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
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]