(Circulation. 1997;95:2250-2253.)
© 1997 American Heart Association, Inc.
Articles |
Influence of Inhaled Nitric Oxide on Systemic Flow and Ventricular Filling Pressure in Patients Receiving Mechanical Circulatory Assistance
the Department of Medicine, Cardiology Division (J.M.H.), Johns Hopkins Medical Institutions, Baltimore, Md; the Cardiovascular Division, Boston Medical Center (W.S.C.); and the Department of Anesthesia (S.K.S., S.C.B.), the Respiratory Therapy Division (E.G.), and the Department of Surgery, Division of Cardiac Surgery (G.S.C.), Brigham and Women's Hospital, Boston, Mass.
Correspondence to Joshua M. Hare, MD, Johns Hopkins Hospital, Cardiology Division, 600 N Wolfe St, Carnegie 568, Baltimore, MD 21287-6568. E-mail jhare{at}welchlink.welch.jhu.edu
Background In patients with left ventricular (LV) dysfunction, inhaled nitric oxide (NO) decreases pulmonary vascular resistance (PVR) but causes a potentially clinically significant increase in left atrial pressure (LAP). This has led to the suggestion that inhaled NO may reach the coronary circulation and have a negative inotropic effect. This study tested an alternative hypothesis that LAP increases because of volume shifts to the pulmonary venous compartment caused by NO-induced selective pulmonary vasodilation.
Methods and Results The Thermo Cardiosystems Heartmate is an LV assist device (LVAD) that can be set (by controlling pump rate) to deliver fixed or variable systemic blood flow. Eight patients (between 1 and 11 days after LVAD implantation) were administered inhaled NO (20 and 40 ppm for 10 minutes), and LAP, systemic flow, and pulmonary arterial pressure were measured in both fixed and variable pump flow modes. In both modes, inhaled NO lowered PVR (by 25±6% in the fixed mode, P<.001, and by 21±5% in the variable mode, P<.003). With fixed pump flow, LAP rose from 12.5±1.2 to 15.1±1.4 mm Hg (P<.008). In the variable flow mode, LAP did not increase and the assist device output rose from 5.3±0.3 to 5.7±0.3 L/min (P<.008).
Conclusions A selective reduction in PVR by inhaled NO can increase LAP if systemic flow cannot increase. These data support the hypothesis that with LV failure, inhaled NO increases LAP by increasing pulmonary venous volume and demonstrate that inhaled NO has beneficial hemodynamic effects in LVAD patients.
Key Words: ventricles • heart failure • assist device • vasodilators • hypertension, pulmonary
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