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    11 views9 pages

    Pharmacology Lecture 06

    Uploaded by

    Arleen Matinca

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    of 9
    Lecture & GENERAL ANESTHETICS OBJECTIVES Define the following terms: * Amnesia Inhalation anesthesia Minimal alveolar concentration Analges General anesthesia © Intravenous anesthesia Stages of anesthesia ‘You should be able to: Define the main inhalational and intravenous anesthetic agents and describe their pharmacodynamic properties Describe the relationship between the blood:gas partition coefficient of an anesthetic and the speed of onset (and offset) of inhalation anesthesia Describe how changes in pulmonary ventilation and blood flow can influence the speed of onset (and offset) of inhalation anesthesia Describe the pharmacokinetics of the commonly used intravenous anesthetics LOCAL ANESTHETH OBJECTIVES Describe the following: ‘The mechanism of blockade of the nerve impulse by local anesthetics ‘The relation between pH, pKa and the onset or intensity of blockade The relation between nerve fiber size and susceptibility to blockade Use-dependent blockade GENERAL ANESTHETIC AGENTS THEORIES OF ANESTHESIA * Many simple, unreactive compounds produce narcotic effects, the extreme example being the inert gas xenon, * Anesthetic potency is closely correlated with lipid solubility (Overton-Meyer correlation(, not with chemical structure. * Earlier theories of anesthesia postulate interaction with the lipid membrane bilayer. Recent work favours interaction with ligand-gated membrane ion channels, * Most anesthetics enhance the activity of inhibitory GABA,-receptors and many inhibit activation of excitatory receptors, such as glutamate and nicotinie acetycholine receptors PHARMACOLOGICAL BFFECTS OF ANESTHETIC AGENTS * Anesthesia involves three main neurophysiological changes: unconsciousness, loss of response to painful stimulation and loss of reflexex. * At supra-anesthetic doses, all anesthetic agents can cause death by loss of cardiovascular reflexes and respiratory paralysis ‘* At the cellular level, anesthetic agents affect synaptic transmission rather than axonal conduction. The release of excitatory transmitters and the response of the postsynaptic receptors are both inhibited. GABA-mediated inhibitory transmission is enhanced by most anesthetics ‘+ Though all parts of the nervous system are affected by anesthetics, the main targets appear to be the talamus, cortex and hippocampus. + Most anesthetic agents (with exceptions stich as ketamine and benzodiazepines) produce similar neurophysiological effects and differ mainly in respect of their pharmacolinetic properties and toxicity. + Most anesthetics cause cardiovascular depression, by effects on the myocardium and blood vessels as well as on the nervous system. Halogenated anesthetics are likely to cause cardiac arrhythmias, accentuated by circulating catecholamines. PHARMACOKINETIC PROPERTIES OF INHALATION ANESTHETIC + Rapid induction and recovery are important properties of an anesthetic agent, allowing flexible control over the depth of anesthesia. : ‘+ Speed of induction and recovery are determined by two properties of the anesthetic: solubility in blood (blood: gas partition coefficient) and solubility in fat (lipid solubility) + Agents with low blood:gas partition coefficients produce rapid induction and recovery (eg. nitrous oxide, desflurane); agents with high blood: gas partition coefficients show slow induction and recovery (e.g. halothane, ether). * Agents with high lipid solubility (e.g, halothane) accumulate gradually in body fat and may produce a prolonged hangover if used for a long operation + Some halogenated anesthetics (especially halothane and methoxyflurane) are metabolised. This is not very important in determining their duration of action, but contributes to toxicity (e.g. renal toxicity associated with fluoride production with methoxyflurane — no longer used). INDIVIDUAL INHALATION ANESTHETIC! + The main agents in current use in developed countries are halothane, nitrous oxide, isoflurane, enflurane, desflurane and sevoflurane. Ether is largely obsolete * Halothane: > Widely used agent » Potent, non-explosive and non-irritant, hypotensive; may cause dysthytmias; about 30% metabolised > Hangover likely, because of high lipid solubility > Risk of liver damage and malignant fever if used repeatedly. «Nitrous oxide: > Low potency, therefore must be combined with other agents > Rapid induction and recovery > Good analgesic properties > Risk of bone marrow depression with prolonged administration © Enflurane: > Halogenated anesthetic similar to halothane > Less metabolism than halothane therefore there is less risk o¢ toxicity > Faster induction and recovery than halothane (less accumulation in fat) > Some risk of epilepsy-like seizures + Isoflurane: > Similar to enflurane but lacks epileptogenic property > May precipitate myocardial ischaemia in patients with coronary disease > Inritant to respiratory tract © Desflurane and sevoflurane are similar to isoflurane but have faster onset and recovery and lack respiratory irritation © Ether: > Obsolete except where modem facilities are not available > Easy to administer and control > Slow onset and recovery, with postoperative nausea and vomiting > Analgesic and muscle relaxant properties > Highly explosive > Initant to respiratory tract. INTRAVENOUS ANESTHETIC AGENTS, * Most commonly used for induction of anesthesia, followed by inhalation agent + Thiopenthal, etomidate and propofol are most commonly used; all act within 20-30 seconds if given intravenously © Thiopenthal: > Barbiturate with very high lipid solubility > Rapid action because of rapid transfer across blood-brain barrier; short duration (about 5 minutes) because of redistribution, mainly to muscle > Slowly metabolised and liable to accumulate in body fat; therefore may cause prolonged effect if given repeatedly > No analgesic effect > Narrow margin between anesthetic dose and dose causing cardiovascular depression > Risk Etomidate: > Similar to thiopenthal but more quickly metabolised > Less risk of cardiovascular depression > May cause involuntary movements during induction > Possible risk of adrenocortical supression Propofol: > Rapidly metabolised > Very rapid recovery; no cumulative effect > Useful for day-case surgery Ketamine: > Analogue of phencyclidine, with similar properties > Action differs from other agents; probably related to effect on NMDA-type glutamate receptors Onset of effect is relatively slow (2-5 minutes) Produces ‘dissociative’ anesthesia, in which patient may remain conscious, though amnesic and insensitive to pain High incidence of dysphoria, hallucinations, ete during recovery; used mainly for ‘minor procedures in children. vv v isoutue pur wisodjeue pod ssonposg ‘orsnyly stomuuoo se asn 0} @IqISSOq ostoqereu Apprdey Sis WORST Tw wRET SasTIPD, rexnwodonp {nw _ueyp_uosssaidap Sromandsos pue sejoseaotpsv9 ssa, ynOs io} uae wonaNpuy se posm AlaptAy SALON ‘uoneajfes pue anwos ‘asneu aanezodonsog Araxosas Sutmofjo} say HOUT IOLOHOAS wworssaudap Azojeardsax pute sejnasesorpse) uuorssaudns eamuo20usspy 4940991 pte wortonput Suuimp sid9ya Krow19K3 uotssaidap A1orwuidsay pur seynaserorpre) SL0ddda ASWAACV NIV surafe soipo wep samois | umjozepiyy = ‘Aroaooa1 Suump uountos sjsayjo-1oye 2suo Mmojg auureey Kranooar sey Kian Yasuo seg | yoyodoug Aaanooan sey

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