Normal Heart Sound Intensity Relationship
The relative intensity of S1 versus S2 varies by auscultation location—S1 is normally louder than S2 at the apex, while S2 is normally louder than S1 at the base of the heart.
Location-Dependent Intensity Patterns
The intensity relationship between first and second heart sounds follows a predictable anatomical pattern based on proximity to the valves generating each sound:
At the Cardiac Apex
- S1 is normally louder than S2 because the apex overlies the mitral valve, where mitral valve closure (the primary component of S1) generates maximum intensity 1
- This is the standard reference point for assessing S1 intensity in clinical practice 2
At the Base (Aortic and Pulmonic Areas)
- S2 is normally louder than S1 at the second right intercostal space (aortic area) and second left intercostal space (pulmonic area) 1
- The proximity to the semilunar valves (aortic and pulmonic) makes S2 predominant in these locations 3
Physiologic Basis
The intensity difference reflects the underlying hemodynamics and valve closure mechanics:
- S1 generation: Occurs with closure of the atrioventricular valves (mitral and tricuspid), with mitral closure (M1) preceding tricuspid closure (T1) by approximately 0.03 seconds 4
- S2 generation: Results from closure of the semilunar valves (aortic and pulmonic), with higher closing pressures typically making S2 sharper and higher-pitched than S1 5
- The energy content of both sounds concentrates below 150 Hz, though S2 contains greater amplitude above 150 Hz due to vibrations within the great vessels 5
Clinical Pitfalls and Pathologic Variations
When S1 Becomes Abnormally Loud
- Early systolic mitral valve prolapse produces an S1 amplitude ratio (S1/A2) of 6.2 ± 3.1 compared to normal controls at 1.4 ± 0.7 2
- Mitral stenosis delays M1 timing (Q-M1 interval of 0.10 seconds versus normal 0.06 seconds), which can reverse normal S1 splitting 4
When S2 Becomes Abnormally Loud or Altered
- A single loud S2 suggests congenitally corrected transposition (L-TGA), where both semilunar valves close simultaneously 3
- Soft or absent aortic component (A2) of S2 indicates severe aortic stenosis 3
- Fixed splitting of S2 during both inspiration and expiration suggests atrial septal defect 3
When S1 Becomes Abnormally Soft
- Flail mitral leaflet without normal coaptation produces an S1/A2 ratio of only 0.3 ± 0.5, making S1 barely audible 2
- Acute severe mitral regurgitation may produce a diminished S1 6
Practical Assessment Technique
Use the "inching" method for accurate sound identification: