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Volatile Anesthetics and Ischemic Myocardium

Halothane and isoflurane decrease subendocardial blood flow and myocardial lactate extraction, produce contractile dysfunction, and cause electrocardiographic changes in the presence of a coronary stenosis concomitant with declines in coronary perfusion pressure.[51] [281] [282] Regional ischemia during isoflurane- or halothane-induced reductions in perfusion pressure is functionally indicated by the appearance of paradoxical systolic lengthening and post-systolic shortening.[51] [283] Contractile dysfunction in the region distal to a critical coronary stenosis is more severe during isoflurane anesthesia than during halothane anesthesia, coincident with higher flows in the normal zone and lower flows in the ischemic zone.[282] [284] These findings suggest that coronary vasodilation produced by isoflurane may cause a detrimental redistribution of coronary blood flow away from ischemic myocardium if hypotension is allowed to occur.

The adverse effects of volatile anesthetics on ischemic myocardium are avoided if coronary perfusion pressure is restored. Subendocardial blood flow in the perfusion bed distal to a critical coronary stenosis is reduced during isoflurane-induced declines in arterial pressure, but treatment of hypotension with phenylephrine restores subendocardial blood flow to values observed before the administration of isolflurane. [285] [286] The transmural distribution of coronary blood flow between the subendocardium and subepicardium (endo/epi ratio) decreases during isoflurane anesthesia despite control of arterial pressure. Administration of phenylephrine to maintain arterial pressure at a constant level increases subepicardial blood flow more than subendocardial flow. This increase in subepicardial perfusion accounts for the decline in the endo/epi ratio in the absence of an absolute reduction in subendocardial flow. Restoration of coronary perfusion pressure to baseline levels during isoflurane anesthesia also increases coronary collateral blood flow and normalizes myocardial oxygen tension in the ischemic zone.[256]

Investigations in dogs with steal-prone anatomy (i.e., complete occlusion of a coronary artery with collateral flow from an adjacent vessel having a critical stenosis) have repeatedly demonstrated that isoflurane and halothane do not alter collateral-dependent or ischemic zone myocardial blood flow,[287] [288] [289] [290] [291] endo/epi distribution,[287] [288] or the electrocardiogram[287] when diastolic arterial pressure is held constant. Coronary collateral perfusion is unchanged during isoflurane or halothane anesthesia in dogs at a mean arterial pressure of 50 mm Hg.[292] Coronary steal does not occur in a chronically instrumented canine model of coronary artery disease with isoflurane,[289] [291] halothane,[290] desflurane,[293] or sevoflurane[294] independent of coronary stenosis severity or coronary collateral development.[288] [289] [290] [291] The findings also refute earlier evidence in dogs with amaroid constrictor-induced augmentation of the coronary collateral circulation, suggesting that isoflurane reduces collateral blood flow and causes coronary steal in vivo.[295] These effects of volatile anesthetics are in marked contrast to those obtained with adenosine, a potent coronary vasodilator that produces coronary steal when arterial pressure is maintained at control


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Figure 7-17 Occluded compared with normal and occluded compared with stenotic zone myocardial blood flow in dogs with steal-prone coronary artery anatomy in the conscious state (C), during 1.1 and 1.9 minimum alveolar concentrations (MACs) of isoflurane (I) anesthesia, during adenosine (A) infusions (0.54 and 1.08 mg/min), and during maintenance of heart rate and arterial pressure at conscious values during the highest doses (BP). Isoflurane does not cause coronary steal, in contrast to significant (P < .05 [*]) reductions in blood flow to collateral-dependent myocardium produced by adenosine. (Adapted from Hartman JC, Kampine JP, Schmeling WT, Warltier DC: Actions of isoflurane on myocardial perfusion in chronically instrumented dogs with poor, moderate, or well-developed coronary collaterals. J Cardiothorac Anesth 4:715–725, 1990.)

levels in models of multivessel coronary artery disease ( Fig. 7-17 ).[289] [291] [296]

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