premature ventricular complexes

Origin of Ectopic Beats

• Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation
• The rate of depolarisation decreases from top to bottom:
  • fastest at the sinoatrial node
  • slowest within the ventricles
• Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above
• However, if an ectopic focus depolarises early enough — prior to the arrival of the next sinus impulse — it may “capture” the ventricles, producing a premature contraction

Premature contractions (“ectopics”) are classified by their origin

• atrial (PACs)
• junctional (PJCs)
• ventricular (PVCs)

Definition and Classification

• VPCs/PVCs:
  • Ectopic beats arising from the ventricles, not conducted via the usual conduction pathways, resulting in early heartbeats with a widened QRS complex
  • Mechanism
    • Enhanced Automaticity: Spontaneous depolarization of ectopic foci in the ventricles.
    • Re-Entry: Abnormal electrical circuits within scarred or ischemic tissue.
    • Triggered Activity: Depolarizations occurring after a normal action potential, often due to calcium overload.
• Classification:
  • By Frequency: Occasional, frequent (>30/hour), or high burden (>10,000 beats/day or >10% of total heartbeats).
  • By Pattern:
    • Bigeminy: A VPC follows every normal beat (1:1 pattern).
    • Trigeminy: A VPC follows every two normal beats (2:1 pattern).
    • Quadrigeminy: A VPC follows every three normal beats.
    • Couplets: Two consecutive VPCs.
    • Triplets: Three consecutive VPCs, indicating a brief run of non-sustained ventricular tachycardia.
    • Multifocal VPCs: Different morphologies indicating multiple ectopic foci.
    • Unifocal VPCs: Similar morphology indicating a single ectopic focus

ECG Diagnostic Criteria:

• Originates from an ectopic ventricular focus, causing wide QRS complexes (>120 ms) due to slow conduction through cardiac myocytes.
• No preceding P wave as the impulse does not originate from the atria.

Compensatory Pause:

• A pause observed after a VPC
  • where the sum of the intervals around the VPC equals twice the normal sinus interval.
• For a full compensatory pause to occur, there are 2 necessities:
  • There must be a stable sinus rhythm. Sinus arrhythmia must not be seen.
  • There must be ventriculoatrial block (the VPC must not interrupt the sinus rhythmicity) or ventriculoatrial conduction occurs but fails to reset the sinus node.
• Not seen in
  • irregular rhythms (e.g., atrial fibrillation)
  • interpolated VPCs
  • Atrial Premature Beat (APB) – If a compensatory pause occurs after an APB, it suggests the APB did not reset the sinus node.

Clinical significance

• Structurally Normal Hearts:
  • Usually benign and not associated with adverse outcomes
  • No treatment is required unless symptomatic.
• Structural Heart Disease:
  • Frequent PVCs (>10,000/day) may indicate an increased risk of heart failure, arrhythmias, or sudden cardiac death, particularly in patients with underlying heart conditions.
  • PVC Burden < 5%: onsidered low and benign, especially in structurally normal hearts. Typically does not require intervention unless symptomatic.
  • PVC Burden 5-10%: Intermediate burden. May be asymptomatic or mildly symptomatic. Requires clinical correlation; further evaluation might be needed if there are symptoms or suspicion of structural heart disease.
  • PVC Burden > 10%: Considered high burden and clinically significant, particularly if sustained. Associated with an increased risk of developing PVC-induced cardiomyopathy, even in patients without underlying structural heart disease.
  • ECG ‘R on T Phenomenon’:
    • occurs when a PVC falls on the T wave of the preceding beat, which is a vulnerable period of ventricular repolarization.
    • Increases the risk of ventricular arrhythmias, including ventricular tachycardia (VT) and ventricular fibrillation (VF), both of which can be life-threatening.
    • Particularly concerning in the setting of myocardial ischemia, structural heart disease, or QT prolongation. (see below)

Differential Diagnosis:

• Not all wide QRS complexes are VPCs; they can also result from:
  • Ventricular pacemaker activity (except His bundle pacing).
  • Aberrant conduction of supraventricular impulses.
  • Wolff-Parkinson-White (WPW) syndrome.

Etiology and Risk Factors

• Cardiac Causes:
  • Cardiomyopathies (dilated, hypertrophic)
  • ischemic heart disease
  • myocarditis
  • mitral valve prolapse.
• Non-Cardiac Causes:
  • Stimulants: Caffeine, alcohol, nicotine, cocaine, amphetamines.
  • Electrolyte imbalances: Hypokalemia, hypomagnesemia, hypercalcemia.
  • Medications: Digoxin, tricyclic antidepressants, sympathomimetics.
  • Hypoxia, hypercapnia, stress, and increased adrenergic stimulation.

Clinical Presentation

• Symptoms:
  • Asymptomatic in many cases.
  • Commonly experienced as ‘missed beats’ or palpitations.
  • Palpitations, skipped beats, dizziness, or lightheadedness.
  • Dyspnea or angina in patients with underlying heart disease.
  • Syncope or presyncope in rare cases with sustained VPCs.

Evaluation

1. ECG:
   • VPCs appear as early, widened QRS complexes without preceding P waves
   • Morphology helps localize the origin (e.g., LBBB pattern suggests right ventricular origin).
2. Holter Monitoring:
   • 24-hour or extended monitoring to quantify VPC burden and assess patterns like bigeminy and trigeminy.
3. Echocardiography:
   • To evaluate underlying structural heart disease or cardiomyopathy.
4. Laboratory Tests:
   • Electrolytes, thyroid function, and drug screening if indicated.

Management

• Lifestyle Modifications: Reduce stimulants (caffeine, alcohol), manage stress, and correct electrolyte imbalances.
• Pharmacological Therapy:
  • Beta-Blockers: First-line for symptomatic VPCs, especially in structurally normal hearts.
  • Calcium Channel Blockers: Alternative for those intolerant to beta-blockers.
  • Antiarrhythmics (Class Ic, e.g., flecainide): Used cautiously; contraindicated in structural heart disease.
  • Amiodarone: Reserved for refractory cases or in those with significant structural heart disease.
• Catheter Ablation:
  • Considered in high-burden VPCs (>10% of total heartbeats) or when VPCs cause cardiomyopathy.

Prognosis and Complications

• Benign VPCs: Generally have a good prognosis if no structural heart disease is present.
• Frequent or Complex VPCs:
  • Associated with increased risk of cardiomyopathy
  • ventricular tachycardia
  • sudden cardiac death, especially in patients with heart disease.
• Reversible Cardiomyopathy: Often resolves after successful ablation.