Inhaled nitric oxide improves hemodynamics in patients with acute pulmonary hypertension after high-risk cardiac surgery

Severe pulmonary hypertension and right-sided circulatory failure (RSCF) re present an increasing cause of morbidity and mortality in patients undergoi ng high-risk cardiac surgery. Increased pulmonary vascular resistance in th e setting of cardiopulmonary bypass (CPB) may further lead to decreased blo od flow across the pulmonary vascular bed; thereby decreasing left ventricu lar filling and cardiac output. Current management techniques for RSCF incl ude both nonspecific vasodilator and inotropic agents (often limited by sys temic hypotension) and the placement of right ventricular assist devices (a ssociated with increased perioperative morbidity). Inhaled nitric oxide (NO i) represents a novel, specific pulmonary vasodilator that has been proven efficacious in these clinical settings. We evaluated 34 patients in 38 operations who underwent cardiac surgery at Columbia Presbyterian Medical Center, and who received NOi (20 ppm) through a modified ventilatory circuit for hemodynamically significant elevations in pulmonary vascular resistance. Nine patients underwent cardiac transplan tation, three patients bilateral lung transplantation, 16 patients left ven tricular assist device placement and 10 patients routine cardiac surgery. Patients receiving NOi exhibited substantial reductions in mean pulmonary a rtery pressure (mPAP) (34.6 +/- 2.0 to 26.0 +/- 1.7 mmHg, p < 0.0001), with improvements in systemic hemodynamics, mean arterial pressure (68 +/- 3.1 to 75.9 +/- 2.0 mmHg, p = 0.006). In five cases, patients could not be wean ed from CPB until NOi was administered. Patients were maintained on NOi fro m 6 to 240 h postoperatively (median duration 36 h). Inhaled NO induces substantial reductions in mPAP and increases in both car diac index and systemic blood pressure in patients displaying elevated pulm onary hemodynamics after high-risk cardiac surgery. NO is, therefore, a use ful adjunct in these patients in whom acute pulmonary hypertension threaten s right ventricular function and hemodynamic stability.