Dr Jain T Kallarakkal
MD, DM, FRCP
 Sounds produced by the heart during a cardiac
cycle
 Easily detected with a stethoscope or
phonocardiograph
 First heart sound - S1
 Second heart sound - S2
 Third heart sound - S3
 Fourth heart sound - S4
 S1: signals the onset of ventricular contraction
whish occurs 50-60 msec after the initiation of
ventricular systole frequency ranging from
100-120 Hz.
 Best heard at apex and lower left sternal
border
 Has mitral (M1) and tricuspid (T1)
components
 Small low frequency muscular vibrations
 Large high frequency vibrations of mitral
valve closure (M1)
 High frequency tricuspid valve closure (T1)
which occurs 20-30 msec after M1
 Small low frequency vibrations of accelerated
blood flow into great vessels
 Luisada: Sound produced by prominent
tensing of left ventricular walls, septum and
mitral valve apparatus
 Leatham: Sudden tensing of closed mitral
valve apparatus leading sudden deceleration of
blood setting the surrounding cardiac
structures into vibration
 Loud
 Soft
 Variable intensity
 Tachycardia or Hyper dynamic states
 Mitral / tricuspid stenosis
 Short PR interval
 Atrial myxoma
 Left to right shunts: Atrial septal defect, Ventricular septal defect,
Patent ductus arteriosus
 Ebstein’s anomaly
 Hypertension
 Thin chest wall
 Low cardiac output states
 Long PR interval
 Severe mitral / tricuspid regurgitation
 Calcified mitral stenosis
 Flail mitral leaflets
 Significant aortic stenosis
 Left bundle branch block
 Atrial fibrillation
 Extrasystoles
 Complete heart block
 Mobitz type I heart block
 Pulsus paradoxus
 Right bundle branch block
 Ventricular premature ectopic from left ventricle
 Left ventricular pacing
 Ideoventricular rhythm from left ventricle
 Wolss Parkinson White syndrome
 Tricuspid stenosis
 Ebstein’s anomaly
 Left bundle branch block
 Paced beats
 Ventricular premature ectopic from right
ventricle
 Left atrial myxoma
 Mitral stenosis
 Left bundle branch block
 Right ventricular pacing
 S2: Sudden deceleration of retrograde blood
flow in the aorta and pulmonary artery which
sets the cardiohemic system into vibration
 Best heard at the base
 Louder and high pitched than S1 (120-150Hz)
 Has aortic (A2) and pulmonary (P2)
components
 Hang out interval: Though the right and left
ventricular systoles are equal in duration, the
pulmonary artery incisura is delayed in
relation to the aortic incisura, primarily due to
a larger interval separating the pulmonary
artery incisura from the right ventricular
pressure compared with the same left sided
event. This internal is termed as hang out
interval
 Occurs because left ventricular contraction
slightly precedes that of right ventricular
contraction
 Hence aortic valve closes before pulmonary valve
 Increases at end inspiration because of increased
filling of right ventricle which further delays
pulmonary valve closure
 Disappears on expiration
 Loud A2: Systemic hypertension, Coarctation
of aorta, Ascending aortic aneurysm,
Tetrology of Fallot, Transposition of great
arteries
 Loud P2: Pulmonary artery hypertension,
Pulmonary artery dilatation
 Low cardiac output
 Aortic regurgitation
 Calcific aortic stenosis
 Right bundle branch block
 Pulmonary stenosis
 Pulmonary hypertension
 Ventricular septal defect
 Acute mitral regurgitation
Wide fixed split : Atrial septal defect
 Severe aortic stenosis
 Hypertrophic cardiomyopathy
 Left bundle branch block
 Ventricular pacing
 Chronic aortic regurgitation
 VSD: Single loud S2
 PDA: Close split S2
 ASD: Narrow fixed split S2
 Low pitched early diastolic sound
 Best heard at apex with bell
 Coincides with rapid ventricular filling (Lub-
Dub-Dum)
 0.12-0.18 seconds after S2
 Usually pathological in elderly
 Physiological: Children, Athletes, Pregnancy,
