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:
- 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
- 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
- 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:
| Feature | Favors VT |
|---|---|
| AV dissociation | Highly specific |
| Capture/fusion beats | Diagnostic |
| Very wide QRS (>160 ms) | Suggests VT |
| Concordance in precordial leads | Suggests VT |
| History of structural heart disease | Strong predictor |
Rule: When in doubt, treat wide complex tachycardia as VT
ICD Function:
- Detection: Sensed rapid ventricular rate >180 bpm
- Discrimination: Determined ventricular origin (not SVT)
- Anti-tachycardia pacing (ATP): Burst pacing to interrupt reentry - unsuccessful
- Defibrillation: High-energy shock terminated arrhythmia
Treatment
Acute Management:
- Hemodynamically stable post-shock - observation
- Electrolyte repletion (maintain K >4.0, Mg >2.0)
- Continue beta-blocker
VT Prevention:
- Antiarrhythmic drug therapy:
- Amiodarone or sotalol to suppress VT episodes
- Amiodarone preferred with low EF
- Reduces ICD shocks but does not eliminate VT risk
- 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:
| Mechanism | Example | Key Feature |
|---|---|---|
| Enhanced automaticity | Sinus tachycardia | Accelerated intrinsic rate |
| Triggered activity (EAD) | Torsades de pointes | Long QT, pause-dependent |
| Triggered activity (DAD) | Digoxin toxicity | Calcium overload |
| Reentry | AF, VT, AVNRT | Circuit, 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:
- The importance of primary prevention ICD in patients with EF <35%
- Scar-related reentry as the most common mechanism of VT in ischemic cardiomyopathy
- The role of antiarrhythmic drugs and ablation in reducing VT burden