Approach to Ventricular Arrhythmias¶

Chapter 259 | Part 6: Disorders of the Cardiovascular System · Part 6 – Cardiovascular Disorders · Chapter 259

Key Clinical Points¶

Ventricular arrhythmias (VAs) are characterized by a wide QRS complex duration, typically >0.12 s, due to slower conduction through ventricular myocardium.
Monomorphic VT indicates a consistent activation sequence from a single source; Polymorphic VT involves a changing activation sequence.
Torsades de Pointes is a specific form of polymorphic VT associated with QT prolongation, characterized by waxing and waning QRS amplitude.
Beta-blockers are the first choice of therapy for most VAs, particularly exercise-induced and idiopathic arrhythmias.
Amiodarone is the most effective antiarrhythmic drug for suppressing VAs in patients with structural heart disease but carries significant long-term toxicity risks.
Implantable cardioverter-defibrillators (ICDs) are indicated for patients at risk of sudden cardiac death to provide a safety net for life-threatening VT or VF.
Catheter ablation is useful for symptomatic AF, atrial flutter, and recurrent VT associated with poor cardiac function or scar-related substrates.
Idiopathic ventricular arrhythmia occurs in patients with a normal ECG, no structural heart disease, and no genetic syndrome risk.
Syncope without prodrome, during exercise, or with abnormal ECG/structural heart disease warrants concern for VT and risk of sudden death.
Atrioesophageal fistula is a rare but fatal complication of catheter ablation; diagnosis is made by chest CT with water-soluble contrast.

DEFINITION & OVERVIEW¶

• Ventricular Arrhythmias (VAs): Diverse group ranging from benign to life-threatening; can arise from focal sites (myocardial or Purkinje cells) or reentrant circuits (scar tissue or diseased pathways). • Electrocardiography: • Conduction through myocardium is slower than the Purkinje system → QRS duration typically >0.12 s. • Ventricular Tachycardia (VT): ≥ 3 consecutive beats at a rate >100 beats/min. • Idioventricular Rhythm: ≥ 3 consecutive beats at slower rates.

Definition (Harrison's 22e): 'PVCs or VT that occurs in patients with a normal electrocardiogram (ECG), without structural heart disease, and not associated with an underlying genetic syndrome or risk of sudden death.'

• Classification by Morphology: • Monomorphic VT: Same QRS morphology beat-to-beat; indicates consistent activation sequence. • Polymorphic VT: Continually changing Q1S morphology; indicates changing activation sequence. • Ventricular Flutter: Very rapid monomorphic VT with sinusoidal appearance (QRS and T wave indistinguishable). • Ventricular Fibrillation (VF): Continuous irregular activation with no discrete QRS complexes.

• Premature Ventricular Contractions (PVCs): • Unifocal: Origin from same focus → same QRS morphology. • Multifocal: Origin from different sites → varying QRS morphologies. • Ventricular Couplets: Two consecutive ventricular beats.

EPIDEMIOLOGY¶

• Atrial Fibrillation (AF) Risk Factors: • Modifiable: Sedentary lifestyle, obesity, hypertension, smoking, alcohol use, sleep apnea. • Non-modifiable: Genetic predisposition, age. • Psychological: Stress is a known risk factor.

• Exercise and AF Risk: • Males: U-shaped curve; high risk in sedentary lifestyles and extreme endurance athletics (e.g., long-distance running). Moderate exercise shows lower risk. • Females: Linear relationship; risk decreases continuously with increasing exercise activity.

• Caffeine: Modest decrease in AF risk with moderate caffeine intake.

ETIOLOGY & PATHOPHYSIOLOGY¶

• Arrhythmia Mechanisms: • Automaticity: Focal VAs from myocardial or Purkinje cells. • Triggered Activity: Focal VAs. • Reentry: Involves areas of scar (myocardial infarction, cardiomyopathy) or diseased conduction pathways. • Electrolyte Disturbances: e.g., Hyperkalemia. • Drug Effects: Sodium channel blockers, QT-prolonging drugs.

• QRS Morphology and Origin Mapping: • Right Ventricle/Septum: Late activation of LV → prominent S wave in V1 (LBBB-like). • Left Ventricular Free Wall: Prominent positive deflection in V1 (RBBB-like). • Inferior Axis (Dominant R in II, III, aVF): Indicates initial activation of the cranial portion. • Superior Axis (Dominant S in II, III, aVF): Indicates initial activation at the inferior wall.

