Page 674 - Cardiac Nursing

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650 PA R T I V / Pathophysiology and Management of Heart Disease
DISPLAY 27-7 Primary and Secondary Prevention of SCD
Primary prevention of SCD is aimed at preventing the first potentials of the QRS complex; (2) T-wave alternans
potentially fatal arrhythmic event. Primary prevention is (TWA) to measure repolarization alternans, variations in
an elusive goal. Trends in SCD events from the Framing- the vector and amplitude of the T wave; and (3) heart
ham Heart study between 1950 and 1999 show a decline rate variability (HRV; see Chapter 17) to measure
in SCD. The decline in SCD in subjects with no prior his- beat–beat variation of the heart rate assessed by ambula-
tory of heart disease suggests benefits from primary pre- tory monitoring. (From Turakhia, M., & Tseng, Z. H.
vention of lifestyle changes. In patients with coronary [2007]. Sudden cardiac death: Epidemiology, mechanisms,
heart disease, increased use of aspirin, -blockers, ACE and therapy. Current Problems in Cardiology, 32, 501–546.)
inhibitor therapy, lipid management aimed at stabilizing There is also accumulating research evidence to suggest
plaque formation, use of antiplatelet and thrombolytic that there is molecular, genetic, and biochemical
therapy, and coronary revascularization, risk stratifi- indicators of SCD. Genetic mutations have been identified
cation of SCD are believed to be responsible for a in individuals with congenital long QT syndrome and Bru-
decrease in sudden and nonsudden cardiac deaths. gada’s syndrome. (From Myerburg, R. J., & Castellanos, A.
(From Fox, C. S., Evans, J. C., Larson, M. G., et al. (2004). (2006). Emerging paradigms of the epidemiology and
Temporal trends in coronary heart disease mortality demographics of sudden cardiac arrest. Heart Rhythm
and sudden cardiac death from 1950 to 1999—The Society, 3, 235–239.)
Framingham Heart Study. Circulation, 110, 522–527.)
AEDs and prehospital interventions including BLS–ACLS Secondary prevention of SCD is aimed at preventing a re-
have been shown to improve survival after cardiac arrest currence of a potentially fatal arrhythmia or cardiac
also contributing to the decline in SCD. (From Fox, C. S., arrest among patients who have survived a sudden car-
Evans, J. C., Larson, M. G., et al. (2004). Temporal trends diac arrest or arrhythmic event. Patients who have expe-
in coronary heart disease mortality and sudden cardiac rienced one sudden cardiac arrest are at high risk for re-
death from 1950 to 1999—The Framingham Heart Study. current cardiac arrest.
Circulation, 110, 522–527.) The ICD is superior to any other treatment and is the only
Several ICD trials have shown that ICD therapy provides pri- evidence-based therapeutic strategy for secondary
mary protection in a well-defined high-risk subgroup of pa- prevention. Three randomized trials—The Antiarrhythmic
tients. The MADIT II Trial, for patients with prior myocar- Versus Implantable Defibrillators (AVID), Cardiac Arrest
dial infarction and ejection fraction 0.30, showed a 30% Study Hamburg (CASH), and the Canadian Implantable
reduction in overall mortality compared to “conventional Defibrillator Study (CIDS)—all found the ICD to be supe-
antiarrhythmic therapy.” (From Moss, A. J., Zareba, W., rior to antiarrhythmic drugs.
Hall, W. J., et al. [2002]. For the Multicenter Automatic De- • AVID was terminated early because the overall survival
fibrillator Implantation Trial II investigators. Prophylactic rate, for 3 years, in the ICD group was 32% higher than
implantation of a defibrillator in patients with myocardial the drug group. (From The Antiarrhythmics vs.
infarction and reduced ejection fraction. New England Jour- Implantable Defibrillators (AVID) Investigators (1997). A
nal of Medicine, 346[12], 877–883.) The SCD-HeFT trial re- comparison of antiarrhythmic drug therapy with
sults confirmed the benefit of ICD therapy in both implantable defibrillators in patients resuscitated from
ischemic and nonischemic cardiomyopathy patients with near fatal ventricular arrhythmias. New England Journal of
an ejection fraction 0.35 with a 23% reduction in risk of Medicine, 337, 1576–1583.)
all-cause mortality. (From Bardy, G. H., Lee, K. L., Mark, • The CASH study showed a 23% lower mortality rate in
D. B., et al. (2005). Amiodarone or an implantable the ICD group compared to the patients randomized to
cardioverter defibrillator for congestive heart failure. New amiodarone/ metoprolol. (From Kuck, K. H., Cappato, R.,
England Journal of Medicine, 352, 225–327.) The DEFINITE Siebels, J., et al. (2000). Randomized comparison of
trial showed a trend toward reduced mortality in patients antiarrhythmic drug therapy with implantable defibrilla-
with nonischemic dilated cardiomyopathy who receive an tors in patients resuscitated from cardiac arrest: the Cardiac
ICD for primary prevention. (From Kadish, A., Dyer, A., Arrest Study Hamburg (CASH). Circulation, 102, 748–754.)
Daubert, J. P., et al. (2004). Prophylactic defibrillator • The CIDS trial showed similar results, with a 19% reduction in
implantation in patients with non-ischemic dilated mortality in the ICD group compared to patients taking amio-
cardiomyopathy. New England Journal of Medicine, 350, darone. (From Connolly, S. J., Gent, M., Roberts, R. S., et al.
2151–2158.) (2000). Canadian Implantable Defibrillator Study (CIDS): a ran-
Other tests available to help determine the risk of SCD domized trial of the implantable cardioverter defibrillator
include: (1) signal averaged ECG (SAECG) to measure late against amiodarone. Circulation, 101, 1297–1302.)
Medical Management of Survivors ■ Institute medical therapy to prevent arrhythmia recurrence,
of Cardiac Arrest such as antiarrhythmic drug therapy and correction of underly-
ing abnormalities that may have precipitated the cardiac arrest.
Postresuscitation Goals ■ Institute measures that increase functional neurological out-
■ Provide cardiac and respiratory support for optimal tissue per- comes.
fusion, especially to the brain.
■ Transfer the patient to the nearest appropriately equipped emer- Cerebral Resuscitation
gency department and then to a critical care unit. The primary goal of cardiopulmonary-cerebral resuscitation is to
■ Identify the causes of the arrest. retain healthy brain function. Unfortunately, neurologic recovery