Polymorphic ventricular tachycardia

Background

Form of ventricular tachycardia
- Multiple ventricular foci
- QRS complexes with varying morphology
Subtypes include:
- Torsades de pointes
- bidirectional polymorphic VTach (as seen in digoxin toxicity)

Etiologies

Myocardial ischemia (most common)
Acquired or congenital prolonged QT
- TCAs, phenothiazines, Type I antiarrhythmics (quinidine, procainamide)
- Hypokalemia
- Hypomagnesemia
- Elevated intracranial pressure
Brugada syndrome, short QT syndrome, congenital catecholaminergic polymorphic ventricular tachycardia

Clinical Features

Differential Diagnosis

Wide-complex tachycardia

Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)

Regular
- Monomorphic ventricular tachycardia
- PSVT with aberrant conduction:
  - PSVT with bundle branch block^
  - PSVT with accessory pathway
  - Atrial flutter with bundle branch block^
- Sinus tachycardia with bundle branch block^
- Accelerated idioventricular rhythm (consider if less than or ~120 bpm)
- Metabolic
  - Hyperkalemia
  - Digoxin toxicity
  - Severe metabolic acidosis
Irregular
- Atrial fibrillation/atrial flutter with variable AV conduction AND bundle branch block^
- Atrial fibrillation/atrial flutter with variable AV conduction AND accessory pathway (e.g. WPW)
- Atrial fibrillation + hyperkalemia
- Polymorphic ventricular tachycardia
  - Torsades de pointes
  - Nonsustained ventricular tachycardia

^Fixed or rate-related

Evaluation

Evaluate for underlying causes (e.g. electrolyte imbalances, ACS)

ECG Findings

Wide QRS (>100ms or 3 small boxes)
QRS complexes of varied amplitude, axis and duration
- Torsades: QRS complexes appear to twist around isoelectric line
Rapid rhythm (usually 140-160 bpm, but can be up to 300 bpm)
Irregular

Management

Pulseless

See Adult pulseless arrest and Pediatric pulseless arrest

Unstable

Unsynchronized cardioversion (defibrillation) 200J (or 2J/kg for pediatrics)
Correct any electrolyte abnormalities

Stable

Correct any electrolyte abnormalities
Torsades:
- Magnesium sulfate (for Torsades):
  - 1-2gm IV, repeat in 5-15min; then 1-2gm/hr (3-10mg/min) drip
  - Peds: 25-50mg/kg (max 2g) IV
- Isoproterenol, 2-8 mcg/min (if available)
- Overdrive Pacing to goal HR 90-120
  - Note that this is only effective for preventing recurrence of TdP - it will not convert TdP to sinus rhythm
- Consider Lidocaine
- Avoid procainamide, amiodarone (may further prolong QT)
Non-Torsades (baseline QT interval not prolonged)
- Amiodarone, agent of choice in setting of AMI or LV dysfunction
  - 150 mg over 10min (15 mg/min), followed by 1 mg/min drip over 6hrs (360 mg total), then 0.5 mg/min drip over next 18 hrs (540 mg total)
  - Peds: 5mg/kg (max 300mg), may repeat twice
- Procainamide
  - 100 mg q5min until termination of arrhythmia, then start 2-6 mg/min (or 1-2 mg/min for renal/cardiac failure)
  - Max dose 17mg/kg OR widening of QRS >50%
- Lidocaine, 1-1.5mg/kg IV q5min, repeat PRN up to 300mg/hr
- Beta-blockers (e.g. metoprolol 5mg IV q5m x 3) if blood pressure tolerates

Refractory

≥3 episodes within 24 hours considered electrical storm
May require alternate treatment (i.e. β-blockers, sedation, ablation)

Disposition

Admit with cardiology consult, even if back in normal sinus rhythm
- Stable patients may be admitted to ward
  - Pads should remain on patient's chest anticipating need for repeat cardioversion
  - All patients should remain on telemetry or full cardio-respiratory monitoring for recurrent events
- Patients with features of instability or refractory VT are best admitted to CCU or ICU and may require urgent or emergent pacemaker placement

External Links

References

Authors: