3. MURMUR AND Dynamic Auscultation OF Cardiovascular System
ANKUR KAMRA

4. Defining a heart murmur
A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of
Varying
intensity(loudness), frequency (pitch), quality, configuration, and duration

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

6. (1) high flow rate through normal or abnormal orifices,
Leatham has attributed the production of murmurs or turbulence to three main factors:
(1) high flow rate through normal or abnormal orifices,
(2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and
(3) backward or regurgitant flow through an incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these factors is operative

7. CLASSIFICATION
Can be classified into organic, functional and innocent.
Organic refer to structural defect responsible for murmur
Important is that the term innocent and functional are not interchangeable.
Functional murmur should subserve a function like increased flow across aortic valve as in severe AR.
While innocent occur in absence of abnormalities of heart and circulation, more common in children and on right side.

8. Description of a Murmur
Position in the cardiac cycle
Site of murmur ]
Shape of murmur
Intensity
Quality & Pitch
Conduction
Dynamic changes

9. Dynamic Auscultation behaviour and the intensity of the
Listening to the change in character,
behaviour and the intensity of the
heart sounds and murmurs to
physiological and pharmacological
maneuvers…….
“AUSCULTATE WITH ALTERED HEMODYNAMICS”

10. Conditions and interventions
Respiration
Postural Change
Valsalva maneuver
Exercise
Change in Cardiac Cycle length
Pharmacological agents.

11. What happen during respiration
Normal inspiration →
↑ venous return to right side of the heart due to fall in intra thoracic pressure → ↑ stroke volume of right side
Dilatation of pulmonary vascular system causing decrease in pulmonary impedance there by increasing pulmonary hang out interval(>80 ms)
So leads to accentuation of R side murmur

12. RESPIRATION CONTINUE
Normal expiration → ↓ lung volume → ↑ pulmonary venous flow
Therefore, left sided murmurs are loudest during expiration except MR which remain unchanged.
While no change is seen
When complicated by RVF as due to high RVEDP no increase in venous return.
Aortic valvular ES do not vary with respiration
MR murmur do not vary with respiration

13. RESPIRATION CONTINUE Assess changes during normal respiration
Patient should be in semiupright or sitting posture
In RV failure and PHT, no increase in venous return with inspiration, hence no inspiratory augmentation of right sided murmurs and gallops
Absence of respiratory influence is of no particular diagnostic value.
Effects of inspiration may be accentuated by Muller maneuver.

14. STANDING
Auscultation is carried out immediately before and after the change in posture since effects may be quite transient persisting for only 10 – 15 heart beats If patient is unable to sit upright or stand, rapid application of tourniquets at upper thigh level may reduce venous return reproducing similar response

15. STANDING
Rapid standing or sitting up from lying position or rapid standing from squatting posture results in
decreased venous return due to venous pooling in legs and splanchnic vessels leads to-
decreased stroke volume
decreased mean arterial pressure
decrease in heart size
followed by reflex increase in heart rate & systemic resistance

16. standing All murmurs decrease except-
ESM of HOCM becomes louder and longer
Click occurs earlier, murmur becomes longer in MVP while loudness shows variable response

17. Sudden assumption of LYING DOWN POSITION PASSIVE ELEVATION OF LEGS
Increase in venous return → increase R.V. stroke volume → later after several cardic cycles left ventricle volume also increase .
So Systolic murmur of AS,PS,MR, TR & VSD increase.
MVP & HOCM murmurs decrease due to increase in LVEDV and LV size.
Most murmurs diminish with standing due to reduced preload. However, the murmur of HCM becomes louder, and the murmur of MVP lengthens and often is intensified. Similarly, most murmurs become louder with prompt squatting (or usually passive leg raising), while the murmurs of HCM and MVP typically soften and may disappear

