Transthoracic impedance does not decrease with rapidly repeated countershocks in a swine cardiac arrest model.
OBJECTIVE
Successful defibrillation is dependent upon the delivery of adequate electrical current to the myocardium. One of the major determinant of current flow is transthoracic impedance. Prior work has suggested that impedance falls with repeated shocks during sinus rhythm. The purpose of this study was to evaluate changes in transthoracic impedance with repeated defibrillation shocks in an animal model of cardiac arrest due to ventricular fibrillation (VF).


METHODS
VF was electrically induced in anesthetized swine. After 5 min of untreated VF, monophasic or biphasic waveform defibrillation was attempted using a standard sequence of 'stacked shocks' (200, 300, then 360 J, if necessary) administered via adhesive electrodes. If one of the first three shocks failed to convert VF, conventional CPR was initiated and defibrillation (360 J) attempted 1 min later. Strength-duration curves for delivered voltage and current were measured during each shock and transthoracic impedance calculated. Animals requiring a minimum of four shocks were selected for study inclusion. Impedance data from sequential shocks were analyzed using mixed linear models to account for the repeated-measures design and the variability of the initial impedance of individual animals.


RESULTS
Thirteen animals (monophasic waveform, n=7, biphasic waveform, n=6) required at least four shocks to terminate VF (range 4-6). Transthoracic impedance did not change from the first shock in the 13 animals (46+/-8 Omega) to the fourth shock (46+/-9 Omega). In animals receiving more than four shocks, transthoracic impedance likewise did not change significantly from the first to the last shock, which terminated VF. The lack of a significant change in impedance was also observed when animals were analyzed according to defibrillation waveform.


CONCLUSIONS
Transthoracic impedance does not change significantly with repeated shocks in a VF cardiac arrest model. This is likely due to the lack of reactive skin and soft tissue hyperemia and edema observed in non-arrest models.
Niemann
James T
JT
Department of Emergency Medicine, UCLA School of Medicine, Harbor-UCLA Medical Center, Box 21, 1000 West Carson Street, Torrance, CA 90509, USA. jniemann@ucla.edu
Garner
Daniel
D
Lewis
Roger J
RJ
D000818:Animals; D004195:Disease Models, Animal; D004554:Electric Countershock; D017097:Electric Impedance; D006323:Heart Arrest / Q000209:etiology / Q000628:therapy*; D013552:Swine; D013909:Thorax / Q000502:physiology*; D014693:Ventricular Fibrillation / Q000150:complications