Clinical Overview

Right ventricular hypertrophy (RVH) is a pathologic increase in right ventricular muscle mass, most often driven by chronic pressure overload on a chamber that is normally thin-walled and built for a low-pressure circuit (StatPearls, 2024). As with its left-sided counterpart, RVH is fundamentally an anatomic diagnosis. The ECG cannot establish it directly — it can only raise or lower suspicion, and it is a poor tool for the job: even the criteria with the best published performance miss roughly half of confirmed cases (LITFL, 2026; Ley et al., Journal of Clinical Medicine, 2024). A strip carrying this dataset’s “Right Ventricle Hypertrophy” label is therefore asserting an ECG pattern consistent with right-sided hypertrophy, not a confirmed anatomic finding, and a strip without that label does not mean the right ventricle is normal.

The mechanism behind the ECG pattern turns on a simple anatomic fact: in the normal heart the left ventricle is several times more massive than the right, so left-sided depolarization forces dominate the QRS almost completely and the right ventricle’s own electrical contribution is masked (Opti-ECG, 2026; StatPearls, 2024). RVH has to become substantial — the right ventricle approaching or exceeding the electrical weight of the left — before that masking breaks down and the horizontal-plane axis swings rightward and anteriorly. That is why the ECG changes described below (a rightward QRS axis, a taller R wave in V1-V2, a deeper S wave in the lateral leads) are read as reversals of the normal left-dominant pattern, not as an independent new signal (LITFL, 2026; StatPearls, 2024).

Clinically, the pattern shares LVH’s trade-off of being fairly specific but not very sensitive: pooled estimates put sensitivity for standard voltage criteria around 50% against specificity above 90% (LITFL, 2026), and a 300-patient study built around the recently revised >20 mmHg pulmonary hypertension threshold found the full panel of ECG parameters it tested spanned sensitivity 3-98% and specificity 3-100%, averaging 39% sensitivity and 87% specificity (Ley et al., Journal of Clinical Medicine, 2024). The practical translation for a monitoring role is the same as for LVH: a positive finding is meaningful and worth reporting, a negative one does not rule anything out.

RVH itself produces no symptoms; early disease is frequently silent. As right heart pressure or volume overload progresses, patients may develop exertional dyspnea, exertional chest pain, palpitations, exertional syncope, peripheral edema, and right-upper-quadrant discomfort from hepatic congestion; hemoptysis and hoarseness from a compressed recurrent laryngeal nerve (Ortner syndrome) are uncommon but recognized (StatPearls, 2024).

Recognized causes fall into a few groups. Chronic lung disease — COPD and interstitial lung disease — is the most common driver overall (StatPearls, 2024). Pulmonary vascular disease covers pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (CTEPH), where ECG changes track measurably with hemodynamic severity and partly reverse after balloon pulmonary angioplasty (Ley et al., Journal of Clinical Medicine, 2023). Congenital heart disease contributes tetralogy of Fallot, pulmonic stenosis, and Eisenmenger physiology. Left heart disease — mitral stenosis and left ventricular failure — raises pulmonary venous pressure and secondarily loads the right ventricle. Primary tricuspid regurgitation and intrinsic myocardial disease (cardiomyopathy, cardiac amyloidosis) round out the list (StatPearls, 2024; Merck Manual, 2026).

Interpretation Guide

Key Features:

