Selected topics: cardiology commentary
Pulmonary embolism with st segment elevation in leads v1 to v4: case report and review of the literature regarding electrocardiographic changes in acute pulmonary embolism1

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Abstract

A 62-year-old man presented to the Emergency Department (ED) after having three short syncopal episodes earlier that day soon after experiencing acute onset of shortness of breath. He had no significant past medical history and was a nonsmoker. Initially in the Emergency Department he was without any complaints, but then became acutely short of breath and hemodynamically unstable and died despite resuscitative efforts. His electrocardiogram showed ST segment elevations in leads V1 to V4, which is consistent with an anteroseptal myocardial infarction. Autopsy revealed that this patient did not have a myocardial infarction, but rather died of a pulmonary embolism (PE). This case demonstrates how a PE can mimic an anteroseptal myocardial infarction on electrocardiogram. This patient’s lack of risk factors for PE also makes this case unusual.

Introduction

Pulmonary embolism (PE) is a condition that is most often a complication of venous thrombosis, usually involving the veins of the lower extremity or pelvis. Risk factors for venous thrombosis include endothelial injury, hypercoagulability of blood, and stasis (1). Electrocardiogram (EKG) changes associated with PE are variable and range from the classic S1Q3T3 pattern to such nonspecific changes as sinus tachycardia. Rarely, a PE presents without any known risk factors and produces an EKG pattern that mimics that of an anteroseptal myocardial infarction. We describe such a case in this case report. Furthermore, autopsy demonstrated that the coronary arteries and myocardium were free of any evidence of infarction, despite the EKG changes suggestive of such an event. The objectives of this case report include (1) a review of the literature pertaining to the various electrocardiographic manifestations of an acute PE; (2) a demonstration of how acute PE may cause dramatic and uncharacteristic changes on the EKG; (3) a reminder to the reader that a PE is a diagnosis that can mimic other medical conditions, particularly, an anteroseptal myocardial infarction; and (4) a reminder of the usefulness of a bedside echocardiogram in distinguishing between the diagnosis of an acute PE and a myocardial infarction.

Section snippets

Case report

A 62-year-old man presented to the Emergency Department (ED) with facial trauma after suffering a syncopal episode of approximately 20 s in duration. His wife found him unconscious on the bathroom floor making gurgling sounds. The patient had an episode of shortness of breath lasting approximately 20 min prior to his fall. The patient had two more syncopal episodes, lasting 10 s each, while waiting for paramedics to arrive. The patient denied having any chest pain, nausea, vomiting, or diarrhea

Discussion

Pulmonary embolism, defined as “the impaction of material into branches of the pulmonary arterial bed,” usually consists of blood clots (thromboemboli). However, they may also consist of neoplastic cells, fat droplets, air bubbles, and other exogenous materials, such as talc, cornstarch particles, or pieces of i.v. catheters (1). The discussion in this article will be limited to thromboembolic causes of PE.

Pulmonary thromboembolism most commonly occurs as a complication of venous thrombosis,

Acknowledgements

We thank Mrs. Juliette Kuylen for technical support and assistance in the French to English translation of Embolies Pulmonaires Et Ischemie Anteroseptale a L’ electrocardiogramme: Piege Diagnostique. A Propos de Deux Cas. (Pulmonary Embolism and Anteroseptal ischemia on electrocardiogram: Diagnosis trap. About two cases.) Revue Medicalede Bruxelles 1999;20:31–4.

References (13)

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Funds for the materials used in preparing this case report were supplied by the LSU Medical School Department of Medicine, Section of Emergency Medicine.

1

Selected Topics: Cardiology Commentary is coordinated by Theodore Chan, MD, of the University of California San Diego Medical Center, San Diego, California and William Brady, MD, of the University of Virginia, Charlottesville, Virginia

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