Bradyarrhythmias arise from (1) failure of impulse initiation (sinoatrial node dysfunction) or (2) impaired electrical conduction (e.g., AV conduction blocks).
SINOATRIAL (SA) NODE DYSFUNCTION
Etiologies are either intrinsic (degenerative, ischemic, inflammatory, infiltrative [e.g., senile 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, sinus pauses, or exit block. In pts with SSS, periods of tachycardia (i.e., atrial fibrillation/flutter) 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. In SSS, treat associated atrial fibrillation or flutter as indicated in Chap. 123.
Impaired conduction from atria to ventricles may be structural and permanent, or reversible (e.g., autonomic, metabolic, drug-related)—see Table 122-1.
TABLE 122-1ETIOLOGIES OF ATRIOVENTRICULAR BLOCK ||Download (.pdf) TABLE 122-1ETIOLOGIES OF ATRIOVENTRICULAR BLOCK
|Carotid sinus hypersensitivity ||Vasovagal |
|Hyperkalemia ||Hypothyroidism |
|Hypermagnesemia ||Adrenal insufficiency |
|Beta blockers ||Adenosine |
|Calcium channel blockers ||Antiarrhythmics (class I and III) |
|Digitalis ||Lithium |
|Endocarditis ||Tuberculosis |
|Lyme disease ||Diphtheria |
|Chagas’ disease ||Toxoplasmosis |
|Syphilis || |
|Congenital heart disease ||Kearns-Sayre syndrome (OMIM #530000) |
|Maternal SLE ||Myotonic dystrophy |
|SLE ||MCTD |
|Rheumatoid arthritis ||Scleroderma |
|Amyloidosis ||Hemochromatosis |
|Sarcoidosis || |
|Lymphoma ||Radiation |
|Mesothelioma ||Catheter ablation |
|Melanoma || |
|Degenerative || |
Coronary Artery Disease
|Acute MI || |
Prolonged, constant PR interval (>0.20 s) (See Fig. 122-1A). May be normal or secondary to increased vagal tone or drugs (e.g., beta blocker, diltiazem, verapamil, digoxin); treatment not usually required.
Bradyarrhythmias. (Modified from BE Sobel, E Braunwald: HPIM-9, p. 1052.)
Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped, then sequence is repeated (See Fig. 122-1B and Fig. 122-1D). 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.
Fixed PR interval with occasional dropped beats, in 2:1, 3:1, or 4:1 pattern; the QRS complex is usually wide. 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. 122-1C). 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).
For a more detailed discussion, see Spragg DD, Tomaselli GF: The Bradyarrhythmias: Disorders of the Sinoatrial Node, Chap. 274, p. 1466; and Chap. 275, and Spragg DD, Tomaselli GF: The Bradyarrhythmias: Disorders of the Atrioventricular Node, p. 1470, in HPIM-19.