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Thromboembolic disease is derived from Virchow’s triad of alterations in blood flow, vascular endothelial injury, and alterations in constituents of the blood. Risk factors include antithrombin deficiency, protein C deficiency, protein S deficiency, factor V Leiden, prothrombin gene deficiency, non-O ABO blood group, dysfibrinogenemia, elevated factor VIII, elevated factor IX, elevated factor XI, hyperhomocysteinemia, cancer, antiphospholipid syndrome, infection, inflammatory disorders, nephrotic syndrome, obesity, smoking, trauma, surgery, immobilization, central venous catheter, pregnancy, hormonal therapy, and travel.1


Acute pulmonary embolism (PE) causes physical obstruction of blood flow and release of humoral factors such as serotonin, thrombin, and histamine.2 Hypoxic vasoconstriction leads to elevated pulmonary vascular resistance. Increased afterload consequently causes right ventricular dilation, hypokinesis, tricuspid regurgitation, and right heart failure.2 Further dilation of the right ventricle causes leftward bowing of the intraventricular septum. This causes left diastolic dysfunction, with decreased left diastolic filling. Further dilation of the right ventricle causes cardiac ischemia due to decreased subendocardial perfusion.2 Acute pulmonary embolism typically originates from deep venous thrombosis of the lower extremities. Locally, this thrombosis can progress and cause venous congestion and fluid sequestration. This can compromise oxygen delivery to the limb, causing edema, pain, and cyanosis.


The increased use of computed tomography (CT) for evaluation of pulmonary embolism has not shown to improve outcomes and is not cost effective.3-9 Therefore, decision-making tools have been developed to determine patients who will be benefit from additional testing (Table 10-1)10-12.

TABLE 10-1Predictive Criteria for Thromboembolic Disease

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