1. DYNAMIC AUSCULTATION FOR CARDIAC MURMURS
Dr. Benny J. Panakkal
Senior Resident
Dept. of Cardiology
Govt. Medical College
Kozhikode.

2. RESPIRATORY VARIATION MULLER MANEUVER VALSALVA MANEUVER
SUSTAINED HANDGRIP
POSTURAL CHANGES
POST – VPC / LONG DIASTOLE OF AF
PHARMACOLOGICAL MANEUVERS – AMYL NITRITE
PRESENTATION OUTLINE

3. RESPIRATORY VARIATION

4. RESPIRATORY VARIATION
INSPIRATION
1. Normal inspiration → dilatation of pulmonary vascular system and ↑ venous return to right side of the heart → frank-starling mechanism → ↑ stroke volume 2. ↑ stroke volume also aided by ↓ RV outflow impedance 3. Respiratory variation most marked in sitting and standing position 4. Normal or slightly deep breaths allowed. Very deep respirations → Partial Valsalva phenomenon
RESPIRATORY VARIATION
Muller's is exaggerated normal respiration

5. RESPIRATORY VARIATION
MULLER MANOEUVRE
Methods to elicit
Close nose with finger in mouth → suck the finger with closed glottis
Suck on a mouthpiece hooked to mercury manometer for 10 secs at mm Hg negative pressure
Increases right heart flow for longer periods compared to respiration
All right sided events ↑ with inspiration
Except pulmonary ejection click
RESPIRATORY VARIATION

6. PULMONARY EJECTION CLICK
• In inspiration → ↑ RV preload → ↑ RV end-diastolic pressures → pulmonary valve may partially open up just BEFORE systole → ↓ overall excursion of the pulmonary valve → reduced intensity of ejection sound
• PAH – RV end-diastolic pressures still remain considerably lower than pulmonary artery diastolic pressures, hence the ejection click variation with respiration is absent
Different pathologies → different variations
Pulmonary valve stenosis and idiopathic dilatation of pulmonary arteries → ejection click varies with respiration
PAH – ejection click does not vary with respiration
RESPIRATORY VARIATION

7. RESPIRATORY VARIATION
EXPIRATION
Normal expiration → ↓ lung volume → ↑ pulmonary venous flow
Therefore, left sided murmurs are loudest during expiration and diminish or remain unchanged during inspiration
THE SECOND HEART SOUND DURING RESPIRATION
Widening of normal splitting of second heart sound (wide variable splitting)
Delayed electrical activation – RBBB
Prolonged mechanical systole – Pul. Stenosis
Prolonged hangout interval – Idiopathic dilatation of Pulmonary Artery
RESPIRATORY VARIATION

8. THE SECOND HEART SOUND DURING RESPIRATION
Wide fixed splitting (ASD)
Pulmonary impedance is almost minimum to incorporate the ↑ pulmonary blood flow → inspiration therefore does not cause a further fall in impedance and hence does not cause a further separation of A2 and P2 → thereby appearing fixed
Paradoxical splitting of S2
Inherently delayed A2 component due to
Delayed electrical activation – LBBB
Delayed mechanical systole – Aortic Stenosis
RESPIRATORY VARIATION

9. RESPIRATORY VARIATION
VALSALVA MANOEUVRE
Forced exhalation against a closed glottis
As if to have a bowel movement
Examiner places a hand on the patient’s abdomen to make sure the abdominal muscles are tightened
Alternative method – blow into a mercury manometer to maintain a pressure of ≥ 40 mmHg
Usually continued for around 10 secs
If done for > 10 secs, chance of syncope
Make sure patient isn’t blowing using his cheeks → false negatives
RESPIRATORY VARIATION

10. RESPIRATORY VARIATION
PHASES
Phase I
Strain phase – blood squeezed from the lung into the left heart → transient ↑ in SBP
Subsequent ↓ in right sided cardiac output → ↓ left sided cardiac output → ↓ SBP
Sympathetic stimulation with vasoconstriction and tachycardia
Phase II
Release of strain → ↑ right sided blood flow → followed gradually by ↑ left sided blood flow
Right sided murmurs ↑ in 1-4 cardiac cycles, left sided ↑ by cardiac cycles
Overshoot of SBP due to previous sympathetic stimulation and vasoconstriction → reflex bradycardia
RESPIRATORY VARIATION

