Disturbances of Sinoatrial Node Function

Abstract

The spectrum of human cardiac performance is amazingly broad with cardiac output varying 10–20-fold between that measured during the deepest of sleep to that seen at peak of exercise. In large part this tremendous cardiac reserve is modulated both by cardiac contractility as well as the heart rate itself. While many factors can affect contractility, heart rate as almost entirely regulated by the autonomic mediation of the sinoatrial (SA) node pacemaker. While uninhibited enhancement of sympathetic tone can result in normal sinus rates over 200/min in many young health individuals, uninhibited and un hindered parasympathetic (vagal) tone can completely suppress all SA nodal activity, even when there is no intrinsic abnormality of the node itself. Consequently, “SA node dysfunction,” manifested as symptomatic sinus pauses or SA nodal exit block, may not represent true intrinsic SA node disease, but instead, could merely result from dramatic neurogenic influences exerted by the autonomic nervous system (Figure 9-1). Therefore, one of the challenges facing the electrophysiologist in evaluating assumed abnormalities of the SA node is distinguishing between intrinsic SA node disease and functional (physiological) disturbances of SA node function related to extrinsic influences such as the autonomic nervous system.