Heart murmurs can be produced by turbulence in blood flow caused by abnormalities in heart valves or structures. A murmur is described by its timing in the cardiac cycle, location, intensity, quality, and radiation pattern. A mid-systolic murmur is the most common murmur and can be caused by ventricular outflow obstructions like aortic stenosis, dilation of the aorta/pulmonary trunk, accelerated flow, or innocent murmurs from normal anatomical variations. Diastolic murmurs include early diastolic murmurs like aortic regurgitation and high-pressure pulmonary regurgitation, and mid-diastolic murmurs caused by stenosis of the mitral or tricuspid valves. Flow murmurs

1. Heart murmurs

2. Definition of murmur
• “Relatively prolonged series of audible vibrations”
• Characterized by the timing in cardiac cycle,
intensity (loudness), frequency (pitch), quality,
configuration, duration and direction of radiation.

3. How is a murmur produced and
heard?

4. How is a murmur produced?
Sound is produced by vibration
Turbulence generated in the blood column vibrations set
up in the vessel wall & cardiac structures murmurs

5. How is a murmur produced?
L = linear dimension (internal
diameter In pipes)
V = mean fluid velocity
Q = volumetric flow rate
A = pipe cross-sectional area
m = dynamic viscosity of the fluid
n = kinematic viscosity [m/ r]
r = density of the fluid
Q = V1*A1= V2*A2
Q = P/R
[Re >4000 turbulent flow]
Re => Turbulence =>
murmur

6. Auscultation of murmur
Other factors affecting auscultation of murmur
• Distance from chest wall, position of patient
• Underlying soft tissue, lung, fluid
• Quality of apparatus

7. Auscultation of murmur
Upper 3rd L St-C Jn
4th L cos. cart. in L St.
border
4th RICS

8. How to describe a murmur?

9. Description of a Murmur
• Position in the cardiac cycle
• Site of murmur [max. intensity]
• Intensity
• Quality & Pitch
• Conduction
• Dynamic changes

10. Position in the cardiac cycle
early systolic
mid systolic
• Systolic murmur late systolic
pan/holo systolic
early diastolic
• Diastolic murmur mid diastolic
pre systolic
• Continuous murmur

11. Site of murmur
Systolic Diastolic Continuous
Apex MR MS, Flow mur.
LLSB TR, VSD TS, Flow mur. RSOV to RV,
RLSB- RSOV to
RA, Cor AVF
ULSB PS PR, AR PDA- 1 & 2
LICS,
APW- 3 LICS
URSB AS
Others

12. Intensity- Grading
FREEMAN & LEVINE GRADING
GRADE 1- faintest murmur which can be
heard only with special effort.
GRADE 2- soft but readily audible
GRADE 3- loud without thrill
GRADE 4- loud with thrill
GRADE 5- heard with steth partially off the
chest
GRADE 6- heard with steth held off the
chest wall.

13. Quality & Pitch
• Depends on two factors
1. Pressure difference or gradient- Gr pitch
2. Amount of Flow- Flow pitch
PITCH Hz Flow Pr Gr QUALIT
Y
E.g.:
LOW 25-125 rumbling MDM-
MS
MEDIUM 125-
300
harsh AS
HIGH >300 blowing MR,AR

14. Conduction of murmur
Site to which conducted aids in diagnosis
• MS localized to apex
• MR conducted to axilla and back; LLSB in MVP-MR
• AS conducted to Carotids

15. Classification & types of
murmurs

16. Classification & types of murmurs
early systolic
mid systolic
• Systolic murmur late systolic
pan/holo systolic
early diastolic
• Diastolic murmur mid diastolic
pre systolic
• Continuous murmur

17. Systolic Murmurs

19. Midsystolic murmur
• Most common murmur heard in everyday practice.
• Starts at an interval after S1 and ends before S2.
• It could be PATHOLOGICAL
INNOCENT/PHYSIOLOGICAL
• 5 settings
1. Ventricular outflow obstruction
2. Dilation of aorta and pulmonary trunk
3. Accelerated systolic flow into aorta or pulmonary trunk
4. Innocent midsystolic murmur( including those due to
morphological changes of valve with no obstruction)
5. Some forms of MR

