Chapter 23: Heart Valves and Heart Sounds; Valvular and Congenital Heart Defects

Hearts Sounds diagram


Written By: Razaullah Khattak (DPT Medical Professional)

Student Source Reference: Guyton and Hall Textbook of Medical Physiology

Chapter: 23

To read more about Role of the kidneys in long term, check out Chapter 19:

https://mednotesbyrazaullah.blogspot.com/2026/08/chapter-19-role-of-kidneys-in-long-term.html

Heart Sounds 

The mechanical function of the heart valves is fundamentally tied to the acoustic phenomena produced during the cardiac cycle. Under normal conditions, the opening of heart valves is completely silent their abrupt closure generates distinct vibrations that propagate through surrounding cardiac tissues and blood vessels to reach the chest wall. The first heart sound (S1) marks the onset of ventricular systole as the atrioventricular (mitral and tricuspid) valves snap shut, causing tense valve structures and adjacent ventricular blood to reverberate. Conversely, the second heart sound (S2) signals the end of systole, produced by the sudden closure and elastic recoil of the taut semilunar (aortic and pulmonary) valves. Low-frequency third and fourth heart sounds may also occur in specific diastolic filling phases, though they are often below the human audible threshold and best detected via phonocardiography.

When heart valves are structurally damaged most commonly due to autoimmune scarring from rheumatic fever their physical dynamics alter dramatically, resulting in valvular stenosis, regurgitation, or a combination of both. These valvular lesions disrupt laminar blood flow, creating high-velocity turbulent jets that produce audible heart murmurs during specific phases of systole or diastole. To maintain effective systemic cardiac output despite structural defects, the heart engages several compensatory mechanisms, including progressive chamber hypertrophy and fluid retention to elevate venous return. Valvular pathology advances past a critical threshold, compensatory limits are exceeded, precipitating left ventricular failure, severe pulmonary edema, and marked reduction in overall cardiac reserve.

Mechanism and Dynamics of Normal Heart Sounds

  • Heart valve closing produces audible diagnostic sounds.
  • Valve opening normally produces no audible sound.
  • First sound occurs at ventricular systole onset.
  • First sound results from atrioventricular valve closure.
  • Second sound occurs at ventricular systole end.
  • Second sound results from semilunar valve closure.
  • Valve leaflet slapping does not cause heart sounds.
  • Cushioning blood prevents significant valve leaflet slapping sound.
  • Sound results from vibration of taut closed valves.
  • Blood backflow causes abrupt closure of AV valves.
  • Taut chordae tendineae prevent backward valve leaflet bulging.
  • Elastic recoil causes blood reverberation inside ventricular walls.
  • Semilunar valve closure recoils blood into arterial trunks.
  • Vibrations transmit along vessels to the chest wall.

Duration, Pitch, and Auscultation Characteristics

  • Duration of normal heart sounds exceeds 0.10 second.
  • First heart sound duration is approximately 0.14 second.
  • Second heart sound duration is approximately 0.11 second.
  • Taut semilunar valves vibrate for a shorter duration.
  • Audible pitch ranges between 40 and 500 Hz.
  • Inaudible vibrations peak around 20 cycles per second.
  • Phonocardiograms record low-frequency inaudible cardiac vibrations.
  • Second heart sound has higher frequency than first.
  • Greater arterial wall tautness increases second sound pitch.
  • Stethoscope auscultation identifies valvular sound chest surface areas.
  • Sound areas do not lie directly over physical valves.
  • Aortic area lies upward along the ascending aorta.
  • Pulmonic area lies upward along the pulmonary trunk.
  • Mitral area aligns with left ventricular cardiac apex.
  • Tricuspid area lies directly over the right ventricle.

Diastolic and Atrial Heart Sounds

  • Weak third heart sound occurs during mid-diastole.
  • Third sound results from inrushing ventricular blood reverberation.
  • Early diastolic ventricles lack sufficient wall tension.
  • Low frequency renders third sound mostly inaudible naturally.
  • Fourth sound occurs during active atrial contraction phase.
  • Atrial sound frequency remains under 20 cycles second.
  • Phonocardiogram detects third sound in some healthy people.

