Why the study?
Does nitrous oxide affect central hemodynamics and left ventricular systolic and diastolic performance in patients undergoing coronary artery bypass surgery?
Does nitrous oxide affect central hemodynamics and left ventricular systolic and diastolic performance in patients undergoing coronary artery bypass surgery?
The administration of nitrous oxide during coronary artery bypass surgery may induce regional wall motion abnormalities and diastolic dysfunction following cardiopulmonary bypass.
N2O was associated with hemodynamic depression and post-CPB wall motion changes in CABG; hypothesis-generating for avoidance and outcome impact.
We investigated the effects of nitrous oxide (N2O) on central hemodynamics and left ventricular systolic and diastolic function in 25 patients undergoing coronary artery bypass surgery. All patients were receiving beta-blockers and had good left ventricular function. Global and regional systolic left ventricular performance and diastolic function were determined by computer-assisted analysis of transesophageal echocardiographic (TEE) images, and mitral Doppler flow profiles, respectively. The patients were anesthetized with fentanyl and ventilated with oxygen in air. Hemodynamic and TEE measurements were obtained before and after the introduction of N2O in oxygen (60%/40%), before and after cardiopulmonary bypass (CPB). N2O reduced mean arterial pressure, heart rate, stroke volume, and cardiac output both before and after CPB. Left ventricular global area ejection fraction (GAEF) was not changed by the introduction of N2O, either before or after CPB. N2O induced a significant change in regional wall motion after, but not before CPB, as assessed by the relationship between segmental area ejection fraction (SAEF) and GAEF. Analysis of the mitral flow profile indicated an increase in early diastolic relaxation in the pre-CPB period after introduction of N2O, that was absent in the post-CPB period. We conclude that N2O induces regional wall motion abnormalities and possibly diastolic dysfunction post-CPB.
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Houltz et al. (1995) studied this question.
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