Cardiovascular · Year 1 · from Cardiovascular

Case 2: Ventricular Tachycardia in Ischemic Cardiomyopathy

Patient Presentation

Demographics: 58-year-old male

Chief Complaint: Palpitations and near-syncope

History of Present Illness: A 58-year-old male with history of prior inferior STEMI (5 years ago, treated with PCI to RCA) and ischemic cardiomyopathy (EF 30%, has ICD) presents with sudden onset of rapid palpitations while sitting at his desk. He felt lightheaded and "almost passed out" but remained conscious. His ICD delivered a shock and his symptoms resolved. He reports no chest pain, dyspnea, or preceding symptoms. He has been compliant with his medications including metoprolol, lisinopril, and atorvastatin.

Physical Examination:

  • Post-shock: BP 118/72 mmHg, HR 68 bpm (regular), RR 16/min, SpO2 98% on room air
  • General: Alert, appears fatigued but comfortable
  • Cardiovascular: Regular rhythm, no murmurs, ICD pocket visible in left pectoral region
  • Lungs: Clear

Workup

  • ICD Interrogation:
  • Sustained monomorphic VT at 210 bpm detected
  • Duration: 45 seconds before therapy
  • Anti-tachycardia pacing (ATP) unsuccessful
  • Shock delivered at 35J - successful termination
  • Stored electrogram shows wide complex tachycardia with RBBB morphology
  • ECG (post-event):
  • Sinus rhythm, 68 bpm
  • Q waves in II, III, aVF (inferior MI)
  • LBBB at baseline
  • Labs:
  • K 4.2, Mg 2.0
  • Troponin mildly elevated (likely demand ischemia)
  • BNP 380 pg/mL
  • Echocardiogram: EF 28%, inferior and posterior akinesis, no new abnormalities

Diagnosis

Sustained monomorphic ventricular tachycardia - appropriate ICD therapy delivered Substrate: Scar-related reentry from prior inferior MI

Cardiac Arrhythmias Correlation:

Mechanism of Monomorphic VT:

  1. Reentry Around Scar Tissue:
  • Prior MI created heterogeneous scar tissue
  • Surviving myocyte bundles within scar form slow conduction channels
  • Creates substrate for reentrant circuit
  • Fixed circuit = uniform (monomorphic) QRS morphology
  1. Components of Scar-Related Reentry:
  • Central isthmus: Slow conducting channel through scar
  • Entrance site: Where impulse enters isthmus
  • Exit site: Where impulse emerges to activate ventricle
  • QRS morphology determined by exit site location
  1. Why Monomorphic?
  • Fixed anatomic circuit
  • Each beat follows same path
  • Consistent QRS appearance beat-to-beat
  • Contrast with polymorphic VT (multiple foci or shifting circuit)

ECG Features of VT:

  • Wide QRS (>120 ms) - ventricular origin
  • AV dissociation (P waves independent of QRS)
  • Capture/fusion beats if present (pathognomonic)
  • Monomorphic: Uniform QRS morphology

Distinguishing VT from SVT with Aberrancy:

FeatureFavors VT
AV dissociationHighly specific
Capture/fusion beatsDiagnostic
Very wide QRS (>160 ms)Suggests VT
Concordance in precordial leadsSuggests VT
History of structural heart diseaseStrong predictor

Rule: When in doubt, treat wide complex tachycardia as VT

ICD Function:

  1. Detection: Sensed rapid ventricular rate >180 bpm
  2. Discrimination: Determined ventricular origin (not SVT)
  3. Anti-tachycardia pacing (ATP): Burst pacing to interrupt reentry - unsuccessful
  4. Defibrillation: High-energy shock terminated arrhythmia

Treatment

Acute Management:

  1. Hemodynamically stable post-shock - observation
  2. Electrolyte repletion (maintain K >4.0, Mg >2.0)
  3. Continue beta-blocker

VT Prevention:

  1. Antiarrhythmic drug therapy:
  • Amiodarone or sotalol to suppress VT episodes
  • Amiodarone preferred with low EF
  • Reduces ICD shocks but does not eliminate VT risk
  1. Catheter Ablation:
  • Consider for recurrent VT despite drug therapy
  • Maps and ablates critical isthmus of reentry circuit
  • Can eliminate or reduce VT burden

ICD Management:

  • Appropriate shock - device functioning properly
  • Program to maximize ATP before shock (reduces painful shocks)
  • Adjust detection parameters if needed

Optimize Heart Failure Therapy:

  • Ensure on guideline-directed medical therapy
  • Consider cardiac resynchronization if criteria met

Clinical Pearl

Arrhythmia Mechanisms Summary:

MechanismExampleKey Feature
Enhanced automaticitySinus tachycardiaAccelerated intrinsic rate
Triggered activity (EAD)Torsades de pointesLong QT, pause-dependent
Triggered activity (DAD)Digoxin toxicityCalcium overload
ReentryAF, VT, AVNRTCircuit, unidirectional block

Clinical Significance of This Case: This patient's ICD functioned as intended - detecting and terminating a potentially fatal arrhythmia. Without the ICD, sustained VT at 210 bpm could have degenerated to ventricular fibrillation and sudden cardiac death. This case illustrates:

  1. The importance of primary prevention ICD in patients with EF <35%
  2. Scar-related reentry as the most common mechanism of VT in ischemic cardiomyopathy
  3. The role of antiarrhythmic drugs and ablation in reducing VT burden

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