Pathology of Rheumatic Valvular Lesions

  • Rheumatic fever causes most acquired heart valve lesions.
  • Rheumatic fever is an autoimmune post-streptococcal disease.
  • Group A hemolytic streptococci initiate primary throat infections.
  • Bacterial proteins trigger persistent systemic antibody production.
  • Antibodies cross-react with vulnerable cardiac valve tissues.
  • Inflammatory fibrinous lesions form along valve leaflet edges.
  • High mechanical stress makes mitral valve most vulnerable.
  • High aortic pressure makes aortic valve second most damaged.
  • Low right heart pressures reduce tricuspid damage severity.
  • Chronic inflammation causes permanent fibrous valve leaflet fusion.
  • Fused leaflets preventing forward flow define valvular stenosis.
  • Scarred non-closing leaflets cause valvular backflow regurgitation.

Acoustic Characteristics of Heart Murmurs

  • Valvular abnormalities create turbulent flow sound murmurs.
  • Aortic stenosis creates high-velocity systolic jet flow.
  • Aortic stenosis generates high left ventricular systolic pressure.
  • Turbulent aortic blood jet produces harsh systolic murmur.
  • Severe aortic stenosis murmur causes chest wall thrill.
  • Aortic regurgitation causes high-pitched diastolic blowing murmur.
  • Backward aortic flow jets into low-pressure resting ventricle.
  • Mitral regurgitation creates high-frequency blowing systolic murmur.
  • Mitral regurgitation sound transmits primarily to apex area.
  • Mitral stenosis creates low-frequency diastolic rumbling murmur.
  • Weak pressure gradient causes low-intensity mitral stenosis murmur.
  • Mid-diastolic ventricular filling enables audible sound reverberation.

Circulatory Dynamics in Aortic Valvular Disease

  • Aortic stenosis impedes left ventricular blood ejection.
  • Aortic regurgitation permits blood backflow during diastole.
  • Both aortic defects reduce net forward stroke volume.
  • Increased workload forces left ventricular muscle hypertrophy.
  • Regurgitation causes massive left ventricular chamber enlargement.
  • Severe stenosis raises ventricular peak pressure to 400 mmHg.
  • Regurgitation stroke volume can reach 250 milliliters total.
  • Decreased arterial pressure triggers renal fluid retention compensation.
  • Increased blood volume raises venous return to heart.
  • Hypoxia stimulates red blood cell mass production gradually.

Decompensation and Pulmonary Edema in Aortic Lesions

  • Early adaptation maintains normal resting systemic cardiac output.
  • Critical workload threshold causes left ventricular dilation eventually.
  • Failing left ventricle depresses overall net cardiac output.
  • Depressed output causes blood damming inside left atrium.
  • High left atrial pressure increases pulmonary vascular pressure.
  • Mean left atrial pressure above 25 mmHg causes edema.
  • Severe pulmonary fluid accumulation impairs alveolar oxygen transfer.

Dynamics of Mitral Valvular Disease

  • Mitral stenosis impedes left atrial blood emptying.
  • Mitral regurgitation allows systolic backflow into atrium.
  • Both mitral lesions elevate mean left atrial pressure.
  • Chronically elevated atrial pressure causes pulmonary tissue edema.
  • Enlarged lymphatic vessels protect lungs up to 25 mmHg.
  • Atrial wall stretching predisposes to circus excitatory signals.
  • Atrial fibrillation frequently complicates late-stage mitral stenosis.
  • Fibrillation abolishes atrial primer pump function completely.
  • Renal fluid retention increases systemic venous return compensation.
  • Pulmonary arteriolar constriction raises pulmonary artery pressure.
  • Elevated pulmonary pressure causes right ventricular muscle hypertrophy.

Effect of Exercise on Valvular Heart Disease

  • Exercise increases peripheral venous return to heart drastically.
  • High venous return exacerbates underlying valvular dynamics abnormalities.
  • Mild resting valvular disease causes severe exercise symptoms.
  • Exercise in aortic lesions precipitates acute heart failure.
  • Exercise in mitral lesions triggers lethal pulmonary edema.
  • Valvular dysfunction severely reduces overall functional cardiac reserve.
  • Restricted cardiac output causes rapid skeletal muscle fatigue.
Disclaimer: This content is for educational purposes only and not a substitute for professional medical advice.

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