S Wave

The S wave is any downward (negative) deflection that follows an R wave in the QRS complex. It represents the later phase of ventricular depolarization, particularly the activation of the posterobasal ventricular walls.

Electrical Genesis

The S wave represents the final phase of ventricular depolarization:

• Vector III (Terminal Depolarization): Activation of posterobasal right and left ventricular free walls, including the basal right septal mass and crista supraventricularis
• Direction: Resultant electrical force is directed rightward and posteriorly, away from left precordial leads
• Magnitude: Small compared to earlier vectors, reflecting the smaller muscle mass of the basal regions
• Left Ventricular Mass Effect: The larger the left ventricular muscle, the deeper the S wave in V1 and V2

Normal S Wave Distribution

S wave depth varies systematically across ECG leads:

• Right Precordial Leads (V1-V2): Deep S waves are normal - depolarization travels away from these electrodes toward the larger left ventricle
• Mid-Precordial Leads (V3-V4): Transition zone where R wave height equals S wave depth (R/S ratio = 1)
• Left Precordial Leads (V5-V6): S waves are minimal or absent - depolarization travels toward these electrodes
• Limb Leads: S wave depth varies with cardiac axis; deep S in lead I suggests right axis deviation

S Wave Nomenclature

• Uppercase "S": Denotes a large (≥5mm) negative deflection after R wave
• Lowercase "s": Denotes a small (<5mm) negative deflection after R wave
• Terminal s: Small S wave at end of QRS, seen in some lateral leads with counterclockwise rotation
• Slurred S: Widened, notched S wave seen in bundle branch blocks

Left ventricular hypertrophy causes increased QRS voltages, particularly deep S waves in right precordial leads and tall R waves in left precordial leads.

Pathophysiology

• Increased Muscle Mass: Thickened LV wall generates larger electrical forces during depolarization
• Prolonged Depolarization: More muscle requires longer time to depolarize, widening QRS slightly
• Vector Magnitude: Larger leftward and posterior forces create deeper S waves in right-facing leads (V1-V3)
• Repolarization Changes: Secondary ST-T changes (strain pattern) due to altered repolarization sequence

Voltage Criteria for LVH

LV Strain Pattern

Accompanies voltage criteria in severe LVH:

• ST Depression: Downsloping ST segment in lateral leads (I, aVL, V5-V6)
• T Wave Inversion: Asymmetric T wave inversion in lateral leads
• Mechanism: Delayed repolarization from endocardium to epicardium due to increased wall thickness
• Prognosis: Strain pattern associated with worse outcomes - indicates significant hypertrophy

Causes of LVH

• Hypertension: Most common cause - chronic pressure overload
• Aortic Stenosis: Severe pressure overload from fixed obstruction
• Aortic Regurgitation: Volume overload with combined pressure load
• Hypertrophic Cardiomyopathy: Primary genetic disorder with massive hypertrophy
• Athletic Heart: Physiologic hypertrophy in endurance athletes (no strain pattern)

Right ventricular hypertrophy causes deep S waves in LEFT precordial leads (V5-V6), opposite to the pattern seen in LVH.

Diagnostic Criteria for RVH

RVH requires at least 2 of the following:

• Right Axis Deviation: ≥ +110° (required for diagnosis)
• Dominant R in V1: R wave ≥ 7 mm or R/S ratio > 1 in V1
• Deep S in V5 or V6: S wave ≥ 7 mm or R/S ratio < 1 in V5-V6
• QRS Duration: < 120 ms (changes not due to RBBB)

Supporting Criteria

• Right Atrial Enlargement: P pulmonale (peaked P > 2.5 mm in II)
• RV Strain Pattern: ST depression and T wave inversion in V1-V4, II, III, aVF
• S1S2S3 Pattern: Dominant S waves in leads I, II, and III (extreme right axis)
• Deep S in Lateral Leads: Deep S waves in I, aVL, V5-V6

