Harvey's Garden

Ventricular tachycardia

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  • Epidemiology & Risk Factors

    • Structural Heart Dz: Prior MI (scar tissue re-entry) = Most common cause. Dilated/Hypertrophic CM.
    • Electrolytes: Hypokalemia, Hypomagnesemia.
    • Drugs: Antiarrhythmics (Class IA, III), TCAs, Digoxin toxicity.
    • Congenital: Long QT syndrome (Romano-Ward, Jervell-Lange-Nielsen), Brugada syndrome.

  • Clinical Features

    • Symptoms: Palpitations, dyspnea, lightheadedness, syncope, chest pain.
    • Signs: Cannon A-waves (AV dissociation), hypotension (if unstable), signs of HF.
    • Presentation:
      • Non-sustained VT (NSVT): &lt 30 sec, self-terminating.
      • Sustained VT: >30 sec or hemodynamic collapse.
      • Monomorphic: Consistent QRS shape (scar-mediated).
      • Polymorphic: Varying QRS shape (Torsades de Pointes/Ischemia).

  • Diagnosis

    • Initial/Confirmatory: 12-lead ECG (if stable).
      • Findings: Wide complex tachycardia (QRS > 120ms), rate > 100 bpm.
      • Specific for VT: AV dissociation (P waves unrelated to QRS), Fusion beats, Capture beats.
      • Concordance: Precordial leads (V1-V6) all positive or all negative.
    • Labs: Electrolytes (K+, Mg2+), Troponin (r/o ischemia), Tox screen.
    • Post-Conversion: TTE (assess EF/structural dz), Ischemia workup (Cath/Stress).

  • Differential Diagnostics

    • SVT with Aberrancy: Diff by presence of P waves preceding QRS, response to vagal maneuvers/adenosine (SVT slows/terminates, VT usually doesn’t—Caveat: Adenosine can be used diagnostically in stable wide-complex tach per recent ACLS, but proceed w/ caution).
    • VFib: Disorganized chaotic rhythm, no pulse.
    • WPW (Antidromic): Wide complex, regular.
    • Hyperkalemia: Wide QRS, sine wave pattern.

  • Management

    1. Unstable (Hypotension, AMS, Shock, Ischemic CP, Acute HF):
      • Synchronized Cardioversion (sedate if conscious).
      • Note: If Pulseless -> Treat as VFib -> Defibrillation (Unsynchronized) + CPR + Epi.
    2. Stable Monomorphic VT:
      • First-line: IV Amiodarone (150 mg bolus -> drip).
      • Second-line: Procainamide (preferred in WPW), Lidocaine (ischemia-associated), Sotalol.
      • Note: If refractory-> Cardioversion.
    3. Polymorphic VT (Torsades):
      • IV Magnesium Sulfate.
      • Overdrive pacing / Isoproterenol (to shorten QT).
      • Correct ‘lytes (K > 4.5, Mg >2.0).
    4. Long-Term:
      • ICD: Indicated if EF < 35% (primary prevention) or hx of sustained VT/cardiac arrest (secondary prevention).
      • Meds: Beta-blockers (Metoprolol/Carvedilol), Amiodarone.

  • Complications

    • Degeneration into Ventricular Fibrillation (VFib).
    • Sudden Cardiac Death (SCD).
    • Cardiogenic Shock/Hemodynamic collapse.

Brugada syndrome

  • Epidemiology & Risk Factors
    • Autosomal dominant inheritance.
    • Loss-of-function mutation in the SCN5A gene encoding the cardiac voltage-gated sodium (Na+) channel (Nav1.5).
    • ↓ Inward Na+ current disrupts the cardiac action potential, creating repolarization heterogeneity (epicardium vs. endocardium) primarily in the right ventricular outflow tract.
    • Sets the stage for phase 2 reentry, predisposing the heart to polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF).
    • Predominantly affects Asian males.
    • Triggers: Fever, sleep/high vagal tone, sodium channel blockers (e.g., flecainide), TCAs, cocaine, alcohol.
  • Clinical Features
    • Often asymptomatic (incidentally found on ECG).
    • Recurrent syncope.
    • Nocturnal agonal respirations.
    • Sudden cardiac death (SCD) or ventricular fibrillation (VF), classically occurring during sleep or rest.
  • Diagnosis
    • Initial/Key Labs: Baseline ECG. Basic metabolic panel (rule out electrolyte abnormalities).
    • Classic ECG Findings:
      • Pseudo-Right Bundle Branch Block (RBBB).
      • “Coved-type” ST-segment elevation ≥ 2 mm followed by a negative T wave in the right precordial leads (V1–V3) = Type 1 pattern.
    • Confirmatory/Gold Standard:
      • Clinical diagnosis (Type 1 ECG + clinical criteria like syncope/family hx of SCD).
      • Provocative testing: IV administration of sodium channel blockers (flecainide, procainamide, ajmaline) to unmask the classic ECG pattern in suspected pts with normal/equivocal resting ECGs.
      • Genetic testing for SCN5A mutation (supportive, but not required for dx).

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