Acute pulmonary embolism: part II: risk stratification, treatment, and prevention.

Pulmonary embolism (PE) presents with a wide clinical spectrum, from asymptomatic small PE to lifethreatening major PE that causes hypotension and cardiogenic shock (Table). Traditionally, our risk assessment is done by gestalt. However, a more precise risk assessment can be obtained by using a formal clinical scoring system, such as the Geneva Prognostic Index.1 The Geneva Prognostic Index uses an 8-point scoring system and identifies 6 predictors of adverse outcome: 2 points each for cancer and hypotension and 1 point each for heart failure, prior deep vein thrombosis (DVT), arterial hypoxemia, and ultrasound-proven DVT. As points accumulate, prognosis worsens. Remarkably, hypoxemia accounts for only 1 of 8 points. Physical examination, ECG, chest radiograph, CT scan, and echocardiogram2 can provide evidence of right ventricular dysfunction, a key prognostic marker of high risk and increased major adverse clinical events. The most recent development in prognostication is the use of biomarkers such as troponin elevation,3 which indicates right ventricular microinfarction, and elevations of pro-B–type natriuretic peptide4 and B-type natriuretic peptide, which indicate right ventricular overload.5,6 On physical examination, general clinical appearance is useful, but young patients may appear deceptively well despite massive PE. Clues to right heart failure include distended jugular veins, an accentuated pulmonic heart sound, and a tricuspid regurgitation murmur. The ECG may show a classic S1Q3T3 pattern but more often will demonstrate a less commonly recognized sign of right ventricular strain, T wave inversion in leads V1 through V4. New incomplete or complete right bundle-branch block is a very useful sign of right ventricular dysfunction. The chest radiograph may show enlarged pulmonary arteries, especially an enlarged right descending pulmonary artery, indicating pulmonary hypertension. Although the chest CT scan is performed primarily to detect or exclude PE, information about right ventricular dilatation can also be gleaned in the phase of the scan in which the right and left ventricles are imaged. If the right ventricle is as large as the left ventricle, then right ventricular dilatation attributable to right ventricular dysfunction can be confidently diagnosed. The echocardiogram is a low-yield diagnostic tool in patients with PE, because it will usually be normal. However, in acutely ill patients, the echocardiogram is quite useful because it can often help differentiate right ventricular dysfunction typical for PE from other catastrophic illnesses, such as pericardial tamponade, dissection of the aorta, and acute myocardial infarction. Among patients in whom the diagnosis of PE is established, the echocardiogram provides rapid and accurate risk stratification. Moderate or severe right ventricular hypokinesis, pulmonary hypertension, a patent foramen ovale, and free-floating right-heart thrombus are markers for a high risk of death or recurrent PE.