Sevoflurane metabolic effects are seen when approximately 5% of the dose is metabolized by the liver, catalyzed by cytochrome P450 (2E1) enzyme.
While Sevoflurane metabolic effects are studied we see that, it is broken down to hexafluoro isopropanol (HFIP) and fluoride ions. Hexafluoro isopropanol is conjugated with glucuronic acid to form HFIP glucuronide and excreted by the kidneys.
No toxicity has been reported. However, in the presence of sodalime or baralyme it is degraded to various compounds (A to F).
Compound A is produced in larger amounts, it may affect renal function but is not reported clinically. Fresh gas flows should be greater than 2 lit/minute and sodalime should never be dry.
Given below is an extract from Miller’s Anesthesia 7th edition, about Sevoflurane metabolic effects –
The effects of sevoflurane on myocardial contractility have also been shown to be virtually indistinguishable from those produced by isoflurane in dogs.
Sevoflurane caused less myocardial depression than an equivalent halothane MAC in pigs did and produced less myocardial depression than enflurane did in humans as evaluated by echocardiography.
Sevoflurane decreased contractile function to approximately 40% to 45% of control values at 1.75 MAC in the presence and absence of autonomic nervous system tone as determined by regional preload recruitable stroke work in dogs.
This magnitude of myocardial depression agreed with previous data for isoflurane and desflurane in an identical experimental model.
Thus, the vast majority of evidence collected to date indicates that isoflurane, desflurane, and sevoflurane depress the contractile state to similar degrees in normal ventricular myocardium.
All modern volatile anesthetics cause concentration-related decreases in arterial pressure. The mechanism by which these anesthetics reduce arterial pressure differs between anesthetics.
The decreases in arterial pressure produced by halothane and enflurane were attributed to reductions in myocardial contractility and cardiac output, whereas isoflurane, desflurane, and sevoflurane decrease arterial blood pressure primarily as a result of reductions in LV afterload.
Thus, isoflurane, desflurane, and sevoflurane maintain cardiac output because these anesthetics produce less pronounced reductions in myocardial contractility and greater decreases in systemic vascular resistance in humans than halothane or enflurane does.