. Dose dependent decrease in BP.

Intravenous anesthetics:

Intravenous anesthetics Propofol : Anti-emetic in action thus no postoperative nausea and vomiting. Suited for day care surgery - residual impairment is less marked It is used for sedation in intensive care units

Intravenous anesthetics:

Intravenous anesthetics Etomidate : New induction anesthetic but a poor analgesic. Rapid onset and duration of action ~ 5-10 mins Little CVS and respiratory depression Motor restless and rigidity more common

Intravenous anesthetics:

Intravenous anesthetics Etomidate : No repeated injections or infusions as it suppresses the production of steroids from the adrenal gland. Proconvulsant and emetic. CVS stability is the main advantage over barbiturates.

Intravenous anesthetics:

Intravenous anesthetics Ketamine : Induces dissociative anesthesia – profound analgesia, cataleptic state, immobility, amnesia with light sleep and feeling of dissociated from the body . Acts by blocking NMDA receptors Characterized by analgesia, immobility and amnesia.

Intravenous anesthetics:

Intravenous anesthetics Ketamine : Increase the cerebral blood flow and increase the ICT Respiration is not depressed and reflexes are not abolished. Heart rate, cardiac output and BP are elevated due to sympathetic stimulation.

Intravenous anesthetics:

Intravenous anesthetics Ketamine : Emergence delirium, hallucinations and involuntary movements occurs in 50% cases during recovery It is useful for burn dressing and trauma surgery Dangerous for hypertensive and IHD.

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Anesthetic Duration I.V mins Analgesia Muscle relaxation Others Thiopental 5 - 10 --- --- Respiratory depression Propofol 5-10 --- --- Respiratory depression Ketamine 5-10 +++ --- Hallucinations Midazolam 5-20 --- +++ Amnesia Fentanyl 5-10 +++ --- Respiratory depression

Intravenous anesthetics:

Intravenous anesthetics Neuroleptanalgesia : characterized by general quiescence, psychic indifference and intense analgesia without total unconsciousness Fentanyl - short acting Opioid Droperidol – long acting Neuroleptic

Intravenous anesthetics:

Intravenous anesthetics Neuroleptanalgesia : characterized by analgesia, decreased motor functions, suppressed autonomic reflexes, cardiovascular stability with mild amnesia.

Intravenous anesthetics:

Intravenous anesthetics Neuroleptanalgesia : It causes drowsiness but responds to commands Respiratory depression and extra pyramidal s/s seen Used for endoscopies, angiographies and minor operations.

Intravenous anesthetics:

Intravenous anesthetics Midazolam Opioids - fentanyl

Nitrous Oxide:

Nitrous Oxide Prepared by Priestly in 1776 Anesthetic properties described by Davy in 1799 Characterized by inert nature with minimal metabolism Colorless, odorless, tasteless, and does not burn

Nitrous Oxide:

Nitrous Oxide Simple linear compound Not metabolized Only anesthetic agent that is inorganic

Nitrous Oxide:

Nitrous Oxide Major difference is low potency MAC value is 105% Weak anesthetic, powerful analgesic Needs other agents for surgical anesthesia Low blood solubility (quick recovery)

Nitrous Oxide Systemic Effects:

Nitrous Oxide Systemic Effects Minimal effects on heart rate and blood pressure May cause myocardial depression in sick patients Little effect on respiration Safe, efficacious agent

Nitrous Oxide Side Effects:

Nitrous Oxide Side Effects Manufacturing impurities toxic Hypoxic mixtures can be used Large volumes of gases can be used Beginning of case: second gas effect End of case: diffusion hypoxia

Halothane:

Halothane Synthesized in 1956 by Suckling Halogen substituted ethane Volatile liquid easily vaporized, stable, and nonflammable

Halothane:

Halothane Most potent inhalational anesthetic MAC of 0.75% Efficacious in depressing consciousness Very soluble in blood and adipose Prolonged emergence

Halothane Systemic Effects:

Halothane Systemic Effects Inhibits sympathetic response to painful stimuli Inhibits sympathetic driven baroreflex response (hypovolemia) Sensitizes myocardium to effects of exogenous catecholamines-- ventricular arrhythmias Johnson found median effective dose 2.1 ug/kg Limit of 100 ug or 10 mL over 10 minutes Limit dose to 300 ug over one hour Other medications

