Cardiovascular system

All inhalational anesthetic agents depress the myocardium, but cardiac output is maintained with isoflurane because of the substantial reduction in systemic vascular resistance and slight increase in heart rate. Isoflurane decreases vascular tone in all vascular beds, and the decrease in arterial pressure may reduce perfusion to vital organs that already have a compromised circulation. No decrease in arterial pressure or increase in heart rate has been reported at the low concentrations required for sedation. Isoflurane, like all other sedative agents, must be administered carefully in patients who are hypovolemic or have a very unstable cardiovascular system.

Isofurane is a coronary vasodilator, and redistribution of coronary blood flow will occur in the presence of fixed stenotic lesions of the coronary arteries. It has been suggested that this may result in poor endocardial perfusion, the 'coronary steal effect'. However the incidence of myocardial ischemia is not more frequent after isoflurane anesthesia and it is now accepted that inspired concentrations of less than 0.5 per cent isoflurane are safe even in patients with a history of coronary artery disease (Slogoff.., etal 1991.).

Isoflurane does not predispose the heart to arrhythmias and unlike halothane does not increase the probability of ventricular arrhythmias following administration of either epinephrine (adrenaline) or aminophylline. However, it is possible that interactions may occur with other drugs affecting the heart.

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