The Effect of Nitrous Oxide on Left Ventricular Pump Performance and Contractility in Patients with Coronary Artery Disease: Effect of Preoperative Ejection Fraction

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Abstract

To elucidate the effects of nitrous oxide (N2O) on left ventricular (LV) pump performance and contractility, 28 patients undergoing coronary artery bypass graft surgery were studied, of whom 15 had depressed global LV function at preoperative catheterization. Trans-esophageal echocardiography and simultaneous hemodynamic measurements were used to assess LV preload, afterload, and systolic performance during inhalation of 100% oxygen (O2) and 60% N2O:40% O2. Systolic function indices were expressed as a percent of the predicted value for observed end-systolic stress to provide estimates of LV contractility. In the entire study population, N2O reduced pump performance (cardiac index 2.4 ± 0.8 to 2.2 ± 0.6 L·min−1·m−2; P < 0.02). Heart rate and mean arterial pressure were reduced (67 ± 13 to 64 ± 13, P < 0.01, and 87 ± 9 to 80 ± 15, P < 0.005) as were left and right ventricular stroke work index. Preload, as measured by end-diastolic stress, was unchanged but afterload, as measured by end-systolic stress, tended to decrease (88 ± 31 to 78 ± 28, P = 0.053). In the 13 patients with normal preoperative LV function, mean arterial pressure and LV stroke work index decreased significantly (91 ± 8 to 84 ± 14, P < 0.04, and 40 ± 13 to 34 ± 10, P < 0.04, respectively) and end-systolic stress tended to decrease (P = 0.054). In the depressed LV function group, central venous pressure increased and cardiac index and right ventricular stroke work index decreased (9 ± 3 to 10 ± 4, P < 0.02; 2.2 ± 0.6 to 2.0 ± 0.5, P < 0.01; and 4.3 ± 2.6 to 3.1 ± 1.9, P < 0.02, respectively). Despite decreases in end-systolic stress in both groups, during N2O inhalation differences between the normal and depressed LV function groups became evident with respect to fractional shortening and percent of area change (27 ± 8 vs 18 ± 6%; P < 0.002, and 46 ± 12 vs 33 ± 9%, P < 0.002, respectively) that were not detected during O2 inhalation. In parallel, significant differences in fractional shortening and percent of area change as a percent of that predicted from end-systolic stress during O2 inhalation increased between groups after N2O inhalation (82% vs 62% and 85% vs 66%, both P < 0.005). Thus, inhalation of 60% N2O:40% O2 caused a small but statistically significant reduction in cardiac pump performance, and exacerbated depressed myocardial contractility in patients with depressed preoperative LV function. Although no adverse clinical consequences were observed, assessment of whether newer anesthetic regimens better preserve function of the diseased left ventricle is warranted.

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