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 Electrocardiography), 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 Clinical and Electrocardiographic Features of Common Arrhythmias 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 Clinical and Electrocardiographic Features of Common Arrhythmias). 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.
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) monomorphic R or Rs in lead AVR, (3) concordance of QRS with monophasic R or S waves in V1-V6 (Fig. 125-1. Algorithm for Differentiation of Ventricular Tachycardia (VT) from Supraventricular Tachycardia (SVT)).
| TREATMENT | ||
TachyarrhythmiasPrecipitating causes (listed earlier) should be corrected (Tables 125-1 Clinical and Electrocardiographic Features of Common Arrhythmias and 125-2 Commonly Used Antiarrhythmic Drugs). If pt is hemodynamically compromised (angina, hypotension, CHF), proceed to immediate cardioversion. Do not cardiovert sinus tachycardia; exercise caution if digitalis toxicity is suspected. Initiate drugs as indicated in the tables; follow ECG intervals (esp. QRS and QT). Reduce dosage for pts with hepatic or renal dysfunction as indicated in Table 125-2 Commonly Used Antiarrhythmic Drugs. Drug efficacy is confirmed by ECG (or Holter) monitoring, stress testing, and, in special circumstances, invasive electrophysiologic study. 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 torsade de pointes ventricular tachycardia (Table 125-1 Clinical and Electrocardiographic Features of Common Arrhythmias) is most common with class IA and III 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 (AF)Evaluate potential underlying cause (e.g., thyrotoxicosis, mitral stenosis, excessive ethanol consumption, pulmonary embolism). Pts with rheumatic mitral stenosis, hypertrophic cardiomyopathy, or CHA2DS2-VASc score ≥2 (1 point each for CHF, hypertension, diabetes, vascular disease, age 65-75, female gender; 2 points each for age 75, history of stroke or TIA) should receive anticoagulation; may also consider for CHA2DS2-VASc score of 1. Use warfarin (INR 2.0-3.0) or in absence of mitral stenosis or mechanical heart valve, consider direct-acting oral anticoagulants (DOACs) that do not require prothrombin time monitoring-e.g., dabigatran (150 mg bid; 75 mg bid for creatinine clearance [CrCl] 15-30 mL/min), rivaroxaban (20 mg daily; 15 mg daily for CrCl 15-50 mL/min), apixaban (5 mg bid; 2.5 mg bid for 2 of the following: age >80, weight <60 kg, creatinine ≥1.5 md/dL), or edoxaban (60 mg daily for CrCl 60-90 mL/min; 30 mg daily for CrCl 15-60 mL/min). Bleeding effects of warfarin can be reversed with prothrombin complex concentrate, fresh frozen plasma, and/or vitamin K. Reversal agents for some DOACs are also now available, if needed for severe bleeding or prior to urgent invasive procedures (idarucizumab for dabigatran, andexanet alfa for rivaroxaban and apixaban). Control ventricular rate (60-80 beats/min at rest, <100 beats/min with mild exercise) with beta blocker, calcium channel blocker (verapamil, diltiazem), or digoxin. Consider cardioversion (100-200 J) after ≥3 weeks therapeutic anticoagulation, or acutely if no evidence of left atrial thrombus by transesophageal echo, especially if symptomatic despite rate control. Initiation of class IC, III, or IA agents prior to electrical cardioversion facilitates maintenance of sinus rhythm after successful procedure. Class IC (Table 125-2 Commonly Used Antiarrhythmic Drugs) drugs are preferred in pts without structural heart disease, and class III drugs are recommended in presence of left ventricular dysfunction or coronary artery disease. Anticoagulation should be continued for a minimum of 3 weeks after successful cardioversion. Consider catheter-based ablation (pulmonary vein isolation) for recurrent symptomatic AF if sufficiently responsive to pharmacologic measures (more effective in pts with paroxysmal AF: ∼60% success at maintaining sinus rhythm after first ablation, 70-80% after additional ablation). Rare late complications of ablation include pulmonary vein stenosis (presents with dyspnea or hemoptysis) and atrio-esophageal fistula (consider if fever, neurologic symptoms, or chest pain arise). |
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). Associated tachyarrhythmias are of two types:
- Narrow QRS “orthodromic” tachycardia (antegrade conduction through AV node). Treat cautiously with IV adenosine or beta blocker, verapamil, or diltiazem (Table 125-2 Commonly Used Antiarrhythmic Drugs).
- Wide QRS complex “antidromic” tachycardia (antegrade conduction through accessory pathway); wide complex tachycardia may also be associated with AF with a very rapid (>250/min) ventricular rate, which can degenerate into VF. If hemodynamically compromised, immediate cardioversion is indicated; otherwise, treat with IV procainamide or ibutilide (Table 125-2 Commonly Used Antiarrhythmic Drugs), not beta blocker, verapamil, diltiazem, digoxin, or amiodarone.
- Refer to electrophysiologist to consider catheter ablation of accessory pathway for long-term prevention of tachycardia.