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  Consider pulmonary embolism (PE) in patients with complaints of dyspnea, chest pain, hemoptysis, or syncope.

  
  
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  Dyspnea, pleuritic chest pain, or tachypnea is present in 92% of patients with PE.

  
  
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  If PE is considered in the differential, use clinical decision rules (PERC, Wells, Geneva) to help guide decisions regarding the patient work-up.

  
  
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  Consider thrombolytics in hemodynamically unstable patients with confirmed PE.

Pulmonary embolism (PE) is a potentially life-threatening condition associated with a partial or complete obstruction of the pulmonary artery caused by a thrombus that breaks off from a peripheral vein, migrates via the right side of the heart, and lodges in the pulmonary artery circulation. About 90% of emboli originate from venous thrombi in the lower extremities and pelvis. The presence of emboli in the pulmonary vasculature blocks normal blood flow to the lung and increases pulmonary resistance. This, in turn, increases pulmonary artery pressure and right ventricular pressure. When greater than 50% of the vasculature is occluded, the patient experiences significant pulmonary hypertension and acute cor pulmonale. Undetected, this leads to long-term morbidity and death.

PE is the third most common cause of death from cardiovascular disease, with approximately 650,000 cases of PE occurring per year in the United States. The diagnosis is frequently missed, with 30% of cases diagnosed antemortem. Massive PE occurs in only 5% of cases, but has an associated mortality rate of 40%. Overall, mortality is 3–10% if treated and 15–30% if untreated.

History

The classic triad of chest pain, dyspnea, and hemoptysis is present in fewer than 20% of patients. Dyspnea is the most common symptom associated with PE, occurring in up to 80% of confirmed cases, with 67% experiencing rapid onset of shortness of breath. Pleuritic chest pain is present in 52% of patients, but substernal chest pain is present in <20%. Other symptoms include fainting, cough, palpitations, hemoptysis, and calf/thigh pain or swelling.

Risk factors for deep vein thrombosis (DVT) and PE are inherited or acquired and continue to follow Virchow’s triad described in 1856: venous stasis (eg, bed rest >48 hours, long-distance auto or air travel, recent hospitalization), alterations in coagulation (eg, malignancy, previous PE/DVT, pregnancy, or protein C deficiency), and vascular injury (eg, trauma, recent surgery, central lines, IV drug use). Ninety-four percent of all patients with PE have one or more risk factors.

Physical Examination

Tachypnea (≥ 20/min) is one of the most sensitive clinical findings, with a prevalence of 70% in PE confirmed cases. Tachycardia (≥100/min) has a prevalence of 26%. Pulse oximetry is frequently normal in patients with a PE and cannot be used to exclude the diagnosis. Lung examination may be clear or may reveal rales, whereas extremity examination is useful only if signs of a DVT are present. Rectal examination for blood is useful to assess bleeding risk if anticoagulation becomes necessary.

Laboratory

Although many patients with PE are hypoxic (PaO₂ < 80 mmHg), this is not universally true. The A-a gradient can be used as an indirect measure of ventilation-perfusion V/Q abnormalities, although 15% of patients with PE have a normal A-a gradient.

D-dimer is a fibrin degradation product that circulates in a patient with a dissolving fibrin thrombus. It is found in the serum within 1 hour and stops circulating after 7 days. Multiple d-dimer tests exist with varying sensitivities and specificities, but a negative d-dimer test (enzyme-linked immunosorbent assay or turbidimetric) in patients with a low pretest probability implies a risk for PE of less than 1%.

Troponin and brain natriuretic peptide have been studied in the context of PE, and at this time their value may be limited to risk stratification only.

Electrocardiogram

An electrocardiogram (ECG) is useful to rule out a primary cardiac etiology and is neither specific nor sensitive for PE. Approximately 30% of patients with PE have a normal ECG. Sinus tachycardia is present in up to 36% of patients with PE. The classic S1Q3T3 combination of findings (S wave in lead I, Q wave in lead III, and T wave inversion in lead III) is present in <20% of patient with confirmed PE. Right-sided heart strain seen as T-wave inversions in the anterior leads (v1–v4) may be present in massive PE.