Ventricular Tachycardia: Diagnostic Evaluation and Risk Stratification
Learning Objective
Apply diagnostic and classification criteria to evaluate and risk-stratify patients with ventricular arrhythmias and sudden cardiac death (SCD) risk.
1. Introduction and Scope
Ventricular tachycardia (VT) is a wide-complex tachycardia originating below the His-Purkinje system. Early, accurate differentiation of VT subtypes and stability status drives both emergent interventions and long-term SCD prevention.
- VT classification: monomorphic vs. polymorphic (includes Torsades de Pointes)
- Hemodynamic stability guides urgency: stable vs. unstable VT
- Pharmacist role: verify ECG measurements, interpret risk tools, coordinate multidisciplinary care
Key Pearl
Structured risk stratification bridges acute management and chronic SCD prevention.
2. Clinical Manifestations and Hemodynamic Assessment
Presentation ranges from benign palpitations to cardiac arrest. Assess symptoms and perfusion markers rapidly to distinguish stable from unstable VT.
A. Signs and Symptoms
- Palpitations, chest discomfort, dyspnea—suggest preserved perfusion
- Presyncope/syncope—transient cerebral hypoperfusion (often SBP <90 mm Hg)
- Cardiac arrest—pulseless VT/VF
B. Hemodynamic Parameters
- Blood pressure: systolic <90 mm Hg indicates hypotension
- Mental status: agitation, confusion, or unresponsiveness
- Skin perfusion: cool, mottled extremities
- Urine output: <0.5 mL/kg/hr signals end-organ hypoperfusion
- Laboratory adjuncts: lactate elevation, troponin rise
C. Stability Classification
- Unstable VT: hypotension, altered mental status, shock, ongoing ischemia, or cardiac arrest—requires immediate cardioversion/defibrillation
- Stable VT: preserved perfusion, minimal symptoms—allows time for diagnostic evaluation and pharmacotherapy
Clinical Pearl
Reassess stability every 2–5 minutes; sedated or ventilated patients may mask decompensation.
3. ECG Interpretation in Ventricular Tachycardia
ECG criteria distinguish VT from supraventricular tachycardia with aberrancy and subtype of VT, guiding treatment choices.
| Feature | Monomorphic VT | Polymorphic VT | Torsades de Pointes (TdP) |
|---|---|---|---|
| Rhythm | Regular | Irregular | Irregular, cyclic QRS axis change |
| QRS Duration | >120 ms (typically >140-160 ms) | >120 ms, variable | >120 ms, variable |
| QRS Morphology | Uniform, consistent beat-to-beat | Beat-to-beat variability in shape/axis | “Twisting of the points” around baseline |
| AV Relationship | AV dissociation common; fusion/capture beats | AV dissociation usually present | AV dissociation usually present |
| Ventricular Rate | Usually 100-250 bpm | Often >200 bpm, can be very rapid | Typically 150-250 bpm |
| QT Interval (Baseline) | Variable, may be normal or prolonged | Often normal; prolonged in specific channelopathies | Markedly prolonged (QTc >500 ms) |
| Common Triggers/Etiologies | Structural heart disease (scar, ischemia), channelopathies | Acute ischemia, electrolyte imbalance (K+, Mg++), channelopathies (e.g., Brugada, CPVT) | Drug-induced QT prolongation, hypokalemia, hypomagnesemia, congenital Long QT Syndromes |
A. Monomorphic VT
- Regular rhythm; QRS duration >120 ms
- Uniform QRS morphology
- AV dissociation, fusion beats, capture beats
B. Polymorphic VT
- Irregular rhythm; beat-to-beat variability in QRS morphology and axis
- Ventricular rate often >200 bpm
- Common triggers: acute ischemia, electrolyte disturbances, channelopathies
C. Torsades de Pointes (TdP)
- Subtype of polymorphic VT with cyclic “twisting” of QRS axis around the baseline
- Predisposed by QTc >500 ms
- Etiologies: drug-induced QT prolongation, hypokalemia, hypomagnesemia, congenital long QT syndromes
D. QTc Measurement Techniques
- Bazett formula (QT/√RR) – overcorrects at high heart rates
- Fridericia formula (QT/RR1/3) – preferred in tachycardia
- Manual measurement: use lead II or V5–V6; average 3–5 beats
Key Pearl
Always confirm automated QTc manually when QRS >120 ms or baseline abnormalities exist.
