Altered Cardiac Oxygen Extraction, Lactate Production and Coronary Blood Flow After Large Dose Transthoracic DC Countershocks

Although problems such as hypotension and pulmonary edema complicate the use of transthoracic DC countershocks, the mechanisms are not clear. In anesthetized dogs at 1 minute after only two defibrillator shocks there was a brief rise in coronary sinus lactate, exceeding arterial concentrations. Larger rises in lactate were seen after five shocks, indicating myocardial production of lactate. By contrast in eight animals given dummy shocks the heart always extracted lactate. At 2 minutes after five shocks mean myocardial oxygen extraction (6.5 +/- 0.6 mL/100 mL/100 mL blood; n = 4; P < 0.001), and remained so until 3 minutes after shocks, without significant increase in the lipid peroxidation product malondialdehyde in coronary sinus or arterial blood. Great cardiac venous blood flow, measured by thermodilution, rose after five shocks, and the heart rate pressure product also increased at 1-2 minutes. This transient failure of oxygen extraction, in the presence of arterial normoxia, hyperemia, and increased cardiac work, is best accounted for by a central effect of countershocks on myocardial cellular respiration.