Pulseless Electric Activity

Abstract

Sudden cardiac arrest (SCA) remains an important public health challenge. Despite a dramatic decrease in the age-adjusted risk of SCA, the cumulative number of fatal SCAs in the United States remains large. Estimates range from 450 000 fatal SCAs per year; a figure in the range of 300 000 to 370 000 per year is likely the best current estimate.1 SCA appears to account for ≈50% of all cardiovascular deaths,2 and it is estimated that 50% of the SCAs are the first clinical expression of previously undiagnosed heart disease.2,3 Most out-of-hospital cardiac arrests (80%) occur in private homes or other living facilities.4 Electric mechanisms associated with SCA are broadly classified into tachyarrhythmic and nontachyarrhythmic categories, the latter including pulseless electric activity (PEA; formerly referred to as electromechanical dissociation), asystole, extreme bradycardia, and other mechanisms often associated with noncardiac factors (Table). The first approaches to the problem of SCA focused on ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). An early impact on the prevention and treatment of VF and VT was realized in patients with acute coronary syndromes >50 years ago,5 followed by the development of strategies for responding to out-of-hospital cardiac arrest, implantable cardioverter-defibrillators, and defibrillation by lay responders. View this table: Table. Tachyarrhythmic and Nontachyarrhythmic Cardiac Arrest Data from the Seattle emergency rescue system6 and elsewhere7–9 have identified progressive reductions in the number of responses to SCA over 2 to 3 decades. This change was due primarily to a reduction in the number of ventricular tachyarrhythmic events identified by emergency medical services responders. In the Seattle data, the incidences of PEA and asystole had not changed over the 3 decades of observation and therefore have emerged as proportionately more frequent mechanisms than VT/VF. Whether this also reflects the …