20. Ventricular outflow obstruction
Phasic flow across left and
right outflow tract
• Isovolumic contraction (b)
• Maximal ejection (c)
• Start of relaxation and reduced
ejection (d)
• Isovolumic relaxation (e)
• LV filling, rapid phase (f)
• Slow LV filling (diastasis) (g)
• Atrial systole or booster (a)

21. AS
• IVC S1 ventricular pressure
increases opening of Aorta and
pulmonary valve ejection
commences and murmur begins
• Ejection increases murmur
becomes crescendo
• Ejection declines murmur in
decrescendo
• Murmur ends before
ventricular pressure drops
below aortic pressure at which
aortic valve and pulmonary
valve closes generating a2 and
p2

22. AS
• Harsh, crescendo-decrescendo
MSM
• Early sys peak short duration vs.
Late systolic peak long duration
• Always Symmetrical [vs. PS]
• ES absent in calcific valves, sub
and supra valvular AS
• Length and loudness do not
necessarily corresponds to
severity but length more
suggestive of severity than other
murmurs
S4
Reverse
splitting S2

23. AS
• Gallaverdin phenomenon/
hourglass phenomenon
Lower n (aortic) vs. Higher n
(mitral) periodic vibrations of stiffened
non calcific aortic valve
• Differentiating from MR
MR AS [ Gallaverdin]
Apical mid sys/ Holosystolic Apical mid sys
A2 buried in late sys
vibrations
Clear S2 heard
P/PVC unchanged P/PVC mur =
End of Long cycles in AF
unchanged
End of Long cycles
in AF =

24. AS
Postextrasystolic enhancement results from the variable interaction of three
factors:
1) Increase in the contractile state (inotropism) of the ventricular muscle
which is more evident if there is hypertrophy and/or depressed
ventricular function.
2) The pause provides longer filling time for the ventricle, which is more
consequential in hypertrophic ventricles (e.g., aortic stenosis) than in
ventricular volume overload states (e.g., mitral regurgitation).
3) Lastly, there is more time for arterial runoff, and in the case of aortic
regurgitation, more backflow into the ventricle. This effect lowers the
arterial diastolic pressure and the impedance to forward flow
(afterload) in the beat following the pause.

25. AS
Valvular AS Supra
valvular
Sub valvular
BP difference nil RUL > LUL Nil
Thrill Max 2 RICS;
Supra sternal &
carotids
Max Right
carotid
Mid LSB
Ejection
sound
Present Absent Absent
Murmur
Maximum
2 RICS 1 RICS Mid LSB
Assoc AR +/- rare +/-

26. HOCM
• Dynamic LVOT obstruction
• Factors increasing gradient
– LV Contractility
• Exercise
• Cathecolamines
• Digitalis
– Ventricular Volume
• Valsalva
• Standing
• Nitroglycerine/ Amyl nitrate
• Tachycardia
– Aortic impedance and pressure
• Sustained Handgrip
• Passive Leg Raise

27. PS
• Murmur brought on by a phasic
ejection click; radiates up &
left
• As severity increases length
increases and P2 becomes soft
(abruptness of closure reduced),
S2 split widens, S4
• Loses symmetry becomes kite
shaped
• May engulf A2 and P2 may be
inaudible; may be confused with
VSD

28. PS

29. Other causes of MSM
Dilation of Aorta & Pulmonary trunk
• Short soft midsystolic murmur
• Left sided murmurs in marfan’s syndrome, syphilis
• Right sided murmurs in idiopathic dilation of pulmonary
artery, pulmonary hypertension
MSM of Hyperdynamic circulation
• Normal aorta or pulmonary trunk but increased flow
• Anaemia, pregnancy, fever, thyrotoxicosis

30. Other causes of MSM
OS-ASD
• Rapid flow across pulmonary valve to dilated pulmonary
trunk
Pure AR
• Due to Accelerated LV ejection

31. Physiological causes
Innocent systolic murmur
• Still’s murmur
• Pulmonary mid systolic murmur
• Peripheral pulmonary systolic murmur
• Supraclavicular or brachiocephalic systolic murmur
• Aortic sclerosis
• Systolic mammary soufflé

