Kürkciyan et al1 have written an interesting and very informative article demonstrating the high mortality associated with cardiac arrest caused by pulmonary embolism (PE). They believe that a mechanism involving obstruction of pulmonary circulation and liberation of vasoconstrictive mediators increases right ventricular afterload and leads to cardiogenic shock. Indeed, the development of right-sided heart failure and circulatory shock as a result of a massive increase in pulmonary vascular resistance is a medical emergency and requires prompt management. The therapy of this condition may include surgery or the administration of thrombolytics. However, there is recent evidence supporting the use of inhaled nitric oxide (iNO) in the treatment of massive PE. This selective pulmonary vasodilator may attenuate the effects of humoral mediators, such as endothelin,2,3 which are released during PE. In fact, iNO significantly lowered pulmonary artery pressure and increased the cardiac output in cases of severe PE.4,5 Also, my colleagues and I have shown that a low dose of iNO (3 ppm) attenuated the hemodynamic changes and blunted the release of thromboxane A2 (a potent pulmonary vasoconstrictor) after air embolism in dogs.6,7 Although extrapolating these findings to the clinical situation is still a matter of debate, we believe that iNO could partially reverse the circulatory collapse caused by massive PE and should be used as a coadjuvant therapy.
Tanus-Santos JE, Moreno, Jr H. Treatment of Massive Pulmonary Embolism. Arch Intern Med. 2001;161(3):481. doi:
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