Pathophysiology

• RV Dominance: Hypertrophied RV creates forces that oppose normal leftward vectors
• Axis Shift: Electrical axis shifts rightward as RV forces increase
• Lateral S Waves: Deep S in V5-V6 as depolarization moves away from lateral leads toward hypertrophied RV
• Strain: RV strain pattern indicates severe hypertrophy with pressure overload

Common Causes

• Pulmonary Hypertension: Most common cause in adults
• Chronic Lung Disease: Cor pulmonale from COPD, pulmonary fibrosis
• Pulmonary Embolism: Acute or chronic thromboembolic disease
• Mitral Stenosis: Increased RV pressure from left atrial hypertension
• Congenital Heart Disease: Tetralogy of Fallot, pulmonary stenosis, ASD
• ARVC: Arrhythmogenic right ventricular cardiomyopathy

Right Bundle Branch Block (RBBB)

RBBB creates characteristic wide, slurred S waves in lateral leads:

• Wide Slurred S in I, V5, V6: Terminal S wave >40 ms in duration
• Mechanism: Delayed right ventricular depolarization creates late rightward forces
• RSR' in V1-V2: Characteristic "M" pattern with terminal R wave in right precordial leads
• QRS Duration: ≥ 120 ms for complete RBBB, 100-119 ms for incomplete RBBB
• S Wave Duration > R Wave: In lateral leads, the S wave amplitude may exceed the preceding R wave

Left Bundle Branch Block (LBBB)

LBBB affects S wave morphology differently:

• Deep S or QS in V1-V2: Absent R wave with deep QS complex in right precordial leads
• Absent Septal Q Waves: No small q waves in lateral leads (I, aVL, V5-V6)
• Mechanism: Septal depolarization occurs right-to-left (reversed), eliminating normal septal forces
• Broad Monophasic R in V5-V6: No S wave in lateral leads - smooth R wave without notching
• QRS Duration: ≥ 120 ms with broad, notched morphology

Clinical Significance

• RBBB: Often benign in young adults; may indicate RV strain (PE, pulmonary HTN) or structural disease in older patients
• LBBB: Almost always indicates underlying cardiac disease (CAD, cardiomyopathy, HTN, aortic valve disease)
• New LBBB + Chest Pain: Consider STEMI equivalent - urgent cardiology consultation
• Bifascicular Block: RBBB + left axis deviation suggests two-level conduction disease

The S1S2S3 pattern refers to dominant S waves in limb leads I, II, and III, indicating extreme right axis deviation.

Definition and Recognition

• Lead I: S wave deeper than R wave is tall (R/S < 1)
• Lead II: S wave deeper than R wave is tall
• Lead III: S wave deeper than R wave is tall
• Axis: Typically > +120° to +180° (far right axis)

Clinical Associations

• Right Ventricular Hypertrophy: Most common cause - chronic RV pressure overload
• Acute Pulmonary Embolism: Part of classic PE triad (S1Q3T3 pattern)
• Chronic Pulmonary Disease: Cor pulmonale with RV strain
• Normal Variant: Rarely seen in thin, tall individuals with vertical heart orientation
• Left Posterior Fascicular Block: Can produce similar pattern with right axis

Pulmonary Embolism (S1Q3T3)

Classic ECG pattern of acute PE (present in only ~20% of cases):

• S wave in Lead I: Deep S wave indicating right axis shift
• Q wave in Lead III: Q wave with T wave inversion in III
• T inversion in Lead III: Right ventricular strain
• Additional Findings: Sinus tachycardia, right axis deviation, RBBB, T wave inversion in V1-V4

Differential Diagnosis of S1S2S3

The transition zone is where R wave height equals S wave depth (R/S ratio = 1), normally occurring at V3 or V4.

