This document describes techniques for dynamic auscultation of the heart by altering circulatory dynamics through physiological and pharmacological maneuvers. Some key techniques discussed include respiration, postural changes, Valsalva maneuver, isometric exercise, and use of vasoactive agents. Various maneuvers cause changes in heart sounds and murmurs due to effects on hemodynamics, ventricular volumes, and pressures. For example, inspiration augments murmurs on the right side of the heart while expiration accentuates some left-sided murmurs. The Valsalva maneuver and post-premature ventricular contractions also cause characteristic changes heard on auscultation.

1. DYNAMIC AUSCULTATION

2. • This is a technique of altering circulatory
dynamics by means of a variety of
physiological and pharmacological maneuvers
and determining their effects on heart sounds
and murmurs

3. Interventions most commonly employed are
• Respiration
• Postural changes
• Valsalva maneuver
• Isometric exercise
• Premature ventricular contractions
• Vasoactive agents-
amyl nitrite ,methoxamine ,phenylephrine

4. RESPIRATION
• History
• Pontain in1866 was the first to note the
normal respiratory variation in splitting of the
second heart sound .
• In 1954 leatham brought pontain’s
observations to clinical attention through
emphasis on their significance

5. • Hemodynamics
• On inspiration the intra thoracic pressure
decreases and results in augmentation of right
heart blood flow and decrease in left heart flow
• Murmurs generated in the right heart there fore
generally become louder on inspiration and those
in left heart chambers decrease as a result of
reduced left heart flow as well as increased
insulation by the air filled lungs

6. • Second heart sound
• Respiration alters the splitting and loudness of second
heart sound
• In normal young adults in supine position
inspiration S2 split increase
expiration split narrows and s2 becomes single
• Failure of S2 to fuse in EXP may occur in normal
children and 15 to 20 % of young adults
• In up to 50% of normal adults > 50 yr single audible S2
is seen in supine position both in INSP and EXP

7. • During inspiration A2 becomes softer because
1. aortic pressure decreases
2. increased lung space between
heart and chest wall
• During ispiration P2 becomes soft in 2nd LICS
and
• Louder in lower LSB ( increased flow in the
pulmonary artery has greater effect lesser
deree of lung space interposed in this area )

8. Heart sounds
Accentuated during
Inspiration
• RVS3 and RVS4
• Tricuspid OS
Expiration
• LVS3 and LVS4
• mitral OS

9. Pulmonary ejection click
• Inspiration diminish intensity of valvular PEC
• PA diastolic pressure is very low
• Inspiration causes elevation of RV DP
• RV late diastolic Pr almost equlises PA diastolic
Pressure
• Causes partial presystolic opening of PV
• Less upward motion of valve during systole

11. MURMURS
• Respiration exerts more pronounced and consistent
alterations on murmurs of right side than left side
• Especially tricuspid murmurs 100% sensitivity, 88%
specificity
• Inspiration increases venous return to right side of
heart
• Expiration increases venous return to left side of heart

12. Murmurs accentuated during
Inspiration
• TS
• TR (Carvallo’s sign)
• PR
• Mild or moderate PS
• Severe PS no further
increase in gradient
Expiration
• MS
• MR
• AS
• AR
• VSD
• Pericardial rub (AP
diameter)

13. MVP
• MSC and systolic murmur occur earlier during
systole in inspiration
• Inspiratory reduction in LV size
• Increased redundancy of MV
• Increase valvular prolapse

15. • IHSS murmur may decrease in loudness and
intensity with inspiration
• This is because of inspiratory increase in Lv
transmural pressure, with resultant decrease
in LVOT obstruction

16. • In general it is best to assess respiratory
variation during normal respiration.
• Effects of inspiration on auscultatory findings
may be accentuated by Muller maneuver
• Converse of Valsalva Maneuver
• Forced inspiration against closed glottis
• Forcibly inspires while the nose is held closed
and mouth is firmly sealed for about 10 sec.

17. • Patients who have pulmonary hypertension and
severe RVF may not demonstrate inspiratory
augmentation of Rt heart murmurs and gallops
• This is due to high Rt heart filling pressures that
does not allow venous return to increase in
inspiration
• By requesting these patients to stand and by
repeating cardiac ausculation we can appreciate
the expected respiratory changes

18. • Widens split S2 and augments murmur and
filling sound originating in right side of the
heart.

