Endocardial and transcutaneous cardiac pacing, calcium chloride, and epinephrine in postcountershock asystole and bradycardias.

Clinically, asystole or a bradyarrhythmia may follow countershock of ventricular fibrillation (VF) in up to 40% of attempts. This study evaluated the effects of artificial cardiac pacing, calcium chloride (CaCl2), and epinephrine in postcountershock asystole/bradycardia. Micromanometer catheters were positioned in the aorta (Ao) and right atrium (RA) of ten dogs and VF induced by right ventricular (RV) stimulation. After 2 min of VF, a 400-J countershock was given. In six animals, asystole or a pulseless bradyarrhythmia followed one countershock. In four animals, up to three countershocks were needed to terminate VF and resulted in asystole or a pulseless bradyarrhythmia. Thirty seconds after termination of VF, cardiac pacing was begun in all animals using conventional RV endocardial pacing (RVEP) or a transcutaneous transthoracic pacing (TTP) technique. RVEP and TTP produced ventricular depolarizations, but electrical capture was never associated with Ao pressure fluctuations. After 2 min of pacing, CaCl2 was given and chest compressions and artificial ventilations (CPR) initiated. CaCl2 had no effect on CPR pressures. After 2 min of CPR, RVEP and TTP were again studied; capture without Ao pressure fluctuations was seen in all animals. Epinephrine was then given and CPR reinstituted. Epinephrine produced a significant increase in CPR Ao systolic pressure (58 +/- 13 to 84 +/- 24 mm Hg, p less than .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 +/- 4 to 34 +/- 8 mm Hg, p less than .001). Within 94 +/- 53 sec after epinephrine, spontaneous circulation was restored in eight animals.(ABSTRACT TRUNCATED AT 250 WORDS)