Ventricular Tachycardia

1) Definitions of Ventricular Tachycardia

Nonsustained VT (NSVT) = at least 3 beats of VT that lasts < 30 seconds (if less than 3 beats, those are just PVCs)
Sustained VT = 30 seconds
Accelerated idioventricular rhythm - basically like VT but with rate < 100
Monomorphic VT - all QRS complexes have same height and morphology (can be sustained or nonsustained)
Polymorphic VT - differing QRS complexes. Can be associated with long QT interval (=Torsades de pointes) or normal QT.

2) Definition of VT Storm

Variable definitions used, but essentially refers to multiple episodes of VT/VF within a short period of time.
One commonly used definition is 3 or more episodes of VT over 24 hours
Management essentially involves finding and treating the etiology/inciting factor (although often none found), especially new myocardial ischemia, as well as antiarrhythmics (most often amiodarone and lidocaine), and potentially VT ablation (see below).
“Incessant VT” refers to hemodynamically stable VT that lasts several hours.

3) Evaluation of Wide Complex Tachycardia - Differentiating VT vs SVT with aberrancy
Factors that favor VT on EKG:
* AV dissociation proves VT *

Dissociated p waves (i.e. p waves that have no clear relation to the QRS)
Fusion beat = impulse from above the ventricles conducts down to ventricles and fuses with ventricular beat --> hybrid beat that is wider than a normal QRS but narrower than a VT beat
Capture beats = impulse from above ventricles “captures” (see normal, narrow QRS)

Also suggestive of VT (but not definitive):

Extreme right axis deviation
Very wide QRS (>160 ms)
Concordance in precordial leads (all QRS in same direction in leads V1-V6).

On history:

Age < 35 - usually SVT, > 35 - usually VT
Presence of structural heart disease (e.g. CAD and MI) --> very strong indicator of VT (>95% in one series)

** If unsure if VT or SVT, always treat as if VT!!! Reason is that majority of wide complex tachycardia is VT (~80%) and treatment for VT often works for SVT, but treatment for SVT can be catastrophic for VT (i.e. adenosine, beta blockers/CCBs can cause cardiovascular collapse in VT)

4) Underlying etiologies for VT and Mechanisms of Tachyarrhythmias
1. Increased Automaticity – accelerated spontaneous generation of action potentials from irritable myocardium
- Hypoxia or Ischemia – this generally needs to be ruled out, not only with troponins but often with cardiac cath
- Electrolyte abnormalities, particularly Hyperkalemia – results in increased cardiac tissue excitability
- Acidemia
- Hyperadrenergic state – i.e. Sepsis, Hyperthyroid state
- Meds – Vasopressors, Digoxin
2. Re-entry – fixed substrate with scar/fibrous tissue that will always predispose to VT
- Prior MI
- Cardiomyopathy

3. Triggered Activity – QRS falling on T-wave – occurs with prolonged QT interval
- Electrolytes – Hypokalemia, Hypomagnesemia, Hypocalcemia
- Drugs that prolong QT interval – many antiarrhythmics, Antibiotics, Antipsychotics, etc

5) Review Antiarrhythmic Classes
1. Class I = Sodium channel blockers - inhibit depolarization of action potential

IA = Intermediate binding/dissociation – Procainamide, Quinidine
IB = Rapid binding/dissociation – Lidocaine
IC = Slow binding/dissociation – Flecainide, Propafenone (contraindicated in patients with CAD due to the CAST trial showing increased mortality in post-MI patients)

2. Class II = Beta blockers

3. Class III = Potassium channel blockers - prolong repolarization phase.

** Cause prolongation of QT interval **

Sotalol – also a beta blocker
Ibutilide
Amiodarone – also blocks Na channels, calcium channels, K, and adrenergic receptors

4. Class IV = Calcium channel blockers – slow AV and sinus nodes (nondihydropyridines ) – Verapamil, Diltiazem

6) Management of VT - Antiarrhythmics and more
First step is determining if stable or unstable. If unstable with pulse --> synchronized cardioversion. If pulseless --> defibrillation + CPR (ACLS algorithm)

If stable but having frequent runs of VT - can try antiarrhythmics.

Lidocaine - 100 mg bolus, can rebolus (usually not more than 1-2 times max), then drip 1-4 mg/min. Boluses of lidocaine are limited by CNS toxicity (see below)
Amiodarone - 150 mg bolus over 10 mins, then usually 1 mg/min x 6 hrs, then 0.5 mg/min. Careful for hypotension (due to solvent) which occurs in ~26% of cases. Advantage of amiodarone is that you can rebolus multiple times (e.g. 10 times per day or more) as opposed to lidocaine.

Also important to search for underlying precipitants and correct what you can:
- Rule out active ischemia
- Correct electrolyte abnormalities if any (K, Mg, Ca)
- Optimize CHF (e.g. diuresis)

Lidocaine Toxicity
Dose-dependent CNS toxicity - can get altered mental status, slurred speech/dysarthria, and CNS excitation (tremors, seizures) followed by CNS depression (decreased mental status and unconsciousness, respiratory depression). Must follow levels in all patients - have narrow therapeutic range (~1-5 mcg/mL)

7) Brief Overview of VT catheter ablation

In general, it is very successful and often curative for idiopathic VT, i.e. VT in the absence of structural heart disease. It is only moderately successful for VT in the setting of structural heart disease, and is typically used as an adjuct to ICD (not as a replacement) in an effort to improve quality of life by decreasing the number and frequency of ICD shocks.

(Chanu Rhee MD, 7/2/10 & 11/2/10)