The Ventricular Depolarization Gradient: Effects of Exercise, Pacing Rate, Epinephrine, and Intrinsic Heart Rate Control on the Right Ventricular Evoked Response

Abstract

A new pacing technique is described that permits high fidelity recording of the paced ventricular evoked response, including cardiac depolarization. Integration of the paced R wave yields the ventricular depolarization gradient (GD), which is dependent on activation sequence and the spatial dispersion of activation times. GD was studied in 27 dogs to determine the effects of treadmill exercise at fixed rate pacing (n = 10), elevation of heart rate in the absence of stress (n = 20), epinephrine at fixed rate (n = 6), and exercise in the presence of normal chronotrophic response (n = 7). Low level exercise (1 mph, 2 min, 15 degrees) at a fixed heart rate produced significant (P less than 0.0005) decreases in GD that averaged -10.8 +/- 4.0% (mean +/- SD). The rate of change in GD was faster at the onset of exercise than at its cessation (P less than 0.0005). Artificial elevation of heart rate at rest produced significant (P less than 0.0005) increases in GD; mean sensitivity of GD to rate was 0.27 +/- 0.12%/beats/min. Intravenous injection of epinephrine produced significant (P less than 0.001) decreases in GD at two dosage levels (2.5 and 5.0 micrograms/kg) when evaluated at two baseline pacing rates (150 and 190 beats/min); mean changes in GD were -20.64 +/- 0.53% (2.5 micrograms/kg at 150 beats/min), -25.19 +/- 4.20% (5.0 micrograms/kg at 150 beats/min), -14.18 +/- 5.19% (2.5 micrograms/kg at 190 beats/min), and -24.22 +/- 4.94% (5.0 micrograms/kg at 190 beats/min). Sensitivity of GD to epinephrine was dose-dependent (P less than 0.01) at each baseline rate, but was independent (P greater than 0.05) of the rate itself. In the presence of a normal chronotropic response, GD remained unchanged (P greater than 0.5) during exercise in spite of significant elevation in heart rate (105.0 to 167.1 beats/min, P less than 0.001). These data suggest the presence of an intrinsic negative-feedback control mechanism that maintains GD constant in the healthy heart during homeostatic disturbance. Applications in closed-loop rate adaptive pacing are described.

Changes in Evoked QT Intervals According to Variations in Atrioventricular Delay and Cardiac Function in Patients With Implanted QT-Driven DDDR Pacemakers

“…One possibility is that they are dependent on changes in autonomic tone caused by changes in cardiac function. [5][6][7][8][9][10][11] When the AV delay setting is inadequate, the QT interval may be shortened by activation of the sympathetic nervous system. The QT interval may be prolonged when cardiac function is improved by optimizing the AV delay.…”

“…[2][3][4] The amplitude and duration of the T wave are influenced by heart rate and autonomic nervous tone. [5][6][7][8][9][10][11] The ventricular depolarization gradient is inversely dependent on sympathetically mediated stress and directly dependent on pacing rate. 11 Activation of the sympathetic nervous system during exercise causes an increase in heart rate and shortening of the QT interval.…”

“…The QT interval has been used as a sensor for rateresponsive pacing [5][6][7][8][9][10][11] and is measured by an implanted pacemaker as the duration from the ventricular-pace to the T-sense point, which is the steepest point of the intracardiac T wave. [5][6][7][8][9][10] As the optimal AV delay can be predicted from the measurement of the evoked QT interval, automatic setting of the optimal AV delay can be achieved by means of the QT sensor of the implanted pacemaker.…”

Eine neue Methode zur Effektivitätskontrolle in der Herzschrittmachertherapie

“…Ziel und Zweck dieses auch als Effektivitätserken-nung bezeichneten Verfahrens ist es beispielsweise, die lebensbedrohlichen Risiken eines Reizschwellenanstieges auf Grund entzündlicher Reaktionen oder einer Elektrodendislokation zu verringern. Mit Hilfe zweier getrennter Elektroden läßt sich das angestrebte Ziel zwar ohne Schwierigkeiten erreichen [2], bislang sind jedoch alle Anstrengungen gescheitert, die Stimulationselektrode gleichzeitig als Aktuator wie auch als Sensor zu verwenden. Der Grund hierfür liegt in der Polarisierbarkeit elektrochemischer Elektroden.…”

Acute Effects of a Class IA Antiarrhythmic Drug on the Ventricular Evoked Response Amplitude in Patients with Cardiac Pacemakers

“…The evoked response amplitude is the intracardiac depolarization immediately following an effective pacing stimulus [1, 3]. Although the evoked response amplitude has been studied for many years, there is limited information concerning its variability [3, 4].…”