18. Squatting leads to- Increases venous return & Stroke Volume
Sudden change from standing to squatting
leads to-
Increases venous return & Stroke Volume
Increase of systemic vascular resistance due to kinking of iliac artery and reduction of pressure of gravity
Increase of systemic Arterial pressure with transient bradycardia
Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure

19. Squatting
Increased venous return and CO - augments most murmurs (AS,PS,MR,AR,VSD) Right heart murmurs do so earlier
Increased left ventricular volume - decreases murmur of HOCM and delayed murmur and click of MVP
Ejection murmur of TOF↑ due to increase pulmonary blood flow and decrease in right to left shunt

20. Other postural changes
Assumption of L Lateral Position Causes closeness of heart to chest wall and transient rise of HR. So leads to – Increased murmur of MS, MR and austin flint murmur of AR Early appearance of click and systolic murmur of MVP due to increasec HR.

21. Sitting up and leaning forward
causes more closeness of base of heart to chest wall so AR and PR murmurs more readly audible
PRONE POSITION & KNEE CHEST POSITION
Bring heart close to chest wall making pericardial rub more prominent

22. Valsalva Maneuver
Relatively deep 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

23. VALSALVA MANEUVER Forced expiration against closed glottis
Manometer method:
Patient blows into the mercury manometer and maintains 40 mmHg for 15 seconds
Valsalva equivalent:
Patient pushes back against examiner’s hand which is pressed downward on mid abdomen.
The maneuver is demonstrated and patient practices the maneuver before assessment of murmur
Caution : Not to be performed in IHD as it will reduce Coronary Blood Flow.

24. PHASES OF VALSALVA
PHASE 1-due to increase in intra thoracic pressure there is transient rise in LV output and systemic arterial pressure but there occurs fall in HR
phase 2(stain phase)- decrease in venous return first to right then to left leads to decrease in systolic, diastolic and pulse pressure and reflex tachycardia

25. PHASE 3- cessation of staining result in-
sudden increase in systemic venous return
but transient decrease in arterial pressure due to fall in intra-thoracic pressure
PHASE 4- return to pre valsalva
a transient overshoot of systemic arterial pressure
Reflex bradycardia

27. PHASE BP HR 1
INCREASE
DECREASE 2
INCRESAE 3 4

28. EFFECTS ON MURMUR PHASE1 –as stroke volume fall there is decrease in –
systolic murmur of AS, PS, MR, TR
diastolic murmur of AR PR MS TS
PHASE2- reduction in LV volume and size leads to-
increase in systolic murmur of HOCM
increase in degree of MVP prolapse

29. PHASE 3- sudden increase in SVR leads to increase in right side murmurs
PHASE 4-left side murmur comes to control levels and may transiently increase.
ASD, MS and CHF – Phase 1 and 3 are normal but there is absence of decrease in arterial pressure tracing during phase 2 and overshoot of BP does not occur in phase 4 that leads to SQUARE WAVE RESPONSE ie. Instead of four phases there is only two phase.

30. The Muller Maneuver
Converse of Valsalva Maneuver Less frequently employed Forcibly inspires while the nose is held closed and mouth is firmly sealed for about 10 sec. Augments murmur and filling sound originating in right side of the heart.

31. ISOMETRIC EXERCISE
Use calibrated handgrip device or tennis ball or rolled up BP cuff.
Measure the maximum effort.
Patient exerts 70 – 100% of this maximum for about 30 seconds
Simultaneous handgrip using both hands
Valsalva maneuver during handgrip should be avoided

32. ISOMETRIC EXERCISE
Hemodynamic changes: Significant increase in Arterial pressure Heart rate Cardiac output LV filling pressure LV size

33. Isometric Exercise
Systolic Murmur of AS reduced due to reduced gradient across aortic valve
AR , MR , VSD – increased due to increase systemic vascular resistance
MDM of MS – increased due to Increased CO
Syst Murmur of HOCM reduced
MVP murmur + click delayed

34. ISOMETRIC EXERCISE
Avoid in those with ventricular arrhythmias and myocardial ischemia
Contraindicated in recent myocardial infarction, uncontrolled hypertension, cerebrovascular disease, suspected aortic dissection

35. Cardiac cycle length changes post PVC and AF
↑ preload will increases ventricular filling and size
Also in addition there is secondry increase in ventricular contractibilty of new beat and transient increase in arterial pressure.  

