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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 . . . [Full Text of this Article]