• Rate: not a defining feature — RVH is a chamber and morphology finding superimposed on whatever rate accompanies it
• Rhythm: not a defining feature — the pattern is described against an underlying supraventricular rhythm and says nothing about where the impulse originates
• P waves: often show the companion finding of right atrial enlargement — a peaked P wave at or above 2.5 mm in lead II, called P pulmonale — which supports the picture but is not itself a QRS voltage criterion and can occur without RVH (LITFL, 2026)
• PR interval: within normal limits unless a separate, coexisting AV conduction abnormality is present
• QRS complex: the defining feature, and unlike LVH’s leftward voltage sums, RVH criteria center on reversing the normal rightward masking described above. Every mm threshold below is deflection on the printed strip, so confirm the calibration marker first. R/S ratio and R-wave height in V1: an R/S ratio above 1 in V1, or an R wave at or above roughly 6-7 mm, in the absence of another explanation (StatPearls, 2024; LITFL, 2026; Opti-ECG, 2026). QRS duration: stays under 120 ms; a wide QRS with R dominance in V1 points to right bundle branch block instead, not RVH, and the voltage criteria here were not derived for that setting (Opti-ECG, 2026; LITFL, 2026). Right axis deviation: sources disagree on the exact cut-off — StatPearls states greater than 90°, LITFL and other teaching sources state 110° or beyond (StatPearls, 2024; LITFL, 2026; Opti-ECG, 2026). Dominant S wave in V5-V6: at or above roughly 7 mm deep, or R/S ratio below 1 (LITFL, 2026; Opti-ECG, 2026). “R in V1 or V2 + S in I or aVL − S in V1” (the same lead combination reported in older literature as the Butler-Leggett score): read positive above 0.6 mV, with 52% sensitivity and 97% specificity for a pulmonary-hypertension-defining mean pulmonary artery pressure above 20 mmHg in one cohort; an optimized cut-off above 0.12 mV raised sensitivity to 75% at the cost of specificity falling to 80% (Ley et al., Journal of Clinical Medicine, 2024). Time to R-wave peak in V1 (the intrinsicoid deflection): prolonged beyond 35 ms/0.035 s, a threshold confirmed independently by both a clinical reference source and a dedicated diagnostic-accuracy study, with the latter reporting 61% sensitivity and 85% specificity for this measurement alone (StatPearls, 2024; Ley et al., Journal of Clinical Medicine, 2024). qR pattern in V1: a small q wave preceding the dominant R in V1, described as a marker of more severe RVH (StatPearls, 2024; Opti-ECG, 2026)
• ST segment: the strain pattern — ST depression in the right precordial leads V1-V4 and, distinctly from LVH’s lateral distribution, in the inferior leads II, III, and aVF (LITFL, 2026; StatPearls, 2024; Merck Manual, 2026)
• T waves: asymmetric T wave inversion in that same right precordial and inferior distribution, the second half of the strain pattern, and — as with LVH — a secondary repolarization change rather than an independent ischemic finding (LITFL, 2026)
• QT interval: not part of any of the named criteria above and not independently diagnostic here. Where a coexisting right bundle branch block widens the QRS, read the two measurements together rather than reporting an isolated QT prolongation
• Other findings: an S1S2S3 pattern — dominant S waves across leads I, II, and III alongside a far-right axis — is a recognized but relatively uncommon marker; one CTEPH cohort found it in only 7-8% of tracings regardless of treatment status (Ley et al., Journal of Clinical Medicine, 2023). Incomplete or complete right bundle branch block is common in RVH, but no ECG criteria set on this page is validated for use when RBBB is already present (LITFL, 2026)

Key Leads

• Leads V1 and V2 – The core of the picture: the R/S ratio and R-wave height criterion, the “R + S − S” composite score, the time-to-R-peak measurement, and the strain pattern’s right precordial ST depression and T wave inversion all read from here, so a poorly recorded V1 electrode changes several criteria at once (StatPearls, 2024; Ley et al., Journal of Clinical Medicine, 2024; LITFL, 2026)
• Leads V5 and V6 – The mirror image of V1-V2: a dominant, deep S wave here is the other half of the reversed R/S relationship that defines the pattern (LITFL, 2026; Opti-ECG, 2026)
• Lead II – Carries the P pulmonale threshold (peaked P wave ≥2.5 mm), the companion right atrial finding that supports but does not itself establish RVH (LITFL, 2026)
• Leads I and aVL – Supply the S-wave terms for the “R in V1/V2 + S in I/aVL − S in V1” score and, together with lead III, the limb leads whose relative deflections define right axis deviation and the S1S2S3 pattern (Ley et al., Journal of Clinical Medicine, 2024; LITFL, 2026)
• Leads V1-V4 and II, III, aVF read together – The strain distribution, which is why it is described separately from LVH’s: right-sided strain sits across the right precordial leads and the inferior leads, not the lateral leads (LITFL, 2026; StatPearls, 2024)