11. RESPIRATORY VARIATION
ABNORMAL PHASES
If absent overshoot → suspect
Mild LV dysfunction
Autonomic failure
If absent ↓ in SBP during strain phase
Overt CCF
Large L → R shunt
Transient ↓ in coronary blood – contraindicated in k/c/o myocardial ischemia or recent infarction
RESPIRATORY VARIATION

12. RESPIRATORY VARIATION
EFFECTS
All murmurs, both left and right sided → ↓ in intensity : except
Mitral Valve Prolapse (MVP)
↓ LV volume → earlier leaflet prolapse → ↑ intensity and duration of murmur
Manoeuvre is unreliable → not to be completely relied upon → variable responses obtained
Hypertrophic obstructive cardiomyopathy (HOCM)
Dynamic obstruction → ↑ with a ↓ in LV volume
Highly specific but not very sensitive sign
RESPIRATORY VARIATION

13. MITRAL STENOSIS – AN EXCEPTION FOR VALSALVA MANOEUVRE
Valsalva causes an overall ↓ in left sided cardiac output → works towards ↓ing the intensity of MS murmur Ensuing tachycardia → incomplete emptying of the LA → backlogging and elevated LA pressures → ↑ in LA-LV gradient → works towards ↑ing the intensity of MS murmur Above to mechanisms cancel each other out → hence, no change in MS murmur
RESPIRATORY VARIATION

14. VALSALVA FOR DIFFERENTIATING A2 AND P2
During strain phase → both A2 and P2 are diminished in intensity During release phase →P2 first returns to baseline intensity, followed later by A2
RESPIRATORY VARIATION
If fixed paradoxical split is present, can be found out by this method.

15. SUSTAINED HANDGRIP

16. METHOD Squeeze examiner’s fingers with one or both hands
Calibrated dynamometer
Duration
Minimum of secs must elapse before a significant change in BP and heart rate is observed
Avoid concomitant Valsalva manoeuvre
SUSTAINED HANDGRIP
Parameter
Handgrip
Dynamic exercise
Heart rate ↑
↑ ↑ ↑
Cardiac output
SBP

17. EFFECTS Systemic vascular resistance
Changes only if strain applied is > 50% of patient’s maximum.
EFFECTS
↑ LV filling pressures
Augmented LV S3 and S4
Systemic vascular resistance
Changes only if strain applied is > 50% of patient’s maximum.
Further, ↑ LV filling pressures AND Augmented LV S3 and S4 seen in patients with LV dysfunction apart from ↑ in heartrate, CO and SBP.
Murmurs that are augmented AR MR
MVP (MR)
VSD
SUSTAINED HANDGRIP

18. EFFECTS Murmurs that are reduced in intensity or show no change AS
HOCM → variable response → hence not a very useful manoeuvre in this condition
Reason for variable response in HOCM
↑ SVR tends to ↓ the gradient
Tachycardia tends to ↑ the gradient
SUSTAINED HANDGRIP
CANCEL EACH OTHER OUT

19. EFFECTS IN rheumatic mitral stenosis
Tachycardia → incomplete LA emptying → ↑ LA filling pressures → ↑ LA-LV gradient → augmentation of murmur
Helps distinguish between OS and S3/pericardial knock
OS moves closer to A2
S3/pericardial knock does not change position
SUSTAINED HANDGRIP

20. POSTURAL CHANGES

21. PHYSIOLOGY Supine to standing → changes similar to Valsalva manoeuvre
Standing ≈ Valsalva
Squatting ≈ opposite of Valsalva
The quicker the change in posture, the more dramatic the change in murmur
Squatting
Compression of femoral arteries → ↑ mean aortic pressure → ↑ afterload
Compression of leg veins and abdomen → ↑ venous return → ↑ preload
For those unable to perform squatting → passive flexion of both legs towards abdomen in supine position mimics squatting mediated hemodynamic changes.
POSTURAL CHANGES

22. EFFECTS Standing – all cardiac murmurs ↓ in intensity
Except HOCM and MVP
Changes similar to Valsalva → ↑ on standing
Postural change from supine to standing → venous pooling → ↓ stroke volume → reflex tachycardia and ↑ in SVR
Respiration
Valsalva
Handgrip
Postural change
POSTURAL CHANGES
Require an intact and functioning autonomic nervous system to manifest effects on murmurs.
∴ in chronic CCF, these manoeuvres are not useful.
So are the physical changes in these maneuvers.

