Left and right ventricular hypertrophy and atrial enlargement

What it is

A thicker ventricle has more muscle to depolarise, so it produces larger QRS voltages pointed towards it, a slightly longer activation time, and often secondary repolarisation changes. Left ventricular hypertrophy (LVH) follows pressure or volume load (hypertension, aortic stenosis, hypertrophic cardiomyopathy, aortic or mitral regurgitation) and is a strong marker of cardiovascular risk. On the ECG it appears as tall R waves in the left-facing leads (I, aVL, V5–V6) and deep S waves in the right precordial leads (V1–V2), measured against voltage criteria such as Sokolow–Lyon or Cornell; it may add left axis deviation, left atrial enlargement and a «strain» pattern of down-sloping ST depression with asymmetric T inversion in the lateral leads. Right ventricular hypertrophy (RVH) follows pulmonary hypertension, chronic lung disease, mitral stenosis, chronic thromboembolism or congenital heart disease; because the left ventricle normally dominates, it shows only when it is marked: right axis deviation, a dominant R wave in V1, deep S waves in V5–V6 and right precordial ST-T changes. The atria show in the P wave: right atrial enlargement makes it tall, left atrial enlargement makes it broad and notched with a deep negative terminal part in V1. ECG criteria are specific but not sensitive: a normal ECG does not exclude hypertrophy, and echocardiography is the test that measures it. Young, thin adults often meet voltage criteria without disease.

How to recognise it

• Calibrate first: standard is 10 mm/mV; at half standard the voltages read must be doubled.
• LVH: Sokolow–Lyon (S V1 + R V5 or V6) ≥35 mm, or R in aVL ≥11 mm; Cornell (R aVL + S V3) >28 mm in men, >20 mm in women.
• Supporting LVH features: left axis deviation, QRS slightly prolonged (often 100–120 ms), delayed R-wave peak in V5–V6, left atrial enlargement, lateral strain.
• RVH: right axis deviation (beyond about +90° to +110° in adults), dominant R in V1 (R ≥7 mm or R/S >1), deep S in V5–V6 (persistent S wave), right atrial enlargement, ST depression and T inversion in V1–V3.
• Left atrial enlargement: broad (≥120 ms), notched («M-shaped») P in II; biphasic P in V1 with a terminal negative part ≥1 mm deep and ≥40 ms long.
• Right atrial enlargement: tall, peaked P wave >2.5 mm in II, III, aVF, or >1.5 mm in V1–V2, with normal width.

Why it happens

• More myocardial mass means more depolarising current, so the QRS vector grows and points towards the thick chamber; the left ventricle's lateral and posterior direction gives tall R in V5–V6 and deep S in V1.
• A thick wall takes longer to activate and its subendocardium is relatively ischaemic, so repolarisation changes direction: ST depression and T inversion in the leads with tall R waves (strain).
• The right atrium depolarises first and forms the early P wave (height); the left atrium forms the late P wave (width and the terminal negative part in V1).

Step by step

1. Check calibration and lead placement — half standard or misplaced leads distort every voltage.
2. Measure S in V1, R in V5 or V6, R in aVL and S in V3 in mm — apply Sokolow–Lyon and Cornell, adjusting for sex.
3. Look at the lateral ST-T for strain — it adds weight to the voltage and to the patient's risk.
4. Work out the axis — left deviation supports LVH, right deviation is the key sign of RVH.
5. Look at V1 for a dominant R wave and at V5–V6 for persistent S waves — the chest-lead pattern of RVH.
6. Read the P wave in II and V1 for height, width and the terminal negative part — this shows which atrium is enlarged.
7. Put it in context: blood pressure, murmur, lung disease, age and build — and confirm with an echocardiogram.

Criteria at a glance

Differential and pitfalls

• Dominant R in V1 is not always RVH: also right bundle branch block, posterior infarction, left-sided accessory pathway, hypertrophic cardiomyopathy, dextrocardia, lead misplacement and a normal child.
• Strain looks like ischaemia; compare with old tracings, and in chest pain still look for new or dynamic ST change and measure troponin.
• Left bundle branch block and ventricular pacing make voltage criteria unreliable; do not diagnose LVH from them.
• False positives: thin young adults and athletes; false negatives: obesity, COPD, pericardial or pleural effusion and breast tissue lower the voltage.
• In COPD, RVH may show only as right axis, low voltage, P pulmonale and poor R-wave progression rather than a tall R in V1.
• Very high voltage with deep narrow Q waves or giant T inversion in a young patient suggests hypertrophic cardiomyopathy, not simple hypertension.

Next step

• Request a transthoracic echocardiogram to measure wall thickness, chamber size, valves and pulmonary pressure.
• LVH: measure blood pressure properly (consider ambulatory readings), look for aortic stenosis, and assess cardiovascular risk and target-organ damage.
• RVH or right atrial enlargement: look for pulmonary hypertension, chronic lung disease, mitral stenosis, chronic thromboembolism and congenital shunts.
• Call a senior or cardiology the same day for hypertrophy with syncope, exertional chest pain, a loud murmur or a family history of sudden death.
• Left atrial enlargement raises the risk of atrial fibrillation: ask about palpitations and look at rhythm on follow-up.

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Elsewhere in DurgiPedia

• ECG basics: waves, intervals and leads
• The cardiac electrical axis
• Physiology of hypertension

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Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: Left Ventricular Hypertrophy (StatPearls (NCBI Bookshelf), 2026); Right Ventricular Hypertrophy (StatPearls (NCBI Bookshelf), 2024); Left Atrial Enlargement (StatPearls (NCBI Bookshelf), 2025).

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