4. Risk Stratification Tools for SCD Prevention
Beyond acute classification, integrate imaging and electrophysiology to predict long-term risk and guide ICD decisions.
A. Left Ventricular Ejection Fraction (LVEF)
- Echocardiography: widely available, rapid
- Cardiac MRI: superior spatial resolution, scar characterization
- Guideline threshold: LVEF ≤35% for primary prevention ICD
B. Electrophysiology Study (EPS)
- Programmed stimulation to assess inducibility of sustained VT/VF
- Positive inducibility correlates with higher SCD risk
- Best predictive value in ischemic cardiomyopathy
C. Cardiac MRI Scar Quantification
- Late gadolinium enhancement (LGE) identifies myocardial fibrosis
- Scar burden and distribution predict arrhythmic events independent of LVEF
D. Integrative Risk Models
- MADIT and MUSTT scores combine LVEF, EPS results, scar metrics
- Emerging multimodal algorithms refine risk beyond single parameters
Clinical Pearl
In patients with borderline LVEF (36–40%), MRI scar assessment can tip the balance toward ICD implantation.
5. Clinical Decision-Making Algorithms
A stepwise pathway streamlines from presentation to risk-based intervention.
Clinical Decision-Making Algorithm for Ventricular Tachycardia
Patient Presentation
Patient with Ventricular Arrhythmia
Step 1: Hemodynamic Assessment
Assess hemodynamic status (stable vs. unstable)
Unstable VT Pathway
Requires immediate intervention.
Step 3: Immediate Synchronized Cardioversion / Defibrillation
Stable VT Pathway
Allows time for diagnostic evaluation.
Step 2: ECG Interpretation
Obtain 12-Lead ECG; Differentiate VT Subtype (Monomorphic/Polymorphic/TdP)
Step 4: Stable VT Management
Correct Reversible Causes, Obtain Imaging (Echo/MRI), Consider Electrophysiology Study (EPS)
Step 5: Long-Term Risk Stratification
Integrate LVEF, Scar Burden, EPS into Risk Model for ICD/Ablation Decisions
Step 6: Multidisciplinary Review
Coordinate Pharmacist Review: Drug Interactions, QTc, Electrolytes, Device Programming Adjuncts
- Assess hemodynamic status (stable vs. unstable)
- Obtain 12-lead ECG; differentiate VT subtype (mono vs. polymorphic vs. TdP)
- For unstable VT: synchronized cardioversion or unsynchronized defibrillation
- For stable VT: correct reversible causes, obtain imaging (echo/MRI) and consider EPS
- Integrate LVEF, scar burden, and EPS into risk model to guide ICD and ablation decisions
- Coordinate pharmacist review: drug-induced QT prolongation, electrolyte repletion, device programming
Key Pearl
Algorithmic pathways must be individualized to patient comorbidities and evolving evidence.
6. Pitfalls, Pearls, and Controversies
Common errors include misclassifying wide-complex tachycardias and overreliance on LVEF alone.
Mimics
SVT with aberrancy vs. VT – use AV dissociation, specific QRS morphology criteria (e.g., Brugada, Vereckei), and capture/fusion beats to distinguish. When in doubt, treat as VT, especially in patients with structural heart disease.
LVEF Cutoff Debates
Nonischemic cardiomyopathy patients may benefit from ICDs at higher LVEF thresholds (e.g., >35%) if other risk factors like significant myocardial scar on CMR or inducible VT on EPS are present. Current guidelines are evolving in this area.
QTc Variability
The choice of QTc correction formula (Bazett, Fridericia, Hodges, etc.) remains controversial, especially in extremes of heart rate or in the presence of wide QRS complexes. Fridericia is generally preferred for tachycardia, but manual verification and clinical context are key.
Clinical Pearl
A significant proportion of SCD occurs in patients with preserved LVEF—novel risk markers (e.g., CMR scar, genetic testing, autonomic markers) are needed and are areas of active research.
References
- Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. J Am Coll Cardiol. 2018;72(14):e91-e220.
- Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997-4126.
- Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659.
- Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J. 2007;28(5):589-600.
- Drew BJ, Ackerman MJ, Funk M, et al. Prevention of Torsade de Pointes in Hospital Settings: A Scientific Statement From the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047-1060.
- Di Marco A, Brownstein JS, Cadrin-Tourigny J, et al. Left Ventricular Ejection Fraction and Long-Term Outcomes in Patients With Nonischemic Cardiomyopathy. J Am Coll Cardiol. 2020;75(3):267-278.