23. POST-VPC / LONG DIASTOLE IN AF
No active patient cooperation required
Intactness of ANS not required

24. POST-VPC / LONG DIASTOLE IN AF
PHYSIOLOGY
Effects observed 1. ↑ preload → frank-starlings law → ↑ contractility 2. ↓ aortic diastolic pressure
POST-VPC / LONG DIASTOLE IN AF

25. POST-VPC / LONG DIASTOLE IN AF
EFFECTS
Aortic stenosis (valvular, supravalvular and discrete subvalvular)
↑ forward flow
↑ gradient between LV and aorta
↑ intensity of the murmur
HOCM
Variable effects due to opposing influences of (↑ preload) and (↑ contractility with ↓ aortic impedance)
Also, associated MR murmur may interfere with intensity estimation
POST-VPC / LONG DIASTOLE IN AF

26. POST-VPC / LONG DIASTOLE IN AF
EFFECTS
Mitral regurgitation
No change in intensity
↑ preload and contractility is compensated by ↓ afterload, thereby preferentially pushing the extra volume of blood into the aorta rather than the LA
There still is an ↑ regurgitant flow into the LA in the isovolumetric contraction phase of LV
However, the regurgitant flow in the later part of systole to LA is ↓
Why TR murmur does not follow the same principles of MR?
↓ afterload after a VPC is a feature specific for the systemic circulation
Further, the pulmonary circulation is already a very low impedance circulation, hence any further drop in the RV afterload would be clinically subtle, it at all present.
POST-VPC / LONG DIASTOLE IN AF

27. PHARMACOLOGICAL MANEUVERS
AMYL NITRITE INHALATION

28. AMYL NITRITE INHALATION
PHYSIOLOGY
Method
Hold ampoule in a tissue wrap near the patient’s nose and mouth
Break ampoule and ask patient to take 3 deep breaths
Actions
Onset – within 15 secs
Duration – 30 secs
BP returns to normal in 1-2 minutes
Reflex tachycardia occurs by secs after inhalation
AMYL NITRITE INHALATION

29. AMYL NITRITE INHALATION
EFFECTS
↓ afterload Initial ↓ in preload Reflex tachycardia → ↑ in stroke volume
AMYL NITRITE INHALATION
Initially, no increase in stroke volume

30. AMYL NITRITE INHALATION
EFFECTS
All LVOT systolic murmurs ↑ in intensity
Aortic stenosis
Valvular
Supravalvular
Discrete subvalvular
HOCM
Aortic regurgitation murmurs → softens
MR murmur
Decreases in intensity
CONTRAST WITH POST VPC STATE
AMYL NITRITE INHALATION
•In post-VPC state, there is ↑ in preload and ↓ in afterload. If the afterload had remained the same, the absolute regurgitant volume (which translates as the flow) through mitral valve would have ↑. But since there is also a ↓ in afterload, the amount of extra volume that needed to be regurgitated to LA gets diverted to the aorta. The effect of ↑ in preload gets cancelled out by the effect of ↓ in afterload and hence the intensity of the MR murmur does not change.
•In amyl nitrite inhalation, there is primarily a ↓ in afterload with a ↓ in preload. Supposing the afterload had remained the same, the ↓ in preload itself would have reduced the regurgitant volume and hence the intensity of murmur. But here, the ↓ in afterload further decreases the regurgitant volume and hence the intensity of murmur.

31. CONGENITAL HEART DISEASE
VSD
PDA
TOF
Differentiating PS with intact ventricular septum vs. TOF with PS
PS murmur increases while the latter decreases
Differentiating between valvular MS vs. Austin Flint murmur
MDM of valvular MS increases while the latter decreases
AMYL NITRITE INHALATION
Murmur intensity decreases because the ↓ systemic vascular resistance ↑ the flow through the systemic circulation and ↓ the flow through the shunt
↓ in pulmonary flow murmur due to ↑ in R→L shunt

32. THANK YOU