• Specific Conditions: • Sinusoidal VT: Caused by hyperkalemia, sodium channel blocker toxicity, or severe global myocardial ischemia. • Torsades de Pointes: Polymorphic VT in context of QT prolongation; characterized by waxing and waning QRS amplitude and shifting axis.

CLINICAL FEATURES¶

• Symptoms: Palpitations, dizziness, exercise intolerance, lightheadedness, syncope, or sudden cardiac arrest. • Asymptomatic Presentation: Irregular pulse/heart sounds on exam, or detected on routine ECG/exercise test.

• Pseudobradycardia: • Occurs during bigeminy (every other beat is a PVC). • Result: Pulse measurements are erroneously low because PVCs may not generate a separate pulse wave.

DIFFERENTIAL DIAGNOSIS¶

Wide-Complex Tachycardia: Must distinguish VT from SVT with aberrancy (use QRS morphology, axis, and response to adenosine).
Syncope: Distinguish VT-induced hypotension from benign causes (vasovagal episodes, orthostatic hypotension).
Ventricular Flutter: Distinguish from sinusoidal VT (caused by electrolyte/drug effects).
Polymorphic vs. Monomorphic VT.
Ventricular Fibrillation vs. Sustained VT.
Idiopathic vs. Structural Disease-associated Arrhythmias.

INVESTIGATIONS & DIAGNOSIS¶

12-Lead ECG: Obtain even if asymptomatic; identify Q waves (prior MI), ventricular hypertrophy (HCM), or genetic markers (LQTS, Brugada, SQTS).
Imaging Studies: • Transthoracic Echocardiography (TTE): Initial evaluation of ventricular function and structure. • Cardiac Magnetic Resonance Imaging (CMR): Use gadolinium contrast to detect areas of delayed enhancement (scar), especially in patients with monomorphic VT.
Coronary Evaluation: Assess for atherosclerotic coronary artery disease based on age and risk factors.
Arrhythmia Recording: ECG, ambulatory/implanted monitors, or electrophysiologic study (EPS) to identify the arrhythmia substrate.

MANAGEMENT & TREATMENT¶

Pharmacologic Therapy: • Beta-blockers: First choice for most VAs, especially exercise-induced and idiopathic arrhythmias. • Amiodarone: Most effective for suppressing VAs in patients with structural heart disease; carries significant long-term toxicity risks.
Device Therapy: • Implantable Cardioverter-Defibrillators (ICDs): Indicated for patients at risk of sudden cardiac death; provides a safety net to terminate life-threatening VT or VF.
Catheter Ablation: • Indications: • Symptomatic AF (Table 1). • Symptomatic atrial flutter. • Recurrent VT associated with poor cardiac function or scar-related substrates.

PROGNOSIS & COMPLICATIONS¶

ICD Complications: • Unnecessary Therapy: Most common; caused by SVT, electrical noise, or lead fracture. • Infection: Occurs in ≈ 1% of patients. • Psychological: Risk of posttraumatic stress disorder from repeated shocks.
Ablation Complications: • Atrioesophageal Fistula: Rare but fatal; diagnosis by chest CT with water-soluble contrast.

KEY PEARLS & CLINICAL TRAPS¶

• QRS Width: ≥ 0.12 s is the hallmark of ventricular origin. • Amiodarone: Most effective for structural heart disease but requires monitoring for long-term toxicity. • Syncope Warning: Syncope without prodrome, during exercise, or with abnormal ECG/structural heart disease is a high-risk indicator for VT. • Ablation Safety: Atrioesophageal fistula must be ruled out via CT if suspected after ablation.

Reference Tables¶

TABLE 258-3 Recommendations for Catheter Ablation in Patients with Atrial Fibrillation (AF) CLASS 1¶

Harrison's 22e, p.1954

CLASS	LEVEL OF EVIDENCE	RECOMMENDATIONS
1	A	In patients with symptomatic AF in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred, and continued rhythm control is desired, catheter ablation is useful to improve symptoms.
	A
1	A	In patients with symptomatic or clinically significant atrial flutter, catheter ablation is useful for improving symptoms.
	B
2a	B	In patients (other than younger with few comorbidities) with symptomatic paroxysmal or persistent AF who are being managed with a rhythm-control strategy, catheter ablation as first-line therapy can be useful to improve symptoms.
259	Approach to Ventricular Arrhythmias William H. Sauer, Usha B. Tedrow