19. POSTURAL CHANGE
RAPID STANDING
• Decrease in venous return, thus stroke volume
and the ensuing reflex increses the cardiac
rate and systemic vascular resistance
immediately

20. • Width of the splitting become reduced
• No change in patients with true fixed split
Decrease in intensity
• RVS3 and RVS4
• LVS3 and LVS4

21. Decrease in intensity
• Semilunar valve stenosis
• AV valve regurgitation murmurs
• VSD
• Most functional systolic murmurs

22. • Since LV EDV is decreased
Increase in murmurs
• HOCM(95% sensitivity, 84%
specificity)
• Early MSC and murmur of
MVP

23. • Physiological changes that cause increase in
obstruction in LVOT include a smaller
ventricular size and reflex inotropic stimulus
from increased catecholamines

24. SQUATTING
• Sudden change from standing to squatting
position
• Increase venous return and augmentation of
peripheral resistance due to kinking of femoral
arteries simultaneously
• Squatting abruptly increases ventricular preload
and afterload
• Arterial pressure rise may cause transient reflex
bradycardia

25. Increase in stroke volume causes augmentation
of
• S3 and S4(of both ventricles)
• Right sided systolic murmurs
• AS
• Diastolic murmur of MS augmented due to
increase in CO with increased flow across
mitral valve

26. Elevation of arterial pressure
• Increase in aortic reflux AR
• Increase in MR volume
• Increase in LT to RT shunt in VSD
• Increase in blood flow through RVOT in TOF

27. Combination of elevated arterial pressure and
venous return
• Increase LV size and reduce LVOT obstruction
• Decrease murmur in HOCM(95% sensitivity,
85% specificity)
• Click and murmur of MVP delayed

29. LEFT LATERAL RECUMBENT POSITION
Accentuate intensity of
• S1
• LVS3 and LVS4
• OS of MS
• Murmurs of MS and MR
• Click and murmur of MVP
• Austin Flint murmur

30. SITTING AND LEANING FORWARD
• Accentuate AR and PR murmur (mechanical)

31. Lying flat or passive leg raising in
supine position
• Results in increase in venous return with
sequential increase in right and then left
ventricular end diastolic volumes, stroke
volume, and ejection velocities

32. • Augmented
• Valvular AS/PS murmurs
• TR murmur
• S3 and S4
• Diminished
• EDM of AR
• Murmur of HOCM
• MVP murmur and click
are delayed

33. ISOMETRIC EXERCISE
• This can be carried out by using a calibrated
handgrip device or a handball
• Better to carryout bilaterally
• Performed in supine posture
• Should be sustained for 30 to 40 secs
• Valsalva maneuver during the handgrip must be
avoided
• Contraindicated in patients with myocardial
ischemia and ventricular arrhythmias, severe
HTN, cerebral ischemia

34. • Hemodynamic effects
• Increases cardiac contractility
cardiac output
arterial pressure
without significant change in ventricular
chamber size

35. Isometric exercise results in significant increase
in
• Systemic vascular resistance
• Arterial pressure
• Heart rate
• COP
• LV filling pressure
• Heart size

36. • Systolic murmur of AS diminished –reduction
of pressure gradient across AV
• Diastolic murmur of AR and systolic murmurs
of rheumatic MR and VSD increases
• LVS3 and LVS4 accentuated
• Diastolic murmur MS becomes louder –
increase in flow across valve

37. Increase LV volume
• Systolic murmur of HOCM decreased
• Click and murmur of MVP delayed

38. VALSALVA MANEUVER
• Forced expiration against a closed glottis
Standard test consists of asking the patient to
blow against an aneroid manometer and
maintain a pressure of 40mmhg for 30seconds

39. • 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
• Normal response has four phases

40. PHASE I
• Intrathoracic pressure rises
• Transient increase in LV output and SBP

41. PHASE II STRAINING PHASE
• Systemic venous return decrease
• Filling of right and then left side reduced
• Stroke volume reduced
• Mean arterial and pulse pressures falls
• Reflex tachycardia

42. Since LV volume is reduced
• Murmur of HOCM increased(65% sensitivity,
95% specificity)
• Systolic click and murmur of MVP commence
earlier

43. PHASEIII VALSALVA RELEASE
• Brief sudden Decrease SBP
• Due to sudden decrease in intra thoracic
pressure

44. • Phase IV
• Over shoot of SBP due to increased venous
return and reduced systemic vascular
resistance
• Followed by reflex bradycardia

