Patient outcomes following defibrillation with a low energy biphasic truncated exponential waveform in out-of-hospital cardiac arrest.

PRIMARY OBJECTIVE

To determine the outcome of patients with out-of-hospital cardiac arrest and ventricular fibrillation as the presenting rhythm while using automated external defibrillators (AEDs) that delivered non-escalating, impedance-compensated low-energy (150 J) shocks.

MATERIALS AND METHODS

AEDs delivering low-energy biphasic truncated exponential (BTE) shocks were employed in an emergency medical services (EMS) system in which first-arriving personnel - police, firefighters or paramedics - delivered the initial shocks. Patients were classified according to their response to shocks: restoration of sustained spontaneous circulation (ROSC) without need for epinephrine and other advanced life support (ALS) interventions; and ALS, those requiring epinephrine in all instances. The primary end-point was neurologically-intact discharge survival. Secondary end-points were ROSC with shocks only and the call-to-shock time interval.

RESULTS

Of 42 patients with VF arrest treated with BTE shocks, 35 were bystander-witnessed. Of these 35, 14 (38%) regained a sustained ROSC on-scene with shocks only, needing no epinephrine for ROSC. All 14 survived to discharge home. Of the remaining 21 patients needing ALS intervention, only two (9.5%) survived to discharge. Overall, 16/35 patients (46%) survived to discharge home, an outcome comparable to our experience with patients treated with escalating high-energy monophasic waveform shocks.

CONCLUSIONS

Low-energy (150 J) non-escalating biphasic truncated exponential waveform shocks terminate VF in out-of-hospital cardiac arrest with high efficacy; patient outcome is comparable with that observed with escalating high-energy monophasic shocks. Low-energy shocks, in addition to high efficacy, may confer the advantage of less shock-induced myocardial dysfunction, though this will be difficult to define in the clinical circumstance of long-duration VF provoked by a pre-existing diseased myocardial substrate.