Heart Sounds: S1, S2, S3, S4, and Murmurs

Complete tutorial on heart sounds - the mechanisms of S1, S2, S3, S4, splitting, and the auscultation of murmurs. Anatomic basis of normal and abnormal cardiac acoustics.

This content is for informational purposes only. Always consult a healthcare professional.

Heart sounds are the acoustic manifestations of cardiac mechanical activity. Understanding their origin and characteristics is essential for cardiac auscultation and diagnosis of valvular and structural heart disease.

Normal Heart Sounds

First Heart Sound (S1)

Timing: Beginning of systole (after QRS complex)

Mechanism: Closure of the mitral and tricuspid valves

Components:

  • M1: Mitral valve closure (loudest at apex)
  • T1: Tricuspid valve closure (loudest at left lower sternal border)

Interval M1-T1: Normally 20-30 ms (tricuspid closes after mitral)

Characteristics:

  • Lower pitched than S2
  • Best heard at the apex (mitral) and left lower sternal border (tricuspid)
  • Coincides with the carotid upstroke (carotid pulse)
S1 Intensity Cause
Loud Short PR interval, mitral stenosis, hyperdynamic state
Soft Long PR interval, heart failure, mitral regurgitation, obesity
Variable Atrial fibrillation, complete heart block

Second Heart Sound (S2)

Timing: End of systole (after T wave)

Mechanism: Closure of the aortic and pulmonary valves

Components:

  • A2: Aortic valve closure (loudest at right upper sternal border)
  • P2: Pulmonary valve closure (loudest at left upper sternal border)

Physiologic splitting:

  • Inspiration: A2-P2 interval widens (40-60 ms)
  • Expiration: A2-P2 interval narrows (10-30 ms)

Mechanism of splitting:

  • Inspiration increases venous return to the right heart
  • Right ventricular ejection is prolonged
  • Pulmonary valve closure is delayed
S2 Splitting Pattern Cause
Physiologic Widens on inspiration, narrows on expiration Normal
Wide, fixed Splitting constant with respiration Atrial septal defect
Wide, variable Wide splitting, varies with respiration RBBB, pulmonary stenosis
Paradoxical (reverse) Splitting narrows on inspiration, widens on expiration LBBB, aortic stenosis
Single No audible splitting Tetralogy of Fallot, pulmonary atresia

S2 intensity:

  • Loud A2: Systemic hypertension
  • Loud P2: Pulmonary hypertension
  • Soft S2: Aortic stenosis (calcified valve)

S3 Gallop

Timing: Early diastole (after S2, during rapid ventricular filling)

Mechanism: Rapid ventricular filling abruptly limited by the ventricular wall

Characteristics:

  • Low-pitched, dull sound
  • Best heard at the apex with the bell
  • Normal in children and young adults (< 40 years)
  • Pathologic in older adults

Left-sided S3:

  • Best heard at apex, left lateral decubitus position
  • Indicates: LV dysfunction, volume overload, heart failure
  • Associated with: Dilated cardiomyopathy, mitral regurgitation
  • Ventricular gallop

Right-sided S3:

  • Best heard at left lower sternal border
  • Indicates: RV dysfunction, pulmonary hypertension
  • Associated with: Cor pulmonale, pulmonary embolism

S4 Gallop

Timing: Late diastole (just before S1)

Mechanism: Atrial contraction against a stiff, noncompliant ventricle

Characteristics:

  • Low-pitched, soft sound
  • Best heard at the apex with the bell
  • Always pathologic (indicates diastolic dysfunction)

Left-sided S4:

  • LV hypertrophy (hypertension, aortic stenosis)
  • Hypertrophic cardiomyopathy
  • Acute myocardial infarction
  • Atrial gallop

Right-sided S4:

  • RV hypertrophy (pulmonary hypertension, pulmonary stenosis)
  • Best heard at left lower sternal border

Extra Heart Sounds

Ejection Click

Timing: Early systole (after S1)

Mechanism: Opening of a stenotic semilunar valve or the sudden halt of a dilated great vessel

Click Location Cause
Aortic Apex (radiates) Bicuspid aortic valve, aortic stenosis
Pulmonary Left upper sternal border Pulmonary stenosis, pulmonary hypertension

Mid-Systolic Click

Timing: Mid-to-late systole

Mechanism: Prolapse of the mitral valve (or tricuspid)

