Heart Sounds

Overview

The Normal Cardiac Cycle and Sound Timing

S1 — First Heart Sound ("lub")

• Duration: ~0.14 seconds
• Frequency: 25–45 Hz (low-pitched, relatively prolonged — "lub")
• Best heard: Mitral area (cardiac apex, 5th intercostal space, midclavicular line) and tricuspid area (lower left sternal border)
• S1 contains both M1 (mitral) and T1 (tricuspid) components; normal splitting of S1 can occasionally be heard

"S1 is classically loud in the early phases of rheumatic MS and in patients with hyperkinetic circulatory states or short PR intervals." — Harrison's Principles of Internal Medicine, 22nd Ed.

S2 — Second Heart Sound ("dub")

• Duration: ~0.11 seconds (shorter than S1 because semilunar valves are tauter)
• Frequency: ~50 Hz (higher-pitched than S1 — "dub")
• Best heard: Aortic area (2nd right intercostal space) and pulmonic area (2nd left intercostal space)

Splitting of S2

Note: P2 is considered loud when its intensity exceeds A2 at the base — a sign of pulmonary hypertension.

S3 — Third Heart Sound

• Frequency: Very low (~20–40 Hz) — barely audible; recorded more easily on phonocardiogram
• Pitch: Low, dull ("lub-dub-ta")
• Best heard: With the bell of the stethoscope at the LV apex (left-sided S3) or lower left sternal border (right-sided S3, louder on inspiration)

"An S3 is equally prevalent among heart failure patients with preserved and reduced LV ejection fraction." — Harrison's, 22nd Ed.

S4 — Fourth Heart Sound

• Frequency: Very low (~20 Hz or less) — rarely audible at bedside
• Creates a "ta-lub-dub" rhythm (gallop)
• Best heard: Cardiac apex (left-sided), lower left sternal border (right-sided)

Auscultation Areas

Additional Sounds

Ejection Sound (Ejection Click)

• Timing: High-pitched, early systolic sound coinciding with the upstroke of the carotid pulse
• Causes: Bicuspid aortic valve, bicuspid pulmonic valve, or dilation of the aortic/pulmonary root
• Key feature of pulmonic ejection sound: It is the only right-sided sound that decreases with inspiration (opposite of most right-sided sounds)

Opening Snap (OS)

• Timing: Early diastole, shortly after S2 (very short A2–OS interval)
• Cause: Sudden opening of a stenotic mitral valve
• Clinical significance: Classic for rheumatic mitral stenosis
• The shorter the A2–OS interval, the higher the left atrial pressure (more severe MS)

Pericardial Knock

• High-pitched diastolic sound, slightly later than OS
• Occurs in constrictive pericarditis due to abrupt cessation of ventricular expansion

Quick Mnemonics

Summary Table

Mechanism of Heart Sounds

Understanding What Generates Sound

1. Sudden deceleration of blood when valves close or ventricular walls stop blood movement
2. Vibration of taut valve leaflets and chordae tendineae under sudden tension
3. Reverberation of blood bouncing between the valve and the adjacent cardiac/vascular walls
4. These vibrations spread through adjacent tissues to the chest wall and are detected by the stethoscope

Mechanism of S1 (First Heart Sound)

Step-by-step sequence:

Ventricular systole begins
        ↓
Ventricular pressure rises above atrial pressure
        ↓
Blood surges BACK toward the atria → pushes AV valves shut
        ↓
Valve leaflets bulge toward the atria
        ↓
Chordae tendineae become taut → ABRUPTLY halt the bulging
        ↓
Elastic recoil of chordae + leaflets → blood bounces BACK into ventricle
        ↓
Blood, valve leaflets, and ventricular walls vibrate
        ↓
Vibrations travel through chest wall → heard as "LUB"

Key structural contributors:

• Mitral valve leaflets + chordae tendineae (dominant component — M1)
• Tricuspid valve leaflets + chordae tendineae (T1, slightly delayed)
• Ventricular myocardium and adjacent great vessel walls amplify the vibration

Why is S1 low-pitched and long?

Mechanism of S2 (Second Heart Sound)

Step-by-step sequence:

End of ventricular ejection
        ↓
Ventricular pressure drops below aortic/pulmonary artery pressure
        ↓
Blood in the aorta/PA surges BACK toward the ventricle
        ↓
Semilunar valve cusps catch this backflow → valve snaps shut
        ↓
Cusps bulge BACK toward the ventricle
        ↓
Elastic recoil → blood bounces BACK into the aorta/PA
        ↓
Blood reverberates between arterial wall and semilunar valve
        ↓
Vibrations travel up the arterial walls → heard as "DUB"

Key structural contributors:

• Aortic valve cusps → A2 component (normally heard first)
• Pulmonic valve cusps → P2 component (slightly delayed, especially on inspiration)
• Arterial walls (aorta and pulmonary artery) act as the resonating chambers

Why is S2 higher-pitched and shorter than S1?

