Ventricular Premature Complex
Contents
- 1 1. What is a Ventricular Premature Complex (VPC)?
- 2 2. Which of the following ECG features is characteristic of a VPC?
- 3 3. What usually follows a VPC on the ECG?
- 4 4. Which of the following is NOT typically associated with VPCs?
- 5 5. A pattern where a VPC occurs after every normal beat is known as:
- 6 6. What defines a couplet in the context of VPCs?
- 7 7. Three or more consecutive VPCs at a rate >100 bpm are termed:
- 8 8. What is a fusion beat?
- 9 9. Which of the following is an appropriate first-line treatment for symptomatic frequent VPCs?
- 10 10. Why are frequent VPCs concerning in patients with structural heart disease?
- 11 ECG Characteristics
- 12 Patterns of Occurrence
- 13 Types Based on Morphology
- 14 Clinical Relevance
- 15 Clinically significant
- 16 Management
- 17 Prognosis
- 18 Prognostic Implications Vary by Context
- 19 VPC-Induced Cardiomyopathy
- 20 VPCs During Exercise or Recovery
- 21 VPCs in ECG – Risk Stratification (20 Key Points)
1. What is a Ventricular Premature Complex (VPC)?
A. A premature beat originating from the atria
B. A premature beat originating from the AV node
C. A premature beat originating from the ventricles
D. A pause following a normal sinus beat
✅ Correct Answer: C
Explanation:
VPCs (also called PVCs – Premature Ventricular Contractions) are early depolarizations originating in the ventricles. They bypass the normal conduction pathway, resulting in abnormal, widened QRS complexes without preceding P waves.
2. Which of the following ECG features is characteristic of a VPC?
A. Narrow QRS complex
B. P wave before each QRS
C. Wide, bizarre QRS complex
D. Long PR interval
✅ Correct Answer: C
Explanation:
Because VPCs originate in the ventricular myocardium, the impulse takes longer to travel, producing a wide (>120 ms) and often bizarre-looking QRS complex.
3. What usually follows a VPC on the ECG?
A. Atrial fibrillation
B. A compensatory pause
C. Shortened QT interval
D. PR prolongation
✅ Correct Answer: B
Explanation:
VPCs are usually followed by a full compensatory pause, as the sinus node timing is unaffected, and the next normal sinus beat arrives on schedule.
4. Which of the following is NOT typically associated with VPCs?
A. Hypokalemia
B. Myocardial ischemia
C. Digoxin toxicity
D. Hyperthyroidism
✅ Correct Answer: D
Explanation:
While VPCs can occur in various conditions, hyperthyroidism is more commonly linked with atrial arrhythmias like atrial fibrillation. VPCs are typically associated with ischemia, electrolyte imbalance, and digitalis toxicity.
5. A pattern where a VPC occurs after every normal beat is known as:
A. Trigeminy
B. Bigeminy
C. Couplet
D. Quadrigeminy
✅ Correct Answer: B
Explanation:
Bigeminy is a rhythm in which every second beat is a VPC — a normal beat followed by a VPC repeatedly.
6. What defines a couplet in the context of VPCs?
A. Two VPCs from different foci
B. Two VPCs in a row
C. VPC with a supraventricular beat
D. Two VPCs with compensatory pauses
✅ Correct Answer: B
Explanation:
A couplet refers to two consecutive VPCs. It’s important as it may indicate increased ventricular irritability.
7. Three or more consecutive VPCs at a rate >100 bpm are termed:
A. Ventricular fibrillation
B. Supraventricular tachycardia
C. Ventricular tachycardia
D. Paroxysmal atrial tachycardia
✅ Correct Answer: C
Explanation:
Ventricular tachycardia (VT) is defined as three or more VPCs in a row at a rate >100 bpm. It may be sustained (>30 sec) or non-sustained.
8. What is a fusion beat?
A. Simultaneous atrial and ventricular beat
B. Beat with features of both sinus and VPC
C. Two VPCs fused together
D. Ventricular beat with a hidden P wave
✅ Correct Answer: B
Explanation:
A fusion beat is when a sinus beat and a VPC occur simultaneously, producing a hybrid QRS complex. It’s a sign of ventricular origin during arrhythmia.
9. Which of the following is an appropriate first-line treatment for symptomatic frequent VPCs?
A. Amiodarone
B. Digoxin
C. Beta-blockers
D. Calcium channel blockers
✅ Correct Answer: C
Explanation:
Beta-blockers are the first-line for symptomatic VPCs, especially in post-MI patients or those with structural heart disease. Antiarrhythmics like amiodarone are used in resistant or high-risk cases.
10. Why are frequent VPCs concerning in patients with structural heart disease?
A. They improve cardiac output
B. They indicate AV nodal reentry
C. They may degenerate into ventricular fibrillation
D. They resolve spontaneously with rest
✅ Correct Answer: C
Explanation:
In patients with underlying cardiomyopathy or ischemic heart disease, frequent VPCs can be a warning sign and may lead to ventricular tachycardia or ventricular fibrillation, both of which are life-threatening.
