VOLATILE ANESTHETICS AND CARDIAC ELECTROPHYSIOLOGY
Cardiac Conduction
Volatile anesthetics slow the rate of sinoatrial node discharge
by direct and indirect effects on sinoatrial node automaticity.[173]
[197]
These actions may be altered in vivo by vasoactive
drugs or autonomic nervous system activity.[198]
Halothane, enflurane and, to some extent, isoflurane shorten the cardiac action
potential and effective refractory period in normal Purkinje fibers,[197]
[199]
[200]
but
these
agents prolong His-Purkinje and ventricular conduction times.[197]
[200]
[201]
Halothane,
enflurane, and isoflurane also prolong atrioventricular conduction time and refractoriness.
[200]
[202]
[203]
When combined with the direct actions of volatile anesthetics on sinoatrial node
discharge, the data suggest that volatile anesthetics have the potential to produce
bradycardia and atrioventricular conduction abnormalities. However, primary disturbances
in atrioventricular conduction leading to second- or third-degree atrioventricular
block in humans probably do not occur with volatile anesthetics in the absence of
conduction
disease or drugs that directly prolong the atrioventricular conduction time.[204]
[205]
Volatile agents may have proarrhythmogenic or antiarrhythmogenic
actions against abnormal cardiac electrophysiologic mechanisms produced by myocardial
ischemia or infarction. Halothane, enflurane, and isoflurane have been shown to
be cardioprotective against ventricular fibrillation produced by coronary artery
occlusion[206]
[207]
and reperfusion.[208]
Protective effects against
ouabain-induced arrhythmias have also been demonstrated during halothane anesthesia.
[209]
Volatile anesthetics may also exert antiarrhythmic
effects by opposing subsidiary pacemaker activity in infarcted myocardium.[199]
Conversely, halothane and, to a lesser extent, isoflurane may be arrhythmogenic
in Purkinje fibers in experimental myocardial infarction by facilitating reentrant
activity or increasing temporal dispersion of refractory period recovery.[199]
[210]
These actions may be related to inhibition
of slow Na+
current in false tendon fibers and induction of reentry of
premature impulses into more refractory Purkinje fibers in the border zone of an
ischemic area.[211]
Halothane, enflurane, and isoflurane
prolong the QTc
interval in humans.[212]
These data suggest that patients with idiopathic or acquired long QT syndrome may
be at greater risk of developing torsade de pointes tachycardia[213]
during anesthesia with these agents.
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