AJP - Heart and Circulatory Physiology, Vol 257, Issue 4 1180-H1183, Copyright © 1989 by American Physiological Society

ARTICLES

Mechanisms responsible for decline in transthoracic impedance after DC shocks

S. J. Sirna, R. A. Kieso, K. J. Fox-Eastham, J. Seabold, F. Charbonnier and R. E. Kerber
Cardiovascular Center, University of Iowa, Iowa City 52242.

To test the hypothesis that tissue hyperemia and edema in the current pathway cause a decrease in transthoracic impedance (TTI) following direct current (DC) shock, the thoracic-skin and skeletal blood flow and blood volume were measured in anesthetized dogs after three 100-J shocks. TTI declined 11% (P less than 0.01) after DC shocks. Blood flow increased 10-fold in skeletal muscle from 0.9 +/- 0.2 to 11.3 +/- 2.6 (SE) ml.100 g-1.min-1 (P less than 0.05). Blood flow did not change outside the current pathway. Blood volume increased in skin in the current pathway from 7.6 +/- 1.5 ml/100 g preshock to 17.5 +/- 2.0 ml/100 g (P less than 0.01) at 60 min after shock; skeletal muscle blood volume did not change. We also determined postshock tissue weight before and after 72 h of drying at 70 degrees C. The percentage decline from wet weight after drying was 68.4 +/- 3.4% in the current pathway vs. 64 +/- 3.8% outside the pathway (P less than 0.05), indicating the tissue in the current pathway was more edematous. Finally, hindlimb edema was induced by deliberate overperfusion. As hindlimb circumference (edema) increased, impedance declined. We conclude that increases in tissue blood flow or tissue blood volume or tissue edema contribute to the decline in transthoracic impedance after DC shock.