During cardiac arrest, global myocardial ischemia accounts for post resuscitation myocardial dysfunction. Based on earlier studies by Ditchey et al (J Am Coll Cardiol 1994) and by Tang et al. (Circulation 1995) we investigated the effects of non specific beta-adrenergic blockade on the outcomes of cardiopulmonary resuscitation (CPR) in an established rat model of cardiac arrest.
Ten Sprague-Dawley rats were randomized to receive either propranolol (1mg/kg) or saline placebo at 15 minutes prior to inducing ventricular fibrillation (VF). VF was untreated for 8 minutes. CPR, including chest compression and mechanical ventilation, was started at 8 minutes and defibrillation was attempted after 6 minutes of CPR.
All animals were successfully resuscitated. Post resuscitation myocardial function, as measured by the rate of left ventricular pressure development at 40 mmHg (dP/dt40), was significantly better after pretreatment with propranolol in comparison with placebo. The number of post resuscitation ectopic ventricular beats was also significantly reduced and, importantly, the duration of survival was significantly increased (TableTable
Duration of survival, dP/dt40 (mmHg/sec) and ventricular premature beats (VPB) after resuscitation.TreatmentdP/dt40 120 min, PRdP/dt40 240Number of VPBDuration of survivalPropranolol5760±540**5450±570**55±28*62±10**Control4870±1604510±39092±3320±17
PR = post resuscitation.**
p=0.05 vs Control).
Non-specific beta-adrenergic receptor blocking agent does not decrease the success of resuscitation but reduces both the severity of post-resuscitation myocardial dysfunction and improves survival of animals resuscitated after prolonged cardiac arrest.
Use of beta-adrenergic bloking agent during cardiopulmonary resuscitation.
G.A. Cammarata, None.