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Chapter 125: Tachyarrhythmias

INTRODUCTION

Tachyarrhythmias 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) heart failure, (3) hypoxemia, (4) hypercapnia, (5) hypotension, (6) electrolyte disturbances (e.g., hypokalemia and/or hypomagnesemia), (7) drug toxicity (digoxin, drugs that prolong the QT interval), (8) caffeine consumption, (9) ethanol consumption.

DIAGNOSIS

Examine ECG for evidence of ischemic changes (Chap. 113), prolonged or shortened QT interval, characteristics of Wolff-Parkinson-White (WPW) syndrome (see below), or ST elevation in leads V1–V3 typical of Brugada syndrome. See Table 125-1 for diagnosis of tachyarrhythmias; always identify atrial activity and relationship between P waves and QRS complexes. To aid the diagnosis:

  • Obtain long rhythm strip of lead II, aVF, or V1. P waves can be made more evident by intentionally doubling the ECG voltage.

  • Place accessory ECG leads (e.g., right-sided chest leads) to help identify P waves. Record ECG during carotid sinus massage (Table 125-1). Note: Do not massage both carotids simultaneously.

  • For intermittent symptoms, consider 24-h Holter monitor (if symptoms occur daily), a pt-activated or continuously recording event monitor over 2–4 weeks, or, if symptoms are very infrequent but severely symptomatic, an implanted loop monitor. A standard exercise test may be used to provoke arrhythmias for diagnostic purposes.

TABLE 125-1Clinical and Electrocardiographic Features of Common Arrhythmias
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TABLE 125-1 Clinical and Electrocardiographic Features of Common Arrhythmias
RHYTHM ATRIAL RATE FEATURES CAROTID SINUS MASSAGE PRECIPITATING CONDITIONS INITIAL TREATMENT
Narrow QRS complex
Atrial premature beats — P wave abnormal; QRS width normal — Can be normal or due to anxiety, CHF, hypoxia, caffeine, abnormal electrolytes (↓K+ ↓Mg2+) Remove precipitating cause; if symptomatic: beta blocker
Sinus tachycardia 100–160 Normal P wave contour Rate gradually slows Fever, anxiety, pain, anemia, dehydration, CHF, hyperthyroidism, COPD Remove precipitating cause; if symptomatic: beta blocker
AV nodal tachycardia (reentrant) 120–250 Absent or retrograde P wave Abruptly converts to sinus rhythm (or no effect) Can occur in healthy individuals Vagal maneuvers; if unsuccessful: adenosine, verapamil, beta blocker, cardioversion (100–200 J). To prevent recurrence: beta blocker, verapamil, diltiazem, digoxin, class IC agent, or catheter ablation
Focal atrial tachycardia 130–200 P contour different from sinus P wave; AV block may occur; automatic form shows “warm-up” in rate in first several beats AV block may ↑ Digitalis toxicity; pulmonary disease; scars from prior cardiac surgery or ablation

If digitalis toxic: hold digoxin, correct [K+]

In absence of digoxin toxicity: slow rate with beta blocker, verapamil, or diltiazem; can attempt conversion with IV adenosine; if unsuccessful, consider cardioversion; for long-term suppression, consider class I or III antiarrhythmic or catheter ablation

Atrial flutter

Atrial fibrillation

260–300

>350

“Sawtooth” flutter waves; 2:1, 4:1 block

No discrete P; irregularly spaced QRS

↑ AV block with ↓ventricular ...

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