Halothane Systemic Effects:

Halothane Systemic Effects Decreases respiratory drive-- central response to CO 2 and peripheral to O 2 Respirations shallow-- atelectasis Depresses protective airway reflexes Depresses myocardium-- lowers BP and slows conduction Mild peripheral vasodilation

Halothane Side Effects:

Halothane Side Effects “Halothane Hepatitis” -- 1/10,000 cases fever, jaundice, hepatic necrosis, death metabolic breakdown products are hapten-protein conjugates immunologically mediated assault exposure dependent

Halothane Side Effects:

Halothane Side Effects Malignant Hyperthermia-- 1/60,000 with succinylcholine to 1/260,000 without halothane in 60%, succinylcholine in 77% Classic-- rapid rise in body temperature, muscle rigidity, tachycardia, rhabdomyolysis, acidosis, hyperkalemia, DIC most common masseter rigidity family history

Halothane Side Effects:

Halothane Side Effects Malignant Hyperthermia (continued) high association with muscle disorders autosomal dominant inheritance diagnosis--previous symptoms, increase CO2, rise in CPK levels, myoglobinuria, muscle biopsy physiology--hypermetabolic state by inhibition of calcium reuptake in sarcoplasmic reticulum

Halothane Side Effects:

Halothane Side Effects Malignant Hyperthermia (continued) treatment--early detection, d/c agents, hyperventilate, bicarb, IV dantrolene (2.5 mg/kg), ice packs/cooling blankets, lasix/mannitol/fluids. ICU monitoring Susceptible patients-- preop with IV dantrolene, keep away inhalational agents and succinylcholine

Enflurane:

Enflurane Developed in 1963 by Terrell, released for use in 1972 Stable, nonflammable liquid Pungent odor MAC 1.68%

Enflurane Systemic Effects:

Enflurane Systemic Effects Potent inotropic and chronotropic depressant and decreases systemic vascular resistance-- lowers blood pressure and conduction dramatically Inhibits sympathetic baroreflex response Sensitizes myocardium to effects of exogenous catecholamines-- arrhythmias

Enflurane Systemic Effects:

Enflurane Systemic Effects Respiratory drive is greatly depressed-- central and peripheral responses increases dead space widens A-a gradient produces hypercarbia in spontaneously breathing patient

Enflurane Side Effects:

Enflurane Side Effects Metabolism one-tenth that of halothane-- does not release quantity of hepatotoxic metabolites Metabolism releases fluoride ion-- renal toxicity Epileptiform EEG patterns

Isoflurane:

Isoflurane Synthesized in 1965 by Terrell, introduced into practice in 1984 Not carcinogenic Nonflammable,pungent Less soluble than halothane or enflurane MAC of 1.30 %

Isoflurane Systemic Effects:

Isoflurane Systemic Effects Depresses respiratory drive and ventilatory responses-- less than enflurane Myocardial depressant-- less than enflurane Inhibits sympathetic baroreflex response-- less than enflurane Sensitizes myocardium to catecholamines -- less than halothane or enflurane

Isoflurane Systemic Effects:

Isoflurane Systemic Effects Produces most significant reduction in systemic vascular resistance-- coronary steal syndrome, increased ICP Excellent muscle relaxant-- potentiates effects of neuromuscular blockers

Isoflurane Side Effects:

Isoflurane Side Effects Little metabolism (0.2%) -- low potential of organotoxic metabolites No EEG activity like enflurane Bronchoirritating, laryngospasm

Sevoflurane and Desflurane:

Sevoflurane and Desflurane Low solubility in blood-- produces rapid induction and emergence Minimal systemic effects-- mild respiratory and cardiac suppression Few side effects Expensive Differences

Intravenous Anesthetic Agents:

Intravenous Anesthetic Agents First attempt at intravenous anesthesia by Wren in 1656-- opium into his dog Use in anesthesia in 1934 with thiopental Many ways to meet requirements-- muscle relaxants, opoids, nonopoids Appealing, pleasant experience

Thiopental:

Thiopental Barbiturate Water soluble Alkaline Dose-dependent suppression of CNS activity--decreased cerebral metabolic rate (EEG flat)

Thiopental:

Thiopental Redistribution

Thiopental Systemic Effects:

