S Wave

The S wave is the negative (downward) deflection after the R wave in the QRS complex. It is the tail end of ventricular depolarization. The impulse leaves the sinus node, crosses the atria, pauses at the AV node, runs down the His–Purkinje system and then lights up the ventricular myocardium. The basal and posterior walls fire last. Their terminal forces are what make the S wave.

A lead writes a negative deflection when the net force points away from its positive electrode. Leads V1–V2 face the right ventricle. The bigger left ventricular forces run away from them, so you see deep S waves. Leads V5–V6 face the lateral left ventricle. The forces run toward them. Result: tall R waves with little or no S.

• Depth reflects: ventricular mass, the direction of the net force, conduction timing and electrode position.

When S depth or the crossover lead moves, mass, conduction or heart position has changed. Read it against the patient in front of you and the last tracing.

How to Measure the S Wave

1. Standardize the tracing: 25 mm/s and 10 mm/mV (1 mm = 0.1 mV; 1 small box = 40 ms).
2. Choose a steady baseline: use 3–5 beats; in atrial fibrillation or another irregular rhythm, average several beats.
3. Measure depth: from the isoelectric baseline (PR or TP segment) to the deepest point of the S, in mm, in V1–V6.
4. Find the transition zone: the first precordial lead where R equals S. Normal is V3–V4.
5. Measure duration: the S in I and V6, from the start of the S to its return to baseline, and the QRS in the widest lead.
6. Check the frontal plane: S waves in I, II and III, and the axis.

Think of a deep S as a voltage marker for hypertrophy. Left ventricular hypertrophy (LVH) deepens the S waves in V1–V2. Right ventricular hypertrophy (RVH) deepens them in V5–V6 and leaves a dominant R wave in V1.

ECG Criteria

• LVH voltage: S in V1 plus R in V5 or V6 ≥35 mm (Sokolow-Lyon). Cornell: R in aVL plus S in V3 >28 mm in men and >20 mm in women.
• LVH support: LV strain (downsloping ST depression and asymmetric T inversion in I, aVL, V5–V6), left atrial enlargement and a prolonged R-wave peak time in V5–V6.
• RVH: deep S in V5–V6 with a dominant R in V1, a right axis (+90° to +180°), RV strain and P pulmonale. Thresholds for each feature are on the R Wave page. No single feature is diagnostic.

Causes

Clinical Significance

• LVH: this is what long-standing pressure or volume overload looks like. High voltage with a strain pattern makes the finding stronger.
• RVH: the tracing reflects right-sided pressure overload. A new RV pattern in an acutely ill patient? Think pulmonary embolism or acute RV failure.

Look-Alikes

Don't be fooled. LBBB (QS in V1–V2), posterior MI (R-dominant V1–V2) and lead misplacement can all imitate these patterns. See Differential Diagnosis & Mimics.

One ventricle activates late. That is bundle branch block. The QRS widens and the S waves change shape, most clearly in V1–V2 and the lateral leads. Full criteria and management are on the QRS Complex page.

ECG Criteria

• Complete RBBB: QRS ≥120 ms; rSR′, rsR′ or rsr′ in V1–V2; and a wide, slurred S wave in I and V6 (longer than 40 ms, or wider than the R wave).
• Incomplete RBBB: RBBB pattern with a narrower QRS. The threshold is on the QRS Complex page.
• LBBB: QRS ≥120 ms; QS or deep rS in V1–V2; no septal q wave in I, V5 or V6 (a narrow q can occur in aVL); and a broad, notched R in I, aVL, V5–V6 with little or no S.

Mechanism

• RBBB: the right ventricle fires late. That late activation makes a terminal rightward force, seen as a terminal R′ in V1 and a wide S in I and V6.
• LBBB: septal activation runs right to left. The normal early septal forces disappear, so V1–V2 record a QS or a deep S.

Clinical Significance

• RBBB: often benign in young adults. Older patient, or new dyspnea? Consider RV strain from pulmonary embolism or pulmonary hypertension.
• LBBB: usually means underlying heart disease. New LBBB alone is not a STEMI equivalent.
• New LBBB with chest pain: run the Smith-modified Sgarbossa criteria on the ST Segment & Ischemia page before you decide. The criteria are not a rule-out. High clinical suspicion of occlusion MI? Activate the STEMI pathway per local protocol, even when the criteria are not met. For current acute coronary syndrome management, see the 2025 ACC/AHA guideline.
• Bifascicular block: RBBB with left anterior fascicular block (left axis) or left posterior fascicular block (right axis) suggests conduction disease at two levels. See the Cardiac Axis page.

S1S2S3 is a dominant S in leads I, II and III. It puts the frontal axis in the extreme (northwest) range, past simple right axis deviation. S1Q3T3 is the S in I plus a Q wave and T-wave inversion in III. Neither pattern points to one diagnosis.

ECG Criteria

• S1S2S3: S waves in I, II and III. All three limb leads go negative only when the axis sits roughly between −90° and −150°, the extreme or northwest range. Simple right axis deviation (+90° to +180°) makes lead III positive, so it does not produce S1S2S3.
• S1Q3T3: S in I, Q in III and T-wave inversion in III. It may appear with sinus tachycardia, T-wave inversion in V1–V4 and RBBB.