Fever
 Pathological: Left ventricular failure, Severe
mitral / tricuspid regurgitation, Severe aortic
regurgitation, Large left to right shunts
 Soft and low pitched
 Pre systolic or atrial gallop
 Best heard at apex with bell
 0.11 seconds prior to S1
 Caused by atrial kick into a non compliant
ventricle
 Always pathological
 LVH (Hypertension, Aortic stenosis,
Hypertrophic obstructive cardiomyopathy)
 Coronary artery disease
 Cannot occur in atrial fibrillation
 Three or four sounds resembling the center of
a horse
 S3 gallop
 S4 gallop
 Summation gallop
 Scratchy leathery high pitched sound
 Best heard at end inspiration leaning over
 Three phases: mid systolic, mid diastolic and
pre systolic
 Confusing with Hamman’s sign
 Viral pericarditis
 Pyogenic pericarditis
 Tuberculous pericarditis
 Dressler’s syndrome
 Acute rheumatic fever
 Systemic lupus erythematosus / Rheumatoid arthritis
 Uremia
 Ball valves: Opening sound louder than
closing sound
 Tilting disc valves: Only closure sound heard
 Bileaflet valves: Closure sound well heard
 Usually high frequency
 Ejection sound
 Seen with bicuspid aortic valve, pulmonic
stenosis and mechanical prosthetic valves
 High frequency
 Click
 Seen with mitral valve prolapse
 Occurs earlier with Valsalva maneuver or
squatting
 Opening snap: seen with mitral stenosis.
Occurs when movement of anterior mitral
leaflet suddenly stops at point when LV
pressure drops below left atrial pressure
 Pericardial knock: seen with chronic
constrictive pericarditis
 Mitral stenosis
 Tricuspid stenosis
 Severe mitral regurgitation
 Atrial septal defect
 Large ventricular septal defect
 Tetrology of Fallot
 Abnormal or ectopic heart sound
 Produced by turbulent flow across an
abnormal valve, septal defect or outflow
obstruction
 Also occur when stroke volume is increased
 Where best heard
 Systolic or diastolic
 Timing and character
 Intensity
 Pitch
 Best heard with bell or diaphragm
 Conducted or not
 Variation with respiration
 Variation with posture
 Dynamic auscultation
 I – Very soft
 II – Soft
 III – Loud
 IV – Loud with thrill
 V – Very loud with thrill
 VI – Very loud even heard when stethoscope is
slightly away from chest wall
 Occur during whole or part of systole
 Early systolic murmurs: Small ventricular septal defect, Acute
severe mitral regurgitation, Acute severe tricuspid regurgitation
 Ejection systolic murmurs: Atrial septal defect, aortic stenosis,
pulmonary stenosis, severe aortic regurgitation, Hypertrophic
obstructive cardiomyopathy
 Late systolic murmurs: Mital valve prolapse, Tricuspid valve
prolapse, Papillary muscle dysfunction
 Pan systolic murmurs: mitral regurgitation, tricuspid regurgitation,
Ventricular septal defect
 I – Very soft
 II – Soft
 III – Loud
 IV – Loud with thrill
 Early diastolic murmurs: Aortic regurgitation,
Pulmonary regurgitation
 Mid diastolic murmurs: Mitral stenosis,
Tricuspid stenosis
 Late diastolic murmurs: Mitral stenosis,
Tricuspid stenosis, Atrial myxoma
 Patent ductus arteriosus
 Aorto pulmonary window
 Tricuspid / pulmonary atresia
 Anomalous left coronary artery from
pulmonary artery
 Pericardial friction rub
 Mammary soufflé
 Rupture of sinus of Valsalva
 Venous hum
 Usually ejection systolic murmur
 Normal S1 and S2
 Normal cardiac impulse
 No hemodynamic abnormality
 Carey-coomb’s murmur
 Infective endocarditis
 Atrial thrombus
 Atrial myxoma
 Carey-coomb’s murmur – Acute rheumatic
valvulitis
 Austin Flint murmur – Chronic aortic
regurgitation
 Graham Steel murmur
 Ritan’s murmur – in complete heart block
 Docks murmur
 Mill wheel murmur
 Stills murmur
 Gibson’s murmur – Patent ductus arteriosus
murmur
Heart sounds and murmurs

Heart sounds and murmurs

  • 1.
    Dr Jain TKallarakkal MD, DM, FRCP
  • 2.
     Sounds producedby the heart during a cardiac cycle  Easily detected with a stethoscope or phonocardiograph
  • 3.
     First heartsound - S1  Second heart sound - S2  Third heart sound - S3  Fourth heart sound - S4
  • 4.
     S1: signalsthe onset of ventricular contraction whish occurs 50-60 msec after the initiation of ventricular systole frequency ranging from 100-120 Hz.  Best heard at apex and lower left sternal border  Has mitral (M1) and tricuspid (T1) components
  • 5.
     Small lowfrequency muscular vibrations  Large high frequency vibrations of mitral valve closure (M1)  High frequency tricuspid valve closure (T1) which occurs 20-30 msec after M1  Small low frequency vibrations of accelerated blood flow into great vessels
  • 6.
     Luisada: Soundproduced by prominent tensing of left ventricular walls, septum and mitral valve apparatus  Leatham: Sudden tensing of closed mitral valve apparatus leading sudden deceleration of blood setting the surrounding cardiac structures into vibration
  • 7.
     Loud  Soft Variable intensity
  • 8.
     Tachycardia orHyper dynamic states  Mitral / tricuspid stenosis  Short PR interval  Atrial myxoma  Left to right shunts: Atrial septal defect, Ventricular septal defect, Patent ductus arteriosus  Ebstein’s anomaly  Hypertension  Thin chest wall
  • 9.
     Low cardiacoutput states  Long PR interval  Severe mitral / tricuspid regurgitation  Calcified mitral stenosis  Flail mitral leaflets  Significant aortic stenosis  Left bundle branch block
  • 10.
     Atrial fibrillation Extrasystoles  Complete heart block  Mobitz type I heart block  Pulsus paradoxus
  • 11.
     Right bundlebranch block  Ventricular premature ectopic from left ventricle  Left ventricular pacing  Ideoventricular rhythm from left ventricle  Wolss Parkinson White syndrome  Tricuspid stenosis  Ebstein’s anomaly
  • 12.
     Left bundlebranch block  Paced beats  Ventricular premature ectopic from right ventricle
  • 13.
     Left atrialmyxoma  Mitral stenosis  Left bundle branch block  Right ventricular pacing
  • 14.
     S2: Suddendeceleration of retrograde blood flow in the aorta and pulmonary artery which sets the cardiohemic system into vibration  Best heard at the base  Louder and high pitched than S1 (120-150Hz)  Has aortic (A2) and pulmonary (P2) components
  • 15.
     Hang outinterval: Though the right and left ventricular systoles are equal in duration, the pulmonary artery incisura is delayed in relation to the aortic incisura, primarily due to a larger interval separating the pulmonary artery incisura from the right ventricular pressure compared with the same left sided event. This internal is termed as hang out interval
  • 16.
     Occurs becauseleft ventricular contraction slightly precedes that of right ventricular contraction  Hence aortic valve closes before pulmonary valve  Increases at end inspiration because of increased filling of right ventricle which further delays pulmonary valve closure  Disappears on expiration
  • 17.
     Loud A2:Systemic hypertension, Coarctation of aorta, Ascending aortic aneurysm, Tetrology of Fallot, Transposition of great arteries  Loud P2: Pulmonary artery hypertension, Pulmonary artery dilatation
  • 18.
     Low cardiacoutput  Aortic regurgitation  Calcific aortic stenosis
  • 19.
     Right bundlebranch block  Pulmonary stenosis  Pulmonary hypertension  Ventricular septal defect  Acute mitral regurgitation Wide fixed split : Atrial septal defect
  • 20.
     Severe aorticstenosis  Hypertrophic cardiomyopathy  Left bundle branch block  Ventricular pacing  Chronic aortic regurgitation
  • 21.
     VSD: Singleloud S2  PDA: Close split S2  ASD: Narrow fixed split S2
  • 22.
     Low pitchedearly diastolic sound  Best heard at apex with bell  Coincides with rapid ventricular filling (Lub- Dub-Dum)  0.12-0.18 seconds after S2  Usually pathological in elderly
  • 23.
     Physiological: Children,Athletes, Pregnancy, Fever  Pathological: Left ventricular failure, Severe mitral / tricuspid regurgitation, Severe aortic regurgitation, Large left to right shunts
  • 24.
