1. Initial Assessment and Stratification

Rapidly determine hemodynamic status and ECG phenotype to guide immediate therapy.

A. Hemodynamic Stability

• Stable: Adequate blood pressure, mentation, and organ perfusion.
• Unstable: Hypotension, shock, altered mental status, or ongoing myocardial ischemia.

B. ECG Classification

• Monomorphic VT: Regular wide QRS complex (>120 ms) with uniform morphology. AV dissociation may be present.
• Polymorphic VT: Beat-to-beat variation in QRS morphology and/or axis.
• Torsades de Pointes (TdP): A specific form of polymorphic VT characterized by a prolonged QT interval and a “twisting” QRS morphology around the isoelectric baseline.

2. Synchronized Cardioversion and Defibrillation

The patient’s hemodynamic status dictates the choice of electrical therapy modality and initial energy settings.

A. Unstable Monomorphic VT (with a pulse)

• Synchronized Cardioversion: Initiate with biphasic energy at 50–100 Joules. Escalate energy levels as needed if the initial shock is unsuccessful.
• Provide brief sedation (e.g., etomidate, midazolam, or propofol) if the clinical situation allows time, to improve patient comfort.

B. Pulseless VT/Ventricular Fibrillation (VF), Unstable Polymorphic VT, or Torsades de Pointes

• Unsynchronized Defibrillation: Deliver a high-energy shock (e.g., biphasic 200–360 Joules, or device maximum) as per Advanced Cardiovascular Life Support (ACLS) guidelines.
• Resume chest compressions immediately after shock delivery, minimizing interruptions.

C. Key Considerations for Electrical Therapy

• Synchronization is crucial in patients with a pulse to avoid delivering a shock during the vulnerable period of the T-wave, which could precipitate VF.
• In pulseless rhythms (VT/VF), synchronization is not possible or necessary; deliver maximal defibrillation energy promptly.

3. Pharmacotherapy of Stable Ventricular Tachycardia

For hemodynamically stable VT, select intravenous antiarrhythmic drugs based on their efficacy, the presence of underlying structural heart disease, and their safety profile.

A. Monomorphic VT

1. Amiodarone (Class III)

• Mechanism: Primarily blocks potassium channels, prolonging action potential duration. Also exhibits sodium channel, calcium channel, and beta-blocking properties.
• Dosing: 150 mg IV infused over 10 minutes, followed by a continuous infusion of 1 mg/min for 6 hours, then 0.5 mg/min.
• Monitoring: ECG (QTc interval, heart rate for bradycardia), blood pressure (for hypotension), liver function tests, and thyroid function (with long-term use).
• Pearls: Generally preferred in patients with structural heart disease or heart failure. Infuse the loading dose slowly to minimize hypotension.

2. Procainamide (Class IA)

• Mechanism: Blocks sodium channels, slowing conduction velocity and prolonging action potential duration.
• Dosing: 20–50 mg/min IV infusion until VT terminates, QRS complex widens by >50% from baseline, hypotension develops, or a total of 17 mg/kg has been administered. Maintenance infusion: 1–4 mg/min.
• Monitoring: Continuous ECG (QRS duration, QT interval), blood pressure. Monitor renal function, as its active metabolite NAPA is renally cleared.
• Pitfall: Avoid in patients with severe heart failure or a baseline prolonged QT interval due to proarrhythmic risk.

3. Lidocaine (Class IB)

• Mechanism: Blocks sodium channels, particularly effective in ischemic tissue by shortening action potential duration in diseased cells.
• Dosing: Initial bolus of 1–1.5 mg/kg IV. May repeat 0.5–0.75 mg/kg every 5–10 minutes up to a total dose of 3 mg/kg. Follow with a maintenance infusion of 1–4 mg/min.
• Monitoring: Neurologic status (for signs of toxicity like seizures, paresthesias, confusion), liver function (as it’s hepatically metabolized).
• When to choose: Particularly useful for VT associated with acute myocardial ischemia. Generally has a lower risk of proarrhythmia compared to Class IA or IC agents.

B. Polymorphic VT (non-Torsades de Pointes)

If polymorphic VT is suspected to be ischemia-mediated, initial management may be similar to monomorphic VT. Consider amiodarone or lidocaine. Aggressively treat myocardial ischemia. If QTc is prolonged, manage as Torsades de Pointes.

4. Torsades de Pointes (TdP) Specific Management

Management of TdP focuses on terminating the arrhythmia, preventing recurrence by addressing QT prolongation, and correcting bradycardia-dependent triggers.

• Unstable or Pulseless TdP: Treat with immediate unsynchronized defibrillation as per ACLS guidelines.
• Intravenous Magnesium Sulfate: Administer 2 grams IV as a bolus over 1–2 minutes, regardless of serum magnesium levels. This can be followed by a maintenance infusion of 1–2 g/hr if TdP is recurrent.
• Overdrive Pacing: If TdP is recurrent or refractory, temporary transvenous pacing at rates of 90–110 beats per minute can shorten the QT interval and suppress TdP. Atrial pacing is preferred if AV conduction is intact.
• Isoproterenol Infusion: If temporary pacing is unavailable or while awaiting pacing, an isoproterenol infusion (1–5 µg/min, titrated to heart rate) can be used to increase heart rate and shorten the QT interval. Use with caution in patients with active ischemia.
• Discontinue QT-Prolonging Agents: Immediately identify and discontinue all medications known to prolong the QT interval.

