ADDED SOUNDS.pptx

AA

1. ADDED SOUNDS

2. The Opening Snap H igh-frequency E arly diastolic sound Timing : usually occurs 0.03-0.15 s after the S 2 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

3. 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

4. The Opening Snap

5. 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.

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

7. 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 Brad y cardia – Long A2-OS

8. 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 2 ND component at Apex soft loud inspiration louder softer standing narrows wider

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

10. 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 presen t.`

11. Pericardial knock Dominic J Corrigan in 1842 QUALITY : High-pitched early diastolic sound Timing : 0. 10 - 0.1 2 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

12. 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.

13. 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

14. Hammans crunch QUALITY : series of crunching sound s 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

15. CLICK

16. 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

17. 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

18. 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

19. 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.

20. 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

21. 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 3 rd LLSB and poorly transmitted D/D : tricuspid valve closure sounds

22. 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 S 1 ] Deep inspiration.

23. 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

24. 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.

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

26. 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

27. 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

28. S 1 -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

29. HCM After the upstroke of the carotid pulse M ay 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

30. 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 S 1 -- 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 M itral position - a prominent opening click occurs 0.05 to 0.15 seconds after A 2 Narrowing of this interval indicates an elevation of left atrial pressure, which can be caused by either relative MS or MR .

31. 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 A 2 . Prosthetic Valve Sounds

32. Prosthetic Valve Sounds

33. THANKYOU