Why can't Left Ventricular Hypertrophy (LVH) or Right Ventricular Hypertrophy (RVH) criteria be applied in patients with Left Bundle Branch Block (LBBB), Wolff-Parkinson-White (WPW) syndrome, hyperkalemia, or those experiencing drug effects?

Why LVH/RVH Criteria Cannot Be Used in LBBB, WPW, Hyperkalemia, and Drug Effects

Standard ECG voltage criteria for ventricular hypertrophy rely on normal ventricular depolarization patterns, and these conditions fundamentally alter QRS morphology and amplitude through different mechanisms—making the voltage measurements unreliable or completely invalid.

The Core Problem: Altered Depolarization Patterns

All standard LVH and RVH criteria depend on measuring R-wave and S-wave amplitudes in specific leads, which reflect the normal sequence and direction of ventricular activation. When this sequence is disrupted, the voltage measurements lose their diagnostic meaning 1.

Left Bundle Branch Block (LBBB)

The ECG diagnosis of LVH should generally not be attempted when LBBB is present 1.

• LBBB causes the left ventricle to activate abnormally through cell-to-cell conduction rather than the rapid His-Purkinje system, fundamentally altering QRS morphology and voltage patterns 1
• Both LVH and LBBB independently alter QRS patterns in similar ways—widening the QRS complex and changing voltage distributions—making it impossible to distinguish which abnormality is causing the observed changes 1
• Studies show conflicting results, with some reporting that the diagnosis should not be attempted at all, while others suggest limited criteria may work 1
• The prevalence of anatomic LVH in patients with LBBB is extremely high (up to 90% in autopsy series), which confounds specificity estimates 1
• Exception: Only in highly specific circumstances—when QRS duration exceeds approximately 155 ms AND there is left atrial abnormality AND precordial voltage criteria are met—can LVH be diagnosed with reasonable specificity, though sensitivity remains very low 1

Common pitfall: Conventional LBBB criteria (QRS ≥120 ms) may falsely diagnose LBBB in cases of LVH with intraventricular conduction delay, creating a circular diagnostic problem 2.

Wolff-Parkinson-White (WPW) Syndrome

WPW syndrome creates pre-excitation that mimics multiple ECG abnormalities, including ventricular hypertrophy and bundle branch blocks 3.

• The accessory pathway causes early ventricular activation (delta wave), which alters the initial QRS vector and changes R-wave and S-wave amplitudes in unpredictable ways 3
• WPW can produce pseudo-infarction patterns, pseudo-hypertrophy patterns, and pseudo-bundle branch block patterns—all of which invalidate standard voltage criteria 3
• The degree of pre-excitation varies with autonomic tone and heart rate, making measurements inconsistent 3
• No reliable algorithm exists for diagnosing ventricular hypertrophy in the presence of WPW with its variable pre-excitation patterns 3

Hyperkalemia

Hyperkalemia progressively widens the QRS complex and increases voltage amplitude through direct effects on myocardial depolarization, creating false-positive voltage criteria.

• Elevated potassium levels slow phase 0 of the cardiac action potential, widening the QRS and creating tall, peaked T waves
• The widened QRS increases measured voltages (particularly R-wave amplitude) independent of actual ventricular mass
• Hyperkalemia can mimic bundle branch blocks and other conduction abnormalities, further confounding interpretation
• The ECG changes are dynamic and reverse with potassium correction, proving they are not related to structural hypertrophy

Drug Effects

Multiple cardiac medications alter QRS morphology and voltage through effects on sodium and potassium channels, invalidating voltage measurements.

• Class I antiarrhythmic drugs (sodium channel blockers) widen the QRS complex, artificially increasing voltage measurements
• Drugs affecting repolarization (Class III agents, tricyclic antidepressants) can alter QRS-T patterns that mimic strain patterns
• Digoxin causes characteristic ST-T changes that can be confused with LVH strain patterns
• These effects are dose-dependent and reversible, demonstrating they are not structural changes

The Underlying Principle

The fundamental issue is that LVH/RVH voltage criteria were derived and validated in patients with normal conduction systems 1. When depolarization is altered by:

• Conduction system disease (LBBB): Changes the sequence of activation
• Accessory pathways (WPW): Creates abnormal early activation
• Electrolyte abnormalities (hyperkalemia): Slows conduction velocity
• Pharmacologic effects: Modifies ion channel function

...the relationship between ventricular mass and surface ECG voltage is fundamentally disrupted 1.

Clinical Implications

• Use echocardiography when ventricular hypertrophy assessment is clinically important in patients with these conditions 4
• Do not report LVH/RVH based on voltage criteria when any of these confounding conditions are present
• Document the limitation explicitly: "LVH criteria cannot be assessed in the presence of LBBB" (or WPW, etc.)
• For LBBB specifically, only apply the highly specific criteria (QRS >155 ms + left atrial abnormality + voltage criteria) if diagnosis is critical, understanding sensitivity will be very low 1