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  • Third most common cardiovascular cause of death in the United States.

  • May present with one or more of the following: dyspnea, pleuritic chest pain, hemoptysis, syncope.

  • Tachypnea, tachycardia, hypoxia may be present (alone or in any combination).

  • Risk stratification with clinical scores, cardiac biomarkers, and right ventricular imaging is key for management.


Pulmonary venous thromboembolism (VTE), often referred to as PE, is a common, serious, and potentially fatal result of thrombus formation within the deep venous circulation that then migrates to the pulmonary circulation. PE is the third leading cause of death among hospitalized patients. Management demands a vigilant systematic approach to diagnosis and an understanding of risk factors so that appropriate therapy can be initiated.

Many substances can embolize to the pulmonary circulation, including air (during neurosurgery, from central venous catheters), amniotic fluid (during active labor), fat (long bone fractures), foreign bodies (talc in injection drug users), parasite eggs (schistosomiasis), septic emboli (acute infective endocarditis), and tumor cells (renal cell carcinoma). The most common embolus is thrombus, which may arise anywhere in the venous circulation or right heart but most often originates in the deep veins of the lower extremities. Pulmonary emboli will develop in 50–60% of patients with proximal DVT; half of these embolic events will be asymptomatic. Approximately 50–70% of patients who have symptomatic pulmonary emboli will have lower extremity DVT when evaluated.

Risk factors for PE include venous stasis, injury to the vessel wall, and hypercoagulability (Virchow triad). Venous stasis increases with immobility (obesity, stroke, bed rest—especially postoperative), hyperviscosity (polycythemia), and increased central venous pressures (low cardiac output states, pregnancy). Vessels may be damaged by prior episodes of thrombosis, orthopedic surgery, or trauma. Hypercoagulability can be caused by medications (oral contraceptives, hormonal replacement therapy) or disease (malignancy, surgery) or may be the result of inherited gene defects (factor V Leiden, prothrombin mutation) or acquired thrombophilias (protein C and protein S deficiency, antithrombin deficiency, antiphospholipid antibodies).

PE has multiple physiologic effects. Thrombus occlusion of greater than 20–25% of vascular bed causes right ventricular dilation or dysfunction and increased pulmonary vascular resistance. Vascular obstruction increases physiologic dead space (wasted ventilation) and leads to hypoxemia through right-to-left shunting, decreased cardiac output, and surfactant depletion causing atelectasis.


A. Symptoms and Signs

The clinical diagnosis of PE is notoriously challenging because the clinical symptoms and signs are similar to those of other cardiopulmonary conditions. Dyspnea and chest pain on inspiration are common. Diagnosis primarily relies on clinical prediction scores to calculate the pretest probability of PE. Wells score is most commonly used and quantifies clinical risk assessment, allowing separation of patients into low, intermediate, or high probability groups, or PE-likely versus PE-unlikely groups (Table 9–18).

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