How do you differentiate slow ventricular tachycardia from metabolic dysrhythmia?

Differentiating Slow Ventricular Tachycardia from Metabolic Dysrhythmia

When confronted with a wide-complex tachycardia that could represent either slow VT or a metabolic/electrolyte-induced dysrhythmia, prioritize identifying AV dissociation, fusion beats, and specific QRS morphologic criteria—but critically, metabolic dysrhythmias typically present with electrolyte abnormalities (particularly hyperkalemia) that cause QRS widening without the classic VT morphologic features. 1, 2

Key Distinguishing Features

Definitive VT Criteria (Present in Either Slow or Fast VT)

• AV dissociation with ventricular rate exceeding atrial rate is pathognomonic for VT and proves the diagnosis, though visible in only 30% of cases 1, 3, 2
• Fusion complexes (merger of conducted supraventricular and ventricular beats) are pathognomonic for VT 1, 3, 2
• Capture beats demonstrate VT definitively 3, 2
• Look for irregular cannon A waves in jugular venous pulse and variable loudness of first heart sound on physical exam—these indicate AV dissociation 1

QRS Morphology Favoring VT (Regardless of Rate)

• R-S interval >100 ms (onset of R wave to nadir of S wave) in any precordial lead strongly suggests VT 1, 2
• Initial R wave in lead aVR implies VT 1, 3, 2
• Initial R or Q wave >40 ms in aVR suggests VT 1, 3, 2
• Concordance (all QRS complexes in precordial leads V1-V6 either all positive or all negative) implies VT 1, 3
• R-wave peak time ≥50 ms in lead II suggests VT 1, 3, 2
• QRS width >0.14 seconds with RBBB pattern or >0.16 seconds with LBBB pattern favors VT 1

Metabolic Dysrhythmia Characteristics

Clinical Context Suggesting Metabolic Cause

• Electrolyte abnormalities (particularly hyperkalemia, hypokalemia, hypocalcemia, hypomagnesemia) or metabolic disorders can cause wide QRS complexes that mimic VT 1, 2, 4
• Metabolic dysrhythmias typically lack the specific morphologic VT criteria listed above 2, 4
• The QRS morphology in metabolic dysrhythmias is usually different from classic VT patterns and may show generalized QRS widening without the specific features of VT 4

Hyperkalemia-Specific Features

• Progressive QRS widening with peaked T waves, flattened P waves, and eventual sine-wave pattern 4
• Lacks AV dissociation, fusion beats, or capture beats 4
• QRS widening is typically uniform across all leads rather than showing the lead-specific morphologic criteria of VT 4

Algorithmic Approach

1. First, assess hemodynamic stability and clinical context 1, 3

   • History of MI or structural heart disease strongly favors VT 3, 5
   • Recent medication changes or known electrolyte abnormalities suggest metabolic cause 2, 4

2. Search for pathognomonic VT features 1, 3, 2

   • AV dissociation (look at physical exam and ECG)
   • Fusion or capture beats
   • If present, diagnosis is VT regardless of rate

3. Apply QRS morphology criteria systematically 1, 3, 2

   • Check aVR for initial R wave or R/Q >40 ms
   • Measure R-S interval in precordial leads
   • Assess for concordance
   • Check R-wave peak time in lead II

4. Obtain immediate electrolyte panel 2, 4

   • If severe hyperkalemia present with appropriate ECG changes (peaked T waves, P wave flattening) and absence of VT morphologic criteria, treat as metabolic dysrhythmia
   • If electrolytes normal or VT criteria present, treat as VT

Critical Pitfalls

• Never assume slow rate means benign etiology—slow VT is still VT and requires the same diagnostic rigor 6, 7
• Antiarrhythmic drugs reduce specificity of QRS width criteria, as they can widen QRS in supraventricular rhythms 1, 2
• When diagnosis remains uncertain after systematic evaluation, treat as VT—this is the safer approach, as medications for SVT (particularly verapamil or diltiazem) may precipitate hemodynamic collapse in VT 1, 3
• Hemodynamic stability does not distinguish VT from other causes—VT can be well-tolerated, especially in younger patients 1, 3