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

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Abstract
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, CaCI2 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 < .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 ± 4 to 34 ± 8 mm Hg, p < .001). Within 94 ± 53 sec after epinephrine, spontaneous circulation was restored in eight animals. Of the remaining two animals, one succumbed to a pulseless bradyarrhythmia after one countershock and the other to asystole after multiple countershocks for recurrent VF. Electron microscopic changes in myocardial sections were largely consistent with the duration of ischemia, and there was no intracellular calcium accumulation. Dehiscence of the myocardial intercalated discs was seen in the animal that received multiple countershocks. It is concluded that: (a) pacing in postcountershock asystole/bradycardia may produce electrical capture but not effective cardiac contraction, (b) CaCl2 is of limited value in asystole/bradycardia after countershock and does not facilitate electrical-mechanical coupling during pacing, (c) epinephrine is effective in the management of postcountershock asystole/bradycardia, and (d) asystole after multiple countershocks may be of structural origin and not amenable to therapy.

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