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 DysfunctionRemove or treat extrinsic causes such as contributing drugs or hypothyroidism. Otherwise, symptoms of bradycardia respond to permanent pacemaker placement (Table 124-1 Summary of Guidelines for Pacemaker Implantation in SA Node Dysfunction). In SSS, treat associated atrial fibrillation or flutter as indicated in Chap. 125 Tachyarrhythmias. |
Impaired conduction from atria to ventricles may be structural and permanent, or reversible (e.g., autonomic, metabolic, drug-related)-see Table 124-2 Etiologies of Atrioventricular Block.
Prolonged, constant PR interval (>0.20 s) (see Fig. 124-1A. A). May be normal or secondary to increased vagal tone or drugs (e.g., beta blocker, diltiazem, verapamil, digoxin); treatment not usually required.
Mobitz I (Wenckebach)
Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped, then sequence repeats Fig. 124-1B. A. Seen with drug intoxication (digitalis, beta blockers), increased vagal tone, inferior MI. Usually transient, no therapy required; if symptomatic, use atropine (0.6 mg IV, repeated × 3-4) or temporary pacemaker.
Mobitz II
Fixed PR interval (i.e., no progressive lengthening) with occasional dropped beats, e.g., in 2:1, 3:1, or 4:1 pattern; the QRS complex is usually wide (Fig. 124-1C. A). Seen with MI or degenerative conduction system disease; more serious than Mobitz I-may progress suddenly to complete AV block; permanent pacemaker is indicated.
Third Degree (Complete AV Block)
Complete failure of conduction from atria to ventricles; atria and ventricles depolarize independently (see Fig. 124-1D. A). May occur with MI, digitalis toxicity, or degenerative conduction system disease. Permanent pacemaker is usually indicated, except when reversible (e.g., drug-related or appears only transiently in MI without associated bundle branch block).