The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart.

Abstract

A B S T R A C T Although ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury, the relationship of QRS complex alterations to the ischemic process is poorly understood. In this study we made a beat-to-beat analysis of the QRS complex in terms of ventricular activation time (CT) and R wave voltage (V) in the acutely ischemic porcine myocardium and analyzed the relationship of these responses to changes in the area of ischemic involvement, altered myocardial energy demands, and plasma [K+]o levels.With the onset of ischemia the QRS complex underwent a specific and reproducible biphasic sequence with an initial decrease in CT and V indicating a transient increase in the conduction velocity of the ischemic tissue. Subsequently both CT and V returned briefly to control and then increased dramatically, now indicating a marked decrease in conduction velocity. The time when CT first began to increase (Tc) was shortened by enlarging the area of ischemia or after an inotropic intervention and was lengthened by decreasing the area of ischemia or with administration of propranolol. Moreover Tc was found to be inversely proportional to plasma [K+]o in the range 3.4-8.8 mM, above which the initial decrease in CT and V was no longer present.We conclude that this biphasic sequence of QRS alterations in early myocardial ischemia is attributable to a progressive leakage of potassium out of the ischemic cells which in turn alters both the time-course and transmural pathway of the activation process through the ischemic tissue. These changes are related to both inotropic state and the area of ischemic involvement. INTRODUCTIONAlthough ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury (1, 2) the relationship of QRS complex alterations to the ischemic process is poorly understood. The casual observations of changes in R wave amplitude noticed by some ST segment investigators after coronary artery occlusion in the dog (3-5) as well as the more specific studies of , Scher (9), and Durrer and van der Tweel (10) in the dog and goat suggest that ischemic QRS complex alterations may bear characteristic temporal and/or spatial relationships to the underlying ischemic process.In the present study we have characterized the temporal sequence of QRS complex alterations during early myocardial ischemia in the intact porcine heart, their modification by changes in the area of ischemic involvement, and altered myocardial energy demands, as well as the important role of potassium in their genesis.

Intramural Foci During Long Duration Fibrillation in the Pig Ventricle

“…(1) Purkinje fibers of pigs extend from the subendocardium almost to the epicardium. 30 (2) Purkinje fibers are more tolerant to the global ischemia during long-duration VF than is the working myocardium. 31 (3) Although the refractory period of Purkinje fibers is longer than that of working myocardium at normal heart rates, it is as short as or shorter than that of working myocardium at the rapid activation rates of VF.…”

The Relationship Between Terminal QRS Complex Distortion and Early Low Dose Dobutamine Stress Echocardiography in Acute Anterior Myocardial Infarction

“…During regional myocardial ischemia, the conduction velocity of the activation wave in the Purkinje fibers is prolonged. 29) Thus, electrical activation of the ischemic zone occurs relatively late. Hence, the terminal vector of the QRS over the ischemic zone is less opposed by activation of the rest of the myocardium.…”

Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks

“…While the Purkinje fibers in pigs traverse the ventricular wall and extend nearly to the epicardial surface, [17][18][19]29 in humans the Purkinje fiber system is limited primarily to the endocardial surface 41,42 . Therefore, transmural Purkinje activation would not be expected in humans.…”

“…[11][12][13][14][15] Previous defibrillation studies have demonstrated that in pigs first postshock activation tends to arise closer to the epicardium than the endocardium.11 , 16 In pigs, Purkinje fibers traverse the ventricular wall and extend nearly to the epicardial surface. [17][18][19] Thus, the subepicardial location of the first recorded post-shock electrical activation in pigs raises the possibility that the earliest post-shock activation arises in the specialized conduction system. As a prerequisite for earliest post-shock activation initiating in the specialized conduction system, we tested the hypothesis that the specialized conduction system is active during the first several post-shock activation cycles following defibrillation shocks near the DFT in strength.…”