Patients with pulmonary embolism (PE) present with a wide spectrum of clinical acuity that necessitates different therapeutic strategies. Most patients maintain normal systolic arterial pressure and normal right ventricular function. With therapeutic levels of anticoagulation, they will likely have a benign clinical course. Unfortunately, some PE patients suffer rapid clinical deterioration with adverse clinical events, including death from right ventricular failure or the need for cardiopulmonary resuscitation, mechanical ventilation, or administration of pressors for systolic arterial hypotension. Selected patients will benefit from thrombolysis or surgical embolectomy in addition to anticoagulation.1,2 Severe dyspnea, cyanosis, and syncope indicate life-threatening PE. The clinical examination may reveal signs of acute right ventricular dysfunction, including tachycardia, a low arterial blood pressure, distended neck veins, an accentuated P 2, or a tricuspid regurgitation murmur. On the ECG, T-wave inversion or a pseudoinfarction pattern (Qr) in the anterior precordial leads indicates right ventricular dilation and dysfunction.3 Chest computed tomography or magnetic resonance imaging may not only confirm PE but also demonstrate right ventricular dilation. Echocardiography has emerged as the principal tool for risk stratification in acute PE. From a prognostic point of view, echocardiography helps to classify patients with PE into 3 groups: Low-risk PE (no right ventricular dysfunction), with a hospital mortality of <4%, submassive PE (right ventricular dysfunction and a preserved arterial pressure), with a hospital mortality of 5% to 10%, and massive PE (right ventricular dysfunction and cardiogenic shock), with a hospital mortality of approximately 30%.4 Right ventricular dysfunction on the echocardiogram is an independent and powerful predictor of early death in patients with acute PE.5 Indirect signs are systolic pulmonary …