32. Physiological murmurs
Still’s murmur
• Short buzzing murmur
‘twanging of a rubber band’
• Pure medium frequency by
periodic vibrations of pulmonic
leaflets at their attachment

33. Physiological murmurs
Pulmonary mid systolic murmur &
Peripheral pulmonary systolic
murmur
• Angulation and disparity
between pulmonary trunk and
its branches turbulent flow
• Normally disappears with
maturity of pulmonary bed

34. Physiological murmurs
Supraclavicular or brachiocephalic
systolic murmur
• Aortic origins of major normal
brachiocephalic arteries
• Crescendo-decrescendo, abrupt
onset, short, sometimes
radiating below clavicle
• vs. supra valvular AS – these
murmur are softer below
clavicle and decreases with
shoulder abduction

35. Physiological murmurs
Mammary Soufflé
• Late Pregnancy or puerperium
• Sometimes continuous louder in
systole, distinct gap from S1 [
time for ejected blood to reach
mammary arteries]
• 2 or 3 RICS/ LICS
• Light Pressure augments
murmur becomes continuous;
firm Pr abolishes murmur

36. Pan Systolic/ Holo Systolic Murmur
Flow from a chamber or vessel whose pressure or resistance
throughout systole is higher than pressure or resistance of
the chamber receiving the flow
• Mitral Regurgitation
• Tricuspid Regurgitation
• Ventricular Septal Defect
• Aorto Pulmonary Window
• Patent Ductus Arteriosus with PAH

37. Mitral Regurgitation
• S1 to S2 provided MV remains
incompetent and gradient
remains
Holosystolic
Early systolic
Late systolic
Sometimes MSM
• Radiates to axilla and back
becos jet directed
posterolaterally in LA
LLSB when jet directed against
atrial septum near base of aorta

38. Tricuspid Regurgitation
• LLSB- RA
• Rivero Carvallo’s sign-
Increased VR, increased RV
volume Increased SV velocity of
regurgitant flow
Sometimes TR heard only
during inspiration
Carvallo’s sign disappears in
RV failure
• Diff from organic TR
– PSM vs. ESM
– High n vs. Medium n
– Features of PAH present

39. Ventricular Septal Defect
Depends on site, size and gradient
• Very restrictive VSD- ESM
decrescendo pattern
• Mod and NR VSD- PSM
• Sub arterial VSD- 1 or 2 LICS similar
to PS murmur
• Septal aneurysms- click with LSM or
PSM with late Sys Accentuation
• Large shunt – MDM
• NR VSD with PAH- ESM
• PSM absent in Eissenmenger
Syndrome

40. Other PSM
• Aorto Pulmonary Window with PAH
– Otherwise continuous murmur
– Diastolic component reduced with increasing PAH
• PDA with PAH
– Similar mechanism

41. ESM
Acute Mitral Regurgitation
• Decrescendo murmur
• Non distensible LA , large v
wave approaching LV pressure
in late systole
• Maximum flow early systole
and minimum to nil flow in late
systole

42. Other ESM
• Normal pressure TR, Organic TR
Tall RA v waves reach the level of normal RV pressure in late systole,
so lower rate of regurgitant flow
Moderate to low frequency as compared to high frequency in high
pressure TR
• VSD with PVR or small muscular VSD
-Equalization of pressures in cases of PAH
-Small VSD closes in late systole

43. LSM
MVP
• Leaflets remains competent during early
ventricular contraction but overshoot in
late systole [critical V. dimensions]
• One or more mid systolic clicks precede
murmur [sudden deceleration of the
column of blood against the prolapsed
leaflet or scallops]
• Longer and softer
– Prompt standing after squatting
– Valsalva II
• Short & louder
– squatting
– Sustained hand grip
– Amyl nitrate
Other LSM- papillary muscle dysfunction
Post Pap Muscle . Late systolic cresendo to S2
Barlow’s syndrome refers to the
spectrum of symptoms caused by MVP
[click or murmur alone to palpitations,
chest pain, or syncope]

