1. Dr.G.Gnanavelu Reader in Cardiology Madras Medical College, Chennai 3
DYNAMIC AUSCULTATION
Dr.G.Gnanavelu
Reader in Cardiology
Madras Medical College, Chennai 3

2. DEFINITION
‘Technique of altering circulatory dynamics by means of respiration and variety of physiological and pharmacological maneuvers and determining their effects on heart sounds and murmurs’

3. Auscultatory changes Spontaneously occur during Normal respiration
After premature beats,
long pauses
Myocardial ischemia
May be induced by maneuvers
Postural changes
Muller maneuver Valsalva maneuver
Isometric exercise
Vasoactive agents: Amylnitrite
Phenylephrine

4. 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

5. IMPORTANT REFLEXES INVOLVED IN DYNAMIC AUSCULTATION
RECEPTOR
RECEPTOR LOCATION
STIMULUS
SYMPATHETIC ACTIVITY
PARASYMPATHETIC ACTIVITY
Arterial Baroreceptor
Mechano receptor
Internal carotids and Aortic arch
Increased arterial pressure
Decreased
Increased
Bainbridge
Mechano
receptor
Venoatrial
Increased venous return

6. BARORECEPTOR FEEDBACK LOOP
Sudden decrease in arterial pressure (abrupt standing from supine position) decreases baroreceptor firing, activating sympathetic nerves and inhibiting parasympathetic nerves. This increases cardiac output and SVR which restores normal arterial pressure

7. Relationship between cardiac output, systemic vascular resistance,
mean arterial pressure and central venous pressure
MAP = (CO x SVR) + CVP
CO =
(MAP – CVP)
SVR
SVR =
(MAP – CVP) CO
Increasing SVR increases Mean arterial pressure at any given cardiac output, whereas decreasing SVR decreases MAP at a given cardiac output.

8. PRELOAD
AFTERLOAD
STROKE VOLUME
HEART RATE
INOTROPY

9. RESPIRATION Assess changes during normal respiration
Patient should be in semiupright or sitting posture
More pronounced & consistent alterations on murmur originating from right than from left side of heart
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.

10. POST PREMATURE VENTRICULAR CONTRACTION
Vent. Filling Cardiac
contractility

11. TRANSIENT MYOCARDIAL ISCHEMIA
Hemodynamic changes during spontaneous angina or induced by exercise:
Increase in LVEDP
Papillary muscle dysfunction
Reduced stroke volume
Increase in arterial pressure
Auscultatory changes:
Paradoxic splitting of S2 becomes obvious
S4 may develop during angina
Late or midsystolic murmur of Papillary muscle
dysfunction may appear or gets augmented

12. 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
leading to decreased stroke volume,
decreased mean arterial pressure &
decrease in heart size
followed by reflex increase in heart rate &
systemic resistance

13. 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

14. PROMPT SQUATTING Hemodynamic changes: Increase in venous return and
stroke volume
increase in mean arterial pressure
due to combined effect of increase in cardiac output and systemic vascular resistance due to acute compression of leg arteries

15. PROMPT SQUATTING
Examiner sits on a chair with stethoscope in place while patient is still standing to assess changes occurring within first few beats after squatting
In patients unable to squat, similar circulatory changes can be produced by bending patient’s knees on his abdomen in supine position

16. PRONE POSITION & KNEE CHEST POSITION
Pericardial friction rub becomes louder

17. 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

18. VALSALVA MANEUVER VALSALVA HEART RATE BLOOD PRESSURE MECHANISM Phase I
Onset of
strain
No change
Increases
Increased intrathoracic pressure compresses vessels within thorax producing abrupt increase in arterial pressure
Phase II
Maintenance
of strain
Increase
Systolic & Pulse pressure decrease
Followed by reduced venous return to right atrium leading to decreased cardiac output and systolic pressure. Carotid baroreceptors inhibit vagus nerve and stimulate vasomotor center. Reflex tachycardia and peripheral vasoconstriction result.
Phase III
Release of
Further decrease in blood pressure
Venous return and capacity of pulmonary bed increase abruptly. Arterial pressure further diminishes due to pooling in expanded pulmonary bed
Phase IV
Relaxation
Decrease
Overshoot of systolic pressure & pulse pressure increase
Accumulated venous return reaches left ventricle and increased stroke volume is pumped into constricted systemic vascular bed causing overshoot of arterial pressure. This overshoot is detected by the carotid sinuses resulting in excitatory effect on vagus nerve leading to reflex bradycardia

20. Phase 2 : used to distinguish systolic murmur of fixed vs dynamic LVOT obstruction. (HOCM vs AS). Most other murmurs decrease in intensity
Phase 4 : used to distinguish left sided from right sided murmurs. Right sided murmurs that decrease during phase 2 return to baseline intensity immediately after valsalva release. Left sided murmurs require five to ten cardiac cycles to return to baseline

21. VALSALVA MANEUVER Mechanical and reflex changes depend on
1. level of cardiac function and effective
central blood volume
2. speed and magnitude of baroreceptor
responses to change in arterial
pressure

22. SQUARE WAVE RESPONSE
Persistent elevation of systolic and diastolic pressure with no change in heart rate. There is no overshoot of blood pressure and no bradycardia when straining is stopped. Absence of bradycardia at the end of proceduce is the easiest sign to detect.
Occurs in congestive heart failure and atrial septal defect.

