INHALED NITRIC-OXIDE IN CARDIAC-FAILURE - VASCULAR VERSUS VENTRICULAREFFECTS

Inhaled nitric oxide (INO) is a powerful and selective pulmonary vasod ilator in pulmonary hypertension, including that related to cardiac di sease. Recently, NO was shown to have a direct negative inotropic acti on on the myocardium, but whether INO can impair left ventricular (LV) function is not known. We administered INO during right heart cathete risation in 10 subjects with LV failure and secondary pulmonary hypert ension. INO was delivered for 10 min at concentrations of 10, 20, and 40 ppm in spontaneous respiration. Average age was 49.9 years (range 1 9-59 years), and mean LV ejection fraction EF (LVEF) was 19.9% (range 15-27%). INO produced an average decrease in pulmonary vascular resist ance (PVR) of 40% as compared with baseline (p < 0.0001) with no signi ficant change in systemic vascular resistance (SVR). There was no sign ificant difference in the haemodynamic response to the three doses of INO. The large decrease in PVR was due mainly to an increase in pulmon ary capillary wedge pressure (PCWP). Cardiac index (CI) rose in 7 pati ents and was unchanged in 2. One patient had a marked increase in PAWP and a marked decrease in CI during administration of INO, which rapid ly reversed after discontinuation of INO. This study demonstrates that the administration of INO to patients with impaired cardiac reserve m ay result in marked increase in ventricular preload with little benefi t to pulmonary pressures. In view of the known in vitro effects of NO and the marked haemodynamic changes demonstrated in response to INO in this study, caution should be exercised when using INO in this popula tion.