44. Diastolic Murmurs

46. Early diastolic murmur
• AR murmur
-Soft high frequency early diastolic
murmur with pt sitting & leaning
forward in full held expiration
-3 LICS [ 2 & 3 RICS in root dil]
-musical quality in eversion
-Austin Flint murmur
-Cole- Cecil murmur- AR murmur
in left axilla due to higher position of
apex

47. AR
• Difference between acute and
chronic AR
• Austin Flint Murmur to be
discussed
A/C AR C/C AR
Short mur. -
early
equalization of
diastolic
pressures
Long mur.
Medium n –
velocity less
rapid and
pressure
gradient lower
High n
Associated S4

48. High Pressure PR
• High pitched soft blowing decrescendo
murmur usually lasts throughout diastole
heard in the left upper sternal border
• Associated with loud P2 and other features
of PAH
• PR vs. AR
– Loud P2, murmur begins after P2
– Normal pulse pressure
– Clinical setting
– Squatting and sustained hand grip
increases AR

49. High Pressure vs. Normal Pressure
High Pressure
Normal
pressure
Decrescendo Crescendo
decrescendo
High frequency Medium to low
pitched
Onset immediately
with p2
Delayed in onset
Usu extends
throughout
diastole
Short duration
Features of PAH
present
Usually absent

50. Mid Diastolic Murmur
-Begin At Clear Interval After S2
I Rapid Filling Phase
Av valve obstruction Stenotic AV valves, tumors
Functional obstruction
Abnormal patterns of AV flow increased flow volume
increased flow velocity
II Incompetent Pulmonary Valve [PR with normal PA
Pressure]
III Atherosclerotic extramural coronary arteries

51. Mid Diastolic Murmur
RV
- TS
LV
- MS
- Austin Flint murmur
- Carey-Comb's
OTHERS
-Atrial Myxoma
- TR
- ASD
- VSD
- PDA
- MR

52. MS
• Low n rough rumbling [sound
of distant thunder] MDM
• Localized to apex, better heard
in left lateral position with bell
• Length a severity
• Long murmurs up to S1 even in
long cycles of AF- severe MS
• Late diastolic or Pre systolic
accentuation usually seen in
pliable valves and in NSR [
sometimes in AF]

53. TS
• Similar to MS
• Murmur usually seen associated with AF
• Diff. from MS
– Increases during inspiration [Augmentation of RV volume, RV
Diastolic Pr., Flow rate and gradient across valve]
– LLSB

54. PR with normal PA pressures
• PR assoc with Cong PS, PV IE, repair of RVOT
• Negligible gradient at the start of diastole, gradient
increases especially during the IVR phase of RV when
murmur reaches maximum intensity.
•2 & 3 LICS
•Medium to low pitched
•Delayed in onset
•Short duration
•Ending before S1

55. Austin Flint Murmur
• Severe AR regurgitant jet directed toward the AML
prevent the latter from opening well during diastole
generating turbulent flow
• Low n MDM or late diastolic, best heard at the apex.
• To differentiate from MS
– No OS
– Amyl nitrate inhalation AR, Austin flint murmur

56. Other Mid Diastolic Murmur
• Carey Coomb’s murmurs
– Acute rheumatic fever, mitral valve structures acutely inflamed with some
thickening and edema turbulence of flow during the rapid filling phase.
+ moderate MR [increased mitral inflow in diastole]
– Low pitched short MDM.
– good evidence of active carditis

57. Flow Murmurs
• Increased AV flow
• TR, ASD, MR, VSD, PDA, hyperdynamic circulation
• To differentiate from MS & TS
– Short MDM
– Medium Pitch- increased flow
– Preceded by S3
– Absence of Opening Snap
– Thrill less common

58. Late Diastolic/ Pre-systolic Murmurs
MS
• Higher frequency than MDM
• Sometimes only PSA heard- mild MS
• Generally absent in calcified valves and most of AF [ may
be present during short cycle lengths in AF]
• Cause-
– Increased flow during atrial contraction in late systole
– Increased dp/dt of LV contraction increases turbulence
[ esp. in AF short cycles]

