1. INTRODUCTION AND COMPONENTS
The second heart sound (S2) marks the end of ventricular systole and the onset of diastole. It is produced by the vibrations initiated by the closure of the semilunar valves.
- Components: * A2 (Aortic closure): Higher pressure, heard all over the precordium.
- P2 (Pulmonic closure): Lower pressure, normally heard only at the upper left sternal border (pulmonic area).
- Normal Splitting: During inspiration, increased venous return to the Right Ventricle (RV) delays RV ejection, while decreased pulmonary venous return to the Left Ventricle (LV) hastens LV ejection. This causes A2 to occur earlier and P2 to occur later, resulting in an audible “split.”
2. PATHOPHYSIOLOGY OF S2 ABNORMALITIES
Variations in S2 are determined by:
- Hemodynamics: Volume or pressure overload in the systemic or pulmonary circuits.
- Electrical conduction: Delays in ventricular activation (e.g., RBBB/LBBB).
- Valve Anatomy: Mobility and thickness of the valve leaflets.
3. CLINICAL SIGNIFICANCE OF INTENSITY
The loudness of the components provides clues to underlying pressures:
- Loud P2 (P2 > A2 at the apex or loud at base):
- Pulmonary Arterial Hypertension (PAH) - most common cause.
- Dilated pulmonary artery.
- Thin chest wall.
- Soft/Absent P2:
- Tetralogy of Fallot (TOF).
- Severe Pulmonary Stenosis (PS).
- Pulmonary Atresia.
- Loud A2:
- Systemic Hypertension.
- Transposition of Great Arteries (Aorta is anterior).
- Coarctation of Aorta.
- Soft A2:
- Severe Aortic Stenosis (Calcific or Valvular).
- Aortic Regurgitation.
4. CLINICAL SIGNIFICANCE OF SPLITTING PATTERNS
A. Wide Physiological Split
Occurs when there is a delay in RV contraction or increased RV volume:
- RV Volume Overload: ASD (but usually fixed), Partial Anomalous Pulmonary Venous Connection (PAPVC).
- RV Outflow Obstruction: Pulmonary Stenosis (the split widens as severity increases).
- Electrical Delay: Right Bundle Branch Block (RBBB).
- LV Early Emptying: Mitral Regurgitation, VSD (A2 occurs early).
B. Fixed Wide Split
The split does not vary with respiration.
- Atrial Septal Defect (ASD): Pathognomonic. Equalization of respiratory changes in venous return between both atria via the defect.
- Severe Right Heart Failure.
C. Narrow Split
- Pulmonary Hypertension (P2 occurs earlier due to high back pressure).
- Aortic Stenosis.
D. Paradoxical (Reversed) Split
P2 precedes A2. The split narrows on inspiration and widens on expiration.
- Delayed LV Activation: LBBB, WPW syndrome (Type B).
- LV Outflow Obstruction: Severe Aortic Stenosis, HOCM.
- Severe LV Dysfunction: Ischemic cardiomyopathy.
E. Single S2 (No Split Audible)
- Only one valve present: Truncus Arteriosus.
- One valve atretic: Pulmonary atresia, Tricuspid atresia.
- One component inaudible: Severe PS, TOF (P2 too soft).
- Overlapping components: Eisenmenger Syndrome (P2 occurs early).
- Malposition: D-TGA (Aorta anteriorly masks P2).
5. DIAGNOSTIC UTILITY IN PEDIATRICS
Assessment of S2 is critical for bedside diagnosis:
- Screening for PAH: A loud, palpable P2 is often the first clinical sign of pulmonary hypertension in VSD/PDA patients.
- Severity of PS: The wider the split and the softer the P2, the more severe the stenosis.
- Severity of TOF: A single, loud S2 (A2) suggests severe RV outflow obstruction where P2 is not heard.
6. SUMMARY TABLE: S2 IN COMMON CONDITIONS
| Condition | S2 Pattern | Intensity Change |
|---|---|---|
| ASD | Wide Fixed Split | Normal P2 |
| VSD | Wide Split | Loud P2 (if PAH) |
| TOF | Single S2 | Soft/Absent P2 |
| PS | Wide Split | Soft P2 |
| AS | Narrow/Reversed | Soft A2 |
| PAH | Narrow Split | Markedly Loud P2 |