Skip to Main Content


Bradyarrhythmias arise from (1) failure of impulse initiation (sinoatrial [SA] node dysfunction) or (2) impaired electrical conduction (e.g., AV conduction blocks).


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.

TABLE 124-1Summary of Guidelines for Pacemaker Implantation in SA Node Dysfunction


Impaired conduction from atria to ventricles may be structural and permanent, or reversible (e.g., autonomic, metabolic, drug-related)—see Table 124-2.

TABLE 124-2Etiologies of Atrioventricular Block

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.