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Does adenosine-induced hypotension alter myocardial hemodynamics and metabolism in patients undergoing cerebral aneurysm surgery?
Does adenosine-induced hypotension alter myocardial hemodynamics and metabolism in patients undergoing cerebral aneurysm surgery?
Adenosine-induced hypotension during cerebral aneurysm surgery produces a hyperkinetic circulation, increasing coronary blood flow and cardiac output while reducing myocardial oxygen demand.
Adenosine-induced hypotension may favorably alter myocardial hemodynamics in aneurysm surgery; single case leaves open prospective validation.
The effects of adenosine-induced hypotension on central as well as myocardial hemodynamics and metabolism were studied in five neurolept-anesthetized patients without known heart or lung diseases, who were undergoing cerebral aneurysm surgery. Adenosine (217 +/- 32 micrograms.kg-1.min-1) decreased mean arterial pressure 30% from 77 +/- 5 to 54 +/- 3 mm Hg. Cardiac filling pressures and heart rate remained unchanged during hypotension. Adenosine decreased systemic vascular resistance 50 +/- 5% while cardiac index increased 39 +/- 10%. Coronary sinus blood flow increased by 73 +/- 13% from 128 +/- 18 to 224 +/- 36 ml/min with a concomitant decrease in calculated coronary vascular resistance (66 +/- 4%). Both systemic and myocardial arteriovenous oxygen content differences decreased, and myocardial oxygen consumption decreased 42 +/- 9%. There were no alterations in myocardial fractional lactate extraction. Arterial plasma renin activity and arterial catecholamine levels were unaffected by hypotension. It is concluded that adenosine hypotension in this group of patients produced a hyperkinetic circulation in the systemic as well as in the myocardial vascular bed. Cardiac output and coronary sinus blood flow increased at the same time as myocardial oxygen consumption decreased.
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Wall et al. (1988) studied this question.
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