Physiological Pacing: Present Status and Future Developments

Abstract

With the increasing tendency to implant pacemakers not only for life-threatening bradycardias but also for improving cardiodynamics in patients with bradycardia, it soon became apparent that classical VVI pacing is not truly able to optimize circulatory performance. Experience has shown that with ventricular pacing augmentation of cardiac output takes place only initially but is not maintained on a long-term basis, exercise capacity remains markedly reduced, there is only an unsatisfactory influence on the degree and course of heart failure and, in an occasional patient, cardiac function may even deteriorate as compared to the situation prior to pacing. Because the disappointing hemodynamic effect of fixed rate ventricular stimulation was at least partly due to the "unphysiological" mode of pacing provided by those systems which fail to restore AV synchrony and to increase heart rate with changing metabolic requirements, so called physiological pacemakers were developed. These pacing systems either maintain AV-synchrony and/or reestablish some way to adapt the pacing rate (Table I). This study delineates the hemodynamics of the paced heart with special reference to the role of AV relationship and rate control; it describes the clinical experience with physiological pacing and provides some ideas leading to present and future developments for rate adaptive pacing systems.

Atrioventricular Interval Optimization and Exercise Tolerance

“…9,10,[33][34][35][36][37][38][39][40] Cardiac output may increase by nearly 30% in AV synchronous pacing compared to ventricular inhibited single chamber pacing. [41][42][43] However, timing of atrial contraction prior to ventricular systole is an important determinant of cardiac output at rest. The most commonly encountered optimal AV interval in our study was 150 ms with a mean value of 154 6 36 ms. Iwase et al 44 maximal left ventricular filling with an AV interval of 150 ms in patients at rest as assessed by Doppler flow of the mitral valve.…”

Natural History and Predictors of Temporary Epicardial Pacemaker Wire Function in Patients after Open Heart Surgery

“…Whenever possible, AV synchrony should be preserved because of the potential contribution of the atrial contraction to stroke volume [1, 7, 12]. Dual chamber pacemakers offer ‘physiologic’ pacing by maintaining AV synchrony [3]. Earlier models of dual chamber pacemakers operated in an AV sequential (DVI) mode were unable to sense intrinsic atrial events.…”

“…Undersensing of intrinsic atrial events may result in pacemaker discharge during the vulnerable period of the atrium, resulting in atrial fibrillation. Loss of atrial capture may result in a decrease of cardiac output due to loss of AV synchrony [3, 6, 7]. Even though there has been an increase in the use of temporary epicardial pacing wires for AV sequential pacing during open heart surgery in the last decade, to our knowledge there has not been any comprehensive prospective study addressing the reliability and predictors of success of temporary epicardial leads during the postoperative period.…”

“…Temporary cardiac pacing may be required for several days postoperatively to optimize cardiovascular function [1, 2]. The recent increase in the use of temporary dual-chamber demand (DDD) pacemakers mandates adequate sensing and capture of both atrial and ventricular chambers [1, 3]. These wires may also be safely and effectively used for atrial defibrillation and overdrive atrial flutter pace termination after open heart surgery [4, 5].…”

Temporary Cardiac Pacing in the Intensive Care Unit

“…In addition, if retrograde ventriculoatrial conduction is present during ventricular pacing; significant retrograde blood flow into the vena cavae and the pulmonary veins can occur when the atria contract against closed AV valves, further impairing ventricular filling and decreasing cardiac output, as well as causing high pulmonary and central venous pressures. These combined effects may result in a 15 to 20% decrease in stroke volume relative to that in sinus rhythm or with atrial pacing [79][80][81], a decline that may not be significant in indh'iduals with normal cardiac reserve, but may have important hemodynamic consequences in critically ill patients. In the presence of significant diastolic or systolic ventricular dysfunction, loss of AV synchrony may result in even more marked reductions in cardiac output.…”