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65 - Rare syndromes, commotio cordis, sudden death in athletes
- from Part VI - Special resuscitation circumstances
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- By Tommaso Pellis, Cardiac Mechano-Electric Feedback Lab, University Laboratory of Physiology, Oxford, UK, Mark Link, Tufts University School of Medicine, Boston, USA, Charles Antzelevitch, Masonic Medical Research Laboratory, Utica, USA, Peter Kohl, The University Laboratory of Physiology, Oxford, UK
- 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 1148-1198
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- Chapter
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Summary
Introduction
Athletes deliberately expose themselves to extreme environments (such as high altitude mountaineering and deep-sea diving) and physical challenges (from weight lifting to marathon running), which may give rise to the manifestation of rare cardiac conditions, or cause sudden death (SD). Indeed, the renowned Athenian long distance runner Pheidippides suffered SD in 490 BC after running from the battlefield of Marathon to Athens to announce the great victory of the Greeks over the invaders.
An analysis of the very dissimilar physical and environmental conditions to which athletes are exposed, and related health risks, is beyond the scope of this chapter and will not be conducted. Instead, we will focus on SD from cardiac causes.
Incidence
Sudden cardiac death
It is commonly understood, and substantiated by clinical evidence, that regular moderate physical exercise has beneficial cardiovascular effects. Several prospective epidemiological studies consistently associate exercise with a reduced risk of coronary artery disease (CAD) and sudden cardiac death (SCD).
The incidence of SCD in adolescents and young adults (here defined as the age group <35 years) is about 1 in 100 000 per year; this is 100 times less than in the older population (1 in 1000 per year; Fig. 65.1). Predominant causes of SCD in athletes change with age. In those over 35 years of age, the most common etiology is atherosclerotic CAD, often severe and diffuse, even in individuals without known risk factors or symptoms. In contrast, in younger athletes, a variety of cardiac diseases, largely congenital and often rare, account for the majority of SCD.
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
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 395-416
-
- Chapter
- Export citation
-
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).