Third heart sound is a unique heart sound because its perfect physiology to hear it in the young , while the same may denote serious LV dysfunction in patients with myocardial disease.
It is a low pitched early diastolic sound usually correspond to the end of rapid filling phase.The mechanism of genesis of this sound has been debated for many years .(Still I think it is unsettled !)
We know genesis of intracardiac sound is contributed by three factors
- The blood flow
- The valve motion
- The myocardial contractile and relaxyl property
The above three is collectively called cardio-hemic system . When this system vibrates heart sounds are generated .In the genesis of S3 all the three may be important . The only difference is , in physiological S3 the valvular and hemic component play a major role . In pathological S3 the myocardial component has a pivotal role .The distended LV facilitates chest wall impact during the rapid filling phase . It is now accepted LV S3 is generated outside the LV . It was proved elegantly by Shaver et all with sound recording on either side of LV /Chest wall.
It is to be emphasized the mechanism of genesis of S3 is diagonally opposite in physiology vs pathological S3 in some conditions . Rapid AV filling can rarely be responsible for pathological S3 associated with severe LV dysfunction , while chest wall impact can contribute in both physiological as well as pathological S 3 .
One can understand the complexity of genesis of S 3 , as there are too many determinants that contribute in varying degree of acoustics.
Factors determining the intensity of S3 is complex
-
Age,
-
Atrial pressure,
-
Rapidity of flow across the atrio-ventricular valve,
-
Rate of early diastolic relaxation
-
Distensibility of the ventricle,
-
Blood volume,
-
Ventricular cavity size,
-
Diastolic momentum of the heart,
-
Degree of contact (coupling) with the chest wall, thickness
-
Character of the chest wall
-
The position of the patient.
It is ironical, pathological S3 which is a diastolic sound though , still its genesis is largely determined by the systolic function of the heart .This mystery is partially solved as we recognise now , LV S3 is equally common in severe degrees of diastolic dysfunction. In fact , while we were studying the relationship of LVS3 in DCM , it has strongly predicted the presence of severe restrictive pattern in them .
Reference
1.Multimedia of S3
http://www.inovise.com/learn/s3causes.html
2.Importance of S3 in cardiology NEJM 2001 article
http://www.nejm.org/doi/pdf/10.1056/NEJMoa010641
3.Chest wall impact theory of S3 by Shaver
Shaver JA, Salerni R. Auscultation of the heart. In: Hurst, ed. Heart. 8th ed. New York, NY: McGraw-Hill, Inc; 1994:291.
Dr.S.Venkatesan MD 