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Learning Objectives

  • The student will be able to describe the clinical symptoms and signs of patients presenting with pulmonary embolism (PE).

  • The student will be able to define the pathophysiology of PE and the risk stratification of patients diagnosed with thromboembolism.

  • The student will be able to evaluate shock and right ventricular dysfunction as a discriminator of outcome during or after PE.

  • The student will be able to provide a stepwise approach to the treatment of patients diagnosed with acute PE.

The anatomical structure of the pulmonary vasculature predisposes to its ability to filter intravascular substances that develop within, or gain access to, the venous circulation. With respect to this filtering function, several clinical syndromes may occur depending upon the nature and quantity of the filtered intravascular materials as well as the physiological reserve of the individual. Although diverse substances including fat, air, amniotic fluid, tumor cells, and septic material can embolize to the lungs, acute pulmonary thromboembolism is the focus of this chapter because of its overwhelmingly predominant frequency and clinical importance.


Pulmonary embolism and deep venous thrombosis (DVT) represent a continuum of the same underlying disorder of venous thromboembolism (VTE), the abnormal intravascular clotting within the venous system. Pulmonary thromboemboli originate from large thrombi in the deep veins of the lower extremities including the iliac, femoral, superficial femoral, and pelvic veins in 75%-90% of cases. The remaining pulmonary thromboemboli arise from venous thromboses of the upper extremities that are commonly associated with central venous or dialysis catheters, cardiac pacing wires, and other devices. Rates of VTE rise with increasing age, with an approximate doubling of risk over each 10-year interval. The estimated annual incidence of PE in the United States exceeds 600,000 cases, causing or contributing to death in up to 200,000 cases each year (Fig. 27.1). Overall, PE is the third most common cause of death in hospitalized patients. Approximately 10% of patients with acute PE die within the first hour. Subjects presenting with hemodynamic instability defined as right ventricular dysfunction and shock have a worse prognosis (Chaps. 28 and 29), and manifest an in-hospital mortality rate as high as 30%, primarily as a result of recurrent embolism. However, accurate diagnosis and effective treatment significantly reduce the mortality rate to 2%-8%.


(a) Of the ~200,000 deaths/yr from PE in the United States, 13,000 occur in patients who received treatment, while 94% of patients who die of PE do not receive treatment because the diagnosis is not made. (b) The relationship of severity and mortality in patients with multiple or severe PE. Adapted from Wood et al. Major pulmonary embolism: review of a pathophysiological approach to the golden hour of hemodynamically significant pulmonary embolism. Chest. 2002;121:877-905.

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