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The sinoatrial (SA) node serves as the natural pacemaker of the heart and has variable rates in response to parasympathetic and sympathetic stimulation. If the sinus node is dysfunctional or suppressed a subsidiary pacemaker in the atrioventricular node or specialized conduction system will take over leading to a slower junctional or ventricular rhythm. Symptoms of sinus node dysfunction can vary but typically present as fatigue, exercise intolerance, or dyspnea. The diagnostic evaluation includes an investigation into reversible causes of sinus bradycardia, confirmation of sinus node dysfunction with outpatient telemetry monitoring or exercise testing, and possibly cardiac imaging if structural heart disease is suspected. Once irreversible sinus node dysfunction is confirmed, permanent pacemaker implantation is the only reliable therapy for symptomatic bradycardia.
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STRUCTURE AND PHYSIOLOGY OF THE SA NODE
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The SA node region is rather complex in structure. Clusters of myocytes with pacemaker activity are surrounded by fibroblasts, endothelial cells, and transitional cells. These clusters of small fusiform cells in the sulcus terminalis on the epicardial surface of the heart at the right atrial–superior vena caval junction envelop the SA nodal artery. The SA node is structurally heterogeneous, but the central prototypic nodal cells have fewer distinct myofibrils than does the surrounding atrial myocardium, no intercalated disks visible on light microscopy, a poorly developed sarcoplasmic reticulum, and no T tubules. Cells in the peripheral regions of the SA node are transitional in both structure and function. The SA nodal artery arises from the right coronary artery in 55–60% and the left circumflex artery in 40–45% of persons. This feature along with a protective extracellular matrix of connective tissue insulates the SA node from the hyperpolarizing influence of the larger atrium. In addition, the alignment of this complex matrix is associated with nearly unidirectional electrical propagation to the atrium (Fig. 244-1).
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Pacemaker cells spontaneously depolarize in a continuous manner setting the natural rate of depolarization and myocardial contraction. Action potential depolarization in the SA node is normally at a resting rate of 60–100 beats/min. The autonomic nervous system exhibits control over the sinus node, with a preponderance of parasympathetic innervation at baseline. Removal of parasympathetic tone or an increase in sympathetic innervation leads to an increase in rate of depolarization. In denervated hearts, the rate of electrical depolarization (intrinsic heart rate) is approximately 100 beats/min, reflecting the ...