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.
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 ||Download (.pdf) 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
“Sawtooth” flutter waves; 2:1, 4:1 block
No discrete P; irregularly spaced QRS
↑ AV block with ↓ventricular ...