     Soft andlow pitched  Pre systolic or atrial gallop  Best heard at apex with bell  0.11 seconds prior to S1  Caused by atrial kick into a non compliant ventricle
  • 25.
     Always pathological LVH (Hypertension, Aortic stenosis, Hypertrophic obstructive cardiomyopathy)  Coronary artery disease  Cannot occur in atrial fibrillation
  • 26.
     Three orfour sounds resembling the center of a horse  S3 gallop  S4 gallop  Summation gallop
  • 27.
     Scratchy leatheryhigh pitched sound  Best heard at end inspiration leaning over  Three phases: mid systolic, mid diastolic and pre systolic  Confusing with Hamman’s sign
  • 28.
     Viral pericarditis Pyogenic pericarditis  Tuberculous pericarditis  Dressler’s syndrome  Acute rheumatic fever  Systemic lupus erythematosus / Rheumatoid arthritis  Uremia
  • 29.
     Ball valves:Opening sound louder than closing sound  Tilting disc valves: Only closure sound heard  Bileaflet valves: Closure sound well heard
  • 30.
     Usually highfrequency  Ejection sound  Seen with bicuspid aortic valve, pulmonic stenosis and mechanical prosthetic valves
  • 31.
     High frequency Click  Seen with mitral valve prolapse  Occurs earlier with Valsalva maneuver or squatting
  • 32.
     Opening snap:seen with mitral stenosis. Occurs when movement of anterior mitral leaflet suddenly stops at point when LV pressure drops below left atrial pressure  Pericardial knock: seen with chronic constrictive pericarditis
  • 33.
     Mitral stenosis Tricuspid stenosis  Severe mitral regurgitation  Atrial septal defect  Large ventricular septal defect  Tetrology of Fallot
  • 34.
     Abnormal orectopic heart sound  Produced by turbulent flow across an abnormal valve, septal defect or outflow obstruction  Also occur when stroke volume is increased
  • 35.
     Where bestheard  Systolic or diastolic  Timing and character  Intensity  Pitch  Best heard with bell or diaphragm  Conducted or not  Variation with respiration  Variation with posture  Dynamic auscultation
  • 36.
     I –Very soft  II – Soft  III – Loud  IV – Loud with thrill  V – Very loud with thrill  VI – Very loud even heard when stethoscope is slightly away from chest wall
  • 37.
     Occur duringwhole or part of systole  Early systolic murmurs: Small ventricular septal defect, Acute severe mitral regurgitation, Acute severe tricuspid regurgitation  Ejection systolic murmurs: Atrial septal defect, aortic stenosis, pulmonary stenosis, severe aortic regurgitation, Hypertrophic obstructive cardiomyopathy  Late systolic murmurs: Mital valve prolapse, Tricuspid valve prolapse, Papillary muscle dysfunction  Pan systolic murmurs: mitral regurgitation, tricuspid regurgitation, Ventricular septal defect
  • 38.
     I –Very soft  II – Soft  III – Loud  IV – Loud with thrill
  • 39.
     Early diastolicmurmurs: Aortic regurgitation, Pulmonary regurgitation  Mid diastolic murmurs: Mitral stenosis, Tricuspid stenosis  Late diastolic murmurs: Mitral stenosis, Tricuspid stenosis, Atrial myxoma
  • 40.
     Patent ductusarteriosus  Aorto pulmonary window  Tricuspid / pulmonary atresia  Anomalous left coronary artery from pulmonary artery  Pericardial friction rub  Mammary soufflé  Rupture of sinus of Valsalva  Venous hum
  • 41.
     Usually ejectionsystolic murmur  Normal S1 and S2  Normal cardiac impulse  No hemodynamic abnormality
  • 42.
     Carey-coomb’s murmur Infective endocarditis  Atrial thrombus  Atrial myxoma
  • 43.
     Carey-coomb’s murmur– Acute rheumatic valvulitis  Austin Flint murmur – Chronic aortic regurgitation  Graham Steel murmur  Ritan’s murmur – in complete heart block  Docks murmur  Mill wheel murmur  Stills murmur  Gibson’s murmur – Patent ductus arteriosus murmur