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Created: 24/11/2004



Uses: Induction and maintenance of general anaesthesia.

Chemical: Halogenated methyl ether. Structural isomer of Enflurane.


Presentation: Clear colourless liquid, with a pungent smell.

Mode of action: Mechanism of general anaesthesia remains unclear.

Routes: Inhalation, via a calibrated vaporiser. Induction dose 1-4%, maintenance 0.5-3%.


Cardiovascular system: Mild negative inotrope, marked decrease in systemic vascular resistance thus leading to a decrease in mean arterial pressure. Causes a reflex tachycardia. Suggested to cause ‘coronary steal’. Coronary vasodilatation in the presence of fixed coronary arterial stenotic lesions may cause redistribution of blood from the endo- to the epicardium.

Respiratory system: Respiratory depressant. Decreases tidal volume, has little effect on respiratory rate. Decreased response to hypoxia and hypercapnia. Very irritant to respiratory tract. Causes bronchodilatation.

Central nervous system: Principal effect is general anaesthesia; little analgesic effect. Causes increased cerebral blood flow in concentrations >1 MAC.

Abdominal system: Maintains hepatic blood flow.

Genitourinary system: Tone of pregnant uterus is reduced.

Toxicity: Trigger agent for malignant hyperthermia. Isolated reports of hepatotoxicity.

Absorption: Coefficients - Blood/gas: 1.4, oil/gas: 98, MAC: 1.15

Distribution: Initially to areas of high blood flow (brain, heart, liver and kidney). Later to less well-perfused organs.

Metabolism: 0.2% of dose is slowly metabolised in the liver (oxidation/dehalogenation).

Excretion: Principally exhaled unchanged. 0.2% in urine as fluorinated compounds.

Special points: Potentiates action of non-depolarising muscle relaxants.


[i] The use of 0.25% isoflurane premixed in 50% nitrous oxide and oxygen for pain relief in labour.
Ross JA, Tunstall ME, Campbell DM, Lemon JS.
Anaesthesia 1999; 54(12): 1166-72.

[ii] Isoflurane and coronary heart disease
N. M. Agnew et al.
Anaesthesia Volume 57 Issue 4 Page 338  - April 2002


Early studies indicated that isoflurane caused coronary steal and should therefore be avoided in patients with coronary heart disease. Subsequently, more detailed trials have disputed this and have shown that as long as coronary perfusion pressure is maintained, isoflurane does not cause coronary steal or myocardial ischaemia. There is now growing evidence, initially in animal work but more recently in human studies, that isoflurane has myocardial protective properties, limiting infarct size and improving functional recovery from myocardial ischaemia. The mechanism for this protection mimics ischaemic preconditioning and involves the opening of adenosine triphosphate-dependent potassium channels. The few studies comparing the myocardial protection offered by individual anaesthetic agents indicate that isoflurane represents the anaesthetic agent of choice for patients with coronary heart disease.

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