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Although many intravascular objects can occlude the lung vasculature, this chapter considers pulmonary embolism (PE) to occur from clotted blood. Most PEs originate as clots in large veins, as deep venous thromboses (DVTs). This chapter henceforth employs the term venous thromboembolism (VTE) to include PE, DVT, or both.


PE represents the second leading cause of sudden, unexpected, nontraumatic death in outpatients.1–3 Longitudinal epidemiologic studies have consistently found that PE has an incidence of approximately 1 in 1500 per year; the incidence increases geometrically with age to a maximum of 1 in 300 per year at age 80.4,5 The incidence is slightly higher in women and blacks than in males and whites; the incidence is lowest in Asians and Latinos.6 The rate of PE diagnosis does vary slightly with geography, with an increase in the South, and the frequency appears to increase in cold weather.7,8


Pulmonary emboli occur when a proximal portion of a venous clot breaks off, travels through the veins, traverses the right ventricle, and lodges in the precapillary pulmonary arteries. Patients without prior heart or lung disease begin to experience symptoms from PE when approximately 20% to 30% of lung vasculature becomes occluded. Venous thrombi large enough to cause clinically important PE can form in the popliteal, common femoral, superficial femoral, pelvic, axillary, jugular, and great veins. These thrombi usually form in the proximal recesses of venous valves, where blood flow is slowest. Although 75% to 80% of hospitalized patients with PE have image-demonstrated DVT, only 40% of ambulatory ED patients with PE have concomitant DVT.9


Blood plasma exists in equilibrium between liquid and solid phases. The balance between clot formation and clot removal depends upon multiple influences. Rudolph Virchow in 1846 succinctly described three conditions that promote the formation of dangerous blood clots in the veins: stasis of venous blood flow, tissue damage, and increased tendency for the blood to clot, referred to variously as either hypercoagulability or thrombophilia (“the love of clotting”).


PE alters the patient’s intrapulmonary blood flow, but measuring lung perfusion in the ED is not possible (techniques are seldom available outside of a research laboratory). Hypoxemia is one consequence of ventilation–perfusion (V̇/Q̇) abnormality that can be measured. Most conditions that cause difficulty breathing and hypoxia in ED populations do so by limiting ventilation, and the severity of hypoxemia correlates with the proportion of airways obstructed. In contrast, PE obstructs blood flow, leading to segments of lung with high ventilation relative to perfusion—a condition termed alveolar dead space. Hypoxemia from PE results from redistribution of blood away from the blocked pulmonary arteries and into patent arteries. If PE diverts a large volume of blood into areas of lung with a previously low V̇/Q̇ ratio, then hypoxemia will result. If PE diverts blood into areas of lung with a previously high ventilation–perfusion ratio, then the sum of venous–to–fresh air mixing will increase, and in ...

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