Individual inhalant anaesthetic agents
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INDIVIDUAL INHALANT ANAESTHETIC AGENTS
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Halothane
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Multihalogenated ethane – introduced in 1957
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Rapid induction, recovery, minimal side effects and nonflammability
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About 20 % metabolized - MAC 0.85% - not irritating to the mucous memb.
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Depresses CNS in a dose related fashion – cerebral blood flow may increase → higher CSF pressure. Shivering found during recovery
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Depression of cardiac output and bradycardia – due to vagus activity
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Depresses Minimal neuromuscular blockade and analgesia
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Minimal pathological changes in the liver. Hepatitis may be caused. Some metabolites may cause necrosis
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Kidney unaffected but sometimes as a sequelae to blood flow changes
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Poor muscle relaxation.
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Malignant hyperthermia in pigs and man. Also in other sp.
Isoflurane
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Popular agent.
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MAC – for induction 3-5% and for maintenance – 1.5 – 2.5%
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Flourinated ether. 1% metabolized into fluoride. But not toxic.
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Lesser vasodilatation of the brain. Affects cardiac output less than halothane and has a wider margin of safety.
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Dose dependent depression of the heart and respiration
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Arrhythmias not reported
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Renal function not affected
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Better muscle relaxation than halothane
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Not to be used in animals with a known susceptibility to malignant hyperthermia
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Used in reptiles
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Yet to replace halothane in popularity
Enflurane
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Since 1963
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cardiac depression, decrease cardiac output, decrease arterial BP as good as or higher than halothane
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2-8% metabolized but may not cause fluoride nephrosis.
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Hepatitis reported
Desflurane
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Highly stable – stable at room temp. for > a year
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Boils at close to room temp. and careful vaporization needed
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Low solubility in blood → rapid induction
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0.2% metabolised
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Not popular in humans because of its irritant nature
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Tendency to cause malignant hyperthermia
Methoxyflurane
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Stable compound
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Less prone to cardiac depression, not irritating
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Polyuric renal dysfunction due to fluoride metabolites
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Hence withdrawn
Ether (diethyl ether)
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Colourless volatile liquid. Stored in a cool place but not in refrigerator
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Inflammable – High blood - gas solubility
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Locally refrigerant, anaesthetic, rubefacient, skin antiseptic
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Nausea and vomition during inhalation -- disadvantageous
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Metabolites non toxic
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CNS – slow and unpleasant induction—
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Heart rate and BP decrease due to epinephrine release during induction
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Respiration – Irritant to passage, bronchial and pulmonary complications seen
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Transient depression of liver and kidney – causes metabolic acidosis
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However ether has been in use for more than 100 years
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Chloroform
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Unpleasant odour – Powerful rapid inducer
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Sensitizes myocardium to adrenaline → ventricular fibrillation → sudden death (20 – 30 times more potent than ether)
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Toxicity to liver – necrosis, fatty degeneration
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Kidney – anuria
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Poisoning → acidosis, vomiting, acetonuria, albuminuria, pyrexia, icterus,
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Discontinued
Nitrous oxide
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Colourless gas – kept compressed at 40 atm.
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N2O increases pulmonary ventilation – due to direct stimulation of respiration.
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Increases its own inhalation – (Concentration effect)
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and also that of halothane or enflurane or oxygen when given together (second gas effect)
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MAC > 100% (104 in man to 255 in cat) – weak anaesthetic-
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But strongly analgesic
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An anaesthetic adjuvant
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Last modified: Monday, 18 June 2012, 6:44 AM