VOLATILE ANESTHETICS AND THE CORONARY CIRCULATION
Coronary Vascular Effects In Vitro
Volatile anesthetics can produce direct coronary artery vasodilation
in vitro, but simultaneous reductions in the determinants of myocardial oxygen consumption
(MVO2
), including heart rate, preload,
afterload, and an inotropic state, produced by these agents cause coronary vasoconstriction
in vivo through metabolic autoregulation. Volatile anesthetic-induced alterations
in coronary blood flow also are affected by the reductions in coronary perfusion
pressure produced by these agents. The combination of direct and indirect actions
ultimately determines the net effect of volatile anesthetics on coronary vascular
tone. Halothane, isoflurane, and enflurane cause vasodilation of isolated coronary
arteries.[227]
[228]
[229]
[230]
[231]
[232]
[233]
[234]
Halothane produces greater coronary artery dilation than does isoflurane at equivalent
MACs[228]
[229]
[230]
[232]
[233]
in isolated coronary arteries larger than 2000 µm.[228]
[230]
[231]
[232]
[233]
In contrast, isoflurane causes vasodilation
of predominantly small (<900 µm) canine epicardial coronary arteries.[231]
Halothane may produce greater vasodilator effects in large coronary arteries than
does isoflurane because halothane causes more pronounced suppression of voltage-dependent
Ca2+
current.[235]
The direct negative inotropic effects of volatile anesthetics
cause a reduction in coronary blood flow in isolated, contracting hearts during precise
control of ventricular loading conditions through flow-metabolism coupling.[236]
Under these conditions, a decrease in myocardial oxygen demand is accompanied by
an increase in coronary vascular resistance, findings that may be incorrectly interpreted
as suggesting that volatile agents produce coronary vasoconstriction. However, examination
of the actions of volatile anesthetics on myocardial oxygen extraction and the ratio
of myocardial oxygen delivery to MVO2
reveals that inhalational anesthetics are coronary vasodilators. Halothane and isoflurane
decrease myocardial oxygen extraction and increase the ratio of oxygen delivery to
consumption in isolated, beating hearts.[237]
[238]
[239]
[240]
These
findings indicate that volatile anesthetics produce direct coronary vasodilation
in isolated hearts because myocardial oxygen delivery exceeds MVO2
,
and coronary sinus oxygen tension increases. Halothane, isoflurane, and sevoflurane
cause similar reductions in adenosine-induced coronary flow reserve[241]
in tetrodotoxin-arrested, isolated hearts. Because mechanical work is not performed
in this preparation, these findings support the hypothesis that volatile agents cause
direct coronary vasodilation of similar magnitude.
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