INHALED NITRIC-OXIDE LEADING TO PULMONARY-EDEMA IN STABLE SEVERE HEART-FAILURE

The mechanism of increased pulmonary wedge pressure and cardiac output after nitric oxide inhalation is not clear. Nitric oxide is rapidly inactivated by hemoglobin before it can produce systemic effects.3 Thus, selective nitric oxide pulmonary vasodilator effects led to these preliminary results. The hypothesis is that acute reduction in right ventricular afterload caused an acute increment of right ventricular cardiac output. The acute increment of blood return to the impaired left ventricle not associated with reduction in afterload caused the increase in wedge pressure and consequently pulmonary edema. In addition, acute reduction in right ventricular afterload could lead to redistribution of blood volume to pulmonary circulation. The absence of pulmonary edema in these patients in the nitroprusside study reinforces the importance of selective nitric oxide effects in pulmonary circulation. © 1994.