59. Other diastolic murmurs
• Cabot– Locke Murmur- [Diastolic Flow murmur]
– The Cabot–Locke murmur is a diastolic murmur that sounds similar to
aortic insufficiency but does not have a decrescendo; it is heard best at the
left sternal border. [High flow thru coronary vessels, LMCA, LAD]
– The murmur resolves with treatment of anaemia.
• Dock’s murmur
– diastolic crescendo-decrescendo, with late accentuation, [consistent with
blood flow through the coronary] in a sharply localized area, 4 cm left of
the sternum in the 3LICS, detectable only when the patient was sitting
upright.
– Due to stenosis of LAD

60. Other diastolic murmurs
• Key–Hodgkin murmur
– EDM of AR; it has a raspy quality, [sound of a saw cutting through wood].
Hodgkin correlated the murmur with retroversion of the aortic valve
leaflets in syphilitic disease.
• Rytand’s murmur in complete heart block
– MDM or Late diastolic murmur
– Atrial contraction coincides with the phase of rapid diastolic filling
increased flow short MDM [intermittent].
– Another theory- Delayed V. contraction following A. contraction may lead
to diastolic MR & TR, because AV valve closure does not occur [unless V.
systole supervenes]. When higher V than A pressure during atrial
relaxation, an incompletely closed AV valve may lead to a reverse gradient
with a considerable regurgitation volume.

61. Continuous murmur

62. Continuous murmur
• Begin in systolic and continues without interruption
through the timing of S2 into all or part of diastole
• Flow from zone of higher resistance into lower resistance
without phasic interruption b/w systole & diastole
1. Connection b/w high pressure chamber/vessel & low
pressure chamber/vessel
2. Disturbance in flow patterns in arteries
3. Disturbances in flow patterns in veins

63. Connection b/w high pressure
chamber/vessel & low pressure
chamber/vessel
1. From the aorta
a. Persistent ductus arteriosus
b. Aorto-pulmonary window
c. RSOV
2. From the coronary artery:
1. Coronary arteriovenous fistulae draining into RA, RV, PA
2. ALCAPA
3. Other arteriovenous communications
1. Broncho-pulmonary collaterals
2. Chest wall arteries–pulmonary vessels
3. Peripheral A-V Fistula
4. Others
1. Lutembacher syndrome with restricted ASD

64. PDA
• Gibson’s murmur
• At 1 or 2 LICS
• NR- high frequency soft
murmur peaks around S2
• Mod R- loud coarse machinery
murmur with eddy sounds
S
E
V
E
R
I
T
Y
PDA with no continuous murmur
•Neonates- due to high PVR
•Very small ductus
•Very large ductus & large
VSD- due to equalization of
pulm and sys Pr
•PAH- first dia component
goes, then sys
•AS, CoA- due to low aortic
pressure

65. Continuous murmurs
• APW
– 2 or 3 LICS
– Usually associated with early devp of eissenmenger
• RSOV
– No peaking at S2 seen [peaks in sys or dia.]
– To RA- RLSB
RV- LLSB
RVOT- 3 LICS
• Lutembacher syndrome with restricted ASD
– LLSB [body of RA]

66. Continuous murmurs
• C-AVF
– RA- RLSB or RUSB
– CS- back b/w spine & Lt scapula
– RV inflow- LLSB
– RVOT- Upper to Mid LSB [beat to beat change in murmur may be
present, RV systolic compression, valsalva softens murmur]
– PA- ULSB [no eddy sounds]
• ALCAPA
– Murmur louder in diastole [LV contr. I/C flow]
– Do not peak at S2
– Usu LUSB or RUSB
-LA- ULSB rad to Lt ant ax line
- Lt SVC- upper to mid LSB

67. Disturbance in flow patterns in arteries
• AV Fistula
– Murmur heard in the venous side
• Due to rapid blood flow-
– cervical venous hum, mammary soufflé, hyperthyroidism, hemangioma,
hyperemia of neoplasm (HCC, RCC, Paget’s disease)
• Stenosed arteries with inadequate distal collaterals
– aortic arch vessel occlusions, atherosclerotic carotids, coarctation of aorta,
main pulmonary artery stenosis and periph pulmonary artery stenosis