Differential Diagnosis

• Right Bundle Branch Block (RBBB) — the single most important look-alike, because both patterns put a dominant R wave in V1. Distinguishing clue: RBBB widens the QRS to 120 ms or more with a classic rSR’ morphology, while RVH keeps the QRS under 120 ms with a monophasic R wave and satisfies its own voltage or axis criteria (Opti-ECG, 2026). RBBB can also coexist with RVH, in which case the voltage criteria on this page do not apply.
• Left Ventricle Hypertrophy (LVH) — the opposite chamber, and the opposite precordial pattern. Distinguishing clue: LVH deepens the S wave in V1 and raises the R wave in V5-V6 with a leftward axis, while RVH raises the R wave in V1 and deepens the S wave in V5-V6 with a rightward axis. The strain distribution separates them too: RVH’s strain sits in V1-V4 plus the inferior leads, LVH’s in I, aVL, and V5-V6.
• Right Atrial Hypertrophy (RAH) — the companion atrial finding rather than a competing chamber pattern. Distinguishing clue: an isolated peaked P wave (P pulmonale) at or above 2.5 mm in lead II without any accompanying QRS voltage, axis, or strain criterion describes right atrial involvement alone; RVH requires the ventricular criteria on this page to be present as well, and the two frequently occur together in the same chronic pressure-overload states.
• Axis Right Shift (ARS) — right axis deviation is one of RVH’s own criteria, but it is also a common isolated finding with causes that have nothing to do with right ventricular mass, including normal variation, a thin body habitus, or lead misplacement. Distinguishing clue: right axis deviation without a supporting R/S-ratio, R-wave-height, or strain finding is read as isolated axis deviation, not RVH.
• ST Drop Down (STDD) — the strain pattern is right precordial and inferior ST depression, so the two labels can land on the same tracing. Distinguishing clue: strain is accompanied by RVH’s own voltage or axis criteria and sits in the leads this page describes; an ischemic depression is more often dynamic, tracks with symptoms, and does not require a companion voltage finding to explain it.

Treatment Brief

The ECG pattern itself is not treated. What a monitoring technician or nursing student owns here is measuring it correctly, naming which criterion produced the finding, and not overstating what the tracing can prove.

• Confirm standard calibration and lead placement before applying any criterion here — several of them depend specifically on V1, and a misplaced or poorly recorded precordial electrode changes the answer without changing the patient.
• Measure the QRS duration before crediting a dominant R wave in V1 to RVH. A QRS at or above 120 ms with an rSR’ shape is right bundle branch block, not RVH, and the voltage criteria on this page were not derived for that setting (Opti-ECG, 2026).
• Report which criterion was applied and the measured values, not just the word “RVH.” Sources disagree on the exact axis and R-wave thresholds, so naming the criterion lets the next reader judge the finding on its own terms.
• Do not read a negative ECG as excluding right-sided hypertrophy. Published sensitivity is low across every criterion reviewed here, and echocardiography (or cardiac MRI where indicated) is what establishes or excludes the diagnosis (LITFL, 2026; Ley et al., Journal of Clinical Medicine, 2024).
• Treat right precordial and inferior ST depression with T wave inversion as strain only when a supporting voltage or axis criterion is also present and the pattern is stable. A new or evolving repolarization change in a symptomatic patient is escalated to the provider regardless of whether RVH criteria are met.
• Note the patient’s context — known chronic lung disease, pulmonary hypertension, congenital heart disease, or mitral valve disease all change how confidently the same voltages should be read, and ECG changes in pulmonary hypertension have been shown to partially reverse with effective treatment, so a change from a prior tracing is itself clinically informative (Ley et al., Journal of Clinical Medicine, 2023).

[CLINICAL REVIEW NEEDED: sources disagree on the exact right axis deviation threshold used to support RVH — StatPearls states greater than 90°, while LITFL and other teaching sources state 110° or beyond, and the R-wave-height threshold in V1 is reported as both roughly 6 mm and roughly 7 mm depending on the source. The “R in V1/V2 + S in I/aVL − S in V1” score also carries conflicting published performance across eras and populations: the modern 0.6 mV cut-off reviewed here reached 52% sensitivity, while the same formula under its original 1986 description was reported at 66-89% sensitivity depending on whether the study population had mitral stenosis or cor pulmonale. The direction is consistent across all of these — rightward axis, a taller R wave in V1, and a higher score all support the pattern — but the exact cut-off values and performance figures used in this guide should not be treated as a single settled number.]