Early Transition (V2 or Earlier)

Transition zone shifts leftward (toward V1-V2):

• Posterior Myocardial Infarction: Loss of posterior forces creates early R wave dominance in V1-V2
• Right Ventricular Hypertrophy: Increased RV forces shift transition leftward
• WPW Syndrome Type A: Pre-excitation creates tall R in V1-V2
• Normal Variant: Especially in children and young adults
• Clockwise Rotation: Heart rotates so left ventricle faces more anteriorly

Delayed Transition (V5 or Later)

Transition zone shifts rightward (toward V5-V6):

• Left Ventricular Hypertrophy: Increased LV forces prolong S waves in right-to-mid precordial leads
• Anterior Myocardial Infarction: Loss of anterior forces delays R wave progression
• Left Bundle Branch Block: Altered depolarization sequence shifts transition
• Counterclockwise Rotation: Heart position shifts so left ventricle faces more leftward
• COPD: Hyperinflated lungs create vertical heart orientation

Persistent S Waves (No Transition)

S waves present across all precordial leads:

• Extreme Right Axis Deviation: S waves in all precordial and limb leads
• Severe RVH: Dominant right ventricular forces
• COPD with Cor Pulmonale: Vertical heart with RV enlargement

• Sokolow-Lyon is quick but imperfect: High specificity (~90%) but low sensitivity (<40%) for LVH - many patients with echo-confirmed LVH have normal voltage
• Age matters: S + R voltages normally higher in young adults (age <30: use >40mm cutoff); lower in elderly due to chest wall changes
• Body habitus affects voltages: Thin patients have higher voltages; obese patients have lower voltages - don't over-interpret in extremes
• Deep S in V2-V3 is normal: Don't be alarmed by 15-20mm S waves in V2 in healthy young adults - it's the left ventricle depolarizing away
• Slurred S waves are pathologic: Wide, notched S waves in lateral leads suggest RBBB; measure S wave duration - if >40ms, consider conduction delay
• S wave in aVR: Deep S in aVR is normal and expected; absence suggests lead reversal or dextrocardia
• Poor R progression mimics: Persistent S waves across precordium may be LVH, not anterior MI - check for tall R in V5-V6
• Athletic heart syndrome: Can meet voltage criteria for LVH but lacks strain pattern and has normal repolarization
• S1S2S3 in PE is rare: Only ~20% of PE cases show S1Q3T3 pattern; most common ECG finding in PE is sinus tachycardia
• New RBBB + deep S: In context of dyspnea, consider acute PE causing acute RV strain and new conduction delay

Systematic S Wave Assessment

1. Measure S Wave Depth in V1:
   • Normal: 5-20 mm
   • Deep (>20mm): Consider LVH if tall R in V5-V6
   • Absent: Consider RVH, posterior MI, or WPW Type A
2. Measure S Wave Depth in V5-V6:
   • Normal: Minimal or absent
   • Deep (>7mm): Consider RVH with R/S <1
   • Persistent large S: Check for LVH or delayed transition
3. Calculate Sokolow-Lyon:
   • Add S in V1 + tallest R in V5 or V6
   • >35mm (>40mm if age <30): Consider LVH
   • Must confirm with non-voltage criteria
4. Identify Transition Zone:
   • Where R = S (R/S ratio = 1)
   • Normal: V3 or V4
   • Early (V2): RVH, posterior MI, WPW
   • Late (V5-V6): LVH, anterior MI, LBBB
5. Assess S Wave Morphology:
   • Narrow: Normal depolarization
   • Wide/slurred: Bundle branch block
   • Measure duration: >40ms suggests conduction delay

Common Interpretation Pitfalls

• Mistake #1: Diagnosing LVH on voltage alone - MUST have supporting criteria (LAE, strain, increased RWPT)
• Mistake #2: Missing lead placement errors - check if S waves are unexpectedly absent or present where they shouldn't be
• Mistake #3: Over-calling LVH in young, thin patients - high voltages are normal in this population
• Mistake #4: Confusing poor R progression with persistent S waves - they're different patterns
• Mistake #5: Forgetting age-adjusted criteria - older patients have lower voltages, younger have higher

When to Suspect Technical Error

• S waves in unexpected leads: If S dominant in leads where R should be (e.g., all lateral leads), consider lead reversal
• Absent S in V1-V2: Unless RVH or posterior MI, should have some S wave - check lead placement
• Bizarre S wave morphology: Irregular, jagged S waves may indicate artifact or muscle tremor
• Asymmetric S waves: If one precordial lead has S wave vastly different from adjacent leads, verify placement

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