Abstract
The ultimate goal of cardiopulmonary resuscitation (CPR) for the nearly 500,000 victims of sudden death in the United States is to return the victims to long-term and functional survival. Yet of the approximately 39% of victims who are initially resuscitated successfully, as few as 3% represent hospital survivors [1, 2]. This large fall off in survival reflects what we now recognize as two discrete stages of cardiac resuscitation. The first stage is that of initial resuscitation with re-establishment of a spontaneous circulation. The second is the management of postresuscitation arrhythmias and myocardial failure including a high incidence of recurrent cardiac arrest. We suggest the term postresuscitation myocardial dysfunction for this second stage [3]. These two discrete stages of cardiac resuscitation may therefore call for two distinct therapeutic goals. The first is to restore spontaneous circulation. The second is to secure the effective pumping function of the heart and especially the moderation of dysrhythmic events and myocardial failure.
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References
McGrath RB (1987) In-house cardiopulmonary resuscitation — After a quarter of a century. Ann Emerg Med 16:1365–1368
AHA Medical/Scientific Statement (1991) Improving survival from sudden cardiac arrest: The “Chain of Survival” concept. Circulation 83:1832–1847
Tang W, Weil MH, Sun S et al (1993) Progressive myocardial dysfunction after cardiac resuscitation. Crit Care Med 21:1046–1050
Gazmuri RJ, Weil MH, Bisera J et al (1996) Myocardial dysfunction after successful resuscitation from cardiac arrest. Crit Care Med 24:992–1000
Sun S, Weil MH, Tang W et al (1996) Effect of buffer agents on postresuscitation myocardial dysfunction. Crit Care Med 24:2035–2041
Xie J, Weil MH, Sun S et al (1997) High-energy defibrillation increases the severity of post-resuscitation myocardial dysfunction. Circulation 96:683–688
Tang W, Weil MH, Sun S et al (1995) Epinephrine increases the severity of postresuscitation myocardial dysfunction. Circulation 92:3089–3093
Liberthson RR, Nagel EL, Hirschman JC et al (1974) Prehospital ventricular defibrillation. N Engl J Med 291:317–321
Brown CG, Martin DR, Pepe PE et al (1992) High-Dose Epinephrine Study Group. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. N Engl J Med 327:1051–1055
Stiell IG, Hebert PC, Weitzman BN et al (1992) High-dose epinephrine in adult cardiac arrest. N Engl J Med 327:1045–1050
Brain Resuscitation Clinical Trial II Study Group (1992) A randomized clinical study of calcium-entry blocker (lidoflazine) in the treatment of comatose survivors of cardiac arrest. N Engl J Med 324:1225–1231
Kern BK, Hilwig RW, Rhee KH et al (1996) Myocardial dysfunction after resuscitation from cardiac arrest: An example of global myocardial stunning. J Am Coll Cardiol 28:232–240
De Antonio HJ, Kaul S, Lerman BB (1990) Reversible myocardial depression in survivors of cardiac arrest. Pacing Clin Electrophysiol 13:982–985
Kloner RA, Przyklenk K, Whittaker P (1989) Deleterious effects of oxygen radicals in ischemia/reperfusion. Circulation 80:115–1127
Figueredo VM, Dresdner KP, Wolney AC et al (1991) Postischemic reperfusion injury in the isolated rat heart: effect of ruthenium red. Cardiovasc Res 25:337–342
Bagchi D, Wetscher GJ, Bagchi M et al (1997) Interrelationship between cellular calcium homeostasis and free radical generation in myocardial reperfusion injury. Chem Bio Int 104:65–85
Bolli R (1988) Oxygen-derived free radicals and postischemic myocardial dysfunction (“stunned myocardium”). J Am Coll Cardiol 12:239–249
Murphy JG, Marsh JD, Smith TW (1987) The role of calcium in ischemic myocardial injury. Circulation 75:V–15
Marban E (1991) Myocardial stunning and hibernation. The physiology behind the colloquialisms. Circulation 83:681–688
Opie LH (1989) Reperfusion injury and its pharmacologic modification. Circulation 80: 1049–1062
Burton KP, McCord JM, Ghai G (1984) Myocardial alterations due to free-radical generation. Am J Physiol 246:H776–H783
Burton KP (1988) Evidence of direct toxic effects of free radicals on the myocardium. Free Radical Biol Med 4:15–24
Doherty PW, McLaughlin PR, Billingham M et al (1979) Cardiac damage produced by direct current countershock applied to the heart. Am J Cardiol 43:225–232
Caterine MR, Spencer KT, Pagon-Carlo LA et al (1996) Direct current shock to the heart generates free radicals: An electron paramagnetic resonance study. J Am Coll Cardiol 28: 1598–1609
Kern KB, Hilwig RW, Berg RA et al (1997) Postresuscitation left ventricular systolic and diastolic dysfunction: Treatment with dobutamine. Circulation 95:2610–2613
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© 1999 Springer-Verlag Italia
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Yamaguchi, H., Weil, M.H. (1999). Postresuscitation Myocardial Dysfunction. In: Gullo, A. (eds) Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2145-7_5
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DOI: https://doi.org/10.1007/978-88-470-2145-7_5
Publisher Name: Springer, Milano
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