![]() If telemetry or Holter monitoring fails to demonstrate bradycardia, then an external or implantable long-term event monitor or a loop recorder is warranted. This is achieved by 24-48 Holter monitor or telemonitoring, depending on the severity of the symptoms. ![]() Given the episodic nature of the disease, diagnosis on 12 lead ECG is unusual and prolonged monitoring to detect and document bradycardic episodes is often indicated. There should be clear documentation of bradycardia that correlates with patient’s symptoms to make a diagnosis of sinus node dysfunction. The first step in evaluating sinus node dysfunction is to exclude reversible causes such as electrolyte abnormalities, metabolic abnormalities, or uncontrolled sleep apnea, and removal of possible offending medications (e.g., beta-blockers, calcium channel blockers). Worsening of angina pectoris or congestive heart failure are also reported. Palpitations are usually felt during episodes of tachycardia, after termination of tachyarrhythmias or due to prolonged pauses. Chronotropic incompetence results in fatigue and exercise intolerance. ![]() Rhythms with AF or atrial flutter pose a significant increased risk of thromboembolism, manifesting as transient ischemic attack or cardioembolic stroke, thus carrying the worst prognosis. Renal and gastrointestinal hypoperfusion may result in oliguria and abdominal pain, respectively. The sudden termination of AF in tachy-brady syndrome typically results in a prolonged sinus pause and failure to return to sinus rhythm which can manifest in syncope. Sinus pauses or severe bradycardia results in central nervous system (CNS) underperfusion which manifests in paroxysmal presyncope or syncope. When symptoms do develop, they are usually attributed to hypo-perfusion to vital organs with high oxygen demand. In the early stages, most patients are asymptomatic. The natural history of sinus node dysfunction is usually a slow progression over decades. Several pharmacologic and toxic substances can produce a similar effect on the SA node these include class I to IV antiarrhythmic medications, digoxin, lithium and sympatholytic medications. Increased intracranial pressure (Cushing’s reflex) also causes bradycardia. Obstructive sleep apnea may cause bradycardia by profound hypoxia during episodes of apnea. Furthermore, metabolic derangements such as hypothyroidism, hyperkalemia, hypokalemia, hypocalcemia, hypoxia, and hypothermia can lead to depression of the pacing function of the SA node. These can occur in conditions where there is abnormally increased vagal tone such as carotid sinus hypersensitivity, vasovagal syncope, and autonomic dysfunction. Several external causes that can affect the pacing function of the SA node. Because the SA node is located within the atrial wall, ischemic injury by atherosclerosis of the arteries feeding the SA node is unusual. Infectious agents such as bacterial endocarditis and Chagas disease commonly result in atrioventricular conduction problems rather than sinus node dysfunction. ![]() Damage to SA node or the sinus nodal artery may occur after cardiothoracic surgery from valve replacement, correction of congenital heart disease or heart transplant. Infiltration of the SA node by sarcoidosis, amyloidosis, hemochromatosis, collagen vascular disease or metastatic cancer results in SA node dysfunction. Heart failure and atrial tachyarrhythmias have been shown to induce cellular remodeling of the sinus node in animal models. Recent studies have identified several mutations in the ion channels explaining familial and congenital forms of sick sinus syndrome. While the most common intrinsic factor leading to sinus node dysfunction is age-related degeneration of the SA node, sinus node dysfunction can be a result of congenital disorders, arrhythmias, infiltrative disorders and surgery. The etiologic factors leading to sinus node dysfunction can be classified into two categories: intrinsic pathology to the sinus node itself, typically results from fibrosis of the nodal tissue and external causes that affect the SA node function.
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