Jaok Han

Nonuniform Recovery of Excitability in Ventricular Muscle

Recovery of excitability of ventricular muscle was measured at numerous points in exposed dog ventricles at varying distances along six radial axes from a primary point of stimulation. Temporal dispersion of recovery of excitability at various points equidistant from the point of stimulation was minimal after a basic beat but was increased after an early premature beat. The degree of dispersion following a basic beat was increased by stimulation of the cardiac sympathetic nerves, administration of chloroform, ouabain intoxication, administration of higher doses of quinidine, myocardial ischemia, and hypothermia, but it was decreased by administration of sympathomimetic amines.

Adrenergic Effects on Ventricular Vulnerability

Effects of stimulation of the cardiac sympathetic nerves and intravenous administration of sympathomimetic amines on the multiple response or fibrillation threshold (VMRT) and on other properties of the dog ventricles were compared. Stimulation of the cardiac sympathetic nerves decreased the VMRT. Administration of sympathomimetic amines caused a brief decrease in the VMRT followed by a sustained increase. Temporal dispersion of recovery of excitability and the degree of ventricular vulnerability were closely related; the ventricle was more vulnerable to fibrillation when the dispersion was increased. The hyperkalemic effect of epinephrine was not responsible for the observed changes in ventricular vulnerability.

Temporal dispersion of recovery of excitability in atrium and ventricle as a function of heart rate

Abstract Temporal dispersion of recovery of excitability, measured as the range of local refractory period durations at numerous sites on the atrial and ventricular surfaces, was found to be a direct function of the basic cycle length except at very rapid driving frequencies. In the atrium, spontaneous ectopic activity followed early premature stimuli at slow but not at fast driving frequencies. In the ventricle, the fibrillation threshold was significantly lower at slow than at high basic frequencies. It was concluded that spontaneous closely coupled beats occurring at slow ventricular rates in A-V dissociation may result from asynchrony in the repolarization of adjacent excitable units.

Aberrant A-V Impulse Propagation in the Dog Heart: A Study of Functional Bundle Branch Block

Excessive delay and configurational change of ventricular responses to atrial premature beats, previously attributed to dissociation within the A-V node, were shown to be due to functional block of the right bundle branch. It was found that the refractory period (RP) of the right bundle branch often exceeded the functional refractory period (FRP) of the A-V node at slow heart rates, permitting an early premature atrial response to reach the ventricles before recovery of the right bundle. Vagal stimulation and rapid driving frequencies, by delaying the intranodal transit of the premature response, prevented the exposure of bundle branch block. Epinephrine in low doses sometimes facilitated its occurrence. Premature responses initiated in the His bundle in open heart preparations were commonly blocked in the right bundle under conditions in which atrial premature responses were normally propagated to the ventricles. Evidence was obtained in such preparations that the portion of the right bundle system beyond the site of the block was activated retrogradely from the left side. Under certain conditions the retrograde activation process returned to the His bundle and the atrium as an echo.

Mechanisms of ventricular arrhythmias associated with myocardial infarction.

Abstract Ventricular ectopic beats may be generated during acute myocardial infarction as the result of enhanced automaticity in the His-Purkinje system, focal reexcitation due to the flow of current between myocardial fibers which are repolarized at disparate times, or reentry of the impulse induced by local impairment of excitability and conductivity in the ventricular tissues. The ectopic beats occur more frequently when the basic ventricular rate is slow, and the danger of fatal episodes of ventricular fibrillation is also increased at slow ventricular rates. Fibrillation is more likely to be induced by early ectopic beats in the ventricle during myocardial infarction, because the development of sustained ectopic activity and turbulent impulse propagation is facilitated by increased inhomogeneity of the ventricular tissues with respect to excitability and conductivity. The aggressive prevention and treatment of ventricular ectopic beats and bradyarrhythmia was emphasized as one of the most effective means of preventing life-threatening ventricular fibrillation and lowering mortality rates from acute myocardial infarction. The mechanisms of action of various drugs and the efficacy of increased ventricular rates in suppressing ectopic activity were discussed. It was concluded that the artificial pacing of the heart at relatively rapid rates is a valuable adjunct to the measures used in the management of ventricular arrhythmias associated with acute myocardial infarction.

