Is there a place for inhaled nitric oxide in the therapy of massive pulmonary embolism?

To the Editor:—Dr. Haddad et al. have written an interesting and informative article regarding the beneficial effects of inhaled nitric oxide (inhaled NO) in perioperative and critical care patients. They believe that inhaled NO causes vasodilation that is proportional to the pulmonary vascular resistance in the presence of pulmonary vasoconstriction. Moreover, they have indicated that the effects of inhaled NO on cardiac function are dependent on the degree of right ventricular dysfunction. We would like to mention recent evidence supporting the idea of using inhaled NO in the therapy of massive pulmonary embolism. Selective pulmonary vasodilator therapy with inhaled NO can attenuate effectively the pulmonary vasoconstriction caused by active mediators, such as endothelin-1 and thromboxane A2, which have been implicated in the pulmonary vasoconstriction and cardiodepression seen in pulmonary embolism. Indeed, inhaled NO blunted thromboxane A2 release, lowered pulmonary artery pressure, and increased cardiac output after massive air embolism in dogs and in four cases of pulmonary embolism. Although extrapolating these findings to the clinical situation is still a matter of debate, we believe that these recent findings support the use of inhaled NO during pulmonary embolism. Finally, it is possible to discontinue administration of inhaled NO if anything untoward happens.