Thiopental Systemic Effects Varied effects on cardiovascular system in people-- mild direct cardiac depression-- lowers blood pressure-- compensatory tachycardia (baroreflex) Dose-dependent depression of respiration through medullary and pontine respiratory centers

Thiopental Side Effects:

Thiopental Side Effects Noncompatibility Tissue necrosis--gangrene Tissue stores Post-anesthetic course

Etomidate:

Etomidate Structure similar to ketoconozole Direct CNS depressant (thiopental) and GABA agonist Redistribution

Etomidate Systemic Effects:

Etomidate Systemic Effects Little change in cardiac function in healthy and cardiac patients Mild dose-related respiratory depression Decreased cerebral metabolism

Etomidate Side Effects:

Etomidate Side Effects Pain on injection (propylene glycol) Myoclonic activity Nausea and vomiting (50%) Cortisol suppression

Ketamine:

Ketamine Structurally similar to PCP Interrupts cerebral association pathways -- “dissociative anesthesia” Stimulates central sympathetic pathways

Ketamine Systemic and Side Effects:

Ketamine Systemic and Side Effects Characteristic of sympathetic nervous system stimulation-- increase HR, BP, CO Maintains laryngeal reflexes and skeletal muscle tone Emergence can produce hallucinations and unpleasant dreams (15%)

Propofol:

Propofol Rapid onset and short duration of action Myocardial depression and peripheral vasodilation may occur-- baroreflex not suppressed Not water soluble-- painful (50%) Minimal nausea and vomiting

Benzodiazepines:

Benzodiazepines Produce sedation and amnesia Potentiate GABA receptors Slower onset and emergence

Diazepam:

Diazepam Often used as premedication or seizure activity, rarely for induction Minimal systemic effects-- respirations decreased with narcotic usage Not water soluble-- venous irritation Metabolized by liver-- not redistributed

Lorazepam:

Lorazepam Slower onset of action (10-20 minutes)-- not used for induction Used as adjunct for anxiolytic and sedative properties Not water soluble-- venous irritation

Midazolam:

Midazolam More potent than diazepam or lorazepam Induction slow, recovery prolonged May depress respirations when used with narcotics Minimal cardiac effects Water soluble

Narcotic agonists (opiods):

Narcotic agonists (opiods) Used for years for analgesic action-- civil war for wounded soldiers Predominant effects are analgesia, depression of sensorium and respirations Mechanism of action is receptor mediated

Narcotic agonists (opoids):

Narcotic agonists (opoids) Minimal cardiac effects-- no myocardial depression Bradycardia in large doses Some peripheral vasodilation and histamine release -- hypotension Side effects nausea, chest wall rigidity, seizures, constipation, urinary retention

Narcotic agonists (opoids):

Narcotic agonists (opoids) Meperidine, morphine, alfentanil, fentanyl, sufentanil are commonly used Naloxone is pure antagonist that reverses analgesia and respiratory depression nonselectively-- acts 30 minutes, effects may recur when metabolized

Muscle Relaxants:

Muscle Relaxants Current use of inhalational and previous intravenous agents do not fully provide control of muscle tone First used in 1942-- many new agents developed to reduce side effects and lengthen duration of action Mechanism of action occurs at the neuromuscular junction

Nondepolarizing Muscle Relaxants:

Nondepolarizing Muscle Relaxants Competitively inhibit end plate nicotinic cholinergic receptor Intermediate acting (15-60 minutes): atracurium, vecuronium, mivacurium Long acting (over 60 minutes): pancuronium, tubocurarine, metocurine Difference-- renal function

Nondepolarizing Muscle Relaxants:

Nondepolarizing Muscle Relaxants Tubocurare-- suppress sympathetics, mast cell degranulation Pancuronium-- blocks muscarinics Reversal by anticholinesterase-- inhibit acetylcholinesterase neostigmine, pyridostigmine, edrophonium side effects muscarinic stimulation

Depolarizing Muscle Relaxants:

Depolarizing Muscle Relaxants Depolarize the end-plate nicotinic receptor Succinylcholine used clinically short duration due to plasma cholinesterase side effects-- fasiculations, myocyte rupture, potassium extravasation, myalgias sinus bradycardia-- muscarinic receptor malignant hyperthermia

Slide 107:

Presentation dedicated to my parents

Slide 108:

Thank You

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