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(Circulation. 2006;114:e42-e47.)
© 2006 American Heart Association, Inc.

Clinician Update

Acute Pulmonary Embolism

Part II: Treatment and Prophylaxis

Gregory Piazza, MD; Samuel Z. Goldhaber, MD

From the Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center (G.P.), and the Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital (S.Z.G.), Harvard Medical School, Boston, Mass.

Correspondence to Samuel Z. Goldhaber, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail sgoldhaber@partners.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Case presentation: A 66-year-old man with a history of deep venous thrombosis (DVT) presented with acute dyspnea. He was normotensive, with a resting tachycardia of 110 beats per minute and an oxygen saturation of 76% on room air. The only electrocardiographic abnormality was sinus tachycardia. His brain-type natriuretic peptide (BNP) and cardiac troponin levels were elevated. Chest computed tomography (CT) with contrast demonstrated a large saddle pulmonary embolus and increased diameter of the right ventricle (RV) compared with the left ventricle (LV). The patient received intravenous bolus followed by continuous infusion unfractionated heparin. Within several hours, the patient became progressively more hypotensive and hypoxemic. Bedside transthoracic echocardiography (TTE) showed RV dilatation and hypokinesis. He then received intravenous fibrinolysis, with rapid improvement in hemodynamics and oxygenation. What were the clues that he was likely to suffer from progressive hypotension and hypoxemia?

	Risk Stratification

 
Pulmonary embolism (PE) represents a spectrum of syndromes ranging from small peripheral emboli causing pleuritic pain to massive PE resulting in cardiogenic shock or cardiac arrest. Most patients with PE present with normal blood pressure. However, some may rapidly deteriorate and manifest systemic hypotension, cardiogenic shock, and sudden death despite therapeutic levels of anticoagulation. Risk stratification to identify such patients has emerged as a critical component of care.

The history and physical examination provide the starting point for risk stratification. The International Cooperative Pulmonary Embolism Registry (ICOPER) identified age >70 years, cancer, congestive heart failure, chronic obstructive pulmonary disease, and systolic blood pressure less than 90 mm Hg as . . . [Full Text of this Article]

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