Pulmonary embolism (PE) is defined as a thrombosis that arises in the venous system and subsequently embolizes to the pulmonary arterial circulation. Despite the advent of modern medical therapies, PE remains a commonly occurring condition associated with significant morbidity and mortality. There is a well-established decreased incidence of PE with appropriate prophylaxis and a significant improvement in patient outcome associated with the prompt institution of appropriate therapy; hence, rigorous screening, early diagnosis, effective thromboprophylaxis, and early therapy are warranted.1 In the United States, it is estimated that 600,000 cases of PE occur each year2 with a mortality rate in the first 3 months after diagnosis of greater than 15%.3 Despite our increased knowledge about the condition and ever-increasing technologic sophistication, mortality rates associated with PE remain high and relatively unchanged over the past half century.4 Additionally, autopsy studies continue to demonstrate that the diagnosis of PE is made less than 50% of the time before death.5 Although specific risk factors have been identified for the occurrence of PE and numerous effective prophylactic regimens have been demonstrated, recent studies show that appropriate prophylactic regimens continue to be significantly underused.6
PE results from the detachment and migration of thrombi fragments that lodge within and obstruct blood flow to a single or multiple areas of the pulmonary vascular bed (Figures 21-1 and 21-2). Pulmonary emboli generally origin from the detachment of deep venous thrombi (DVTs) of the proximal lower extremities accounting for up to 50% of PE.7 Less commonly, deep pelvic veins or proximal upper extremity DVTs associated with central venous catheters are the source of pulmonary emboli.8 PE is, therefore, part of the continuum of venothromboembolism (VTE).
Endarterectomy specimen demonstrating obstruction of pulmonary vascular bed.
Pulmonary angiogram demonstrating large left pulmonary artery filling detect.
A cascade of pathophysiologic mechanisms ensues with the pulmonary embolic event that may lead to hypoxemia and cardiovascular compromise. After traveling to the lung, large thrombi may lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. The anatomical obstruction is the primary insult resulting from the PE. The reduction of the cross-sectional area of the pulmonary arterial bed caused by the embolism has been shown to correlate with the degree of physiologic impairment. Pulmonary arterial pressure generally begins to increase with a 25% to 30% occlusion of the pulmonary vascular bed in otherwise normal heart and lungs9; greater than 50% obstruction is generally present before a clinically significant elevation occurs. Increased right ventricular afterload can cause right ventricular dilatation, hypokinesis, tricuspid regurgitation, and eventual right heart failure.10 A normal right ventricle can fail with acute increases ...