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20 - Pharmacology of cardiac arrest and reperfusion
- from Part III - The pathophysiology of global ischemia and reperfusion
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- By Tommaso Pellis, The University Laboratory of Physiology, Oxford, UK, Clinical and Medical Affairs, Biosite Incorporated, San Diego, CA, USA, Jasmeet Soar, The University Laboratory of Physiology, Oxford, UK, Clinical and Medical Affairs, Biosite Incorporated, San Diego, CA, USA, Gavin Perkins, The University Laboratory of Physiology, Oxford, UK, Clinical and Medical Affairs, Biosite Incorporated, San Diego, CA, USA, Raúl J. Gazmuri, The University Laboratory of Physiology, Oxford, UK, Clinical and Medical Affairs, Biosite Incorporated, San Diego, CA, USA
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
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- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 395-416
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- Chapter
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Summary
Introduction
The pharmacology of resuscitation is largely based on anecdotal evidence and descriptive research rather than on objective scientific experimentation. Our understanding of the pharmacokinetics (PK) and pharmacodynamics (PD) of drugs used to resuscitate victims of cardiac arrest is also limited by ethical and experimental constraints.
Animal models of cardiac arrest and cardiopulmonary resuscitation (CPR), jointly with clinical studies, have considerably increased our understanding of the pathophysiology of cardiac arrest and significantly improved our ability to resuscitate victims of cardiac arrest. The great majority of such studies, however, were designed to address interventions to improve resuscitation rather than to investigate the pharmacological profile of drugs used in settings of cardiac arrest and reperfusion. Even less evidence is available on the PK of administration of multiple drugs, a more complex but realistic scenario. During resuscitative efforts, i.e., low flow reperfusion, significant shunting of blood to vital organs occurs. The use of vasopressors in this setting further modifies the patterns of blood flow distribution, in all likelihood affecting the PK of concomitantly administered drugs.
The time from onset of cardiopulmonary arrest until restoration of an effective spontaneous circulation is the single most important determinant of long-term survival and neurological outcome. Prompt initiation of CPR and defibrillation of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) are more likely to alter patient outcome than is pharmacologic management. Nevertheless, treatment with pharmacologic agents is frequently required in patients with VF or VT that is refractory to electrical shocks and in patients with asystole or pulseless electrical activity (PEA).
48 - Prevention and therapy of postresuscitation myocardial dysfunction
- from Part V - Postresuscitation disease and its care
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- By Raúl J. Gazmuri, North Chicago VA Medical Center, IL, USA, Max Harry Weil, Rancho Springs, CA, Karl B. Kern, Tucson, AZ, Wanchun Tang, Palm Springs, CA, Iyad M. Ayoub, North Chicago, IL, Julieta Kolarova, North Chicago, IL, Jeejabai Radhakrishnan, North Chicago, IL
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 829-847
-
- Chapter
- Export citation
-
Summary
Introduction
It is estimated that between 400 000 and 460 000 individuals suffer an episode of sudden cardiac arrest every year in the United States. Yet, the percentage of individuals who are successfully resuscitated and leave the hospital alive with intact neurological function averages less than 10% nationwide. Efforts to restore life successfully are formidably challenging. They require not only that cardiac activity be initially restored but that injury to vital organs be prevented or minimized. A closer examination of resuscitation statistics reveals that efficient Emergency Medical Services systems are able to re-establish cardiac activity in 30% to 40% of sudden cardiac arrest victims at the scene. Yet, close to 40% die before admission to a hospital presumably from recurrent cardiac arrest or complications during transport. Of those admitted to the hospital nearly 60% succumb before discharge, such that only one in four initially resuscitated victims leaves the hospital alive.
Although the causes of postresuscitation deaths have not been systematically investigated, the available information suggests that postresuscitation myocardial dysfunction, hypoxic brain damage, systemic inflammatory responses, intercurrent illnesses, or a combination thereof are the main culprits. The core pathogenic process driving such poor outcome is the intense ischemia of variable duration that organs suffer after cessation of blood flow and the subsequent reperfusion injury that accompanies the resuscitation effort. In addition, the precipitating event of cardiac arrest may also play a role in the postresuscitation phase.