Ventricular Dyrhythmias

Study Notes

An early heartbeat originating in the ventricles, followed by a compensatory pause
Unifocal: one site of electrical impulse generation
Multifocal: multiple sites of electrical impulse generation
Common causes:
- Enhanced automaticity or re-entry mechanisms.
- Increased sympathetic tone, stimulants, medications mimicking sympathetic actions.
- Myocardial ischemia or infarction, hypoxia, acidosis, hyperkalemia.
Pathophysiology:
- Frequent: Occurrence once every 5 minutes or less.
- Non-frequent: Occurrence more than every 5 minutes.
- Couplets: Two consecutive PVCs.
- Ventricular tachycardia: Three or more consecutive PVCs.
- Bigeminy: Every second beat is abnormal.
- Trigeminy: Every third beat is abnormal.
- Quadrigeminy: Every fourth beat is abnormal.
Clinical significance:
- Isolated PVCs: Not immediately significant, but the underlying cause matters.
- Key determinant: Frequency of PVCs.
- R-on-T phenomenon: PVC occurring on the T wave of the previous QRS complex, can trigger repetitive ventricular complexes leading to ventricular tachycardia or fibrillation.
ECG analysis:
- Rate: That of the underlying rhythm.
- Regularity: Depends on PVC frequency, irregularity associated with PVCs.
- P wave: Should be normal.
- PR interval: Should be normal.
- QRS: Abnormal during PVC, otherwise generally normal.
- Origin: Ectopic site in the ventricles.

Fast heartbeat (100-250 bpm) originating from ectopic pacemakers within the ventricles.
Causes:
- Acute coronary syndromes, cardiomyopathy, valvular diseases.
- Atrial or ventricular valve abnormalities.
- Medications causing QT interval prolongation, electrolyte imbalances (hyperkalemia).
- Genetic conditions, R-on-T phenomenon.
Pathophysiology:
- With pulse (non-cardiac arrest): maintained blood flow.
- Pulseless (cardiac arrest): no blood flow.
- Non-sustained: Lasting less than 30 seconds (nonparoxysmal).
- Sustained: Lasting more than 30 seconds.
- Monomorphic VT: One ectopic pacemaker, results in a single type of wide QRS.
- Polymorphic VT: Multiple ectopic pacemakers, multiple different QRS complexes.
  - Torsades de pointes: Gradually alternating shape, size, and direction of QRS complexes.
- Bidirectional VT: Two alternating QRS complexes.
Clinical significance:
- High workload on the heart leading to decreased cardiac output and increased oxygen demand, potentially insufficient to maintain blood flow.
- Not sustainable for long periods.
- Underlying cause of VT is often a pre-existing cardiac issue.
ECG analysis:
- Rate: 100-250 bpm.
- Regularity: Generally regular with slight variations.
- P wave: Absent.
- PR interval: None.
- QRS: Wide complexes, abnormal appearance.
- Origin: Ectopic pacemaker in the ventricles.

Chaotic electrical activity in the ventricles with incomplete depolarization.
Causes:
- Cardiomyopathy, cardiac trauma, hypoxia, acidosis, electrolyte imbalances (hyperkalemia and hypokalemia).
- Medications, electrocution, failed cardioversion, R-on-T phenomenon.
Pathophysiology:
- Coarse VF: Larger deflections on ECG, potentially more oxygenated.
- Fine VF: Smaller deflections on ECG, potentially less oxygenated.
Clinical significance: No cardiac output, cardiac arrest.
ECG analysis:
- Rate: Technically 300-500 bpm but uncoordinated.
- Regularity: None.
- P wave: Absent.
- PR interval: Absent.
- QRS: Absent.
- Origin: Multiple ectopic sites in the ventricles.

Rhythm originating from an ectopic pacemaker in the ventricles, becoming the dominant rhythm.
Causes: Blockage above the ventricles preventing the SA node and AV junction from pacing, forcing the ventricles to take over.
- Sinus arrest, sinoatrial exit block, third-degree AV block, block below the AV node.
Pathophysiology:
- AIVR: Can occur during return of spontaneous circulation (ROSC).
Clinical significance:
- Poor cardiac output alongside the underlying cause, leading to significant hemodynamic instability.
ECG analysis:
- Rate:
  - IVR: 20-40 bpm.
  - AIVR: Over 40 bpm.
- Regularity: Should be regular.
- P wave: Absent.
- PR interval: Absent.
- QRS: Wide.
- Origin: Ventricular pacemakers.

Also known as ventricular standstill.
Complete absence of any ventricular electrical activity.
Causes:
- Failure of all primary escape pacemakers.
- VT or VF refractory to defibrillation.
Pathophysiology:
- Transient asystole: Temporary cessation of electrical activity, often after termination of supraventricular tachycardia or ventricular tachycardia, or medication administration.
Clinical significance: Loss of ventricular activity, no cardiac output.
ECG analysis:
- Rate: None.
- Regularity: None.
- P wave: Mostly absent, may be present if there is an active SA node or AV junction pacemaker.
- PR interval: None.
- QRS: Absent.
- Origin: None.