Cardiac Murmur & Dynamic Auscultation.pptx

1. Cardiac Murmur &
Dynamic Auscultation
Dr Awadhesh Kr Sharma
Professor Cardiology,LPS Institute of Cardiology,Kanpur

2. UNDERSTANDING STETHOSCOPE
• Size of Tubing=10-12 inches
• Ear-tips should point forward and fit
properly
• Chest piece should be held between
straightened index and middle fingers
• Don’t touch the tube or rub it against
the patient’s skin
• Tube should be relatively straight
• Bell for low frequency & diaphragm
for higher frequencies

3. HOLD IT THE RIGHT WAY
Like this – the thumb under the tube keeps
it from rubbing the skin, which causes extra
noise
Not like this – it’s harder to control and
harder to hold gently.

4. DEFINITION OF MURMUR
• Heart murmur results from auditory vibrations caused by increased
turbulence and are defined by their timing with in the cardiac cycle
(Braunwald text book)
• Heart murmurs are caused by audible vibrations that are due to
increased turbulence from accelerated blood flow through normal or
abnormal orifices, flow through a narrowed or irregular orifice into a
dilated vessel or chamber, or backward flow through an incompetent
valve, ventricular septal defect, or patent ductus arteriosus (Harrison
text book)

5. PHYSIOLOGY OF MURMUR PRODUCTION

7. Description of a Murmur
 Timing in the cardiac cycle
 Site of murmur
 Shape of murmur
 Intensity/ Loudness
 Quality & Pitch
 Conduction/ Radiation
 Dynamic changes

8. TIMING OF MURMURS
• SYSTOLIC
• Early systolic i.e Acute severe MR, Acute TR
• Ejection(mid)-systolic i.e. AS, PS, HCMP ➜Late systolic i.e. MVP
• Pansystolic i.e. MR, TR, VSD
• DIASTOLIC
• Early diastolic i.e. AR, PR, Dock’s murmur
• Mid-diastolic i.e. MS, TS, Austin Flint, Carey-coombs, LA myxoma
• Late diastolic / pre-systolic i.e. MS
• CONTINUOUS
• PDA, severe COA, Severe AS with AR

9. TIMING OF COMMON MURMURS
• A – Normal, no murmur
• B – Mid-systolic murmur of AS
• C – Pansystolic murmur of MR
• D – Early diastolic murmur of AR
• E – Mid-diastolic murmur of MS
• F – Continuous murmur of PDA

10. SHAPE OF MURMUR
• CRESCENDO
• Grow louder
• mid-systolic murmur of MVP
• DECRESCENDO
• Grow softer
• early diastolic murmur of AR
• CRESCENDO-DECRESCENDO
• Grow louder than softer
• mid-systolic murmur of AS
• PLATEAU
• Remains uniform throughout
• pan-systolic murmur of MR
JONAS TEXTBOOK OF CARDIOLOGY

11. PITCH & QUALITY OF MURMUR
PITCH Hz Pressure
Gradient
QUALITY E.g.:
LOW 25-125 Less Rumbling,
rough
MDM-MS
MEDIUM 125-300 mix Harsh, rough AS
HIGH >300 high Blowing, soft,
musical
MR,AR

12. LOCATION OF MURMURS
AREA LOCATION SYSTOLIC DIASTOLIC
AORTIC Right 2nd ICS AS, flow murmur AR
PULMONIC Left 2nd ICS PS, flow murmur PR
ERB’S Left 3rd ICS AR, PR, ASD, Dock’s
murmur
TRICUSPID LLSB TR, VSD, HCM TS, ASD
MITRAL Left 5th ICS medial
to MCL
MR MS, Austin Flint,
Carey Coombs
Left infra-clavicular area : PDA, CoA

13. RADIATION OF MURMURS

14. Freeman and Levine Grading of Heart Murmur

15. Murmurs accentuated during
Inspiration
TS
TR (Carvallo's sign)
PR
Mild or moderate PS
Severe PS (no further
increase in gradient)
 No change of murmur on
deep inspiration in RV
failure and severe PAH
Expiration
MS
MR
AS
AR
VSD
Pericardial rub
VARIATION WITH RESPIRATION

16. VARIATION WITH MANEUVRES
• STANDING, VALSALVA
• Decreases venous return and ventricular filling
• Decreases intensity of all murmurs except MVP
• Since outflow obstruction is increased by decreasing preload, it increases the
intensity of HOCM murmur as well
• SQUATTING, LAYING DOWN and LEG RAISING
• Increases venous return and ventricular filling (preload), Hence, increases
cardiac output
• It increases the murmurs of AS, AR, MR and VSD
• It decreases the murmurs of HOCM and MVP

