Harrison’s Manual of Medicine
Preexcitation Syndrome (WPW)
Arrhythmias may appear in the presence or absence of structural heart disease; they are more serious in the former. Conditions that provoke arrhythmias include (1) myocardial ischemia, (2) CHF, (3) hypoxemia, (4) hypercapnia, (5) hypotension, (6) electrolyte disturbances (especially involving K, Ca, and Mg), (7) drug toxicity (digoxin, pharmacologic agents that prolong QT interval), (8) caffeine, (9) ethanol.
DIAGNOSIS Examine ECG for evidence of ischemic changes (Chap. 113), prolonged QT interval, and characteristics of Wolff-Parkinson-White (WPW) syndrome (see below). See Fig. 115-1 for diagnosis of tachyarrhythmias; always identify atrial activity and relationship between P waves and QRS complexes. To aid the diagnosis:
FIGURE 115-1. Tachyarrhythmias. (Reproduced by BE Sobel, E Braunwald: HPIM-9, p. 1052.)
Obtain long rhythm strip of leads II, aVF, or V1. Double the ECG voltage and increase paper speed to 50 mm/s to help identify P waves.
Place accessory ECG leads (right-sided chest, esophageal, right-atrial) to help identify P waves. Record ECG during carotid sinus massage (Table 115-1) for 5 s. Note: Do not massage both carotids simultaneously.
Table 115-1 Clinical and Electrocardiographic Features of Common Arrhythmias
Tachyarrhythmias with wide QRS complex beats may represent ventricular tachycardia or supraventricular tachycardia with aberrant conduction. Factors favoring ventricular tachycardia include (1) AV dissociation, (2) QRS >0.14 s, (3) LAD, (4) no response to carotid sinus massage, (5) morphology of QRS similar to that of previous ventricular premature beats (Table 115-2).
Table 115-2 Wide Complex Tachycardia
Tachyarrhythmias (Table 115-1 and Table 115-3) Precipitating causes (listed above) should be corrected. If pt is hemodynamically compromised (angina, hypotension, CHF), proceed to immediate cardioversion. Note: Do not cardiovert sinus tachycardia; exercise caution if digitalis toxicity is suspected. Initiate drugs as indicated in the tables; follow drug levels and ECG intervals (esp. QRS and QT). Reduce dosage for pts with hepatic or renal dysfunction as indicated in Table 115-3. Drug efficacy is confirmed by ECG (or Holter) monitoring, stress testing, and in special circumstances, invasive electrophysiologic study.
Table 115-3 Antiarrhythmic Drugs
Antiarrhythmic agents all have potential toxic side effects, including provocation of ventricular arrhythmias, esp. in pts with LV dysfunction or history of sustained ventricular arrhythmias. Drug-induced QT prolongation and associated torsades de pointes ventricular tachycardia (Table 115-1) is most common with group IA agents; the drug should be discontinued if the QTc interval (QT divided by square root of RR interval) increases by >25%. Antiarrhythmic drugs should be avoided in pts with asymptomatic ventricular arrhythmias after MI, since mortality risk increases.
Chronic Atrial Fibrillation Evaluate potential underlying cause (e.g., thyrotoxicosis, mitral stenosis, excessive ethanol consumption, pulmonary embolism). Pts with risk factors for stroke (e.g., valvular heart disease, hypertension, CAD, CHF, age >75) should receive warfarin anticoagulation (INR 2.0– 3.0; use caution to keep INR < 3.0 in pts >age 75). Substitute aspirin 325 mg/ d for pts without these risk factors or if contraindication to warfarin exists. Control ventricular rate (60–80 bpm at rest, <100 bpm with mild exercise) with beta blocker, digoxin, or calcium channel blocker (verapamil, diltiazem). Consider cardioversion (after ³3 weeks therapeutic anticoagulation or if no evidence of left atrial thrombus by transesophageal echo), especially if symptomatic despite rate control: use group IA, IC, or III agent (usually initiate with inpatient monitoring), followed, within a few days, by electrical cardioversion (usually 100–200 J). Type IC (Table 115-3) drugs are preferred in pts without structural heart disease and type III drugs are recommended in presence of left ventricular dysfunction or CAD (Fig. 115-2). Anticoagulation should be continued for an additional 3 weeks after successful cardioversion.
FIGURE 115-2. Recommendations for the selection of antiarrhythmic medications to prevent the recurrence of atrial fibrillation. See Table 115-3 for definition of types IA and IC drugs. An atrioventricular nodal blocking agent (i.e., beta blocker, calcium channel blocker, or digoxin) should be added to all type IC and IA agents as well as to dofetilide. LVEF, left ventricular ejection fraction; CHF, congestive heart failure; CAD, coronary artery disease; EF, ejection fraction.
Preexcitation Syndrome (WPW)
Conduction occurs through an accessory pathway between atria and ventricles. Baseline ECG typically shows a short PR interval and slurred upstroke of the QRS (“delta” wave) (Fig. 115-1N). Associated tachyarrhythmias are of two types:
Narrow QRS complex tachycardia (antegrade conduction through AV node): usually paroxysmal supraventricular tachycardia. Treat cautiously with IV verapamil, digoxin, or propranolol (Table 115-3).
Wide QRS complex tachycardia (antegrade conduction through accessory pathway): often associated with AF with a very rapid (>250/min) ventricular rate (which may degenerate into VF). If hemodynamically compromised, immediate cardioversion is indicated; otherwise, treat with IV procainamide, not digoxin, beta blocker, or verapamil.
FIRST DEGREE (See Fig. 115-1J) Prolonged, constant PR interval (>0.20 s). May be normal or secondary to increased vagal tone or digitalis; no treatment required.
SECOND DEGREE Mobitz I (Wenckebach) (See Fig. 115-1M) Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped, then sequence is repeated. 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 (See Fig. 115-1K) 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; a dangerous rhythm—may progress suddenly to complete AV block; pacemaker is indicated.
THIRD DEGREE (COMPLETE AV BLOCK) (See Fig. 115-1L) Atrial activity is not transmitted to ventricles; atria and ventricles contract independently. Seen with MI, digitalis toxicity, or degenerative conduction system disease. Permanent pacemaker is indicated, except when associated transiently with inferior MI or in asymptomatic congenital heart block.
For a more detailed discussion, see Josephson ME, Zimetbaum P: Bradyarrhythmias, Chap. 229, p. 1283; and The Tachyarrhythmias, Chap. 230, p. 1292, in HPIM-15.