46. • PHASE IV OVERSHOOT PHASE
• Murmurs and heart sounds transiently
augmented

48. Square wave response
• Seen in
• Severe LV dysfunction +_ Heart failure
• MS with significant PAH
• ASD with significant L to R shunt
• Apparently normal persons aged above 55 yr

49. • Phase I: Intra thoracic pressure rises with
increase in sys and pul arterial pressures with
no increase in CO
• Phase II: ventricular filling is not decreased
and venous return is maintained during
continued straining. Arterial pressure remains
mildly elevated with insignificant changes in
PP , HR , LV SV , CO

50. • Phase III/IV: post release phase pressures
return to normal pre strain level
• No transient increase invenous return,SV or
over shoot BP rise or reflex brady cardia

51. • The maneuver should be performed with
patient in supine position or upper part of
body elevated no more than 30 degrees
• Strain phase to be limitied to 10 to 12 sec
• Should not be performed in patients with
active myocardial ischemia or cerebral
ischemia and unstable cardiac rhythm

52. 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

54. • Valsalva maneuver is helpful in differentiating
rt sided systolic murmurs from those of the
left side and of considerable importance in
identifying systolic murmur of HOCM

55. • During strain phase
Attenuation of
• S3 and S4
• AS & PS
• MR & TR
• AR & PR
• TS & MS
• Most of the heart sounds and
murmurs decrease in the
strain phase of valsalva

56. • Up on release of valsalva murmurs on the
right side of the heart return to baseline
intensity in 2 to 3 cardiac cycles where as left
sided murmurs donot return to baseline
intensity till 5 to 10 cardiac cycles

57. • Second heart sound
• Normal splitting of S2 narrows during the
strain phase of valsalva and widens markedly
immedaitely during the release phase
• Paradoxical plitting of S2 widens during the
strain phase and then becomes more narrow
during the release phase

58. POSTPREMATURE VENTRICULAR
CONTRACTIONS
Followed by a significant pause
• Increase in ventricular filling
• Augmentation of cardiac contractility- post
extra systolic potentiation
• Onset of LV ejection at a lower diastolic
pressure

59. During postpremature beat – augmented are
• ESM of AS and PS volume
contractility
• HOCM contractility-increase dynamic
LVOT obstruction
increase volume decrease LVOT obstruction
net increase gradient

60. • PSM of MR and of VSD - not altered(relatively
little further increase in mitral valve flow or
change in the LV-LA gradient) (ventricle has
has 2 openings aorta and LA in MR not in AS)
• Systolic murmur of papillary muscle
dysfunction diminish
• Increase in LV size delays systolic click and
murmur of MVP (depend mainly on volume)

62. • Similar auscultatory changes follow prolonged
diastolic pauses in AF
• After a long R-R interval
augmented unchanged
AS/PS TOF
IHSS VSD
TR MR
AR

63. • PR interval variations
• When PR interval becomes abnormal atrial
contribution to ventricles decrease and the
stroke volume falls
• Varying atrial contribution will cause
significant alteration in ESMs
• S1 soft with long PR and loud with short PR

64. PHARMACOLOGICAL AGENTS
AMYL NITRITE INHALATION
• Crush ampule in towel
• take 3-4 deep breaths over 10 – 15 secs
• First 30 secs– Systemic art pressure decrease
• 30 to 60 secs– Reflex Tachycardia
• > 60 secs - positive inotropic effect, SV, EF,
CO,HR and Ejection Velocity
• Significant increase in venous return

65. • S1 augmented
• A2 diminished
• OS mitral and tricuspid valve become louder
• A2 OS interval shortens
• RVS3 and LVS3 augmented –rapidity of
ventricular filling
• LVS3 associated with MR diminished(MR
reduced)

66. Systolic murmurs accentuated are
• HOCM
• AS
• PS
• TR
• Functional systolic murmurs
Increased ventricular contractility and SV

67. Due fall in systemic arterial pressure murmurs
diminished are
• PSM of MR
• PSM of VSD
• EDM of AR
• Austin flint murmur
• Continuous murmur of PDA
• Continuous murmur of AVF

68. Systolic ejection murmur of TOF diminished
• Decrease in arterial pressure
• Increase right to left shunt
• Decrease blood flow in RVOT

69. Reduction cardiac size leads to
• Early appearance of click and murmur of MVP
• Murmur intensity show variable response

