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
RHYTHMATRIAL RATEFEATURESCAROTID SINUS MASSAGEPRECIPITATING CONDITIONSINITIAL 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 tachycardia100–160Normal P wave contourRate gradually slowsFever, anxiety, pain, anemia, dehydration, CHF, hyperthyroidism, COPDRemove precipitating cause; if symptomatic: beta blocker
AV nodal tachycardia (reentrant)120–250Absent or retrograde P waveAbruptly converts to sinus rhythm (or no effect)Can occur in healthy individualsVagal 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 tachycardia130–200P contour different from sinus P wave; AV block may occur; automatic form shows “warm-up” in rate in first several beatsAV 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
  1. Slow the ventricular rate: beta blocker, verapamil, diltiazem, or digoxin
  2. 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 IAa 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 tachycardia100–150At least three distinct P wave shapes with varying PR intervalsNo effectSevere respiratory insufficiencyTreat 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 beatsNo effectCAD, 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 rateNo 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, myocarditisUsually none; for symptoms, use atropine or atrial pacing
Ventricular fibrillation Erratic electrical activityNo effect Immediate defibrillation
Torsade de pointes Ventricular tachycardia with sinusoidal oscillations of QRS heightNo effectProlonged 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
hmom20_ch125_f001.png
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
DRUGLOADING DOSEMAINTENANCE DOSESIDE EFFECTSEXCRETION
Class IA
Quinidine PO: 300–600 mg q6hDiarrhea, tinnitus, QT prolongation, hypotension, anemia, thrombocytopeniaHepatic and renal
ProcainamideIV: 15 mg/kg over 60 minIV: 1–4 mg/minNausea, lupus-like syndrome, agranulocytosis, QT prolongationRenal and hepatic
  PO: 500–1000 mg q4h  
Sustained-release PO: 1000–2500 mg q12h  
Disopyramide PO: 100–300 mg q6–8hMyocardial depression, AV block, QT prolongation anticholinergic effectsRenal and hepatic
Sustained-release PO: 200–400 mg q12h  
Class IB
LidocaineIV: 1–3 mg/kg at 20–50 mg/minIV: 1–4 mg/minConfusion, seizures, respiratory arrestHepatic
Mexiletine PO: 150–300 mg q8–12hNausea, tremor, gait disturbanceHepatic
Class IC
Flecainide PO: 50–200 mg q12hNausea, exacerbation of ventricular arrhythmia, prolongation of PR and QRS intervalsHepatic and renal
Propafenone PO: 150–300 mg q8h Hepatic
Class II
MetoprololIV: 5 mg over 3−5 min × 3 dosesPO: 25–100 mg q6hBradycardia, AV block, CHF, bronchospasmHepatic
EsmololIV: 500 µg/kg over 1 minIV: 50 (µg/kg)/min  
Class III
AmiodaronePO: 800–1600 mg qd × 1–2 weeks, then 400–600 mg/d × 3 weeksPO: 100–400 mg qdThyroid abnormalities, pulmonary fibrosis, transaminitis, bluish skinHepatic
 IV: 150 mg over 10 minIV: 1 mg/min × 6 h, then 0.5 mg/min  
IbutilideIV (≥60 kg): 1 mg over 10 min, can repeat after 10 min—Torsade de pointes, hypotension, nauseaHepatic
Dofetilide PO: 125–500 µg bidTorsade de pointes, headache, dizzinessRenal
Sotalol PO: 80–160 mg q12hFatigue, bradycardia, exacerbation of ventricular arrhythmiaRenal
Dronedarone PO: 400 mg q12hBradycardia, AV block, prolonged QT, exacerbation of heart failure, GI discomfortHepatic
Class IV
VerapamilIV: 5–10 mg over 3–5 minIV: 2.5–10 mg/hAV block, CHF, hypotension, constipationHepatic
  PO: 80–120 mg q6–8 h  
DiltiazemIV: 0.25 mg/kg over 3–5 min (maximum 20 mg)IV: 5–15 mg/h Hepatic
  PO: 30–60 mg q6h  
Other
DigoxinIV: 0.25 mg q2h until 1 mg totalIV, PO: 0.125–0.25 mg qdNausea, AV block, ventricular and supraventricular arrhythmiasRenal
AdenosineIV: 6-mg rapid bolus; if no effect then 12-mg bolus—Transient hypotension or atrial standstill—

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