36. Cardiac cycle length changes
Increased ( L or R vent ejection murmurs ) AS PS HOCM(there is inc in SM but also decrese volume of pulse known as BROCKENBROUGH PHENOMENA) No change for MR , TR DM of AR increases due to transient rise in arterial pressure
Intensity of the ejection systolic murmur increases in aortic stenosis and hypertrophic cardiomyopathy. Carotid pulse volume increases in the former and decreases or remains unchanged in the latter.
The pansystolic murmur of mitral regurgitation, particularly of rheumatic origin, does not usually change. In mitral valve prolapse, post ectopic potentiation causes a rapid rate of ejection and, therefore, an earlier onset of the click and the murmur

38. Amylnitrite Inhalation
Inhalation of Amyl Nitrate
Crush ampoule in towel
take 3-4 deep breaths over 10 – 15 secs
Changes observed-
< 30 secs : Systemic vasodilatation
30 – 60 secs : increase HR & CO
However majority of auscultaory changes are observed in first 30 sec

39. Due to increse in CO-
SM of AS and PS
SM of TR
All functional SM
DM of MS and TS
DM of PR

40. Due to decrease in SVR following murmur are decreased-
SM of MR
DM and austin flint murmur of AR
SM of TOF
Due to decrease LV volume and size –
SM of HCM increases
early appearance of MVP click and murmur but softening of murmur occur due to decrease resistance to LV resistance

41. Amyl Nitrite Inhalation
Augments Diminishes
Aortic stenosis Mitral regurgitation
Pulmonary stenosis TOF
Tricuspid regurgitation Mitral regurgitation
Mitral stenosis Austin Flint
Pulmonary regurgitation Aortic Regurgitation

42. Phenylephrine ↑ BP & SVR ↓ CO & HR – last for 3-5mts
Reduces intensity of S1, A2-OS may widen
Augments the murmurs of VSD, PDA, MR, AR, TOF, Systemic AVF
Diminishes AS, MS & functional murmurs
ESM of HOCM diminishes
Click & murmur of MVP get delayed

43. Methoxamine & Phenylephrine
Opposite effect of Amyl Nitrate
Phenylephrine - due to short duration of action
Systolic pressure elevated by 30 mm Hg
for 3 to 5 mts
EFFECT
Increases systemic arterial pressure
Reflex Bradycardia , decrease CO, decrease Contractility
Caution : Not to be used in patients with CHF or Systemic hypertension.
METHOXAMINE — An increase in systemic vascular resistance and arterial pressure following administration of methoxamine or phenylephrine produces effects opposite to those of amyl nitrite. Both agents cause reflex bradycardia and a lower cardiac output.  The diastolic murmur of aortic regurgitation increases in intensity.  The systolic murmur of mitral regurgitation increases in intensity.  Intensity of the systolic murmur due to a ventricular septal defect and tetralogy of Fallot increases.  The murmurs of aortic stenosis and hypertrophic cardiomyopathy become softer.  The click and murmur of mitral valve prolapse are delayed  In mitral stenosis, the A2-opening snap interval becomes longer due to increased arterial pressure.  An isoproterenol infusion in patients with hypertrophic cardiomyopathy increases intensity of the murmur with little or no change in the carotid pulse volume.

