Coronary Vasodilator Reserve and Autoregulation

Coronary vasodilator reserve, defined as the ratio of peak coronary blood flow after brief coronary artery occlusion (e.g., reactive hyperemia) and baseline flow, is affected by halothane and isoflurane.^[262] Coronary vasodilator reserve is greater during isoflurane than during halothane anesthesia.^[262] This observation suggested that halothane may be a more potent coronary vasodilator than isoflurane because greater baseline coronary vasodilation should be accompanied by a reduced ability to increase coronary blood flow further in response to a brief ischemic episode. However, halothane also reduces the determinants of MVO₂ to a greater degree than does isoflurane in vivo. Peak coronary blood flow during reactive hyperemia and percent flow debt repayment are directly related to the intensity of the ischemic stimulus and the magnitude of oxygen debt accrued during coronary artery occlusion. Differences in coronary vasodilator reserve produced by isoflurane and halothane may reflect differences in the intensity of ischemia during coronary occlusion and not the relative vasodilator efficacy of these volatile anesthetics. ^[236]

Dilation of coronary arteriolar resistance vessels by volatile anesthetics alters pressure autoregulation in the coronary vasculature.^[263] Changes in autoregulation produced by vasoactive drugs, including volatile anesthetics, are typically determined by the slope of the pressure-flow curve generated by progressive constriction of a coronary artery. Changes in these pressure-flow curves demonstrate that autoregulation is disrupted during anesthesia in comparison with the conscious state ( Fig. 7-16 ). Isoflurane produces more profound alterations in autoregulation than does halothane or enflurane, as indicated by greater increases in the slope of the pressure-flow relation. Coronary perfusion pressure also plays a more important role in the determination of coronary blood flow during anesthesia. Although volatile anesthetics impair coronary autoregulation to some degree, these agents do not produce the profound degree of coronary vasodilation and inhibition of autoregulation caused by adenosine or dipyridamole.^{[250] [257] [263]} In contrast to volatile agents,

Figure 7-16 A qualitative description of the effects of volatile anesthetics on the coronary blood flow (CBF)-diastolic pressure relationship demonstrates the effect of adenosine-induced maximal coronary vasodilation in awake and anesthetized dogs. Solid lines are mean slopes determined by linear regression analysis. Dashed lines represent the nonlinear portion of the curve and are estimates. When compared with the findings obtained in awake dogs, the anesthetics affect absolute CBF variably but do not increase the slope of the CBF-diastolic pressure plots. (Adapted from Hickey RF, Sybert PE, Verrier ED, Cason BA: Effects of halothane, enflurane, and isoflurane on coronary blood flow autoregulation and coronary vascular reserve in the canine heart. Anesthesiology 68:21–30, 1988.

205