Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.

The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart.

As a result of theoretic advances made during the past 10 years, it is now feasible to record scalar and vector electrocardiograms in a manner which is independent of body shape and cardiac location. A similar independence of the body's electric inhomogeneities has not yet been achieved. On the contrary, the evidence presented here shows that inhomogeneity phases in the body, especially the intracavitary blood mass, exert a powerful influence on the heart-lead relationship. The particular effect of the intracavitary phase is to augment the manifest strength of normal components of myocardial doublets, and to reduce the manifest strength of tangential components. This augmentation-reduction effect is quantitatively predictable under conditions of simple idealization, and has been confirmed by experiments on electrocardiograpic models. The net effect of the intracavitary phase is probably to produce quasi-vectorial registration of the electromotive forces of the heart, at least during the normal depolarizat...

A Theoretical Analysis of Intracavitary Blood Mass Influence on the Heart-Lead Relationship

The distribution of isopotential lines on the thoracic surface of 15 normal subjects aged 15 to 43 was determined at 10 to 20 instants of time during ventricular activation. At the beginning of the QRS interval a precordial maximum and a dorsal minimum of potential can be observed. Thereafter, the minimum migrates toward the right shoulder and appears then anteriorly in the right subclavicular fossa, while another minimum appears near the mid-sternal line. The two minima finally merge together, and the potential distribution becomes dipolar once again. During the last third of the QRS interval the maximum of potential moves toward the left axillary and dorsal region, while a new maximum appears near the upper end of the sternum. A tentative correlation between surface and intracardiac electrical events can be established on the basis of the most generally accepted descriptions of ventricular activation processes. During some phases of ventricular activation, the potential distribution on the surface of the body is of the dipolar type, and there are no measurable local components; during other phases of ventricular depolarization, however, proximity potentials do appear on the thoracic surface, yielding information about local activation waves. When the ventricular activation is altered, the location and time course of local and dipolar potentials show important modifications.

Distribution of Heart Potentials on the Thoracic Surface of Normal Human Subjects

IN RECENT years, a number of review articles devoted entirely or partly to electrical changes and arrhythmias during ischemia and infarction have appeared (Wit and Bigger, 1975; Coraboeuf et al., 1976; Arnsdorf, 1977; Elharrar and Zipes, 1977; Bigger et al., 1977; Wit and Cranefield, 1978; Lazzara et al., 1978; Carmeliet, 1978; Cranefield and Wit, 1979). Most of what is known about cellular electrophysiological changes is derived from experiments on isolated tissue, either excised at different times after coronary artery occlusion, or taken from normal hearts and superfused with solutions altered in such a way as to imitate conditions occurring in ischemic hearts. (Friedman et al., 1973; Lazzara et al., 1974; Cranefield, 1975). The acquisition of electrophysiological data from intact hearts with the same degree of accuracy as in isolated tissue is limited by the techniques available at present. Therefore the description of the mechanisms for arrhythmias and conduction disturbances observed in intact hearts is based mainly on indirect evidence. Most experimental work on ischemia has been conducted in late stages (hours or days) after occlusion. The changes occurring in the very first minutes after coronary occlusion follow a very rapid time course, and a stable electrical situation is not present. Thus anlaysis of the electrophysiological changes in the very early phase of ischemia is hampered by both the technical difficulties of obtaining reliable recordings from intact hearts and by the rapidly changing electrical conditions.

Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

A study was designed to correlate changes in bipolar epicardial electrograms recorded from normal and acutely infarcted myocardium with the onset of ventricular arrhythmias. Electrodes were sewn to selected sites on the left ventricle, and after control electrograms and ECG's were recorded, the left anterior descending coronary artery was doubly ligated close to its origin. Electrograms recorded from within the infarct initially manifested diminished amplitude and increased duration of the deflection which reflected depolarization. The appearance of ventricular arrhythmias during phase 1 of Harris was associated with the appearance in electrograms recorded from within the infarct of continuous electrical activity which extended beyond the T wave of the preceding beat and preceded the onset of the arrhythmia. During the continuous electrical activity, it was not possible to delineate which deflections of the electrogram reflected depolarization or repolarization and it was suggested that the continuous ele...

A Study of Ventricular Arrhythmias Associated with Acute Myocardial Infarction in the Canine Heart

Curves which represent bundle branch block can usually be identified. More important are those which represent peri-infarction block. Multiple unipolar leads enable identification of the latter from the former, which they may closely resemble in the limb leads, and from intraventricular block of other types. Criteria and examples of peri-infarction block are presented and an incidence and explanation are offered.

Peri-infarction block; electrocardiographic abnormality occasionally resembling bundle branch block and local ventricular block of other types.

Changes in left ventricular activation during the first 10 min. following occlusion of the anterior descending branch of the left coronary artery of dogs were studied by using multiple intramural electrodes. Intramural block and an increase in the amplitude of R were observed routinely in the outermost layers of muscle in the central zone of maximal ischemia as long as the occlusion was maintained. The changes were distinct from those produced by left bundle-branch block. Failure to propagate the accession process in normal fashion seems to be characteristic of ischemic heart muscle.

Activation of the Ischemic Ventricle and Acute Peri-Infarction Block in Experimental Coronary Occlusion

The electrocardiographic effects of injury at the endocardial surface of the left ventricle.

“Body surface” potentials produced by the eccentric dipole in the heart wall of the nonhomogeneous volume conductor

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.

Robert H. Bayley

Papers

Peri-infarction block; electrocardiographic abnormality occasionally resembling bundle branch block and local ventricular block of other types.

Activation of the Ischemic Ventricle and Acute Peri-Infarction Block in Experimental Coronary Occlusion

The electrocardiographic effects of injury at the endocardial surface of the left ventricle.

“Body surface” potentials produced by the eccentric dipole in the heart wall of the nonhomogeneous volume conductor

The Zero of Potential of the Electric Field Produced by the Heart Beat: The Problem with Reference to Homogeneous Volume Conductors