Large increase in cardiac output in a patient with ARDS and acute right heart failure during inhalation of nitric oxide.

Abstract

Inhaled nitric oxide (NO), a selective pulmonary vasodilator, reduces pulmonary artery pressure in patients with acute respiratory distress syndrome (ARDS). In spite of the reduction of right ventricular afterload, the effect of NO on cardiac output remains unclear. A patient with ARDS and echocardiographically determined severe acute right heart failure was treated with increasing concentrations of inhaled nitric oxide (NO). Haemodynamic and gas exchange variables were determined for each concentration of NO. NO treatment was continued for 3 days. During initial right heart failure, administration of NO resulted in a large increase (32%) in cardiac output in a dose-dependent manner. When right ventricular function had improved, inhalation of NO did not increase cardiac output. Our observations suggest that inhalation of NO is likely to increase cardiac output in ARDS when severe acute right heart failure is present.