👉 In practice, ablation is often considered when VT is drug-refractory, recurrent, or causing ICD shocks, provided the patient can safely undergo the procedure.
How isoprenaline (isoproterenol) controls VT ?
The way isoprenaline (isoproterenol) controls VT depends on the mechanism of arrhythmia.
1. Idiopathic VF / Brugada / Early repolarization syndrome
These arrhythmias are triggered by phase-2 reentry or Purkinje PVCs.
At slow heart rates, abnormal repolarization (J-wave accentuation, action potential heterogeneity) favors PVCs and VF.
Isoprenaline (β-agonist) increases sympathetic tone → raises heart rate → shortens action potential duration and suppresses early afterdepolarizations.
This reduces dispersion of repolarization and stabilizes the ventricular myocardium.
Net effect: PVC suppression → VF/VT storm breaks.
2. General mechanism
β-1 stimulation → increases HR and conduction → overrides pause-dependent triggers.
β-2 stimulation → increases calcium influx → suppresses phase-2 reentry in Brugada / ER syndrome.
3. Why not in scar-related VT?
In structural VT (reentry circuits in scar tissue), isoprenaline increases excitability and automaticity → promotes arrhythmia instead of suppressing it.
✅ In short:
Isoprenaline works by increasing heart rate, reducing repolarization heterogeneity, and suppressing PVC triggers, which is why it’s lifesaving in Brugada, idiopathic VF, and early repolarization VT storms but harmful in scar-related VT storms.
Management of VT storm (electrical storm: ≥3 episodes of sustained VT/VF requiring intervention within 24h):
It requires simultaneous acute stabilization and long-term planning:
1. Immediate stabilization
ICD reprogramming: prolong detection intervals, reduce shocks, promote ATP use.
Hemodynamic support: oxygen, IV fluids, vasopressors if hypotensive.
Mechanical circulatory support if unstable (IABP, Impella, ECMO).
2. Antiarrhythmic drug therapy
Amiodarone (IV bolus + infusion) → first-line.
Lidocaine IV (especially in ischemic VT).
Procainamide (if available, especially in idiopathic VT, but limited by hypotension).
Beta-blockers (IV metoprolol, propranolol, or esmolol) → blunt sympathetic drive, very important.
Avoid excessive catecholamines (they aggravate VT).
3. Sympathetic modulation
Sedation (benzodiazepines, propofol, or dexmedetomidine) to reduce adrenergic surge.
General anesthesia if needed for recurrent VT.
Stellate ganglion block / sympathectomy → highly effective in refractory VT storm.
4. Treatment of underlying cause
Acute ischemia → urgent revascularization.
Heart failure decompensation → optimize diuretics/inotropes.
Electrolytes → correct hypokalemia, hypomagnesemia.
Thyrotoxicosis, infection, drug toxicity → treat accordingly.
5. Definitive therapy
Catheter ablation (once stabilized, or emergent if refractory).
Heart transplant in refractory cases with end-stage cardiomyopathy.
✅ In short: Suppress sympathetic tone (sedation, beta-blockade), stabilize hemodynamics, give IV antiarrhythmics (amiodarone ± lidocaine), correct triggers, and consider sympathetic blockade or ablation if refractory.
Contraindications of ventricular tachycardia (VT) ablation can be grouped into absolute and relative:
Absolute contraindications
Inability to obtain vascular access (e.g., severe peripheral vascular disease without alternative access).
Active systemic infection or sepsis.
Uncorrected coagulopathy or severe bleeding disorder.
Patient unwilling or unable to provide consent.
VT that is clearly non-clinical or not inducible, making ablation targetless.
Relative contraindications:
Severe hemodynamic instability that cannot be supported (unless mechanical circulatory support is available).
Severe comorbidities where risks outweigh benefits (e.g., advanced multi-organ failure, end-stage malignancy).
Thrombus in the left ventricle or left atrium (risk of embolization).
Pregnancy (risk from radiation and procedure, unless absolutely necessary).
Recent myocardial infarction (very acute phase, tissue still evolving).
Thanks.
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