Ventricular vulnerability during acute coronary occlusion

Ventricular fibrillation thresholds were determined by delivering gated trains of pulses to the ventricle, spanning the vulnerable period. The coupling interval of premature beats decreased and the number of subsequent repetitive responses increased with an increase in the intensity of gated stimuli. Although fibrillation thresholds were determined before and during coronary occlusion at an identical site unaffected by ischemia, they were consistently lower in the ventricle with an ischemic area. The decrease in fibrillation threshold resulted because the ventricle with an ischemic area could be fibrillated by premature beats with longer coupling intervals and fewer subsequent repetitive responses. It was concluded that reentrant activity and resulting fibrillation are more likely to be induced in the ventricle with an ischemic area because of the increased irregularity in the propagation of premature impulses. This irregularity is a result of a marked depression of excitability and conduction velocity in the ischemic area. The results emphasize the greater chance that premature ventricular beats will induce fibrillation in patients with myocardial infarction.

The role of local disparity in conduction and recovery time on ventricular vulnerability to fibrillation

Summary In experiments on 16 mongrel dogs, conduction time (CT), local refractory periods (RP), and recovery time (RT) of conducted beats were measured in the ventricles under local coronary perfusion and under systemic intravenous infusion with potassium chloride or epinephrine. The values of these parameters found in the locally perfused and in the non-perfused areas and the degree of local dispersion of these values were correlated with ventricular fibrillation thresholds. Regardless of potassium or epinephrine infusion, ventricular vulnerability to fibrillation was significantly lower with local infusions than with systemic infusions. It was found that changes of CT, RP, and RT in either direction would occur with increased and decreased fibrillation thresholds, and they were not directly correlated to ventricular vulnerability to fibrillation. The local dispersion of these parameters between the perfused and non-perfused areas, however, was always increased when ventricular vulnerability was high, and decreased when ventricular vulnerability was low. These results are strong evidence supporting the importance of local dispersion in excitability. The local dispersion was best represented by local variation in the RT of conducted beats, which under all experimental conditions correlated best with ventricular vulnerability. The other electrophysiological parameters seem to be of importance for the ventricular vulnerability when they contribute to an increased or decreased local dispersion of excitability.

Fibrillation Threshold of Premature Ventricular Responses

The degree of temporal dispersion of recovery of excitability of premature ventricular responses, estimated as the range of local refractory periods at various points on the surface of the right ventricle, is greater within a radius of 10 to 15 mm from the stimulated site than at greater distances. The fibrillation threshold of early premature beats is significantly lower than that of responses initiated in fully excitable tissue. The effect of prematurity on the fibrillation threshold is greater at points near the site of origin of the premature response. The observed spatial and temporal relationships suggest that the fibrillation threshold is related inversely to the degree of asymmetry in the excitable field.

Incidence of ectopic beats as a function of basic rate in the ventricle

Abstract The frequency of development of ventricular ectopic beats was studied at different basic frequencies under conditions which facilitate the induction of ectopic beats and fibrillation in the ventricle. Ectopic beats were more frequently induced by coronary occlusion, sudden elevation of the aortic pressure, and hypothermia when the basic frequency was low. The average time of onset of ectopic beats after the start of coronary occlusion decreased with a decrease in basic frequency. Ectopic beats developed more frequently after the second stimulated responses at slow rates of paired-pulse stimulation. The stimulus strength required to induce such ectopic beats was much lower at slower frequencies of paired-pulse stimulation. The results emphasize the importance of selection of an optimum rate of stimulation.

Sino-Atrial Reciprocation in the Isolated Rabbit Heart

Reciprocal beats between sinus node and atrium were studied in isolated rabbit heart tissue by microelectrode techniques. Early premature atrial responses which entered the sinus node frequently emerged to re-excite the atrium as “echoes.” When the premature atrial beats discharged some but not all nodal areas, the atrial echoes, in turn, appeared to re-enter the sinus node. Repetitive reciprocation involving the sino-atrial circuit was occasionally observed. Anatomic and temporal patterns of excitation at multiple recording sites suggest that “entrance” block and slow conduction of premature impulses within the sinus node may explain the observed reciprocation. The results support the hypothesis that self-sustained reciprocation in a sino-atrial circuit might be responsible for some cases of paroxysmal atrial tachycardia.