44. Methoxamine & Phenylephrine
AR , MR , VSD , TOF – Louder SM OF AS, PS and DM of PR and TS -show no changes LV size increases HOCM – Softer Click and Murmur of MVP - Delayed

45. Some general points about murmur before discussing individual murmurs

46. Timing

47. Sometime it is difficult to identify the timing of murmur
Murmur can be timed by simultaneous palpation of the carotid arterial pulse or by identifying S2 at base
Inching technique of Harvey and Levine
In tachycardia carotid sinus massage can slow down heart rate
In case of extra systole indentify the beat that follows pause and then first sound after pause will be S1

48. LENGTH
It generally reflect the pressure difference b/w two sites and this is true for all stenotic lesions like MS, AS, PS or TS
In regurgitant lesion length has no correlation with severity.
In AR length of murmur correlates better then MR but still not as reliable as stenotic lesions

49. CHARACTER
High frequency murmur occur when pressure difference b/w two chambers are high and low pressure difference has low frequency and pitch.
As a general rule regurgitant lesions are high frequency and stenotic are rough or low frequency. Murmur of AV stenosis are of low frequency while semilunar are of mixed frequency
High frequency or soft component of murmur is more widely audible this is reason why AS soft component is audible at apex and mistaken for MR
While low frequency or rough component is audible at site of best audibility of murmur.

50. PITCH Hz
Pr Gr
QUALITY
E.g.:
LOW
25-125
Less
Rumbling,
rough
MDM-MS
MEDIUM
mix
Harsh, rough AS
HIGH
>300
high
Blowing, soft, musical
MR,AR

51. Systolic Murmurs

52. Early Systolic murmurs
Early systolic murmurs begin with S1 and extend for a variable period of time, ending well before S2
1. Acute severe mitral regurgitation
Regurgitation occurs into a normal-sized, relatively noncompliant left atrium and as LV-LA pressure gradient is abolished during late systole, termination of retrograde flow occurs well before S2.
best heard at apical impulse
Caused by:
i. Papillary muscle rupture due to ishemia
ii. Infective endocarditis -destruction of leaflet tissue, chordal rupture, or both

53. iii. Rupture of the chordae tendineae in myxomatous mitral valve disease
iv. Blunt chest wall trauma-papillary muscle contusion and rupture, chordal detachment, or leaflet avulsion.
2.Congenital, small ventricular septal defect-
ventricular size decrease and septum thickness increases which seals off defect
3. VSD with high PA pressure-
high pulmonary resistance will decrease the late shunting
Tricuspid regurgitation with normal PA pressures-
The murmur is soft (grade 1 or 2), best heard at the lower left sternal border, and may increase in intensity with inspiration (Carvallo's sign). Regurgitant "c-v" waves may be visible in the jugular venous pulse.

54. Midsystolic (ejection) murmurs
Mid-systolic murmurs begin at a short interval following S1, end before S2
Murmur is due to flow across LV or RV outflow tract when flow proceeds , murmur increase in in crescendo and when it decrease murmur decrease in decrescendo.
Intensity of murmur depend on cardic output. So when flow and cardic output changes like in various maneuver murmur changes.
Causes are:
1. Innocent: due to flow across normal ventricular outflow tract
2. Functional: dilation of aortic root, pulmonary trunk increase flow into aorta and pulmoary artery
3. Pathologic
are secondary to structural CV abnormalities
e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic stenosis

55. Aortic stenosis
Harsh, medium pitch, loudest in aortic area; radiates along the carotid arteries and apex.
Intensity varies directly with CO
Severity varies with murmur may have an early peaking and short duration or late peaking and prolonged duration.
A/W parvus et tardus
Other conditions which may mimic the murmur of aortic stenosis w/o obstructing flow:
1. Aortic sclerosis
2. Bicuspid aortic valve
3. Dilated aorta
4. Increased flow across the valve during systole

56. Hypertrophic cardiomyopathy
Loudest b/t left sternal edge and apex; Grade 2-3/6
Does NOT radiate into neck; carotid upstrokes are brisk and may be bifid
The murmur will classically increase in intensity with maneuvers that result in increasing degrees of outflow tract obstruction, such as a reduction in preload or afterload (Valsalva, standing, vasodilators) or to an augmentation of contractility (inotropic stimulation). Maneuvers that increase preload (squatting, passive leg raising, volume administration) or afterload (squatting, vasopressors) or that reduce contractility (-adrenoreceptor blockers) decrease the intensity of the murmur