17. VARIATION WITH MANEUVRES
• HAND-GRIP and PHENYLEPHRINE
• Increases total peripheral resistance (afterload)
• Increases murmurs of AR, MR, VSD and MS
• Decreases murmurs of AS, MVP and HOCM
• INHALED AMYL NITRATE
• Vasodilation causes decreased TPR and afterload
• Increases murmurs of AS, MS, PS, MVP and HOCM
• Decreases murmurs of AR, MR and VSD
• SITTING UP and LEANING FORWARD
• Accentuates S2 and increases the murmur of AR
• LEFT LATERAL DECUBITUS POSITION
• Accentuates the murmur of MS

19. AORTIC STENOSIS
• An ejection click (EC) followed by a crescendo-
decrescendo ejection systolic murmur at the
aortic area. Heard best with breath held in
expiration in a leaning forward. Sometimes
radiates to the carotid arteries
• In mild AS, the diamond-shaped murmur has an
early peak whereas In severe AS, the murmur
has a late peak
• Gallavardin phenomenon?
It is the systolic murmur of fibrocalcific AS seen
with aging. It has a harsh and noisy quality in
aortic area but is musical over the apex area.

20. PULMONIC STENOSIS
• An ejection click (EC) followed by a
crescendo-decrescendo ejection
systolic murmur at the pulmonic area,
EC may be absent
• Murmur becomes louder with
inspiration unlike ESM of AS which
becomes softer
• May radiate towards the left clavicle

21. PS with or without VSD
• If IVS is intact, as obstruction
becomes more severe:
• The murmur lengthens
• Peak of murmur moves closer to
S2
• P2 becomes softer
• If VSD is present (e.g. tetralogy
of Fallot / TOF) as obstruction
becomes more severe:
• The murmur becomes shorter
• Peak becomes more closer to S1
• P2 is very soft or absent

22. TRICUSPID REGURGITATION
• A holosystolic murmur (HSM) at
LLSB (tricuspid area) that may
obscure S1
• Heard best with diaphragm with
breath held in inspiration
• Murmur becomes louder with
inspiration (Carvallo sign) unlike
murmur of MR
• Murmur may radiate upwards to
upper left sternal border
• Acute severe TR may present as an
early systolic murmur

23. MITRAL REGURGITATION
• A holosystolic murmur (HSM) at apex area that may
obscure S1
• Heard best with diaphragm
• Murmur may radiate into the precordium or axilla,
due to intra-atrial backflow jet
• Murmur becomes softer with inspiration unlike
murmur of TR (turns loud)
• Murmur of MR is ‘rumbling’ as opposed to musical
quality of fibro-calcific AS

24. VARIANTS OF MR
• Acute severe MR may present as
an early systolic murmur as left
atrium has a normal size with
limited distensibility.
• Papillary muscle dysfunction
(PMD) seen in acute MI may
present as an late systolic
murmur without a preceding
click. Also called ischemic MR

25. MVP
• A mid-systolic click (MSC) followed by a mid-
to-late systolic murmur at the apex area.
• It has a “whooping” musical quality.
• Maneuvers that preload (standing, Valsalva)
or afterload (amyl nitrate):
• earlier onset of click (closer to S1)
• longer murmur duration
• decreased murmur intensity
• Maneuvers that preload (leg elevation,
squatting) or afterload (hand grip) :
• Delayed onset of click (closer to S2),
• Shorten murmur duration
• Increase murmur intensity.

26. HOCM
• A crescendo-decrescendo systolic
murmur at the left sternal border
• Best heard with diaphragm in
standing position.
• Like in AS, there is LVOT*
obstruction but at a sub-valvular
level, due to ASH**
• Aortic valve is not involved so there
is no ejection click, as heard with AS

27. VSD
• A pansystolic murmur (PSM) at the left sternal
border, with a harsh blowing character, becomes
louder with expiration
• There may be an associated systolic thrill, louder
the murmur, smaller the defect
Roger’s murmur – the loud PSM of small VSD
• Murmur of supra-cristal type of VSD is heard in
the pulmonic area
• If pulmonary hypertension is present,
there will be a loud P2 and a right ventricular
heave. But if there is an associated severe
pulmonic stenosis (TOF), P2 will be soft/absent

