Heart sound: Difference between revisions

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* Increasing filling pressure
* Increasing filling pressure
* Reduced compliance (this may be the more important factor)
* Reduced compliance (this may be the more important factor)
An S<sub>3</sub> is associated with reduced prognosis among patients with [[heart failure]].<ref name="pmid11529211">{{cite journal| author=Drazner MH, Rame JE, Stevenson LW, Dries DL| title=Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 8 | pages= 574-81 | pmid=11529211
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=11529211 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>


===S<sub>4</sub>===
===S<sub>4</sub>===

Revision as of 13:50, 26 February 2010

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The location of the heart below the thoracic wall.

In medicine and the physical examination, heart sounds are the "sounds heard over the cardiac region produced by the functioning of the heart. There are four distinct sounds: the first occurs at the beginning of systole and is heard as a "lubb" sound; the second is produced by the closing of the aortic valve and pulmonary valve and is heard as a "dupp" sound; the third is produced by vibrations of the ventricular walls when suddenly distended by the rush of blood from the heart atria; and the fourth is produced by atrial contraction and ventricular filling."[1]

Normal heart sounds

A diagram of the cardiac cycle is available and helps understand the normal heart sounds.[2]

S1

S1, which originates from closure of the mitral and tricuspid valves is normally louder than S2 at the cardiac apex (fifth left intercostal space).[2][3]

The S1 is actually two sounds, closure of mitral (M1) and tricuspid (T1) valves. M1 precedes T1 by 20 to 30 msec. This physiologic splitting is best heard at the lower left sternal border (the tricuspid area). Intervals less than 30 to 40 msec may sound like a single sound.[4] Wide splitting over 60 msec may be heard if:

  • Delayed electrical activation of the right ventricle (Right bundle branch block)
  • Delayed closure of either atrioventricular valve (mitral stenosis or atrial myxoma)

Distinguishing a split S1 from a S4

Distinguishing a split S1 from a S4[5]
  Split S1 S4
Loudest location Triscuspid area
(lower left sternal border)		 Apex
(may be palpable)
Pitch Low
(Best heard with bell)
Interval 20 to 30 msec 50 msec or more[6]
Auscultation maneuvers Left sided S4 (most common type)
• Louder with increased systemic resistance (isometric hand grips)
• Quieter with decreased venous return (sitting or standing position)

More discussion is available online[5]; less experienced examiners will more often confuse these findings.[7]

S2

S2 is normally louder than S1 at the cardiac base (second left intercostal space).[8] "With quiet respiration, A2 will normally precede P2 by 0.02 to 0.08 second (mean, 0.03 to 0.04 sec) with inspiration."[9] Intervals less than 30 to 40 msec will sound like a single sound.<[4]

The S2 is composed of A2 and P2:

  • A2 originates from closure of the aortic valve
  • P2 originates from closure of the pulmonic valve, is best heard at the cardiac base (second left intercostal space), and is quieter than A2.
    • During expiration, A2 and P2 are perceived as a single sound in 90% of people.[10][11]
    • During inspiration, the interval between A2 and P2 lengthens ('splits') and may as long as 60 msecs.[11]

S3

About 10% of asymptomatic adults have an S3; it is more common in younger adults.[12] More discussion is available online.[13]

S4

About 15% of asymptomatic adults have an S3.[12] The S4 is best heard at the cardiac apex. More discussion is available online.[5]

Abnormal heart sounds

Until recently, studies of the pathophysiological correlations with abnormal heart sounds have only studied measures of systolic function.[14] More, recently, studies have included measures of diastolic function and have used multivariable analysis to study physiologic correlates.

S1

More discussion is available online.[2]

A loud S1 may be from:

  • Increased valve gradient mitral stenosis or atrial myxoma)
  • Increased valve flow (left-to-right shunts; high output)
  • Shortened diastole (tachycardia)
  • Short PR intervals (preexcitation syndrome)

S2

More discussion is available online.[9]

  • Fixed split S2 may be from:
  • Paradoxical split S2 may be from
    • Conduction abnormalities: left bundle branch block, artificial RV pacing, preexcitation of the RV
    • Hemodynamic abnormalities: aortic valve stenosis
  • Wide split S2 (> 40 or 50 msec) may be from
    • Conduction abnormalities: right bundle branch block, artificial LV pacing, and preexcitation of the LV
    • Hemodynamic abnormalities: pulmonary stenosis and pulmonary hypertension

S3

More discussion is available online.[13] An S3 can be due to:[15][16]

  • Increasing filling pressure
  • Reduced compliance (this may be the more important factor)

An S3 is associated with reduced prognosis among patients with heart failure.[17]

S4

More discussion is available online.[5] The presence of an S4 correlates with age, ventricular stiffness, and brain natriuretic peptide.[18] However, the S4 may be absent when diastolic dysfunction becomes severe.[19] Interpretation of these studies is hindered by definitions used for diastolic function.

