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CARDIAC
AUSCULTATION
PRESENTOR - DR. RASHI VOHRA
MODERATOR - DR. JAGDISH RAWAT
HISTORY
▪Rene Theophile Hyacinthe Laennec
French physician who discovered the concept
of auscultation and invented the first
stethoscope in 1816.
▪Arthur Leared and George Cammann
Invented the first bi-aural stethoscope in
1852.
STETHOSCOPE
AREAS OF AUSCULTATION
FEATURES OF A SOUND
•SITE
•CHARACTER
•RADIATION
•INTENSITY
•PITCH
•TIMING
CARDIAC CYCLE
The electrical and mechanical cardiac events that occur from the beginning of one heart
beat to the beginning of the next are called the cardiac cycle.
Duration :– 0.8 seconds
CARDIAC CYCLE
Ventricular diastole-Isovolumetric Relaxation
Filling of the Ventricles- Passive filling (70%)
Atrial systole- Active filling of ventricles (30%)
Ventricular systole- Isovolumetric Contraction
Ejection of blood
FIRST HEART SOUND (S1)
▪Due to closure of AV valves (M1T1)
▪Split time between M1T1 < 20 msec, heard as a single
sound
▪S1 barely precedes/coincides with upstroke of carotid
pulsation.
▪Site:- Apex
▪Pitch:- Moderate
FIRST HEART SOUND (S1)
SECOND HEART SOUND (S2)
▪Due to closure of Semilunar valves (A2P2)
▪Split time between A2P2 is 30-60 msec, heard as two
separate sounds
▪Site:- A2- aortic area P2- pulmonary area
▪Pitch:- High
▪Loud A2- systemic hypertension
▪Loud P2- pulmonary hypertension
PHYSIOLOGICAL SPLITTING OF S2
INSPIRATION EXPIRATION
Venous return increases as
thoracic pressure becomes
negative.
LV blood volume dec.
RV blood volume inc.
LV ejection time dec.
RV ejection time inc.
A2 comes EARLY
P2 comes LATE
SPLIT INCREASES
LV blood volume inc.
RV blood volume dec
LV ejection time inc.
RV ejection time dec.
A2 comes late
P2 comes early
SPLIT DECREASES
WIDE SPLITTING OF S2 IN
INSPIRATION
WIDE SPLITTING OF S2 IN
EXPIRATION
(reverse splitting)
WIDE AND FIXED SPLIT OF S2
 ATRIAL SEPTAL DEFECT
AORTIC REGURGITATION
AORTIC VALVE LEAFLET FAIL TO STRIKE EACH OTHER
HENCE A2 IS ABSENT
SINGLE P2
THIRD HEART SOUND (S3)
(VENTRICULAR GALLOP)
▪Due to increased ventricular blood during early
filling phase (passive) which leads to ventricular
vibration
▪Site :- Right Ventricular S3- Tricuspid area
Left Ventricular S3- Apex
▪Pitch :- Low
THIRD HEART SOUND (S3)
PATHOLOGICAL
Inc. in end systolic volume
(Systolic failure of
ventricles)
RVF, LVF
DCMP
Inc. in Atrial
volume
High Cardiac
output
states (MR)
PHYSIOLOGICAL
HEALTHY
YOUNG
ADULTS
PREGNANCY FEVER
ATHLETES
FOURTH HEART SOUND (S4)
(ATRIAL GALLOP)
▪Due to forceful atrial contraction against stiff
ventricle
▪Always PATHOLOGICAL
▪Site:- Right Ventricular S4- Tricuspid area
Left Ventricular S4- Apex
▪Pitch:- Low
FOURTH HEART SOUND (S4)
▪LVH ( Hypertension, AS,HOCM)
▪RVH
▪RCMP
ADDITIONAL HEART SOUNDS
S1 S1
S3 S4
A2P2
EJECTION CLICK
MIDSYTOLIC CLICK OPENING SNAP
PERICARDIAL KNOCK
SYSTOLE DIASTOLE
EARLY MID LATE
ADDITIONAL HEART SOUNDS
NAME CAUSE TIMIMG PITCH
EJECTION CLICK AS
PS
EARLY SYTOLE HIGH
NAME CAUSE TIMIMG PITCH
EJECTION CLICK AS
PS
EARLY SYTOLE HIGH
MID SYSTOLIC CLICK MITRAL VALVE
PROLAPSE
MID-LATE SYSTOLE HIGH
ADDITIONAL HEART SOUNDS
NAME CAUSE TIMIMG PITCH
EJECTION CLICK AS
PS
EARLY SYTOLE HIGH
NAME CAUSE TIMIMG PITCH
OPENING SNAP MS
TS
EARLY DIASTOLE HIGH
ADDITIONAL HEART SOUNDS
NAME CAUSE TIMIMG PITCH
PERICARDIAL RUB ACUTE
PERICARDITIS
MID-LATE DIASTOLE/
EARLY SYSTOLE
HIGH
• Best heard leaning forward/patient holding breath in expiration
• Often disappear (DYANMIC)
• Loudest at lower left sternal border
• Intensity does not increase with increased pressure of stethoscope
PERICARDIAL KNOCK CONSTRICTIVE
PERICARDITIS
MID-DIASTOLE HIGH
PLEURAL RUB
• Not heard in cessation of respiration
• Loudest at lateral parts of chest
• Intensity increases with increased pressure of stethoscope
MURMURS
▪ Murmurs are produced by turbulent flow across an abnormal
valve, septal defect or outflow obstruction.
