Pulmonary embolism (PE) is a relatively common disease, with an estimated annual incidence of 23 cases diagnosed per 100,000 persons in the United States.1
More than 50% of cases are undiagnosed. Untreated PE has a high mortality, although risk for death is reduced significantly with anticoagulation.2
PE refers to obstruction of the pulmonary artery or one of its branches by material (e.g., thrombus, tumor, air, or fat) that originated elsewhere in the body. In this chapter we will discuss PE resulting from thrombus.
Although venous thromboembolism (VTE) is a common disease, underlying pathogenic mechanisms are only partially known, particularly in comparison with those of atherothrombosis. During the past decades, progress was made in the identification and characterization of the cellular and molecular mechanisms that interdependently influence Virchow’s triad. It is now accepted that the combination of stasis and hypercoagulability, much more than endothelial damage and activation, are crucial for the occurrence of venous thrombosis; venous thrombi are mainly constituted by fibrin and red blood cell, and less by platelets.3
Most PEs originate from the deep venous system of lower extremities, iliofemoral veins being the source of most clinically significant PEs; however, upper extremities, pelvic and renal veins, and the right heart, could potentially be the embolic source as well.
After reaching the pulmonary circulation, large thrombi may lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi continue traveling distally and are more likely to produce pleuritic chest pain, presumably by initiating an inflammatory response adjacent to the parietal pleura. Only about 10% of emboli cause pulmonary infarction, usually in patients with preexisting cardiopulmonary disease.
Most patients with acute PE have an identifiable risk factor at the time of presentation.4
Immobilization of only 1 or 2 days may predispose to PE.5
Among patients in whom immobilization was a predisposing factor, 65% were immobilized for more than 2 weeks.6
Other predisposing factors include surgery within the last 3 months, stroke, paresis or paralysis, history of VTE, malignancy, and central venous instrumentation within the last 3 months.4
Additional risk factors identified in women include obesity (BMI ≥29 kg per m2
), heavy cigarette smoking (>25 cigarettes per day), and hypertension.7
The risk for PE in patients hospitalized with heart failure is twice that of hospitalized patients who do not have heart failure, and PE is a frequent cause of death in patients hospitalized with heart disease.8
The lower the ejection fraction, the greater the risk for VTE.10
Based on the clinical presentation, PE can be classified as massive or submassive.
Massive PE causes hypotension, defined as a systolic blood pressure <90 mm Hg or a drop in systolic blood pressure of ≥40 mm Hg from baseline for a period >15 minutes. It is a catastrophic entity that frequently results in acute right ventricular (RV) failure and death. Hypotension results from reduction in cardiac output (CO) owing to increased pulmonary vascular resistance (PVR). PVR is increased from physical obstruction of the vascular bed with thrombus and vasoconstriction, the latter due to the effects of inflammatory mediators and hypoxia. When obstruction of the vascular bed approaches 75%, the right ventricle must generate a systolic pressure in excess of 50 mm Hg and a mean pulmonary artery pressure approximating 40 mm Hg to preserve pulmonary perfusion.11
The normal right ventricle is unable to accomplish this and may eventually fail. Patients with underlying cardiopulmonary disease experience more substantial deterioration in CO than normal individuals.
When death occurs, it is often within 1 to 2 hours of the event, although patients remain at risk for 24 to 72 hours. All acute PEs not meeting the definition of massive PE are considered submassive PE.
A saddle PE is a PE that lodges at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries. Most saddle PEs are submassive. In a retrospective study of 546 consecutive patients with PE, 14 (2.6%) had a saddle PE. Only two of the patients with saddle PE had hypotension.12