References

  1. ↑ Anonymous (2024), Heart sound (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. ↑ 2.0 2.1 2.2 Felner JM (1990). “The First Heart Sound”, Walker HK, Hall WD, Hurst JW: Clinical methods: the history, physical, and laboratory examinations (in English), 3rd. London: Butterworths, 119. LCC RC71 .C63. ISBN 0-409-90077-X.  Library of Congress Cite error: Invalid <ref> tag; name "isbn0-409-90077-X-p119" defined multiple times with different content Cite error: Invalid <ref> tag; name "isbn0-409-90077-X-p119" defined multiple times with different content
  3. ↑ McGee, Steven R. (2007). “The First and Second Heart Sounds”, Evidence-Based Physical Diagnosis, 2nd. Philadelphia: Saunders, 418. ISBN 1-4160-2898-6. 
  4. ↑ 4.0 4.1 Felner JM (1990). “The Second Heart Sound”, Walker HK, Hall WD, Hurst JW: Clinical methods: the history, physical, and laboratory examinations (in English), 3rd. London: Butterworths, 125. LCC RC71 .C63. ISBN 0-409-90077-X.  Library of Congress PDF
  5. ↑ 5.0 5.1 5.2 5.3 Williams ES (1990). “The Fourth Heart Sound”, Walker HK, Hall WD, Hurst JW: Clinical methods: the history, physical, and laboratory examinations (in English), 3rd. London: Butterworths, 129. LCC RC71 .C63. ISBN 0-409-90077-X.  Library of Congress PDF
  6. ↑ Kino M, Shahamatpour A, Spodick DH (1976). "Auscultatory perception of the fourth heart sound: effects of interval form fourth to first sound (S4-S1) and aging.". Am J Cardiol 37 (6): 848-52. PMID 1266747.
  7. ↑ Jordan MD, Taylor CR, Nyhuis AW, Tavel ME (1987). "Audibility of the fourth heart sound. Relationship to presence of disease and examiner experience.". Arch Intern Med 147 (4): 721-6. PMID 3827460.
  8. ↑ McGee, Steven R. (2007). “Auscultation of the Heart: General Principles”, Evidence-Based Physical Diagnosis, 2nd. Philadelphia: Saunders, 415. ISBN 1-4160-2898-6. 
  9. ↑ 9.0 9.1 Felner JM (1990). “The Second Heart Sound”, Walker HK, Hall WD, Hurst JW: Clinical methods: the history, physical, and laboratory examinations (in English), 3rd. London: Butterworths, 122. LCC RC71 .C63. ISBN 0-409-90077-X.  Library of Congress PDF Cite error: Invalid <ref> tag; name "isbn0-409-90077-X-p122" defined multiple times with different content
  10. ↑ McGee, Steven R. (2007). “The First and Second Heart Sounds”, Evidence-Based Physical Diagnosis, 2nd. Philadelphia: Saunders, 422. ISBN 1-4160-2898-6. 
  11. ↑ 11.0 11.1 Harris A, Sutton G (November 1968). "Second heart sound in normal subjects". British heart journal 30 (6): 739–42. PMID 5718983. PMC 487796. [e] PubMed Central
  12. ↑ 12.0 12.1 Collins SP, Arand P, Lindsell CJ, Peacock WF, Storrow AB (2005 Sep-Oct). "Prevalence of the third and fourth heart sound in asymptomatic adults.". Congest Heart Fail 11 (5): 242-7. PMID 16230865.
  13. ↑ 13.0 13.1 Silverman ME (1990). “The Third Heart Sound”, Walker HK, Hall WD, Hurst JW: Clinical methods: the history, physical, and laboratory examinations (in English), 3rd. London: Butterworths, 126. LCC RC71 .C63. ISBN 0-409-90077-X.  Library of Congress PDF
  14. ↑ Marcus GM, Gerber IL, McKeown BH, Vessey JC, Jordan MV, Huddleston M et al. (2005). "Association between phonocardiographic third and fourth heart sounds and objective measures of left ventricular function.". JAMA 293 (18): 2238-44. DOI:10.1001/jama.293.18.2238. PMID 15886379. Research Blogging.
  15. ↑ Shah SJ, Marcus GM, Gerber IL, McKeown BH, Vessey JC, Jordan MV et al. (2008). "Physiology of the third heart sound: novel insights from tissue Doppler imaging.". J Am Soc Echocardiogr 21 (4): 394-400. DOI:10.1016/j.echo.2007.06.007. PMID 17658724. Research Blogging.
  16. ↑ Tribouilloy CM, Enriquez-Sarano M, Mohty D, Horn RA, Bailey KR, Seward JB et al. (2001). "Pathophysiologic determinants of third heart sounds: a prospective clinical and Doppler echocardiographic study.". Am J Med 111 (2): 96-102. PMID 11498061.
  17. ↑ Drazner MH, Rame JE, Stevenson LW, Dries DL (2001). "Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure.". N Engl J Med 345 (8): 574-81. PMID 11529211.
  18. ↑ Shah SJ, Nakamura K, Marcus GM, Gerber IL, McKeown BH, Jordan MV et al. (2008). "Association of the fourth heart sound with increased left ventricular end-diastolic stiffness.". J Card Fail 14 (5): 431-6. DOI:10.1016/j.cardfail.2008.01.010. PMID 18514937. PMC PMC2483506. Research Blogging.
  19. ↑ Meyers DG, Porter IT, Schneider KA, Maksoud AR (2009). "Correlation of an audible fourth heart sound with level of diastolic dysfunction.". Am J Med Sci 337 (3): 165-8. DOI:10.1097/MAJ.0b013e318182ee55. PMID 19282674. Research Blogging.

Bibliography

See also

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