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Challenges in Clinical Electrocardiography
January 19, 2021

Unusual Cause of Cardiac Arrest

Author Affiliations
  • 1University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio
  • 2Division of Cardiovascular Medicine, Department of Medicine, University of Virginia, Charlottesville
  • 3Louis Stokes Cleveland Veterans Affairs Medical Center, Division of Cardiology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio
JAMA Intern Med. 2021;181(4):542-543. doi:10.1001/jamainternmed.2020.8370

A patient in their 40s with a history of remote coronary artery bypass grafting, heart failure with reduced ejection fraction, and poorly controlled insulin-dependent diabetes was admitted to the cardiac intensive care unit with acute decompensated heart failure. The patient’s baseline electrocardiogram (ECG) demonstrated normal sinus rhythm, with normal PR and QRS intervals at 132 and 82 milliseconds, respectively. With poor response to intravenous (IV) diuretics, the patient underwent right heart cardiac catheterization, which demonstrated a low cardiac index, high left ventricular filling pressure, and elevated systemic vascular resistance. The patient’s outpatient use of metoprolol was discontinued, and IV dobutamine (5.0 µg/kg/min) was initiated with continuing aggressive IV diuresis. While defecating on the bedside commode, the patient became lightheaded and unresponsive. The patient’s pulse was barely palpable, and the ECG rhythm showed bradycardia (Figure).

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    1 Comment for this article
    Pharmacology of epinephrine
    Stephan Krahenbuhl, MD, PhD | Clinical Pharmacology & Toxicology, Unversity Hospital Basel, Basel, Switzerland
    Thank you for this instructive article. The authors state that epinephrine is a better choice than atropine to treat this patient due to its positive chronotropic and inotropic effects as well as its vasoconstrictive properties. I agree that epinephrine is a better choice than atropine in this situation, but I disagree with the description of the pharmacological actions of epinephrine. Epinephrine is a beta1 and beta2 sympathomimetic. Stimulation of beta1 adrenoceptors leads to the desired positive chronotropic and inotropic effects, but stimulation of beta2 adrenoceptors causes vasodilation, not constriction. If vasoconstriction is the aim, norepinephrine should be administered, which stimulates beta1 and alpha1 adrenoceptors.