70. Amyl nitrate response useful in distinguishing
• Systolic murmur of AS(^)and MR(v)
• Systolic murmur of TR(^) and MR(v)
• Systolic murmur of PS(^) and TOF(v)
• Systolic murmur of PS(^) and VSD(v)
• Diastolic murmur of MS(^) and Austin flint(v)
• EDM of PR(^) and AR(v)

71. • In HOCM there an additional and earlier( 5 to
10 after inhaltion) augmentation of murmur
due to decrease in LV Vol and sys art pressure
with resultant increase in LVOT obstruction
• This earlier response helps in differentiating
HOCM from valvular AS where murmur
augmentation starts 15 to 20sec after
inhalation

72. METHOXAMINE AND PHENYL EPHRINE
• Increase systemic arterial pressure
• Reflex bradycardia and decreased contractility
and COP
• Contraindicated in CHF and HTN

73. • Methoxamine 3-5 mg IV increase arterial
pressure by 20-40 mm Hg with in 2-3 min
lasting for 30 to 40 min
• Phenylephrine 0.5mg IV elevates systolic
pressure around 30mm Hg for 3-5min
• Phenylephrine preferred due to shorter
duration action

74. • S1 reduced
• A2 becomes louder
• A2 OS prolonged
• S3 and S4 response variable
• Click of MVP occurs later and accentuated

75. Increase in arterial pressures cause following
murmurs louder
• EDM of AR and Austin Flint murmur
• PSM of MR
• VSD
• TOF
• Continuous murmurs of PDA and AVF

76. • Systolic murmur of HOCM softens(^ LV size)
• Click and murmur of MVP delayed(^ LV size)
Decrease in COP diminish
• ESM of AS
• Functional systolic murmurs
• MDM of MS

77. TRANSIENT ARTERIAL OCCLUSION
• Transient external compression of both
brachial arteries
• By bilateral cuff inflation to 20 mm Hg greater
than peak systolic pressure
• Augments the murmurs of MR, VSD, and AR

78. MS
Inspiration, Sudden standing
Dec pulmonary venous return, Reduces LAP
• MDM reduced
• OS softens
• A2-OS gap widen
• Three sequential sounds (A2, P2, and OS) may
be audible
• Exercise ,Squatting ,Amyl Nitrate, isometric
hand grip
MDM accentuated

79. • Valsalva maneuver may show square wave
response
• A2 OS interval directly related to R-R interval

80. MR
• Varies little with respiration
Decrease murmur
• Sudden standing
• Valsalva
• Amyl Nitrate
Augments the murmur
• Squatting
• Isometric Exercise

81. AS
Murmur increases on
• Post PVC beat
• squatting
• Lying flat from standing
Reduces AS murmur
• Valsalva
• Standing
• Handgrip
• Abnormal PR

82. AR
EDM increases on
• Expiration
• sitting up and leaning
forward
• Squatting
• Isometric exercise
• Vasopressors
Decreases with
• Amyl Nitrate
• Valsalva

83. MVP
Murmur and click
earlier(intensity
decreases)
LV Volume decrease
• Standing
• Valsalva
Murmur and click later
LV Volume increase
• Squatting
• Post ectopic
• Isometric Exercise
(intensity increases)

85. HOCM
Increase murmur in
• Expiration
• Valsalva strain
• Standing
• Post ectopic
• Amyl nitrate
Decrease murmur in
• Inspiration
• Sustained Handgrip
• squatting
• Methoxamine

86. • Valsalva strain following amyl nitrate in HCM
• In 20 to 30% of patients systolic murmur of
HCM remains unchanged after valsalva strain
• When valsalva strain is repeated after amyl
nitrate inhalation most of these pts will now
show augmentation
• This maneuver increases the sensitivity of
valsalva for diagnosing HOCM

87. Dynamic auscultation helpful in
• AS X HOCM squatting (^/v)
valsalva/standing (v/^)
• AS x MR handgrip (v/^)
phenyl ephrine (v/^)
post pvc (^/v)
amyl nitrate (^/v)

89. • MS X TS respiration
• MR X TR respiration
• MS X AUSTIN FLINT amyl nitrate(^/v)
• PS X AS respiration
• PS X Small VSD amyl nitrate (^/v)
phynylephrine (v/^)
respiration
• PR X AR squatting (_/^)
sus handgrip (-/^)

90. •Thank you