23. VALSALVA MANEUVER Apart from induced auscultatory changes
Used to assess
Autonomic function
Left ventricular function
Used to treat
Supraventricular tachycardias

24. 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

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

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

27. PHARMACOLOGICAL AGENTS
Commonly two agents are used
Amylnitrite - Vasodilator
Phenylephrine - Vasoconstrictor

28. AMYL NITRITE Patient in supine position; Perform baseline auscultation
0.3 ml ampoule of Amyl nitrite placed in gauze is crushed with gloved hand near patient’s nose
Warn patient that he will smell some vapors smelling like sweet almond or dirty socks
Patient takes three or four deep breaths over 10 to 15 seconds
Preferable to have another person to monitor systolic BP and call the level as drug takes effect
Patient remains in supine position till the effect wears off

29. AMYL NITRITE Hemodynamic changes:
Initial vasodilatation leading to reduction in systemic arterial pressure
Next 1- 2 mins. - Reflex tachycardia and venoconstriction lead to increase in cardiac output and velocity of blood flow

30. AMYLNITRITE vs NITROGLYCERIN
Both lead to reduction in BP due to systemic vasodilatation
Due to reflex tachycardia and venoconstriction Amylnitrite leads to increased venous return
Venous return falls with Nitroglycerine due to venodilatation

31. PHENYLEPHRINE Patient in supine position; Baseline auscultation
Dilute 10 mg vial of Phenylephrine in 250 ml of isotonic saline
0.3 to 0.5 mg IV over 30 sec. Alternately can be given as infusion 0.1 mg/min. infusion stopped once 20 mm Hg rise in BP occurs or when intensity of murmur clearly changes
It has shorter duration of action and elevates BP for only 3 – 5 mins.

32. PHENYLEPHRINE Hemodynamic changes:
Initial increase in BP for 3 – 5 mins.
Followed by reflex bradycardia and decreased contractility and cardiac output
Should not be used in CHF and Hypertension

33. ↓ ↑ IMPORTANT HEMODYNAMIC CHANGES IN MANEUVERS Venous return
Systemic resistance
Stroke volume
Cardiac output
Arterial pressure
Heart rate
Heart size
Standing ↓ ↑
Squatting
Valsalva
Phase II
Isometric
Exercise
Amylnitrite
Phenylephrine

34. RESPIRATION & SPLITTING OF S2
A P
A P
P A
EXPIRATION
INSPIRATION
NORMAL SPLIT
PARADOXICAL SPLIT
(LBBB, AS, HBP)
PERSISTING SPILIT (RBBB, PS)
FIXED SPILIT
(ASD)

35. Pulmonary vascular click (eg. PAH) – No change with inspiration
EJECTION SOUND S1 ES PA S1 ES AP
Aortic ejection sound
(no change with inspiration) S1 ES
A P S1 ES
A P
Pulmonic ejection sound
(decreases with inspiration)
Pulmonary vascular click (eg. PAH) – No change with inspiration

36. S4 S1 vs SPLIT S1 vs S1 ES Maneuver S4 S1 Split S1 S1 AES Respiration
S4 louder in expiration
Obvious during inspiration
No change
Sudden standing
S4 softer; moves closer to S1
Becomes single
Wider, No change in intensity
Lying with passive leg raising
S4 prominent, moves away from S1
Becomes wider

37. S2 OS vs SPLIT S2 Maneuver S2 OS Split S2 Respiration
OS softens & Triple sound sometimes during inspiration
S2 split wider during inspiration
Sudden standing
S2 OS widens
S2 split narrows

38. MITRAL REGURGITATION vs TRICUSPID REGURGITATION
SYSTOLIC MURMUR
MITRAL REGURGITATION vs TRICUSPID REGURGITATION

39. AORTIC STENOSIS vs MITRAL REGURGITATION vs HOCM
SYSTOLIC MURMUR
AORTIC STENOSIS vs MITRAL REGURGITATION vs HOCM
HANDGRIP/ SQUATTING
AMYLNITRITE
BASELINE
VALSALVA
AORTIC STENOSIS MR
HOCM

40. SYSTOLIC MURMUR OF HOCM & MVP
Strain phase of Valsalva
Murmur increases in intensity
Murmur longer but not louder
Amylnitrite
Murmur louder
No change in intensity
Post PVC
Increase in intensity and duration of murmur
Murmur remains unchanged or decreases
Standing
Click occurs earlier, intensity of murmur varies

41. HOCM Gradient and systolic murmur increase
Gradient and systolic murmur decrease
Standing/Squatting
Decrease in Preload
Increase in Preload
Isometric exercise/
Decrease in afterload
Increase in afterload
Contractility
Increase in contractility
Decrease in contractility

43. SYSTOLIC MURMUR PULMONARY STENOSIS vs TETRALOGY OF FALLOT
Maneuver
Pulmonary
stenosis
Tetralogy of
Fallot
Respiration
Augments
No change
Amylnitrite
Decreases

44. SYSTOLIC MURMUR SMALL VSD vs PULMONARY STENOSIS
Maneuver
Small VSD
Pulmonary stenosis
Amylnitrite
Decreases
Increases

45. Diastolic murmur Austin Flint vs Mitral stenosis
BASELINE
AFTER AMYLNITRITE AR MS
Both diastolic murmurs are low frequency; best heard with bell at LV apex in left lateral position.
Austin Flint : soft S1; prominent S3; Diastolic murmur of MS: Loud S1, High frequency OS

46. CONTINUOUS MURMUR VENOUS HUM Compression of neck veins,
Turning head to one side
PATENT DUCTUS ARTERIOSUS

47. Thank you