AA

1. ADDED SOUNDS

3. The Opening Snap
• High-frequency
• Early diastolic sound
• Timing : usually occurs 0.03-0.15s after the S2
• Coincides with the full opening of the mitral valve
• Best heard :
– With the diaphragm of the stethoscope just medial to the cardiac apex
– intensity parallels of M1
– widely transmitted
• Causes
– Mitral and Tricuspid valve stenosis
– Excessive flow through the mitral valve in early diastole as in VSD,MR and thyrotoxicosis

4. The Opening Snap
Mechanism :
• It occurs in the presence of a thickened but mobile leaflets
• High atrial pressures
• High velocity flow across AV valves
• Margolies and Wolferth theory

5. The Opening Snap

6. • Timing : Major factors controlling the duration of isovolumic relaxation
• The pressure at which the aortic valve closes (near systolic pressure).
• The pressure in the LA at the time the mitral valve opens.

7. FACTORS DECREASING INTENSITY OF
OS
• Associated valvular disease.
• MR / AR / AS
• Decreased cardiac output
• Cardiac failure / PAH
• Extensive valve calcification

8. Factor affecting A2-OS interval
• Severity of MS
– Severe MS short A2-OS interval
• Associted valvular heart disease
– AS/ AR – Prolonged
– MR - narrow
• Increased LVEDP
– LV dysfunction– Long A2-OS
• Heart rate
– Bradycardia – Long A2-OS

9. Differentiating P2 and OS
• A triple second sound, in which the three
sounds are close enough together to sound
like a snare drum, implies that an OS is present
as the final component.
A2- P2 A2- OS
2ND component at
Apex
soft loud
inspiration louder softer
standing narrows wider

10. MS with ABSENT OS
• Severe MS with calcification of valve
• Congenital MS
• Associated valvular heart disease

11. Tumor plop
• It is high frequency early diastolic sound heard in left or
right atrial myxomas
• changes with body positions
• MECHANISM :
– arises from the diastolic prolapse of the masses across the AV
valve.
• Associated : diastolic murmur may be present.`

12. Pericardial knock
• Dominic J Corrigan in 1842
• QUALITY : High-pitched early diastolic sound
• Timing : 0.10- 0.12 sec after S2 , with the steep y descent of jugular venous
waveform
• MECHANISM :
– The sudden slowing of blood flow into the ventricle in early diastole that occurs when
the ventricle meets the rigid pericardial sac water hammer effect
– Sail flop phenomenon- sudden tautening of the pericardium sets in to vibrations of the
chambers
• CAUSES
– constrictive pericarditis

13. Pericardial Rub
• QUALITY : Very high pitched, leathery, scratchy in nature, to-and-fro
character. The sound seems very close to the ear
• Typically with three components
– one systolic [at the time of ventricular contraction]
– two diastolic [atrial systole and during rapid early diastolic filling].
• BEST HEARD : between the apex and sternum with the patient leaning
forward or in the knee–chest position holding breath after forced
expiration. Pressure with diaphragm increases intensity.

14. • MECHANISM : inflammation of pericardium causes the walls to rub
against each other with audible friction.
• CAUSES
– Pericarditis (Uremic, acute primary , postoperative , traumatic)
– acute phase of transmural MI
• D/D
– scratchy pulmonic ejection murmur heard in hyperthyroidism (Means-
Lerman sign).
– Superficial, scratchy ejection systolic murmurs in patients with Ebstein
anomaly- Sail sound
Pericardial Rub

15. Hammans crunch
QUALITY : series of crunching sounds synchronous with the cardiac cycles
• Mechanism : presence of air in the pericardium and mediastinum
• Best heard : over the precordium during ventricular systole in left
lateral position
• Causes :
– spontaneous mediastinal emphysema
– tracheobronchial injury
• Trauma
• medical procedures (e.g., bronchoscopy)
• proximal pulmonary bleb rupture.
– Boerhaave syndrome

16. CLICK

17. Ejection sounds
• QUALITY : High-pitched early systolic ejection event
• TIMING : 0.05 sec after S1 , coincides with upstroke of the
carotid pulse.
 Valvular- high pitched sound produced by snapping open of
the stenotic thickened semilunar valve
- Defining the level of RV or LV outflow tract obstruction
- EC disappear as the culprit valve loses its pliability over
time

18.  Vascular or root events- caused by the rapid & forceful ejection of
blood into the great vessels
 Mechanism
 Increased pressure beyond valve
 Increased flow across the valve
 Dialatation of vessel beyond the valve
• BEST HEARD : lower left sternal border than at the base of the heart
Ejection sounds

19. Valvular vs Vascular
Vascular click Valvular click
S2 intensity Loud Normal or diminished
Split Normal or narrow split Wide or reverse split
Palpable artery Often palpable impalpable

20. Aortic Valvular Ejection Sounds
• Mechanism :
– Inherent ability of the deformed valve to move.
– Coincident with the maximal excursion of the domed valve when its elastic
limits are met. Deceleration of the oncoming column of blood sets the
entire cardiohemic system into vibration
– The intensity correlates directly with the mobility of the valve
• TIMING :
– 20 to 40 ms after the onset of pressure rise in the central aorta
– coincident with the sharp anacrotic notch on the upstroke of the aortic
pressure curve
• BEST HEARD : widely transmitted and often heard best at the AA / apex.
• CAUSES :
– Nonstenotic congenital bicuspid valves
– entire spectrum of mild to severe stenosis of the aortic valve.

