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The acceptable zeros of the potential of the electrical fields produced by certain dipole distributions in homogeneous volume conductors is discussed. A bridge circuit is described by which a solution of the three-arm and the four-arm central terminals of Wilson may be solved for a zero of potential of the field produced by an arbitrary distribution of dipoles in a homogeneous volume conductor. An acceptable zero of potential for evaluation of the potentials in a locus on the "body" surface distant from the heart is described.

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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.

We examined the hypothesis that reversal of hyponatremic hyperkalemic electrocardiographic changes through the infusion of saline solutions was due to the action of sodium ion in increasing the action potential rising velocity which is depressed when the cell is exposed to increasing concentrations of potassium. Using standard microelectrode techniques, the rising velocity of canine ventricular cells was shown to increase by 21%, whereas conduction time between two microelectrodes decreased 17% when the sodium concentration of the perfusate was increased from 120 to 163 mM in 2.7 mM potassium solution. When these cells were exposed to identical increases in sodium concentration in a 7.7-mM potassium solution, rising velocity increased 55% (P less than 0.005), whereas interelectrode conduction time decreased 33% (P less than 0.05). Similar changes were noted in experiments on human ventricular cells. These experimental findings are consistent with the hypothesis stated above.