This document provides an overview of cardiac auscultation. It discusses the history of auscultation and the stethoscope. It describes the areas of auscultation on the chest and features of heart sounds such as location, character, and timing. The normal cardiac cycle and sounds S1, S2, S3, and S4 are explained. Additional heart sounds like clicks, opening snaps, and pericardial knocks are covered. Murmurs are defined and systolic and diastolic murmurs are described. The grading of murmurs and the radiation of murmurs is also summarized.

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.

3. STETHOSCOPE

4. AREAS OF AUSCULTATION

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

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

10. FIRST HEART SOUND (S1)

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

26. GRADING OF MURMURS

27. SYSTOLIC MURMURS

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)

34. PULMONARY HYPERTENSION AUSCULTATION

35. RADIATION OF MURMURS

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

38. THANK YOU!!