title: 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.
mesh_terms: D001281:Atrial Fibrillation / Q000209:etiology; D001919:Bradycardia / Q000503:physiopathology* / Q000628:therapy; D002302:Cardiac Output; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D006325:Heart Atria / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D010100:Oxygen / Q000097:blood; D012804:Sick Sinus Syndrome / Q000503:physiopathology / Q000628:therapy; D013318:Stroke Volume
chemical_list: D010100:Oxygen