Chapter 125: Tachyarrhythmias
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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 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.
|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 rate
↓ ventricular rate
|Mitral valve disease, hypertension, pulmonary embolism, pericarditis, post–cardiac surgery, hyperthyroidism; obstructive lung disease, EtOH; atypical atrial flutter usually arises from atrial scars|
Atrial flutter may respond to rapid atrial pacing, and radio frequency ablation highly effective to prevent recurrences; consider ablation for recurrences of atrial fibrillation, especially if class IC or class III agents fail to control
|Multifocal atrial tachycardia||100–150||At least three distinct P wave shapes with varying PR intervals||No effect||Severe respiratory insufficiency||Treat underlying lung disease; verapamil or diltiazem may be used to slow ventricular rate; class IC agents or amiodarone may ↓ episodes|
|Wide QRS complex|
|Ventricular premature beats||Fully compensatory pause between normal beats||No effect||CAD, MI, CHF, hypoxia, hypokalemia, digitalis toxicity, prolonged QT interval (congenital or drug-related)||May not require therapy; if needed for symptomatic suppression, use beta blocker|
|Ventricular tachycardia||QRS rate 100–250; slightly irregular rate||No effect|
Monomorphic: myocardial scar (e.g., prior MI, sarcoid), ARVC, idiopathic outflow tract tachycardias
Polymorphic: Myocardial ischemia, hypertrophic cardiomyopathy, electrolyte disturbances, drug toxicities, genetic arrhythmia syndromes (see “torsade de pointes” below)
If unstable: electrical conversion/defibrillation (≥200 J monophasic, or ≥100 J biphasic)
Otherwise: acute (IV): amiodarone, procainamide, lidocaine; chronic management: usually ICD
Pts without structural heart disease (e.g., focal outflow tract ventricular tachycardia) may respond to beta blockers or verapamil
|Accelerated idioventricular rhythm (AIVR)||Gradual onset and offset; QRS rate 40–120||Acute MI, myocarditis||Usually none; for symptoms, use atropine or atrial pacing|
|Ventricular fibrillation||Erratic electrical activity||No effect||Immediate defibrillation|
|Torsade de pointes||Ventricular tachycardia with sinusoidal oscillations of QRS height||No effect||Prolonged QT interval (congenital or drug-related)|
IV magnesium (1- to 2-g bolus); overdrive pacing; isoproterenol for bradycardia-dependent torsades (unless CAD present); lidocaine
Drugs that prolong QT interval are contraindicated
|Supraventricular tachycardias with aberrant ventricular conduction||P wave typical of the supraventricular rhythm; wide QRS complex due to conduction through partially refractory pathways||Etiologies of the respective supraventricular rhythms listed above; atrial fibrillation with rapid, wide QRS may occur in preexcitation (WPW)||Same as treatment of respective supraventricular rhythm; if ventricular rate rapid (>200), treat as WPW (see text)|
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).
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. 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) 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) 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).
|DRUG||LOADING DOSE||MAINTENANCE DOSE||SIDE EFFECTS||EXCRETION|
|Quinidine||PO: 300–600 mg q6h||Diarrhea, tinnitus, QT prolongation, hypotension, anemia, thrombocytopenia||Hepatic and renal|
|Procainamide||IV: 15 mg/kg over 60 min||IV: 1–4 mg/min||Nausea, lupus-like syndrome, agranulocytosis, QT prolongation||Renal and hepatic|
|PO: 500–1000 mg q4h|
|Sustained-release||PO: 1000–2500 mg q12h|
|Disopyramide||PO: 100–300 mg q6–8h||Myocardial depression, AV block, QT prolongation anticholinergic effects||Renal and hepatic|
|Sustained-release||PO: 200–400 mg q12h|
|Lidocaine||IV: 1–3 mg/kg at 20–50 mg/min||IV: 1–4 mg/min||Confusion, seizures, respiratory arrest||Hepatic|
|Mexiletine||PO: 150–300 mg q8–12h||Nausea, tremor, gait disturbance||Hepatic|
|Flecainide||PO: 50–200 mg q12h||Nausea, exacerbation of ventricular arrhythmia, prolongation of PR and QRS intervals||Hepatic and renal|
|Propafenone||PO: 150–300 mg q8h||Hepatic|
|Metoprolol||IV: 5 mg over 3−5 min × 3 doses||PO: 25–100 mg q6h||Bradycardia, AV block, CHF, bronchospasm||Hepatic|
|Esmolol||IV: 500 µg/kg over 1 min||IV: 50 (µg/kg)/min|
|Amiodarone||PO: 800–1600 mg qd × 1–2 weeks, then 400–600 mg/d × 3 weeks||PO: 100–400 mg qd||Thyroid abnormalities, pulmonary fibrosis, transaminitis, bluish skin||Hepatic|
|IV: 150 mg over 10 min||IV: 1 mg/min × 6 h, then 0.5 mg/min|
|Ibutilide||IV (≥60 kg): 1 mg over 10 min, can repeat after 10 min||—||Torsade de pointes, hypotension, nausea||Hepatic|
|Dofetilide||PO: 125–500 µg bid||Torsade de pointes, headache, dizziness||Renal|
|Sotalol||PO: 80–160 mg q12h||Fatigue, bradycardia, exacerbation of ventricular arrhythmia||Renal|
|Dronedarone||PO: 400 mg q12h||Bradycardia, AV block, prolonged QT, exacerbation of heart failure, GI discomfort||Hepatic|
|Verapamil||IV: 5–10 mg over 3–5 min||IV: 2.5–10 mg/h||AV block, CHF, hypotension, constipation||Hepatic|
|PO: 80–120 mg q6–8 h|
|Diltiazem||IV: 0.25 mg/kg over 3–5 min (maximum 20 mg)||IV: 5–15 mg/h||Hepatic|
|PO: 30–60 mg q6h|
|Digoxin||IV: 0.25 mg q2h until 1 mg total||IV, PO: 0.125–0.25 mg qd||Nausea, AV block, ventricular and supraventricular arrhythmias||Renal|
|Adenosine||IV: 6-mg rapid bolus; if no effect then 12-mg bolus||—||Transient hypotension or atrial standstill||—|