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: 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.

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 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	Slow the ventricular rate: beta blocker, verapamil, diltiazem, or digoxin Consider conversion to NSR (after anticoagulation if chronic) electrically (50–100 J for atrial flutter, ≥200 J for atrial fibrillation) or chemically with IV ibutilide or oral class IC, III, or IA^a agent 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)

^aAntiarrhythmic drug groups listed in Table 125-2.

Abbreviations: ARVC, arrhythmogenic right ventricular cardiomyopathy; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; EtOH, ethyl alcohol; ICD, implantable cardioverter defibrillator; NSR, normal sinus rhythm; WPW, Wolff-Parkinson-White.

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).

FIGURE 125-1

Algorithm for differentiation of ventricular tachycardia (VT) from supraventricular tachycardia (SVT).

Treatment: Tachyarrhythmias

Precipitating causes (listed earlier) should be corrected (Tables 125-1 and 125-2). 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. 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).

Tables

TABLE 125-2: Commonly Used Antiarrhythmic Drugs
DRUG	LOADING DOSE	MAINTENANCE DOSE	SIDE EFFECTS	EXCRETION
Class IA
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
Class IB
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
Class IC
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
Class II
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
Class III
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
Class IV
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
Other
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	—

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