No abstract

The closest analog to propagated excitation of the heart is an electromotive surface. The width of the cardiac electromotive surface was 0.9 ± 0.1 mm and was remarkably constant. The mean epicardial surface component of voltage across the electromotive surface was 62.4 ± 7.2 mv with the chest closed and 74.1 ± 8.3 mv with the chest open. This 18.7% increase is significant ( P < .001) and suggests a shunting effect of the lungs and thorax. Fortuitous measurement of voltage across the electromotive surface yielded nine values in excess of 80 mv and two above 90 mv, suggesting that the true voltage across the electromotive surface is of about the same magnitude as the transmembrane action potential. Cross-fiber activation resulted in a 29.5% reduction in voltage, a 51.8% reduction in conduction velocity and notched QRS complexes. A closed electromotive surface has no external electrical field, suggesting that its voltage is uniform. The voltage between two electrodes, both in advance or toward the rear of a normally propagated open electromotive surface, is caused by an extracardiac current path, since removal of the lung from the epicardial surface greatly reduces this voltage and augments that across the electromotive surface.

The effective refractory period was determined at the surface and in the deeper layers of the dog heart and was correlated with the surface T-waves. A small delay in recovery of cardiac excitability appeared at the surface when T-waves were negative and in the deeper layers when T-waves were positive. Acute injury produced by ligation of the coronary artery caused a marked acceleration of recovery in the deeper layers, sometimes extending to the surface.