The Next Chapter in the High-Dose Epinephrine Story: Unfavorable Neurologic Outcomes?
- Richard O. Cummins, MD, MPH; and
- Mary Fran Hazinski, RN, MSN
- University of Washington; Seattle, WA 98195 Vanderbilt University; Nashville, TN 37212 Requests for Reprints: Richard O. Cummins, MD, MPH, University of Washington, 1959 NE Pacific, Seattle, WA 98195. Current Author Addresses: Dr. Cummins: University of Washington, 1959 NE Pacific, Seattle, WA 98195.
The standard dose of epinephrine used in cardiopulmonary resuscitation, 1 mg given intravenously every 5 minutes, originated from landmark studies by Redding and Pearson in the 1960s [1, 2]. They studied the effects of 1 mg of epinephrine given to dogs weighing 10 kg and established that epinephrine played a critical role in improving blood flow to the heart and brain during cardiopulmonary resuscitation and in restoring spontaneous circulation. The original American Heart Association (AHA) resuscitation recommendations adopted the 1-mg dose for all patients without adjusting for the obvious weight differences between 10-kg dogs and 70-kg humans. In addition, cardiac surgeons had been using 1 mg of intracardiac epinephrine to restart hearts in the operating room for years [3]. An epinephrine dosage of 1 mg given intravenously every 5 minutes seemed to make sense and remained the standard for more than 25 years.
In the 1980s, Brown and colleagues determined that giving 1 mg of epinephrine to a 70-kg patient was no more than homeopathic and should produce little if any effect on blood flow to the heart and brain during cardiopulmonary resuscitation [4-6]. Their dose-response experiments confirmed that the original dose of 0.1 mg/kg used by Redding and Pearson achieved the best hemodynamic effects and should used in human resuscitation.
Persuaded by these animal data, …
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