Effect of Inhaled Nitric Oxide on Hemodynamics in Lambs with 1½ Ventricle Circulation.

Inhaled nitric oxide (NO) is widely used to treat postoperative pulmonary hypertension in congenital heart disease. It is believed that NO increases cardiac output (CO) by decreasing pulmonary vascular resistance (PVR), leading to increased left ventricular preload. However, the effect of NO on CO in patients with 11/2 ventricle circulation remains unclear. To evaluate this, a superior cavopulmonary (SCP) shunt was constructed in 10 juvenile sheep. A PTFE graft was inserted between the superior vena cava (SVC) and the main pulmonary artery (PA). The SVC was clamped at the right atrial junction to establish a 11/2 ventricle circulation. Flows, pressures, and arterial blood gases were recorded before and during inhalation of NO. Mean arterial pressure (46.6 +/- 5.4 to 44.6 +/- 5.9mm Hg; p = 0.06) and left atrial pressure (4.0 +/- 2.5 to 4.0 +/- 2.3mm Hg; p = 1.0) did not change. Mean PA pressure (13.6 +/- 2.4 to 11.7 +/- 2.9mm Hg; p = 0.006) and PVR (5.47 +/- 2.99 to 4.54 +/- 2.61 Wood Units; p = 0.037) decreased significantly. SVC flow (24.8 +/- 11.3 to 22.0 +/- 9.7ml/min/kg; p = 0.09) did not change, and CO decreased (140.2 +/- 37.2 to 132.1 +/- 39.2ml/min/kg; p = 0.033). Arterial PO2 improved (103.72 +/- 29.30 to 132.43 +/- 47.02mm Hg; p = 0.007). In this 11/2 ventricle model, NO surprisingly decreased cardiac output (CO) and did not increase left ventricular preload.