1. Semilunar valves are tauter than AV valves → vibrate at a higher frequency (~50 Hz)
2. The aortic and pulmonary arterial walls are stiffer and more elastic than the ventricular chambers → higher elastic coefficient → faster, shorter vibration (~0.11 sec)

Mechanism of S2 Splitting — Why Inspiration Widens the Gap

INSPIRATION
    ↓
Negative intrathoracic pressure
    ↓
↑ Venous return to RIGHT heart
    ↓
RV stroke volume ↑ → RV takes longer to eject → P2 delayed
    ↓
Simultaneously: ↑ lung vascular capacitance → ↓ pulmonary venous 
return to LEFT heart → LV stroke volume ↓ → aortic valve closes EARLIER (A2 earlier)
    ↓
A2–P2 interval WIDENS → audible splitting on inspiration

Abnormal Splitting Mechanisms:

Mechanism of S3 (Third Heart Sound)

Early diastole: Mitral valve opens
        ↓
Blood rushes rapidly from atrium into ventricle (passive filling phase)
        ↓
Ventricle rapidly distends and decelerates the inflowing blood
        ↓
Abrupt cessation of ventricular wall motion
        ↓
Blood oscillates back and forth between ventricular walls 
(like water rushing into a paper bag — it reverberates)
        ↓
Low-frequency vibration of ventricular walls
        ↓
Heard as a soft, low-pitched "ta" after S2

Why does S3 only appear in the MIDDLE third of diastole?

Why is it pathological in adults?

Mechanism of S4 (Fourth Heart Sound)

Late diastole: Atrial contraction (P wave on ECG)
        ↓
Atrium contracts forcefully
        ↓
Blood is pushed into a STIFF, non-compliant ventricle
        ↓
The ventricle resists sudden filling
        ↓
Sudden deceleration of atrial blood → vibrates the ventricular wall
        ↓
Very low-frequency sound just before S1 ("ta-lub-dub")

Why only in stiff ventricles?

Why is S4 absent in atrial fibrillation?

Comparative Summary of Mechanisms

A2 and P2 — The Two Components of S2

What Are A2 and P2?

Why Does A2 Come Before P2?

Left ventricle has HIGHER pressure than right ventricle
        ↓
LV ejects blood FASTER and FINISHES ejection earlier
        ↓
Aortic valve closes FIRST → A2
        ↓
RV continues ejecting slightly longer (lower pressure system)
        ↓
Pulmonic valve closes SECOND → P2
        ↓
A2 precedes P2 by 20–30 ms (normally)

Physiologic Splitting — Why Inspiration Widens A2–P2

INSPIRATION
│
├─► Negative intrathoracic pressure
│         ↓
│    ↑ Venous return to RIGHT heart
│         ↓
│    RV fills more → needs more time to eject → P2 DELAYED
│
└─► Increased pulmonary vascular capacitance
          ↓
     ↓ Pulmonary venous return to LEFT heart
          ↓
     LV fills less → finishes ejection sooner → A2 EARLIER
          ↓
     A2–P2 gap WIDENS → AUDIBLE SPLITTING on inspiration

EXPIRATION → Both effects reverse → A2 and P2 merge → single S2

Auscultation — Where to Hear Each Component

Normal rule:

A2 > P2 at the base — the aortic component is normally louder because the aortic pressure (~120 mmHg) is much higher than pulmonary pressure (~25 mmHg), producing a sharper valve snap.

A2 Intensity — What Affects It

P2 Intensity — What Affects It

Clinical rule for P2:

P2 is considered abnormally loud when it:

• Is louder than A2 at the base (2nd ICS)
• Can be palpated as a tap at the 2nd left interspace
• Can be heard at the apex (normally P2 is not audible at the apex)

All three indicate pulmonary hypertension until proven otherwise.

Splitting Patterns — Complete Classification

1. Normal (Physiologic) Splitting

• A2 → P2 gap: widens on inspiration, disappears on expiration
• Heard in: Normal individuals, especially young people
• The gap is ~20–30 ms on expiration, widens to ~60 ms on inspiration

2. Wide Splitting (A2 ←—→ P2, always wide, increases on inspiration)

3. Fixed Splitting (A2 → P2 gap: wide and UNCHANGED with respiration)

ASD → left-to-right shunt → RV always volume overloaded
        ↓
P2 is always delayed (RV always has extra volume to eject)
        ↓
On INSPIRATION: venous return ↑ to RA, BUT the ASD allows equalization 
                of pressure → no extra augmentation of RV filling
        ↓
The A2–P2 gap remains FIXED regardless of respiration

Fixed splitting = ASD until proven otherwise.

4. Paradoxical (Reversed) Splitting (P2 → A2, gap widens on EXPIRATION)

LBBB (or other causes of delayed LV activation)
        ↓
LV contracts LATE → aortic valve closes LATE → A2 delayed
        ↓
Now P2 occurs BEFORE A2 (order reversed)
        ↓
On INSPIRATION: P2 moves later (normal mechanism) → 
                P2 moves TOWARD A2 → gap NARROWS
On EXPIRATION:  P2 moves earlier → P2 moves AWAY from A2 → gap WIDENS
        ↓
Splitting heard on EXPIRATION (opposite of normal)

5. Narrow / Single S2 (A2 and P2 fused)

Summary Comparison Table