5. Correction of Reversible Causes

Identifying and correcting underlying reversible causes is critical in the management of all types of ventricular tachycardias and for preventing recurrence.

• Electrolyte Imbalances:
  • Maintain serum potassium (K⁺) > 4.0 mEq/L.
  • Maintain serum magnesium (Mg²⁺) > 2.0 mg/dL.
  • Ensure normocalcemia.
• Offending Drugs: Review the patient’s medication list and discontinue any agents known to prolong the QT interval or precipitate arrhythmias. Common culprits include certain antiarrhythmics (Class IA, III), antipsychotics, antibiotics (macrolides, fluoroquinolones), and antiemetics.
• Myocardial Ischemia/Infarction: If acute ischemia is suspected or confirmed, provide appropriate anti-ischemic therapy (e.g., nitrates, beta-blockers, antiplatelet agents) and consider urgent revascularization (PCI or CABG) as indicated.

6. Device Therapies and Catheter Ablation

For recurrent or refractory VT, or for long-term prevention, device therapies and catheter ablation play a significant role.

A. Temporary Pacing

• Indications: Primarily for bradycardia-dependent Torsades de Pointes to increase heart rate and shorten QT interval. Can also serve as a bridge therapy for recurrent, hemodynamically significant VT that is difficult to control pharmacologically.
• Rate: Typically set at 90–110 beats per minute for TdP suppression.
• Considerations: Requires appropriate sedation and analgesia per institutional protocol.

B. Catheter Ablation

• Indications: Recurrent, drug-refractory monomorphic VT, or as a first-line therapy in some cases (e.g., idiopathic VT).
• Planning: Involves detailed electroanatomic mapping to identify the VT substrate. Requires careful consideration of sedation strategy (conscious sedation vs. general anesthesia) and periprocedural anticoagulation.
• Medication Management: Class I and III antiarrhythmic drugs are often held prior to the procedure to facilitate VT induction and mapping. Post-procedure medication management is guided by ablation success and residual arrhythmia burden.

C. Implantable Cardioverter-Defibrillator (ICD) Therapy

• Secondary Prevention: Indicated for survivors of VT/VF cardiac arrest or hemodynamically significant sustained VT.
• Primary Prevention: Indicated in patients with significantly reduced left ventricular ejection fraction (LVEF ≤ 35%) despite optimal medical therapy (OMT), and other specific high-risk conditions.
• Programming: ICD detection zones and therapies (anti-tachycardia pacing, shocks) should be carefully programmed and tailored to the individual patient to effectively terminate arrhythmias while minimizing inappropriate shocks and patient discomfort.

7. Pharmacokinetic (PK) and Pharmacodynamic (PD) Considerations in Critical Illness

Managing VT in critically ill patients requires attention to altered drug handling.

• Increased Volume of Distribution: Sepsis, shock, and fluid resuscitation can increase the volume of distribution for many drugs, potentially requiring higher loading doses or affecting time to steady state.
• Impaired Hepatic and Renal Clearance:
  • Hepatic dysfunction (common in shock states) can impair the metabolism of drugs like amiodarone and lidocaine.
  • Renal impairment or acute kidney injury can reduce the clearance of procainamide and its active metabolite N-acetylprocainamide (NAPA).
• Continuous Renal Replacement Therapy (CRRT): Drug removal by CRRT is variable and depends on drug properties and CRRT modality/settings. This can lead to unpredictable drug concentrations. Therapeutic drug monitoring and dose adjustments are often necessary.
• Dosing Adjustments: Weight-based dosing and adjustments based on organ function are essential to avoid drug toxicity or sub-therapeutic levels. Close monitoring for efficacy and adverse effects is paramount.

8. Monitoring and Safety

Vigilant monitoring is crucial during acute management and to prevent adverse effects of therapy.

• Continuous ECG/Telemetry: Monitor for VT recurrence, changes in QRS morphology or duration, development of bradyarrhythmias, AV block, and especially QTc interval prolongation.
• QTc Measurement: Measure the QTc interval at baseline and regularly (e.g., every 4–6 hours, or after each dose adjustment) when administering drugs known to prolong repolarization (e.g., amiodarone, procainamide).
• Laboratory Monitoring:
  • Serum electrolytes (potassium, magnesium, calcium) regularly.
  • Liver function tests (LFTs) and renal function panel (BUN, creatinine).
  • Thyroid function tests (for amiodarone therapy, especially long-term).
• Drug Levels: If available and clinically indicated, monitor serum levels of procainamide/NAPA and lidocaine, particularly in patients with organ dysfunction or suspected toxicity.
• Hemodynamics: Closely monitor blood pressure, heart rate, signs of organ perfusion (mental status, urine output), and lactate trends to assess response to therapy and detect deterioration.

9. Stepwise Management Algorithms

10. Pearls, Pitfalls, and Controversies