Heart sounds are produced from a specific cardiac event such as closure of a valve or tensing of a chordae tendineae heart sounds are discrete short audible events from a specific cause different from a heart murmur ID: 1043253
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1. HEART SOUNDS Akhil Suresh
2. Heart sounds are produced from a specific cardiac event such as closure of a valve or tensing of a chordae tendineae.
3. heart sounds are discrete, short audible events from a specific cause — different from a heart murmur.
4. The main normal heart sounds are the S1 and the S2 heart sound. The S3 can be normal, at times, but may be pathologic. S4 heart sound is almost always pathologic
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7. INTENSITY Heart sounds can be described as increased in intensity (loud), decreased in intensity (soft) or absent
8. PITCH Heart sounds can be described as high pitched (heard best with the diaphragm of the stethoscope).
9. POSITIONThe location of the heart sound can help determine the etiology. The standard listening posts (aortic, pulmonic, tricuspid and mitral) apply to both heart sounds and murmurs.
10. the S1 heart sound — consisting of mitral and tricuspid valve closure — is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts
11. TIMING The timing can be described as during early, mid or late systole or early, mid or late diastole.
12. S1Low pitched Heard at the start of systole Precedes carotid pulse Louder at the apex Longer than S2
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14. S1 The first heart sound results from the closing of the mitral and tricuspid valves. The sound produced by the closure of the mitral valve is termed M1, and the sound produced by closure of the tricuspid valve is termed T1.
15. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates to all cardiac listening posts (loudest at the apex) T1 is usually only heard at the left lower sternal border. This makes the M1 sound the main component of S1.
16. The M1 sound occurs slightly before T1. Because the mitral and tricuspid valves normally close almost simultaneously, only a single heart sound is usually heard20 to 30 ms
17. 40% to 70% of normal individuals — as well as in certain cardiac conditions — a “split S1” sound can be appreciated. This occurs when the mitral valve closes significantly before the tricuspid valve, allowing each valve to make a separate audible sound.
18. Inspiration delays the closure of the tricuspid valve in a normal persondue to increased venous returnthereby enhancing the splitting of the S1 sound.
19. SPLIT S1right bundle branch block ventricular tachycardiapremature ventricular contractions
20. RBBBelectrical impulse reach the left ventricle before the right ventricle. Dyssynchrony occurs, resulting in the left ventricle contracting before the right ventriclethus the pressures in the LV rise before that of the right ventricle.
21. This delays the closure of the tricuspid valve, resulting in a split S1 sound.
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23. the electrical impulse reaches the RV before the LV thus the pressure in the RV rises before that of the LV. This forces the tricuspid valve to closed early
24. This results in complete overlap of M1 and T1, and thus no audible split S1 sound
25. RBBB results in a widened split S1, whereas a LBBB results in the absence of a split S1
26. Intensity of S1 Four factors affect the intensity of the first heart sound. Because the M1 portion of S1 is much louder than T1, it is important to discuss what affects the intensity of M1
27. Chest wall thicknessIndividuals with obesity will have a soft S1 thinner people will have a more intense S1.
28. The greater the distance separating the leaflets of the mitral valve at the beginning of systole, the louder the S1 this is affected by the duration of the PR interval on the ECG
29. Length of PR interval PR interval represents part of diastole longer PR interval would result in a longer diastolic filling time.
30. As the LV fills, the pressure gradually increases. This gradual increase in pressure causes the mitral valve leaflets to slowly drift together
31. when ventricular systole occurs in the setting of a long PR interval, the leaflets will be separated by a smaller distance the S1 sound will be softer
32. A short PR interval results in an accentuated S1the mitral valve leaflets will be further apart at the onset of ventricular systole
33. Valve leaflet mobility In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, resulting in an accentuated M1 sound
34. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.
35. Ventricular contraction rateThe faster the heart rate and the faster the rise in ventricular pressure, the louder the S1
36. high flow states such as anemia, thyrotoxicosis or sepsis would result in an accentuated S1. during exercise or any other setting of tachycardia, the S1 will be accentuated.
37. Absent S1
38. S2High pitched Louder at the base Shorter in duration Heard at the end of systole Follows carotid pulse
39. S2The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2.
40. The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heartA2 radiates to all cardiac listening posts (loudest at the right upper sternal border), and P2 is usually only heard at the left upper sternal border
41. the A2 sound is the main component of S2.A split S2 is best heard at the pulmonic valve listening post, as P2 is much softer than A2.
42. S2 is physiologically split in about 90% of people. The S2 heart sound can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting or the absence of splitting
43. The S2 heart sound intensity decreases with worsening aortic stenosis due to immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all
44. Physiologic split Normally, A2 occurs just before P2, and the combination of these sounds make up S2. A physiologic split S2 occurs when the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately
45. Inspiration increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect)decreased return to the left side of the heart hastens the closure of the aortic valve (minor effect), thereby further separating A2 and P2
46. Expiration the distance narrows, and the split S2 is no longer audible.
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48. Paradoxical split paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspirationopposite of the physiologic split S2
49. any setting that delays the closure of the aortic valve severe aortic stenosis hypertrophic obstructive cardiomyopathyleft bundle branch block.
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52. Persistent splitA2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration (due to increased venous return) and less prominent with expiration
53. Any condition that causes a nonfixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2
54. RBBBpulmonary hypertension pulmonic stenosis (delayed P2) severe mitral regurgitation/ventricular septal defect (early A2 closure).
55. RBBBdelay in the closure of the pulmonic valve, and thus a delay in P2, without any effect on A2
56. Mitral regurgitation due to a large proportion of the left ventricular stroke volume entering the left atriumthe left ventricular pressure decreases fasterEarly A2 closure
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58. VSD large proportion of the stroke volume goes into the RV, similarly decreasing LV pressure quickly
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60. The P2 is not affected in severe MR or VSD unless pulmonary hypertension is present
61. Fixed SplitA fixed split S2 is a rare finding on cardiac exam; however, when found, it almost always indicates the presence of an atrial septal defect
62. A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve, and there is no further delay with inspiration
63. During inspiration, as usual, there is an increase in venous return to the right side of the heart and thus increased flow through the Pulmonic valve — delaying its closure
64. The alteration in a person with an ASD occurs during expiration. As the person expires, the pressure in the right atrium decreases because there is less venous return
65. The decreased pressure allows more blood to flow abnormally through the ASD from the high pressured left atrium to the right atriumresulting again in increased flow through the pulmonic valve — again, delaying its closure
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67. fixed split S2 is pathognomonic for the presence of an ASD
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