ECG Characteristics
- Wide QRS complex (>120 ms)
- Bizarre morphology (different from normal QRS)
- No preceding P wave
- T wave direction opposite to QRS
- Usually followed by a full compensatory pause
Patterns of Occurrence
- Isolated VPC: Single premature beat
- Couplet: Two consecutive VPCs
- Triplet: Three consecutive VPCs (may be nonsustained VT)
- Bigeminy: VPC after every normal beat
- Trigeminy: VPC after every two normal beats
- Quadrigeminy: VPC after every three normal beats
Types Based on Morphology
- Unifocal VPCs: All VPCs look the same (same origin)
- Multifocal VPCs: Different morphologies (different origins) → higher risk
Clinical Relevance
- Occasional VPCs in healthy individuals may be benign
- Frequent VPCs (>10% of total beats or >30/hour) need evaluation
- R-on-T phenomenon: VPC falling on preceding T wave → may trigger VT/VF
- High burden VPCs can cause VPC-induced cardiomyopathy
Clinically significant
- VPCs in presence of:
- Structural heart disease (e.g. MI, cardiomyopathy)
- Syncope or palpitations
- Family history of sudden cardiac death
- LVEF < 40%
→ Require urgent cardiology evaluation
Management
- Asymptomatic + normal heart: Often no treatment
- Symptomatic or frequent:
- ✅ Lifestyle: avoid caffeine, stress, alcohol
- ✅ Beta-blockers (1st line)
- Calcium channel blockers (non-dihydropyridine) in some cases
- Antiarrhythmics (e.g., Amiodarone) in selected cases
- Catheter ablation for refractory or high-burden VPCs
Prognosis
- Benign if infrequent and no structural heart disease
- Concerning if:
- High frequency
- R-on-T phenomenon
- Multifocal origin
- Occur during exercise or recovery
Prognostic Implications Vary by Context
| Context | Prognosis |
|---|---|
| Healthy heart, isolated VPCs | Usually benign |
| Post-MI with frequent VPCs | High risk for SCD |
| Dilated cardiomyopathy with VPCs | Worsens prognosis |
| VPC-induced cardiomyopathy | Reversible if burden reduced |
VPC-Induced Cardiomyopathy
- Chronic high-burden VPCs (>10–15% of all beats) can cause:
- LV dysfunction
- Dilated cardiomyopathy
- Reversible with:
- Medical suppression (e.g., beta-blockers)
- Catheter ablation (curative in many)
VPC falling on the preceding T wave can trigger malignant ventricular arrhythmias
Especially dangerous in:
- Ischemia
- Long QT syndromes
- Electrolyte disturbances
VPCs During Exercise or Recovery
- VPCs at peak exercise: May be benign
- VPCs during recovery phase:
- Strongly associated with increased cardiac mortality
- Reflect autonomic imbalance and myocardial vulnerability
| Feature | Risk Level |
|---|
| Isolated VPCs in healthy heart | Low |
| Frequent VPCs with structural heart disease | High |
| R-on-T, polymorphic, exercise-recovery VPCs | Very high |
| VPC-induced cardiomyopathy | Reversible with treatment |
VPCs in ECG – Risk Stratification (20 Key Points)
| # | Parameter | High-Risk Features | Low-Risk Features |
|---|---|---|---|
| 1 | Underlying heart disease | Structural heart disease (e.g. MI, cardiomyopathy) | Normal heart |
| 2 | Frequency | >10,000 VPCs/day or >10% burden | <1% burden, rare |
| 3 | Pattern | Bigeminy, couplets, triplets, runs | Isolated VPCs |
| 4 | Morphology | Polymorphic, multifocal | Monomorphic |
| 5 | VPC timing | R-on-T phenomenon | Occurs after T wave |
| 6 | Exercise stress test | VPCs in recovery phase | VPCs at peak exercise or absent |
| 7 | Symptoms | Syncope, presyncope, palpitations | Asymptomatic |
| 8 | Ejection fraction (EF) | LVEF <40% | LVEF >50% |
| 9 | Response to exercise | Increase in VPCs | Suppression with exercise |
| 10 | 24-hr Holter monitoring | >500 VPCs/hour | <30 VPCs/hour |
| 11 | Couplets/triplets | Present | Absent |
| 12 | Sustained VT history | Present | Absent |
| 13 | Family history of SCD | Present | Absent |
| 14 | VPC burden effect on LV | LV dysfunction (PVC-induced cardiomyopathy) | No effect on LV |
| 15 | Fusion beats | Seen (suggests re-entry) | Absent |
| 16 | QT interval | Prolonged QT with VPCs → torsades risk | Normal QT |
| 17 | Presence of scar (MRI) | Scar/fibrosis seen | Normal myocardium |
| 18 | Response to beta blockers | Poor/no response | Symptom relief |
| 19 | Inducibility on EP study | VT inducible | Not inducible |
| 20 | ICD indication | Meets primary/secondary prevention criteria | Not indicated |
Frequency:
The number of PVCs per minute or hour (PVC burden) is a crucial risk factor. More than 5 PVCs per minute or 10-30 per hour are generally considered frequent.
