Ventricular Arrhythmias

Ventricular arrhythmias are a group of cardiac rhythm disorders originating from the ventricles, the lower chambers of the heart. These arrhythmias are clinically significant because they can lead to hemodynamic compromise, sudden cardiac death, and are often associated with underlying structural heart disease. Among ventricular arrhythmias, Ventricular Tachycardia (VT), Ventricular Fibrillation (VF), and Premature Ventricular Contractions (PVCs) are the most recognized. Understanding their pathophysiology, electrocardiographic patterns, clinical presentation, and management is crucial for effective patient care.

1. Introduction

Ventricular arrhythmias arise when there is abnormal electrical activity within the ventricles. Unlike supraventricular arrhythmias, which originate above the ventricles, these arrhythmias bypass normal conduction pathways, leading to potentially life-threatening situations.

Key Points:

Ventricular arrhythmias can be sustained or non-sustained, symptomatic or asymptomatic.
Common causes include ischemic heart disease, cardiomyopathies, electrolyte imbalances, drug toxicity, and genetic disorders like Long QT Syndrome or Brugada Syndrome.

Electrocardiography (ECG) remains the cornerstone for diagnosing ventricular arrhythmias. Recognizing characteristic patterns helps differentiate VT, VF, and PVCs, guiding urgent and long-term management strategies.

2. Premature Ventricular Contractions (PVCs)

2.1 Definition and Mechanism

PVCs, also known as ventricular extrasystoles, are early depolarizations originating from the ventricles before the next normal heartbeat. They disrupt the regular rhythm of the heart, producing a wide and bizarre QRS complex on ECG.

Mechanisms:

Enhanced Automaticity: Increased spontaneous depolarization of ventricular cells.
Triggered Activity: Afterdepolarizations (early or delayed) leading to extra beats.
Reentry: Circular electrical pathways allowing premature impulses.

2.2 ECG Characteristics

PVCs have distinct electrocardiographic features:

Wide QRS Complex: Usually >120 ms.
Absence of P Wave preceding the PVC.
Compensatory Pause: The pause after a PVC allows the sinus node to reset.
Morphology: Monomorphic PVCs have uniform shape; polymorphic PVCs vary in shape, suggesting multiple ventricular foci.

Common Patterns:

Bigeminy: Every other beat is a PVC.
Trigeminy: Every third beat is a PVC.
Couplets: Two consecutive PVCs.

2.3 Clinical Significance

Usually benign in healthy individuals.
Symptomatic PVCs may cause palpitations, dizziness, or syncope.
Frequent PVCs may indicate structural heart disease or predispose to VT.

2.4 Management

Lifestyle Modification: Reduce caffeine, alcohol, and stress.
Pharmacologic Therapy: Beta-blockers or antiarrhythmic drugs (e.g., amiodarone) if symptomatic.
Electrophysiologic Intervention: Catheter ablation for refractory cases.

3. Ventricular Tachycardia (VT)

3.1 Definition and Classification

Ventricular Tachycardia is a fast heart rhythm originating in the ventricles, usually defined as three or more consecutive ventricular beats at a rate >100 bpm.

Types:

Monomorphic VT: QRS complexes have a consistent morphology.
Polymorphic VT: QRS morphology varies beat-to-beat.
- Torsades de Pointes (TdP): A polymorphic VT associated with prolonged QT interval.

3.2 Pathophysiology

VT usually arises due to:

Reentry circuits in scar tissue post-myocardial infarction.
Increased automaticity in ischemic or injured myocardium.
Triggered activity from afterdepolarizations in electrolyte imbalances.

3.3 ECG Features

Wide QRS Complex (>120 ms).
Rapid Rate: Typically 120–250 bpm.
AV Dissociation: P waves may be independent of QRS.
Capture and Fusion Beats: Occasional normal QRS due to sinus impulse capture.
Monomorphic vs Polymorphic: Stable vs changing morphology.

Example Patterns:

Sustained VT: Lasts >30 seconds or requires termination due to hemodynamic instability.
Non-sustained VT: Lasts <30 seconds and may be asymptomatic.

3.4 Clinical Presentation

Palpitations
Syncope or presyncope
Chest pain
Shortness of breath
Cardiogenic shock in sustained VT

3.5 Complications

Hemodynamic compromise
Progression to Ventricular Fibrillation
Sudden cardiac death

3.6 Management

Acute VT:

Hemodynamically unstable: Immediate synchronized cardioversion.
Hemodynamically stable: Antiarrhythmic drugs such as amiodarone, procainamide, or lidocaine.

