Allen M. Scher

Mechanism of S-T Segment Alteration During Acute Myocardial Injury

Electrocardiograms recorded with a direct-coupled amplifier and recordings of intramyocardial and intracellular potentials were used to determine the nature of the S-T segment shift after myocardial injury. Immediately after coronary artery ligation in the dog, both true S-T and T-Q changes are produced. Lack of responsiveness to the activation wave in the injured area does not account for the initial change in the S-T segment. Changes in the intracellular action potential can be correlated with the electrocardiographic changes. Immediately after injury, cells in the injured area usually repolarize more rapidly than normal cells and this change is significantly correlated with S-T segment shifts. A decrease in resting potential, generally oc curring later than the action potential changes, is similarly correlated with T-Q segment changes.

The Pathway of Ventricular Depolarization in the Dog

Studies of ventricular depolarization with multichannel recording technics permit detailed three dimensional analysis of the process. Activity commences on the mid left septal surface, followed by activity on the right septum. Rapid endocardial excitation follows and leads to endoepicardial activation of the walls. The latest areas activated are in the basal septum. These findings are related to the genesis of the normal QRS. Theories of simultaneous activation and electrocardiographic silent areas are discussed.

Spread of Electrical Activity Through the Wall of the Ventricle

Multipolar recording technics have been employed to record the spread of excitation through the wall of the ventricle. The construction of isochronous planes in a block of tissue aids in visualizing the direction of spread. The results give direct support to the idea of fast endocardial spread followed by syncytial spread through the wall at a slower rate. No evidence is found that the impulse spreads through the individual cardiac muscle bundles.

Factor Analysis of the Electrocardiogram: Test of Electrocardiographic Theory: Normal Hearts

The factor analysis of electrocardiograms from 17 normal individuals indicates that over 95 per cent of all the electrocardiographic “information” is accounted for by 3 factors. In the entire series, all individual leads were more than 93 per cent accounted for by 3 factors. These results indicate that there are no significant voltages at the body surface in normal individuals which can be ascribed to more than 3 internal generators. While these results indicate a 3-function system, they do not indicate a dipolar system since a dipole is a special case of a more general 3-function system.

Ventricular depolarization and the genesis of QRS.

An understanding of electrocardiographic complexes will be achieved when the potential a t a given body-surface point can be predicted from a knowledge of ventricular depolarization and repolarization pathways. To do this for QRS we must have exact information on three factors. First, we must know the time course and magnitude of potential changes across the membranes of the ventricular syncytium as depolarization takes place.’ Second, we must know the pathway of ventricular depolarization. Third, we must understand the basic principles of current flow in volume conductors2 and the modifications of these principles necessitated by the resistive inhomogeneity of the tissues and the irregular shape of the body. The potential Ep a t a given point P in a homogeneous conducting medium is a product (1) of the solid angle fl subtended a t P by the boundary between resting and active tissue, and (2) of the dipole moment per unit area CP across the boundary between resting and active tissue. To determine the solid angle 3, a sphere of radius R is drawn with origin a t P and intersecting all lines from P to the boundary. A is then the area of the sphere within the lines from P to the boundary, and the solid angle is equal to A/RZ. The dipole moment per unit area, CP, is determined by dividing the voltage V across the “cell” membrane by 4 ~ . Then 9 = V / h

The Mechanism of Atrioventricular Conduction

Potentials recorded at various sites in the atrioventricular (A-V) conduction system indicate that conduction is continuously electrical in nature and involves no synapse-like (i.e., chemical) conduction. The region between atrium and atrioventricular node has the slowest conduction velocity (.05 M./sec.) and lowest safety factor. Conduction through the A-V node is at about .12 M./sec. Results demonstrate shapes of potentials recorded extracellularly at various sites within the A-V node, first degree and complete block during rapid atrial stimulation, and echo-like phenomena.

Ventricular excitation in experimental bundle-branch block.

Multipolar recording apparatus has been used to study the pattern of ventricular excitation in experimental bundle-branch block. After block, the wave of activation spreads uniformly from the contralateral ventricle across the septum to the free wall of the homolateral ventricle. Septal activation consumes more time than in the normal. Changes occur in the site and extent of early endocardial activity in the blocked ventricle. Alterations in both septal and mural depolarization contribute to QRS changes. Endocardial depolarization is described during recovery from transient bundle-branch block.

Frequency Analysis of the Electrocardiogram

The frequency analysis of the electrocardiogram reveals that contributions by frequencies of 100 cycles, or higher, per second are less than 10 per cent of the amplitude of the fundamental of the QRS comples, and it thus appears that transistor-driven amplifier-pen recorders presently available are adequate to record all the information contained in the electrocardiogram, if the standard paper speed is doubled, or quadrupled.

Spread of Excitation During Premature Ventricular Systoles

Premature systoles were elicited at many points in the dog heart and the resultant pattern of excitation plotted in detail with a multipolar electrode and a 16-channel oscilloscope. In premature systoles, most of the mural endocardium is excited by a wave travelling at about 1 meter per second. These results indicate that in a normally originating beat the mural endocardium is excited by branched Purkinje tissue, the elements of which conduct at about 1 meter per second. The transmural velocity of the wave of depolarization in premature systoles is about 0.3 meter per second. No evidence was found for intramural penetration of Purkinje fibers. Intramural potentials recorded on stimulation give some insight into normal intramural potentials.

Ventricular excitation in experimental left bundle branch block.

Abstract The pattern and mechanism of ventricular excitation following experimental left bundle branch block was studied in detail by means of a multichannel recording system. After interruption of the main left bundle, the septum is activated from right to left. This depolarization proceeds in orderly fashion with no evidence of intraseptal delay. Single rather than double envelopment of the septum accounts for the septal phases of the prolonged QRS complex. This type of septal activation accounts for more than half the duration of the QRS after LBBB. Mural activation on the blocked side occurs first on the anterior epicardium. The excitation wave apparently reaches this region by muscle conduction across the septum. Initially there is epi-endocardial spread in this region of the mural myocardium. Such a pattern of spread may be one reason why differentiating LBBB and anterior myocardial infarction is sometimes difficult. As the excitation wave proceeds laterally, its direction of spread becomes endo-epicardial. Changes in (1) the earliest activated site, (2) the rate of conduction, (3) the direction of spread, and (4) the sequence of depolarization in the left ventricular wall also contribute to the prolongation of the QRS. The inscription of the QRS complex in a Lead II electrocardiogram is correlated with the order of depolarization. Records from bipolar limb leads further substantiate the similarity between human and canine electrocardiograms.