If possible, discontinuing or modifying the dose of the implicated agent may help stave off the need for permanent pacing. Identifying pharmacologic agents with the potential to exacerbate SND (extrinsic component) is critical. The evaluation and management of patients with symptomatic SND should include a review of the patient's medical regimen. Once the patient is hemodynamically stable, assessment and treatment for any potentially reversible causes should occur, followed by placement of a permanent pacemaker for patients without an identifiable reversible etiology. Unstable patients require immediate pharmacologic therapy and, in most instances, should also receive temporary pacing to increase heart rate and cardiac output. Initial management - The initial management of the patient with symptomatic SND depends on the presence and severity of any signs and symptoms (eg, lightheadedness, presyncope, syncope, dyspnea on exertion or worsening angina) related to the ventricular rate. The higher prevalence of hypertension, coronary artery disease, and atrial fibrillation (AF) in the same group of patients with SND would make it more likely that the pharmacologic regimen of such patients may include beta adrenergic blockers, non-dihydropyridine calcium channel blockers, and antiarrhythmic agents, all of which would potentially exacerbate any underlying SA node dysfunction. The most common of these extrinsic agents are pharmacologic agents. It is important to recognize that there may be an "extrinsic" component to SND compounding the "intrinsic" component inherent to the dysfunctional SA node. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and 'Long-term management' below.) Definitive therapy of irreversible SA node dysfunction requires the implantation of a permanent pacemaker. There is a limited role for pharmacologic intervention in symptomatic and/or hemodynamically unstable sinoatrial (SA) node dysfunction. Specific treatment for the control of symptomatic SND usually involves the implantation of a pacemaker. While some individuals present with frank syncope, patients more commonly report progressive development of symptoms and often equate this with natural aging. In addition, patients with tachycardia-bradycardia syndrome may present with palpitations and other symptoms associated with a rapid heart rate. TREATMENT - Treatment of SND is directed at ameliorating symptoms, which may include lightheadedness, presyncope, syncope, and, less often, dyspnea on exertion or worsening angina. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Definition'.) SND can also be accompanied by AV nodal conduction disturbances and by atrial tachyarrhythmias as part of the tachycardia-bradycardia syndrome. SND may also manifest as chronotropic incompetence with inappropriate heart rate responses to physiologic demands during activity. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation" and "Arrhythmia management for the primary care clinician", section on 'Referral to a specialist'.)ĭEFINITION - SND is a clinical syndrome characterized by chronic sinoatrial (SA) node dysfunction, a sluggish or absent SA nodal pacemaker after electrical cardioversion, and/or depressed escape pacemakers in the presence or absence of atrioventricular (AV) nodal conduction disturbances. The etiologies, clinical manifestations, diagnosis, evaluation, and natural history are discussed in detail separately. The treatment of SND will be reviewed here. (See "Permanent cardiac pacing: Overview of devices and indications".) Treatment of SND is directed at symptoms and typically involves the implantation of a permanent pacemaker. Different forms of SND exist electrophysiologically from inappropriate sinus bradycardia, chronotropic incompetence, sinus pauses, SA exit block and the tachycardia-bradycardia syndrome. The occasional patient may be identified during a standard ECG or ambulatory ECG monitoring performed for another indication. The initial clues to the diagnosis of SND are often derived from taking the history and obtaining a routine electrocardiogram (ECG), though the symptoms (eg, fatigue, lightheadedness, palpitations, presyncope, and/or syncope) and ECG findings are frequently vague and nonspecific. INTRODUCTION - Sinus node dysfunction (SND), also historically referred to as sick sinus syndrome, is characterized by dysfunction of the sinoatrial (SA) node that is often secondary to senescence of the SA node and surrounding atrial myocardium.
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