28. ASD
• A ejection systolic murmur (ESM)
without a preceding click is heard at the
upper sternal border. It is due to the
excessive flow across the pulmonary
valve. It is soft and heard best with a
bell. Louder the murmur, smaller the
defect
• Wide fixed splitting of S2 at pulmonic
area is the most important feature
• A diastolic murmur may be heard at the
LLSB due to increased flow across
tricuspid valve

29. AORTIC REGURGITATION
• In chronic AR, a decrescendo type EDM of
“blowing” quality and high pitch is heard after S2
(or A2) at the left 3rd ICS- Erb’s area
• It is heard best with a diaphragm with breath held
in expiration in a patient leaning forward
• If the AR is due to aortic root dilatation, diastolic
murmur will radiate into the aortic area
• Any maneuver that increases the afterload will
increase the murmur of AR, as it will tend to
favour backflow into the ventricle. i.e. handgrip

30. Aortic regurgitation cont…
• There can also be a mid-systolic murmur with AR,
due to the increased flow across the aortic valve
during systole
• In AR, a third murmur may be heard, called Austin-
Flint murmur, which is a soft mid-to-late diastolic
murmur of low pitch and “rumbling” quality. It is
heard at the apex, best with a bell during expiration
• It is thought to be due to functional mitral valve
stenosis, as backflow jet from aorta presses on the
anterior mitral leaflet to slightly occlude the blood
flow from LA into LV during diastole
• Rarely, an early diastolic murmur, called Cole-Cecil
murmur, may be heard in axilla

31. PULMONARY REGURITATION
• In chronic PR, a decrescendo type early
EDM of “blowing” quality and high pitch is
heard after S2 (or P2) at the pulmonic area
(left 2nd ICS)
• Heard best with a diaphragm with breath
held in inspiration in a supine patient.
Unlike AR, it is not increased by handgrip
maneuver
• It is called Graham Steel murmur.
If PR is with PAH (pulmonary artery HTN),
murmur will have a low pitch, heard with a
bell

32. MITRAL STENOSIS
• Preceded by a high pitch opening snap (OS), then by
a low pitch mid-diastolic murmur that becomes
augmented (high-pitched) before loud S1 (late
diastolic or pre-systolic component)
• MDM is best heard with bell placed lightly over the
apex in left decubitus position
• There may be a diastolic thrill
• Why is there an Opening Snap?
• There is a pressure gradient across the mitral valve
(MV), which causes sharp movement of the tethered
anterior cusp of MV at the time when the flow
commences, resulting in OS.

33. AUSTIN FLINT VS MDM OF MS

34. TRICUSPID STENOSIS
• A Mid diastolic rumble of more high
pitch than mitral rumble
• It is best heard with the diaphragm
placed over the tricuspid area with
breath held in inspiration while lying
supine
• Murmur becomes louder with
inspiration (Carvallo sign) unlike MDM
of MS (softer)
• Tricuspid component (T1) of S1 is loud.
There may be an opening snap.
There may be a diastolic thrill.

35. CAREY COOMB MURMUR
• Feature of mitral valvulitis in acute rheumatic fever, commonly
heard in children who also have fever and anemia
• A short mid-diastolic rumble at the apex
• Usually preceded by an S3 gallop
• S3 gallop is distinguished from the opening snap of MS by the
frequency.

36. CABOT-LOCKE MURMUR
• Feature of severe anemia
• An early diastolic murmur, resembling the murmur of AR, can be
heard at the Erb’s area
• Unlike murmur of AR, it does not have a decrescendo
• It is an innocent murmur that resolves with treatment of anemia
• It is due to the increased flow from aorta to coronary arteries that
arise from the aortic root

37. DOCK’S MURMUR
• Feature of severe stenosis of left anterior descending coronary artery
(LAD)
• A crescendo-decrescendo type diastolic murmur with late
accentuation
• In a sharply localized area: 4 cm left of sternal border in left 4th ICS
• It is detected only if the patient is sitting upright

38. RYTAND MURMUR
• Feature of chronic complete heart block
• A mid-to-late diastolic murmur at the apex
• It is thought that murmur is due to increased flow across AV valves
due to a slow heart rate
• It may also be due to antegrade flow across the closing mitral valve
(when LA is contracting but LV also contracts before it is full)

