++
Bradyarrhythmias arise from (1) failure of impulse initiation (sinoatrial [SA] node dysfunction) or (2) impaired electrical conduction (e.g., AV conduction blocks).
+++
SINOATRIAL NODE DYSFUNCTION
++
Etiologies are either intrinsic (degenerative, ischemic, inflammatory, infiltrative [e.g., amyloid], or rare mutations in sodium channel or pacemaker current genes) or extrinsic (e.g., drugs [beta blockers, Ca++ channel blockers, digoxin], autonomic dysfunction, hypothyroidism).
++
Symptoms are due to bradycardia (fatigue, weakness, lightheadedness, syncope) and/or episodes of associated tachycardia (e.g., rapid palpitations, angina) in pts with sick sinus syndrome (SSS).
++
Examine ECG for evidence of sinus bradycardia (sinus rhythm at <60 beats/min) or failure of rate to increase with exercise (chronotropic incompetence), sinus pauses, or exit block. In pts with SSS, periods of tachycardia (i.e., atrial fibrillation/flutter) also occur. Prolonged ECG monitoring (24–48 h Holter, 30-day loop recorder, or long-term implanted monitor) aids in identifying these abnormalities. Invasive electrophysiologic testing is rarely necessary to establish diagnosis.
++
TREATMENT Sinoatrial Node Dysfunction
Remove or treat extrinsic causes such as contributing drugs or hypothyroidism. Otherwise, symptoms of bradycardia respond to permanent pacemaker placement (Table 124-1). In SSS, treat associated atrial fibrillation or flutter as indicated in Chap. 125.
++
++
Impaired conduction from atria to ventricles may be structural and permanent, or reversible (e.g., autonomic, metabolic, drug-related)—see Table 124-2.
++