22. Significance
• Best audible in aortic area / apex [ mistaken for Loud S1]
• Constant
• Localises obstruction to the valve
• Occurs earlier as severity of stenosis increases.
• May be absent in calcified or immobile valve
• Absence of EC in child makes valvular AS unlikely.
• Persistance of EC in elderly indicates mild stenosis

23. Aortic vascular ejection sounds
• originate from the aortic root
• MECHANISM :
• CAUSES :
– Systemic hypertension
– aortic aneurysm
– aortic root dilatation owing to aortic regurgitation.
• TIMING : Occur later than aortic valvular ejection sounds
• BEST HEARD : Localized 3rd LLSB and poorly transmitted
• D/D : tricuspid valve closure sounds

24. Pulmonary Valvular Ejection Sounds
• Occur at the maximal excursion of the stenotic pulmonary valve
• Causes
– Mild to moderate pulmonary valve stenosis
– idiopathic dilatation of the pulmonary artery
• Localised to pulmonary area . Decreases in intensity with
inspiration
• Ab PEC :
– Severe pulmonary stenosis[PEC fused with the S1 ]
– Deep inspiration.

25. Mechanism of respiratory variation of PEC
• During inspiration RVEDP > PA diastolic pressure
• This produces upward movement of the valve prior
to ejection
• Partically open valve undergoes less excursion prior
to ejection producing soft sound

26. Pulmonary vascular ejection sounds
• Dilatation of the pulmonary artery
– Idiopathic
– severe pulmonary hypertension
• BEST HEARD : Second and third left intercostal spaces
• TIMING : coincide with the complete opening of the
pulmonary valve and occur during the upstroke of the
pulmonary artery pressure recordings
• may not vary substantially during the phases of respiration.

27. EC VS SPLIT S1
S1 - EC Split S1
Best heard PA /AA Apex
Standing intensifies No change
Inspiration softens No change

28. Non ejection click
• QUALITY : Sharp, high-frequency, clicking
• Best over: cardiac apex with the diaphragm, but
can be transmitted widely
• Mechanism : Tensing of the atrioventricular
valves during systole.
• Asso : systolic murmur may or may not follow the
click
• Causes :
– MVP
– Left ventricular aneurysm
– Aneurysm associated with ventricular septal defects

29. • Timing :
– Occur after the upstroke of the carotid pulse
– Variation results from prolapsing of the different areas of the large,
redundant, scalloped mitral leaflets at different times
– Midsystolic clicks occur at the time of maximum prolapse
• Valvuloventricular disproportion: ventricular volume or dimension
associated with prolapse of the valve [click dimension] is relatively fixed
in a given patient.
• Determinants of S1-NEC interval : Ventricular ED volume and rate of
ejection
Non ejection click

30. • S1-click interval and the relative proportion of systole occupied
by the regurgitant murmur vary with maneuvers
• Smaller ventricle - chordae long and redundant – leaflets loose
support and prolapse into atrium
Non ejection click

31. • HCM
• After the upstroke of the carotid pulse
• May result from the contact of the anterior leaflet with the
septum or from the deceleration of blood flow in the left
ventricular outflow tract
• Interval does not change with maneuvers
Pseudo-ejection click

32. Prosthetic Valve Sounds
• Vary depending on the type of valve, its position, and whether or not it is
functioning normally.
• Starr-Edwards
– the loudest
– most distinctive opening and closing clicks
• Aortic position – OC 0.06 to 0.07 seconds after S1
-- coincident with maximal ball excursion
• multiple early systolic clicks - freely moving ball bouncing against the cage
during early systolic ejection
• OC/CC > O.5
• Decrease in intensity of these clicks can occur with valve obstruction or LV
dysfunction
• Mitral position - a prominent opening click occurs 0.05 to 0.15
seconds after A2
• Narrowing of this interval indicates an elevation of left atrial
pressure, which can be caused by either relative MS or MR.

33. • Tilting-disk
– Distinct closing sounds
– Easily heard in both aortic and mitral positions
• softer sound
– Valve dysfunction
– Conditions causing the disk to move to a partially closed position before
the onset of ventricular contraction- LV dysfunction, first-degree AV block
• Tissue prosthetic valves are more similar to normal heart sounds
• Mitral opening sound is audible in approximately 50% of patients at
an interval of 0.07 to 0.11 second after A2.
Prosthetic Valve Sounds

34. Prosthetic Valve Sounds

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