68. Disturbances in flow patterns in veins
Venous hum
• Healthy children, young healthy
adults, pregnancy
• Sitting, Bell, medial aspect of Rt
SCl fossa, with face pulled
leftwards & upwards
disappears when returned to
normal position
• Louder in diastole, +/- high
pitched whine
• Radiation to infra clavicular
areas confuse with other mur.
Check by obliteration

69. Dynamic Auscultation

70. Dynamic Auscultation
It refers to the technique of altering circulatory dynamics by
a variety of physiological and pharmacological maneuvers
and determining the effects of these maneuvers on heart
sounds and murmurs .

71. Intervention
• Position
• Physical maneuvers
• Pharmacological

72. Position
A. Lt Lateral Decubitus
LV impulse [apical sounds, murmurs better heard]
Act of turning increases HR[ MDM & PSA of MS ],
induces PVC [AS murmur vs. MR murmur (n/c)]
B. Sitting leaning forward full held expiration
AR & PR EDM
C. Sitting with legs dangling
Further reduces venous return
If S2 fails to fuse on sitting
D. Elbow Knee Position
Pericardial friction rub

73. Position
E. Standing to squatting and vice versa
– Standing[ venous return, BP ]; [opp. in squatting]
1. All murmurs [except HOCM , MVP earlier]
• HOCM [ LV contractility, after load, preload]
• MVP [ preload, afterload ]
2. A2- P2 , A2-OS , A2-S3 (n/c)
F. Hyperextension of shoulders
supraclavicular Systolic murmurs
G. Stretching of Neck
Venous hum
H. Passive elevation of both legs
Transiently increases venous return, increase S3

74. Physical Maneuvers
Inspiration
• Right sided events become more
prominent
• S2 split appreciable
• RVs3 RVs4 prominent
• Tricuspid sys & dia Mur
increased
• Pulm ejection sound reduced
Expiration
• Left sided events become more
prominent
• Diff AR & PR
• Pericardial friction rub
[exhalation & supine]
• Innocent pulm mid sys murmur
becomes more prominent becos
of reduced AP diameter

75. Inspiration followed by forced exhalation against a closed
glottis for 10 to 20 seconds
Physician has to keep flat of the hand on the abdomen to
provide the patient a force to breathe against
Not attempted in patients with IHD
Normal response has four phases
Valsalva Maneuver

76. Valsalva Maneuver
•initial pulm VR = SV
• I/T Pr directly
transmitted to aorta.
I/T Pr = VR = BP
sympathetic tone HR
Sudden I/T Pr = BP
sudden return of peripherally pooled blood
to the vaso-constricted arterial
system (20 to the increased sympathetic tone)

77. Phase II – Decrease in systemic venous return , systolic
pressure and pulse pressure
• S3 & S4 attenuated
• A2-P2 interval narrows
• All murmurs except MVP / HOCM decrease
Phase III- increased Left murmurs & Phase IV- increased
Right murmurs
Valsalva Maneuver

78. Valsalva Maneuver
I/T Pr = VR = BP
sympathetic tone HR
sudden return of peripherally pooled blood
to the vaso-constricted arterial
system (20 to the increased sympathetic tone)
PHASE II
PHASE IV
MAXIMAL SYMPATHETIC
ACTIVATION
FLAT PART OF
STARLING’S CURVE
HEART
FAILURE
ASD
MS

79. Isometric Exercise
Calibrated Handgrip device or a handball.
Better to carryout bilaterally, sustained for 20-30 secs
Not to be done in arrhythmia / Ischemia
Transient but significant increase in SVR, BP, HR , CO , LV filling
pressure , Heart size
1. LVS3 & LVS4 increases
2. Systolic Murmur of AS reduced – reduced gradient across aortic
valve
3. AR , MR , VSD – increased
4. MDM of MS – increased
5. Syst Murmur of HOCM reduced
6. MVP murmur + click delayed

80. • Few minutes of brisk walking sufficient
• Must be auscultated quickly before effect wears off
– Increases Ms murmur in low output states
– Wide Split of S2 in RVF further widens after exercise
Isotonic Exercise

81. Thank you