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(Circulation. 2003;108:2834.)
© 2003 American Heart Association, Inc.

Review: Clinical Cardiology: New Frontiers

Acute Pulmonary Embolism: Part II

Risk Stratification, Treatment, and Prevention

Samuel Z. Goldhaber, MD; C. Gregory Elliott, MD

From the Cardiovascular Division (S.Z.G.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass, and the Department of Medicine (C.G.E.), Pulmonary and Critical Care Division, LDS Hospital and University of Utah School of Medicine, Salt Lake City, Utah.

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

Key Words: thrombosis • embolism • pulmonary heart disease • thrombosis • thrombolysis

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

	Introduction

 
Pulmonary embolism (PE) presents with a wide clinical spectrum, from asymptomatic small PE to life-threatening 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.

View this table: [in this window] [in a new window]   Risk Stratification

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^2a 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 . . . [Full Text of this Article]

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