39. KEY HODGKIN MURMUR
• Feature of syphilitic aortitis
• An early diastolic murmur, resembling the murmur of AR, but heard
only at the aortic area instead of Erb’s area
• It has a “raspy” quality (saw cutting through wood)
• It is due to the retroversion of aortic valve leaflets during diastole due
to inflammation

40. “Innocent murmur”
• “functional murmur or flow murmur”
• Doesn’t radiate
• Underlying cardiovascular system is entirely normal and murmur is
audible at rest
• Results from normal turbulence occurring during ejection of blood
from heart
• Typical innocent flow murmur arises in pulmonary artery

41. INNOCENT MURMUR CHARACTERSTICS

42. Physiologic murmurs
• Caused by transient increase in blood volume and/or velocity of
ejection
• Common causes-Anemia, anxiety, fever, thyrotoxicosis, pregnancy
• Murmur will no longer audible or become faint (grade 1-2/6)
innocent murmur after correction of increase blood flow or
augmented cardiac contractility

43. EJECTION CLICK (EC)
Results from sudden opening of a stenotic valve
• AORTIC EJECTION CLICK
High-pitched, best heard at the aortic area, but widely audible.
Occurs earlier as severity of stenosis increases ➜Followed by a
systolic murmur and not seen in calcific AS as the cusps are rigid
• PULMONARY EJECTION CLICK
High-pitched, best heard at the pulmonic area with a diaphragm,
softens with inspiration. ➜Coincides with a wave of JVP.

44. MID-SYSTOLIC CLICK (MSC)
• Mitral valve prolapse (MVP)
• Usually followed by a late systolic
murmur
• Results from abrupt halting of
prolapsing mitral valve leaflets
into the atrium by the chordae
• High-pitched, best heard at apex
with diaphragm
• Moves closer to S1 with valsalva
and standing.

45. OPENING SNAP (OS)
• Mitral stenosis (MS), rarely in
tricuspid stenosis
• Occur early in diastole after S2 but
before S3
• May be followed by apical diastolic
rumble in MS
• Results from sudden opening of a
stenotic valve
• High-pitched, best heard at apex by
diaphragm in left decubitus position
“Softer and closer to S2 in severe MS”

46. PERICARDIAL KNOCK (PK)
• Constrictive pericarditis
• Occur early in diastole, after S2
but before S3
• Sharper, higher pitch than S3 and
OS
• Heard widely but best at apex with
diaphragm
• Knock coincides with rapid Y
descent of JVP
• JVP increases with inspiration
(Kussmaul’s sign)

47. TUMOR PLOP
• Myxoma or vegetation in left
atrium
• Causing ventricular in-flow
obstruction
• Occurs in early diastole, after S2
• Low pitch, heard best at apex with
bell
• A diastolic murmur may also be
appreciated

48. PERICARDIAL FRICTION RUB
• A coarse scratching or leathery sound (acute viral pericarditis
and Dressler’s syndrome 24-72 hours after MI)
• Best heard over the bare area of heart with diaphragm with the
breath held in expiration. Vary in intensity over time, and with
position of patient (louder when leaning forward and over)
• No change with respiration. In contrast, pleural rub disappears
when breath is held
• 3 components : presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after a2p2)

49. HAMMAN’S CRUNCH
• A series of precordial crackles that correlate with the heartbeat and
not with respiration
• “Crunching” sounds are produced by the heart beating against air-
filled tissues.
• A finding heard in pneumo-pericardium:
• Following heart surgery
• Vigorous resuscitation
• Iatrogenic i.e. pericardiocentesis, bronchoscopy
• Also in pneumo-mediastinum, spontaneous mediastinal emphysema,
Boerhaave syndrome

50. Physiological maneuver
1. Valsalva
2. Muller
3. Passive leg elevation
4. Sudden standing from
squatting or lying down
5. Sudden squatting
6. Isometric exercise
7. Respiration
Dynamic Auscultation

51. Physiological maneuver
1. Valsalva
2. Muller
3. Passive leg elevation
4. Sudden standing from
squatting or lying down
5. Sudden squatting
6. Isometric exercise
Pharmacological
• Amyl Nitrate inhalation
• Methoxamine/phenylephrine

52. Physiological maneuver
1. Valsalva
2. Muller
3. Passive leg elevation
4. Sudden standing from
squatting or lying down
5. Sudden squatting
6. Isometric exercise
7. Respiration
Pharmacological
• Amyl Nitrate inhalation
• Methoxamine/phenylephrine
Other postural changes
• Left lateral- MS
• Sitting up and leaning forward- AR
• Stretching of neck- venous hum