▪ “Innocent” murmurs are caused by increased volume or
velocity of flow through a normal valve when stroke volume is
increased.
e.g:- pregnancy
athletes with resting bradycardia
children with fever
GRADING OF MURMURS
SYSTOLIC MURMURS
SYSTOLIC MURMURS
▪ EJECTION SYSTOLIC MURMUR
(CRESCEND0-DECRESCENDO MURMUR)
AORTIC STENOSIS
SYSTOLIC MURMURS
▪ PAN SYSTOLIC MURMUR
SYSTOLIC MURMURS
▪EARLY SYSTOLIC MURMUR - ACUTE MR, ACUTE TR
▪LATE SYSTOLIC MURMUR - MITRAL VALVE PROLAPSE
DIASTOLIC MURMURS
▪ EARLY DIASTOLIC MURMUR
(DECRESCENDO MURMUR)
DIASTOLIC MURMURS
▪ MID DIASTOLIC MURMUR
MITRAL STENOSIS
DIASTOLIC MURMURS
▪ CONTINUOS MURMUR
(MACHINERY MURMUR)
PULMONARY HYPERTENSION AUSCULTATION
RADIATION OF MURMURS
ADDITIONAL MURMURS
NAME CAUSE TYPE SITE
KEY HODGKIN AR EARLY DIASTOLIC ERB’S AREA
GRAHAM STEEL PR EARLY DIASTOLIC PULMONARY AREA
AUSTIN FLINT AR MID-LATE DIASTOLE APEX
CAREY COOMB’S ACUTE RHEUMATIC
FEVER
MID DIASTOLE APEX
DOCK’S SEVERE STENOSIS OF
LAD
CONTINUOUS ERB’S AREA
RYTAN’S COMPLETE AV BLOCK MID DIASTOLE APEX
EFFECT OF DIFFERENT MANOUVERS ON
MURMURS
THANK YOU!!

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Cardiac auscultation

  • 1. CARDIAC AUSCULTATION PRESENTOR - DR. RASHI VOHRA MODERATOR - DR. JAGDISH RAWAT
  • 2. HISTORY ▪Rene Theophile Hyacinthe Laennec French physician who discovered the concept of auscultation and invented the first stethoscope in 1816. ▪Arthur Leared and George Cammann Invented the first bi-aural stethoscope in 1852.
  • 5. FEATURES OF A SOUND •SITE •CHARACTER •RADIATION •INTENSITY •PITCH •TIMING
  • 6. CARDIAC CYCLE The electrical and mechanical cardiac events that occur from the beginning of one heart beat to the beginning of the next are called the cardiac cycle. Duration :– 0.8 seconds
  • 7. CARDIAC CYCLE Ventricular diastole-Isovolumetric Relaxation Filling of the Ventricles- Passive filling (70%) Atrial systole- Active filling of ventricles (30%) Ventricular systole- Isovolumetric Contraction Ejection of blood
  • 8.
