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The role of intracardiac volume in controlling electrocardiographic R-wave amplitude changes during acute myocardial ischemia was studied in 24 open-chest dogs. The R-wave amplitude in surface ECG leads 2, V5 and Frank X, Y and Z leads were correlated with hemodynamic, echocardiographic and angiographic changes in a 5-minute circumflex coronary artery ligation and reperfusion model. After coronary ligation, left ventricular end-diastolic diameter and volume increased progressively above control, reached a peak and plateau at 120--130 seconds after ligation and did not return to control levels until more than 5 minutes after release of the occlusion. In contrast, the R-wave amplitude showed a biphasic response to acute ischemia, reaching a nadir (sigma R = 18.2% below control) at 30 seconds after coronary ligation and only subsequently increased to reach a peak (sigma R = 52% above control) at 150 seconds after ligation. In addition, R-wave amplitude returned immediately to control levels within 10 seconds after reperfusion. In six other dogs, both venae cavae were occluded for a 30-second period, beginning 180 seconds after coronary ligation. Although intracardiac volume decreased markedly, R-wave amplitudes increased even more. Thus, the demonstration of discordance between alterations in intracardiac volume and R-wave amplitude in these studies suggests that factors other than intracardiac volume determine R-wave amplitude changes in the course of acute myocardial ischemia.

R-wave amplitude variations during acute experimental myocardial ischemia: an inadequate index for changes in intracardiac volume.