53. 1.Valsalva maneuver
•Exhale forcefully in to a mercury manometer to generate
pressure of 40 mm Hg for 20 sec
•Deep inspiration followed forced expiration against a closed
glottis for 20 seconds

54. Stages
1.Onset of straining
2.Continued straining (Strain phase)
3.End of expiration (Release phase)
4.Recovery (5-10 sec after end of
expiration) (Overshoot phase)

55. Stages
1.Onset of straining
2.Continued straining
3.End of expiration
4.Recovery (5-10 sec after end of
expiration)
VALSALVA PHASE I
• increased intrathoracic pressure-> pulmonary
circulation is squeezed, so blood is pushed to left
heart and there is increase in BP and LV output

56. Stages
1.Onset of straining
2.Continued straining
3.End of expiration
4.Recovery(5-10 sec after end of expir)
VALSALVA PHASE I
• increased intrathoracic pressure-> pulmonary
circulation is squeezed, so blood is pushed to left
heart and there is increase in BP and LV output
VALSALVA PHASE II
• d/t increase intrathoracic pressure, systemic
venous return decrease
• Filling of right and then left side chamber reduced
• Stroke volume reduced
• Mean arterial and pulse pressures falls
• Reflex tachycardia

57. Stages
1.Onset of straining
2.Continued straining
3.End of expiration
4.Recovery(5-10 sec after end of expir)
VALSALVA PHASE I
• increased intrathoracic pressure-> pulmonary
circulation is squeezed, so blood is pushed to left
heart and there is increase in BP and LV output
VALSALVA PHASE II
• d/t increase intrathoracic pressure, systemic
venous return decrease
• Filling of right and then left side reduced
• Stroke volume reduced
• Mean arterial and pulse pressures falls
• Reflex tachycardia
PHASE III VALSALVA RELEASE
• As the pressure on chest is released, allowing
pulmonary vessels and aorta to re-expand causing
a further initial slight fall in SV due to decrease LA
return and increase aortic volume
• Venous blood can once more enter chest and
heart, CO begins to increase

58. Stages
1.Onset of straining
2.Continued straining
3.End of expiration
4.Recovery(5-10 sec after end of expir)
VALSALVA PHASE I
• increased intrathoracic pressure-> pulmonary
circulation is squeezed, so blood is pushed to left
heart and there is increase in BP and LV output
VALSALVA PHASE II
• d/t inc intrathoracic pressure, systemic venous
return decrease
• Filling of right and then left side reduced
• Stroke volume reduced
• Mean arterial and pulse pressures falls
• Reflex tachycardia
PHASE III VALSALVA (RELEASE PHASE)
• As the pressure on chest is released, allowing
pulmonary vessels and aorta to re-expand causing
a further initial slight fall in SV due to decr LA
return and incr aortic volume
• Venous blood can once more enter chest and
heart, CO begins to incr
PHASE IV (OVERSHOOT PHASE)
• Blood pressure over shoots
• increased Vagal stimulation in carotids
• heart rate decrease (bradycardia)

59. Importance of Valsalva
• The Valsalva maneuver is helpful in differentiating right-
sided systolic murmurs from those originating from the left
heart
• Most useful in identifying the systolic murmurs of HOCM
and MVP
• Upon release of the Valsalva maneuver, murmurs from the
right heart generally return to baseline intensity within 2-3
cardiac cycles whereas left sided murmurs generally takes
5-10 cycles
• Not useful in heart failure, ASD and MS

60. 2.Muller’s maneuver
• Nares held closed, patient has to suck forcibly into a
manometer to generate a negative pressure of 40-50 mm Hg
for 10 seconds and see for changes in intensity of murmur at
end of 10 sec
• Nares pinched, mouth firmly sealed, and asked patient to
inspire for 10 sec

61. • Historically used to accentuate right sided murmur
• Objective studies has found not useful
• Infrequently performed

62. Dynamic auscultation helpful in
• AS vs HOCM : Squatting (A/v)/ Post VPCS
Valsalva/Standing (V/A)
• AS x MR : Handgrip (V/A)
Phenyl ephrine (V/A)
Post PVC (A/V)
Amyl nitrate (A/V)
• MS X Austin Flint murmur: Amyl nitrate(A/v)
• PR X AR : Squatting (_/A)
Sustained handgrip (-/A)
• PS X Small VSD : Amyl nitrate (A/V)
Respiration

63. Thanku