  • 9. FIRST HEART SOUND (S1) ▪Due to closure of AV valves (M1T1) ▪Split time between M1T1 < 20 msec, heard as a single sound ▪S1 barely precedes/coincides with upstroke of carotid pulsation. ▪Site:- Apex ▪Pitch:- Moderate
  • 11. SECOND HEART SOUND (S2) ▪Due to closure of Semilunar valves (A2P2) ▪Split time between A2P2 is 30-60 msec, heard as two separate sounds ▪Site:- A2- aortic area P2- pulmonary area ▪Pitch:- High ▪Loud A2- systemic hypertension ▪Loud P2- pulmonary hypertension
  • 12. PHYSIOLOGICAL SPLITTING OF S2 INSPIRATION EXPIRATION Venous return increases as thoracic pressure becomes negative. LV blood volume dec. RV blood volume inc. LV ejection time dec. RV ejection time inc. A2 comes EARLY P2 comes LATE SPLIT INCREASES LV blood volume inc. RV blood volume dec LV ejection time inc. RV ejection time dec. A2 comes late P2 comes early SPLIT DECREASES
  • 13. WIDE SPLITTING OF S2 IN INSPIRATION
  • 14. WIDE SPLITTING OF S2 IN EXPIRATION (reverse splitting)
  • 15. WIDE AND FIXED SPLIT OF S2  ATRIAL SEPTAL DEFECT
  • 16. AORTIC REGURGITATION AORTIC VALVE LEAFLET FAIL TO STRIKE EACH OTHER HENCE A2 IS ABSENT SINGLE P2
  • 17. THIRD HEART SOUND (S3) (VENTRICULAR GALLOP) ▪Due to increased ventricular blood during early filling phase (passive) which leads to ventricular vibration ▪Site :- Right Ventricular S3- Tricuspid area Left Ventricular S3- Apex ▪Pitch :- Low
  • 18. THIRD HEART SOUND (S3) PATHOLOGICAL Inc. in end systolic volume (Systolic failure of ventricles) RVF, LVF DCMP Inc. in Atrial volume High Cardiac output states (MR) PHYSIOLOGICAL HEALTHY YOUNG ADULTS PREGNANCY FEVER ATHLETES
  • 19. FOURTH HEART SOUND (S4) (ATRIAL GALLOP) ▪Due to forceful atrial contraction against stiff ventricle ▪Always PATHOLOGICAL ▪Site:- Right Ventricular S4- Tricuspid area Left Ventricular S4- Apex ▪Pitch:- Low
  • 20. FOURTH HEART SOUND (S4) ▪LVH ( Hypertension, AS,HOCM) ▪RVH ▪RCMP
  • 21. ADDITIONAL HEART SOUNDS S1 S1 S3 S4 A2P2 EJECTION CLICK MIDSYTOLIC CLICK OPENING SNAP PERICARDIAL KNOCK SYSTOLE DIASTOLE EARLY MID LATE
  • 22. ADDITIONAL HEART SOUNDS NAME CAUSE TIMIMG PITCH EJECTION CLICK AS PS EARLY SYTOLE HIGH NAME CAUSE TIMIMG PITCH EJECTION CLICK AS PS EARLY SYTOLE HIGH MID SYSTOLIC CLICK MITRAL VALVE PROLAPSE MID-LATE SYSTOLE HIGH
  • 23. ADDITIONAL HEART SOUNDS NAME CAUSE TIMIMG PITCH EJECTION CLICK AS PS EARLY SYTOLE HIGH NAME CAUSE TIMIMG PITCH OPENING SNAP MS TS EARLY DIASTOLE HIGH
  • 24. ADDITIONAL HEART SOUNDS NAME CAUSE TIMIMG PITCH PERICARDIAL RUB ACUTE PERICARDITIS MID-LATE DIASTOLE/ EARLY SYSTOLE HIGH • Best heard leaning forward/patient holding breath in expiration • Often disappear (DYANMIC) • Loudest at lower left sternal border • Intensity does not increase with increased pressure of stethoscope PERICARDIAL KNOCK CONSTRICTIVE PERICARDITIS MID-DIASTOLE HIGH PLEURAL RUB • Not heard in cessation of respiration • Loudest at lateral parts of chest • Intensity increases with increased pressure of stethoscope
  • 25. MURMURS ▪ Murmurs are produced by turbulent flow across an abnormal valve, septal defect or outflow obstruction. ▪ “Innocent” murmurs are caused by increased volume or velocity of flow through a normal valve when stroke volume is increased. e.g:- pregnancy athletes with resting bradycardia children with fever
  • 28. SYSTOLIC MURMURS ▪ EJECTION SYSTOLIC MURMUR (CRESCEND0-DECRESCENDO MURMUR) AORTIC STENOSIS
  • 29. SYSTOLIC MURMURS ▪ PAN SYSTOLIC MURMUR
  • 30. SYSTOLIC MURMURS ▪EARLY SYSTOLIC MURMUR - ACUTE MR, ACUTE TR ▪LATE SYSTOLIC MURMUR - MITRAL VALVE PROLAPSE
  • 31. DIASTOLIC MURMURS ▪ EARLY DIASTOLIC MURMUR (DECRESCENDO MURMUR)
  • 32. DIASTOLIC MURMURS ▪ MID DIASTOLIC MURMUR MITRAL STENOSIS
  • 33. DIASTOLIC MURMURS ▪ CONTINUOS MURMUR (MACHINERY MURMUR)
  • 36. ADDITIONAL MURMURS NAME CAUSE TYPE SITE KEY HODGKIN AR EARLY DIASTOLIC ERB’S AREA GRAHAM STEEL PR EARLY DIASTOLIC PULMONARY AREA AUSTIN FLINT AR MID-LATE DIASTOLE APEX CAREY COOMB’S ACUTE RHEUMATIC FEVER MID DIASTOLE APEX DOCK’S SEVERE STENOSIS OF LAD CONTINUOUS ERB’S AREA RYTAN’S COMPLETE AV BLOCK MID DIASTOLE APEX
  • 37. EFFECT OF DIFFERENT MANOUVERS ON MURMURS

Editor's Notes

  1. Rashi