Causes

Pulmonary Embolism

Many patients with PE have an abnormal ECG, but the findings are nonspecific. A 2015 systematic review and meta-analysis of 8,209 patients with PE found tachycardia (38%), T-wave inversion in V1 (38%) and ST elevation in aVR (36%) most often. S1Q3T3 was one of six ECG findings that predicted hemodynamic collapse and 30-day mortality.

The transition zone is the precordial lead where R and S are equal (R/S = 1). Normally that is V3 or V4. Shift it toward V1–V2 or toward V5–V6 and the read changes.

Early Transition (V2 or Earlier)

• Posterior MI: lose the posterior forces and V1–V2 turn R-dominant.
• WPW pattern (type A): pre-excitation makes a tall R in V1–V2. See the PR Interval page.
• Normal variant: you see it often in children and young adults.

Late Transition (V5 or Later)

• LVH: high left ventricular forces keep the S waves deep across the mid-precordium. That can push the transition later.
• Anterior MI: lose the anterior forces and R-wave progression falls off. See the R Wave page.
• LBBB: the septum activates differently, so precordial progression changes.

Persistent S Waves (No Transition)

• Severe RVH or extreme right axis: dominant right ventricular forces carry the S waves through V5–V6. The transition comes late or not at all.
• Chronic lung disease with a vertical heart: poor R-wave progression.

Artifact & Lead Misplacement

• Limb lead reversal: flip lead I and you get a deep S in I and a false right axis. Check the P-wave polarity in lead I.
• Precordial misplacement: electrodes placed high or low shift the R and S amplitudes in V1–V3. Compare with the adjacent leads.
• Motion, shivering and transport vibration: these make jagged baselines that can imitate S waves or hide them.

Normal Variants

• Deep S waves in V1–V2 in young, thin or athletic adults.
• A small terminal r wave in V1 or V2 (an rSR′-type pattern) without QRS widening.

Few S-wave findings call for an immediate drug decision. What matters is what the finding signals and who needs to hear about it.

• New RBBB or LBBB with dyspnea, hypotension, syncope or an RV strain pattern: consider PE and acute RV failure. Tell the receiving ED or critical-care team early. Treat per local protocol.
• New LBBB with chest pain: don't dismiss it, and don't call it STEMI by default. Apply the Smith-modified Sgarbossa criteria on the ST Segment & Ischemia page, repeat the 12-lead ECG and activate the STEMI pathway per protocol when the criteria or the clinical picture support it.
• Chronic deep S waves (LVH or RVH) without new symptoms: document it and compare with prior tracings. The pattern alone does not indicate acute treatment.

Obtain serial 12-lead ECGs and any prior tracings. Ask for an echocardiogram or other imaging when RV strain is suspected. Follow local protocols and medical direction.

Pediatrics

• Newborns and infants: right ventricular dominance is physiologic here. A tall R in V1 and a rightward axis can be normal. Compare against age-specific limits, not adult values (Rijnbeek 2001 normal limits).
• Children and adolescents: amplitudes and QRS duration in normal children differ substantially from adult limits. Sex differences exist too. Use age-specific normal limits before you call an S wave abnormal.
• Congenital heart disease: after infancy, a right-sided pattern with deep S waves in V5–V6 needs pediatric cardiology review. That matters most with tetralogy of Fallot or pulmonary stenosis.
• Weight and vital-sign references: see pediatric vital signs for age-based heart rates.

Other Populations

• Athletes: an athlete's LV voltage may meet LVH criteria with normal repolarization. Athletic remodeling should not produce strain-type ST-T changes.
• Older adults and body habitus: lower QRS voltage from obesity, lung disease or pericardial effusion can hide LVH.
• Pregnancy: the growing uterus pushes the diaphragm up and shifts the frontal axis leftward. Precordial voltage and S-wave depth can change with it. New RV strain, S1Q3T3 or tachycardia still calls for PE evaluation. PE risk is higher in pregnancy and the postpartum period.
• Paced rhythms: S-wave voltage criteria don't apply here. Read paced complexes with the QRS Complex page.

1. Confirm the tracing: check standardization (10 mm/mV), lead placement and the patient's identity on the strip.
2. Measure S depth in V1–V2 and V5–V6: from baseline to the deepest point, in mm.
3. Locate the transition zone: note the lead where R equals S. Normal is V3–V4.
4. Measure the QRS: a QRS of 120 ms or more with a wide, slurred S in I and V6 points to bundle branch block.
5. Check the frontal plane: the axis and any S1S2S3 pattern. Look for an inverted lead I that suggests limb reversal.
6. Calculate voltage only when needed: Sokolow-Lyon and Cornell for suspected LVH, then look for strain and atrial enlargement before naming LVH.
7. Compare with the prior ECG and the clinical picture: dyspnea, chest pain, hypotension or syncope change the urgency.
8. Act per Bedside Management: escalate, notify and document the finding and its trend.

Common Pitfalls

• Diagnosing LVH from voltage alone, without strain or other supporting features.
• Calling a deep S in V1–V2 abnormal in a young, thin or athletic patient.
• Naming PE from an S1S2S3 pattern alone, or ruling PE out because the ECG looks normal.
• Dismissing new LBBB in a patient with chest pain, or activating STEMI on LBBB alone without applying Sgarbossa criteria.
• Missing limb lead reversal or precordial misplacement.
• Confusing persistent S waves with poor R-wave progression (see the R Wave page).