Associated murmur: Late systolic murmur (if regurgitation occurs)

Cause: Mitral valve prolapse (MVP), myxomatous degeneration

Maneuvers:

  • Squatting: Click moves later (increased preload)
  • Standing: Click moves earlier (decreased preload)

Opening Snap

Timing: Early diastole (after S2)

Mechanism: Opening of a stenotic mitral valve

Characteristics:

  • High-pitched, snapping sound
  • Best heard at the apex
  • Present in mitral stenosis (pliable valve)

Time interval: A2-OS:

  • Short interval (< 70 ms): Severe mitral stenosis
  • Long interval (> 100 ms): Mild mitral stenosis

Pericardial Knock

Timing: Early diastole

Mechanism: Sudden halt of ventricular filling due to pericardial constriction

Characteristics:

  • Medium-pitched
  • Best heard at the apex
  • Associated with: Constrictive pericarditis

Heart Murmurs

Classification

Characteristic Types
Timing Systolic, diastolic, continuous
Shape Crescendo, decrescendo, plateau, crescendo-decrescendo
Location Aortic, pulmonary, tricuspid, mitral
Intensity Grade 1-6
Pitch High, medium, low
Quality Blowing, harsh, rumbling, musical
Radiation Carotid, axilla, back

Murmur Grading

Grade Description
1/6 Very faint, heard only with effort
2/6 Faint, heard immediately
3/6 Moderate intensity, no thrill
4/6 Loud, palpable thrill
5/6 Very loud, heard with stethoscope edge on chest
6/6 Heard with stethoscope off the chest

Systolic Murmurs

Holosystolic (pansystolic):

Diagnosis Location Radiation Characteristics
Mitral regurgitation Apex Axilla Blowing, high-pitched
Tricuspid regurgitation LLSB Right Increases with inspiration
VSD LLSB Diffuse Harsh

Mid-systolic (ejection):

Diagnosis Location Radiation Characteristics
Aortic stenosis RUSB Carotids Harsh, crescendo-decrescendo
Pulmonary stenosis LUSB Left lung Harsh, with ejection click
HOCM LLSB-apex Variable Increases with Valsalva

Late systolic:

  • Mitral valve prolapse (with click)
  • Papillary muscle dysfunction

Diastolic Murmurs

Early diastolic (decrescendo):

Diagnosis Location Characteristics
Aortic regurgitation LLSB Blowing, high-pitched, decrescendo
Pulmonary regurgitation LUSB Similar, with pulmonary HTN

Mid-to-late diastolic:

Diagnosis Location Characteristics
Mitral stenosis Apex Low-pitched, rumbling, presystolic accentuation
Tricuspid stenosis LLSB Rumbling, increases with inspiration

Continuous Murmurs

  • Patent ductus arteriosus (left infraclavicular, machinery murmur)
  • Arteriovenous fistula
  • Venous hum (cervical, disappears lying down)

Maneuvers Affecting Heart Sounds and Murmurs

Maneuver Physiologic Effect Auscultatory Change
Inspiration ↑ RV preload, ↓ LV preload ↑ Right-sided sounds, ↓ Left-sided
Expiration ↓ RV preload, ↑ LV preload ↓ Right-sided sounds, ↑ Left-sided
Valsalva (strain) ↓ Preload (both sides) MV click moves earlier, HOCM louder, AS softer
Squatting ↑ Preload, ↑ Afterload MV click later, HOCM softer, MR louder
Standing ↓ Preload, ↓ Afterload MV click earlier, HOCM louder
Handgrip ↑ Afterload MR louder, AR louder, AS softer
Amyl nitrite ↓ Afterload AS louder, MR softer, VSD louder

Innocent Murmurs

Type Age Location Characteristics
Still murmur 3-6 years LLSB-apex Vibratory, musical
Pulmonary flow murmur Children LUSB Soft, systolic, ejection
Venous hum Children Infraclavicular Continuous, disappears lying down
Supraclavicular bruit Adolescents Supraclavicular Systolic, from great vessels
Mammary souffle Pregnancy Anterior chest Continuous, from breast vessels
Age Normal Findings
Newborn S2 single (pulmonary resistance high), murmurs from PDA
Children Physiologic S3, innocent murmurs common
Young adults Physiologic splitting of S2
Middle-aged S4 may appear (LV stiffness)
Elderly Aortic sclerosis murmur, S4, reduced S2 intensity