58. MANEUVERS
FIXED LVOT
DYNAMIC LVOT
RESPIRATION
NO CHANGE
MAY INC WITH EXPIRATION
STANDING
DECREASES
INCREASES
SQUATTING
VALSALVA
BROCKENBROUGH
NORMAL
POSTIVE

59. Slow rising and delayed pulse Ejection click S4 Narrow pulse pressure AS MR
Location
Aortic area
Apex
Radiation
Neck
Axilla
Shape
Diamond
Holosystolic
Pitch
Medium
High
Associated signs
Decreased A2
Slow rising and delayed pulse
Ejection click S4
Narrow pulse pressure
Decreased S1
Laterally displaced diffuse PMI S3
POST PVC
INCRESES
NO CHANGE
Isometric Exercise
DECREASES
INCREASES
Amyl Nitrate

60. MVP
HCM
CLICK
PRESENT
ABSENT
POST ECTOPIC BEAT
DO NOT CHANGES
DECREASES
AMYL NITRATE
BI PHASIC
INCREASES

61. Pansystolic (Holosystolic) Murmurs
Are pathologic
Murmur begins immediately with S1 and continues up to S2
1. Mitral valve regurgitation
Loudest at the left ventricular apex
Radiation reflects the direction of the regurgitant jet
i. To the base of the heart = anterosuperior jet (flail posterior leaflet)
ii. To the axilla and back = posterior jet (flail anterior leaflet
Also usually associated with a systolic thrill, a soft S3, and a short diastolic rumbling (best heard in left lateral decubitus
2. Tricuspid valve regurgitation
3. Ventricular septal defect

64. 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
-Austin Flint murmur

65. AR A/C AR C/C 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

66. 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

67. High Pressure vs. 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

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

69. MS Low pitch 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]
OS- leaflet excursion comes to its anatomical limits because of its commissural tethering, part of the column of blood will be decelerated suddenly, along with the doming anterior leaflet.

70. 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

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

72. Late Diastolic/ Pre-systolic MurmursMS
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

74. Valsalva Maneuver

75. DYNAMIC AUSCULTATION Proper assessment requires Good stethoscope
Quiet room
Cooperative patient
Bare chest
Intact autonomic function and normovolemia
Knowledge about the maneuver and the
changes expected

76. THE CAVEATS ARE……… Avoid dynamic auscultation in sick patients
When postures are changed, transition should be abrupt
Continuous auscultation is required, when maneuvres are being elicited
Concentrate on the first few cycles after maneuvres
Realize that each maneuvre induces more than one alterations in hemodynamics

77. early systolic
mid systolic
Systolic murmur late systolic
pan/holo systolic
early diastolic
Diastolic murmur mid diastolic
pre systolic

78. 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

79. 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

80. 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.

81. crescendo, decrescendo, crescendo-decrescendo, plateau
SHAPE
crescendo, decrescendo, crescendo-decrescendo, plateau
The crescendo (grows louder) Configuration of the murmur of chronic AS can be understood in terms of the progressive increase in the systolic pressure gradient between the left ventricle and aorta.
Decrescendo Configuration(decreasing) of the murmur of chronic AR can be understood in terms of the progressive decline in the diastolic pressure gradient between the aorta and the left ventricle.
The crescendo-decrescendo(increasing-decreasing or diamond shape) configuration of the murmur of AS reflects the changes in the systolic pressure gradient between the left ventricle and the aorta as ejection occurs,
The plateau(even or unchanged) configuration of the murmur of chronic rheumatic MR is consistent with the large and nearly constant pressure difference between the left ventricle and the left atrium.