Chronic/Recurrent VT:

Implantable Cardioverter-Defibrillator (ICD)
Catheter ablation for recurrent VT.
Address underlying causes: ischemia, electrolyte abnormalities, heart failure.

4. Ventricular Fibrillation (VF)

4.1 Definition

Ventricular Fibrillation is chaotic, rapid ventricular activity that results in the loss of effective cardiac output. It is a major cause of sudden cardiac death.

4.2 Pathophysiology

Often arises from acute myocardial ischemia or post-myocardial infarction scar tissue.
Reentrant circuits or multiple ectopic foci in ventricles lead to disorganized electrical activity.
VF eliminates coordinated contraction, leading to cardiac arrest if not treated immediately.

4.3 ECG Characteristics

Chaotic, irregular, and wide QRS activity with no discernible P waves or T waves.
Amplitude: Can be coarse (high-voltage) or fine (low-voltage).
Rate: Extremely rapid, often 300–600 bpm in theory.

4.4 Clinical Presentation

Sudden collapse
Absence of pulse
Loss of consciousness
Apnea

4.5 Management

Immediate Defibrillation: The definitive treatment.
Advanced Cardiac Life Support (ACLS) Protocols:
- CPR until defibrillation.
- Epinephrine administration.
- Antiarrhythmic drugs (amiodarone, lidocaine) if defibrillation fails.

Post-Resuscitation Care:

Coronary angiography if myocardial infarction suspected.
Targeted temperature management.
Evaluation for ICD placement.

5. Distinguishing PVCs, VT, and VF

Feature	PVC	VT	VF
Origin	Single ectopic ventricular focus	Ventricular myocardium	Multiple ventricular foci
Rhythm	Irregular	Regular or slightly irregular	Totally irregular
QRS Complex	Wide, bizarre	Wide (>120 ms), monomorphic/polymorphic	Chaotic, no defined QRS
P Wave	Absent before PVC	AV dissociation may be seen	Absent
Clinical Significance	Often benign; palpitations	Life-threatening if sustained	Cardiac arrest; emergent
Treatment	Lifestyle, beta-blockers	Antiarrhythmic drugs, ICD, ablation	Immediate defibrillation

6. Etiology and Risk Factors

6.1 Ischemic Heart Disease

Post-myocardial infarction scar tissue predisposes to reentrant VT.
Acute ischemia may trigger VF.

6.2 Cardiomyopathies

Hypertrophic, dilated, or restrictive cardiomyopathy alters conduction.
Fibrosis and structural remodeling increase arrhythmic risk.

6.3 Electrolyte Imbalances

Hypokalemia, hypomagnesemia, and hypercalcemia can trigger ventricular arrhythmias.
Drugs prolonging QT interval may precipitate torsades de pointes.

6.4 Genetic Disorders

Long QT Syndrome, Brugada Syndrome, Catecholaminergic Polymorphic VT are inherited arrhythmogenic conditions.

6.5 Drug-induced Arrhythmias

Antiarrhythmic drugs, certain antibiotics, and psychotropic medications may increase risk.

7. Advanced ECG Interpretation Techniques

7.1 Identifying VT vs SVT with Aberrancy

Brugada Criteria and Vereckei Criteria help distinguish wide-complex tachycardias.
Features favoring VT:
- AV dissociation
- Fusion or capture beats
- Extreme axis deviation
- Concordant QRS in precordial leads

7.2 Holter Monitoring

Continuous ECG recording for detecting intermittent VT or frequent PVCs.

7.3 Electrophysiology Study

Invasive procedure mapping ventricular foci.
Guides ablation therapy for recurrent arrhythmias.

8. Prognosis and Outcomes

Isolated PVCs: Generally benign in normal hearts.
Sustained VT: Mortality risk higher, especially with underlying cardiomyopathy or ischemia.
VF: Without immediate intervention, mortality approaches 100%.
ICD Placement: Significantly improves survival in high-risk patients.

9. Preventive Strategies

Primary Prevention: Risk stratification in cardiomyopathy and ischemic heart disease.
Lifestyle Interventions: Avoid stimulants, maintain electrolyte balance.
Medical Therapy: Beta-blockers and ACE inhibitors reduce arrhythmic burden in heart failure.
Device Therapy: ICD implantation in high-risk patients with prior VT/VF or severe left ventricular dysfunction.