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Circulation
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Circulation. 2006;114:2754-2756
doi: 10.1161/CIRCULATIONAHA.106.668095
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(Circulation. 2006;114:2754-2756.)
© 2006 American Heart Association, Inc.


Editorial

Measuring Progress in Resuscitation

It’s Time for a Better Tool

Joseph P. Ornato, MD; Mary Ann Peberdy, MD

From the Departments of Emergency Medicine (J.P.O., A.P.) and Internal Medicine, Cardiology (A.P.), Virginia Commonwealth University, Richmond, Va.

Correspondence to Joseph P. Ornato, MD, Professor and Chairman, Department of Emergency Medicine, Virginia Commonwealth University, 401 N 12th St, Room G248, Richmond, VA 23298. E-mail ornato@aol.com


Key Words: Editorials • arrhythmia • cardiopulmonary resuscitation • fibrillation • registries • resuscitation • ventricles


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

Weisfeldt and Becker1 theorize the existence of 3 physiological phases of resuscitation: electrical, circulatory, and metabolic.1 When cardiac arrest occurs because of ventricular fibrillation (VF), myocardial adenosine triphosphate (ATP) levels begin to fall as fibrillating myocardial cells continue to consume ATP at a nearly normal rate.2 During this first 3 to 4 minutes (electrical phase), prompt defibrillation is often all that is required to restore circulation. Soon thereafter, myocardial ATP stores drop to critical levels, and a defibrillation shock will usually terminate ventricular fibrillation, but this frequently results in either asystole or pulseless electrical activity as cells run out of high-energy phosphate fuel. During this circulatory phase, a brief (90 s to 3 minutes) period of effective chest compression before defibrillation can boost myocardial ATP stores and increase the likelihood that a perfusing rhythm will result after a defibrillation shock.3 If the patient remains in cardiac arrest for >8 to 10 minutes, increased cellular ischemic injury develops. Weisfeldt and Becker1 term this the "metabolic phase" of resuscitation, indicating that additional cellular protective measures will likely be needed to restore vital organ function. Thus, the strategic paradigm for resuscitating VF cardiac arrest victims has evolved from "shock first and often" to a time-critical, orchestrated ballet of high-quality cardiopulmonary resuscitation (CPR), defibrillation, and postresuscitation care.

Article p 2760

This new paradigm highlights the importance of high-quality, minimally interrupted CPR to maximize tissue oxygen delivery and intracellular high-energy phosphate levels. Conventional closed-chest CPR is, at best, imperfect, producing hemodynamic changes similar to those . . . [Full Text of this Article]




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