Heart Sounds S1, S2, S3, S4

Introduction

Heart sounds are audible vibrations produced by the cardiac cycle, primarily generated by valve closure, blood flow, and myocardial movement. They are fundamental to cardiovascular assessment, providing critical information about heart function, valvular integrity, and hemodynamics. Traditionally, four heart sounds are recognized: S1, S2, S3, and S4, each reflecting specific phases of the cardiac cycle. Understanding their origin, timing, characteristics, and clinical significance is essential for accurate diagnosis and patient management.

1. Overview of Heart Sounds

Heart sounds are classified as:

S1 (“lub”): First heart sound, associated with AV valve closure.
S2 (“dub”): Second heart sound, associated with semilunar valve closure.
S3: Third heart sound, associated with rapid ventricular filling.
S4: Fourth heart sound, associated with atrial contraction against a stiff ventricle.

Additional sounds include splitting of S2, clicks, murmurs, and rubs, but S1–S4 remain the core auscultatory findings.

2. First Heart Sound (S1)

2.1 Timing

Occurs at the onset of ventricular systole.
Coincides with the QRS complex on ECG.

2.2 Mechanism

Produced mainly by closure of the mitral and tricuspid valves.
Turbulence in blood flow and vibrations of adjacent cardiac structures contribute.
Mitral component precedes tricuspid component (M1 slightly before T1).

2.3 Location of Maximal Intensity

Apex of the heart (mitral valve) in left lateral decubitus position.
Tricuspid area (lower left sternal border) for tricuspid component.

2.4 Characteristics

“Lub” sound: low-pitched, longer duration than S2.
Loudness influenced by valve mobility, ventricular contractility, and chest wall thickness.

2.5 Clinical Significance

Loud S1: mitral stenosis, short PR interval.
Soft S1: mitral regurgitation, first-degree AV block, calcified valves.
Variable S1: atrial fibrillation (loss of atrial contraction).

3. Second Heart Sound (S2)

3.1 Timing

Marks end of ventricular systole, just before diastole begins.
Coincides with the T wave on ECG.

3.2 Mechanism

Produced by closure of aortic (A2) and pulmonary (P2) valves.
Aortic component usually precedes pulmonary component due to higher pressure on left side.

3.3 Splitting of S2

Physiological splitting: during inspiration, P2 delayed → A2-P2 interval increases.
Pathological splitting:
- Wide split: pulmonary stenosis, right bundle branch block
- Fixed split: atrial septal defect
- Paradoxical split: left bundle branch block, aortic stenosis

3.4 Location

Best heard at base of the heart (aortic and pulmonic areas).

3.5 Clinical Significance

Loud A2: systemic hypertension, aortic root dilation
Soft A2: aortic stenosis
Absent P2: pulmonary hypertension, pulmonic stenosis

4. Third Heart Sound (S3)

4.1 Timing

Occurs early in diastole during rapid ventricular filling.
Follows S2 (ventricular “protodiastolic” sound).

4.2 Mechanism

Rapid deceleration of blood entering a compliant ventricle causes vibrations of the ventricular wall and chordae tendineae.
Physiological S3 can occur in children, young adults, and athletes.

4.3 Location and Auscultation

Best heard at apex with bell of stethoscope, patient in left lateral decubitus.
Low-pitched, dull sound, often described as “Kentucky” cadence when combined with S1 and S2.

4.4 Clinical Significance

Physiological S3: young, healthy individuals, pregnant women.
Pathological S3 (ventricular gallop): indicates volume overload or heart failure.
- Common in dilated cardiomyopathy, mitral regurgitation, post-MI
Associated findings: elevated jugular venous pressure, pulmonary congestion.

5. Fourth Heart Sound (S4)

5.1 Timing

Occurs late in diastole, just before S1.
Coincides with atrial contraction (atrial systole).

5.2 Mechanism

Produced by atrial contraction into a stiff or noncompliant ventricle, causing vibrations of ventricular walls.

5.3 Location and Auscultation

Best heard at apex with bell, patient in left lateral decubitus.
Low-pitched, dull sound, often described as “Tennessee” cadence when combined with S1, S2, S3.

5.4 Clinical Significance

Typically pathological in adults:
- Hypertensive heart disease
- Left ventricular hypertrophy
- Aortic stenosis
- Ischemic cardiomyopathy
Rarely physiological in trained athletes with stiff ventricles.

6. Gallop Rhythms

S3 + S1 + S2 → “ventricular gallop” → often heart failure
S4 + S1 + S2 → “atrial gallop” → stiff ventricle, hypertension
S4 + S1 + S2 + S3 → “summation gallop” → severe cardiac dysfunction

7. Heart Sound Modulation

7.1 Effect of Respiration

Inspiration increases venous return → accentuates right-sided heart sounds (physiological S2 splitting).
Expiration accentuates left-sided sounds.

7.2 Body Position

Left lateral decubitus: enhances S3 and S4.
Sitting/leaning forward: accentuates aortic valve sounds.

7.3 Exercise

Increased cardiac output → louder S1
Pathological S3 may become audible in decompensated heart failure

8. Heart Sounds in Valvular Diseases

Valvular Lesion	Heart Sound Changes
Mitral Stenosis	Loud S1, opening snap, S3 in advanced cases
Mitral Regurgitation	Soft S1, pansystolic murmur, S3 may be present
Aortic Stenosis	Soft or delayed S2, ejection click
Aortic Regurgitation	Early diastolic murmur, may be accompanied by S3
Tricuspid Stenosis	Loud S1 at lower left sternal border
Pulmonic Stenosis	Soft S2, ejection click

9. Techniques of Auscultation

9.1 Equipment

Stethoscope bell: low-frequency sounds (S3, S4)
Stethoscope diaphragm: high-frequency sounds (S1, S2, murmurs)

9.2 Systematic Approach

Identify S1 and S2 using timing with pulse or carotid upstroke.
Listen for splitting of S2 at pulmonic area.
Detect low-frequency gallops (S3, S4) with bell at apex.
Assess loudness, pitch, duration, and location.

9.3 Clinical Pearls

Always correlate heart sounds with ECG and hemodynamic context.
Use positioning and maneuvers to enhance subtle sounds:
- Squatting → increases venous return
- Valsalva → reduces venous return, diminishes S3

10. Pathophysiological Correlates

10.1 S1 Abnormalities

Loud: mitral stenosis, short PR
Soft: mitral regurgitation, first-degree AV block

10.2 S2 Abnormalities

Absent or soft: valve calcification, stenosis
Split abnormalities: RBBB, LBBB, ASD

10.3 S3 and S4

Indicators of ventricular compliance, preload, and volume status.
S3: early sign of heart failure
S4: hypertensive or ischemic heart disease

11. Additional Heart Sounds

Ejection clicks: congenital aortic/pulmonic valve stenosis
Opening snaps: mitral stenosis
Pericardial rubs: pericarditis, triphasic sound

12. Heart Sounds and Hemodynamics

S1 intensity correlates with ventricular contractility and valve mobility.
S2 splitting provides insights into right vs. left ventricular systolic timing.
S3 reflects high filling pressures or dilated ventricles.
S4 reflects ventricular stiffness and impaired compliance.

13. Clinical Integration

Heart sounds + ECG + echocardiography → comprehensive assessment.
S1 and S2: basic cardiac rhythm and valve function.
S3 and S4: early markers of heart failure, cardiomyopathy, ischemia.
Used to monitor therapeutic response in heart failure or hypertension.