S3 and S4

Description of third and fourth heart sounds.

1. S3 and S4 DR ANIRBAN DUTTA MODERATOR- DR ARUN PRASATH, DM CARDIOLOGY

2. Introduction Low frequency Low amplitude Diastolic sounds Best heard at cardiac apex S3 can be normal or abnormal S4- mostly pathological

3. S3

4. Follows mitral valve opening and the onset of rapid ventricular filling Occurs near the end of rapid filling wave S3 related to forces during active rapid filling Rapid deceleration of blood during inflow to the left ventricle is translated into vibratory energy , resulting in S3 Physiology of S3

5. Contd …… Coupling of the left ventricle with the inner chest wall is directly related to the presence or absence of an audible S3. May be soft or loud Physiologic S3 is seen in young individuals.

6. Hemodynamics Rapid rate of early LV diastolic filling with normal to slightly elevated LA pressure with normal or increased cardiac output

7. Causes of S3 PHYSIOLOGICAL S3 DIASTOLIC OVERLOAD STATE LV DYSFUNCTION Children Left ventricle-MR,VSD,PDA CCF Young adults Dilated LV Hyperkinetic states with normal heart Right ventricle-TR,ASD Severe LV dysfunction

8. LV S3 vs RV S3 FEATURE LV S3 RV S3 Site Respiration Position Isometric hand grip Associated features Apex Expiration Left lateral Increases Left sided cause for S3 Left lower sternal border Inspiration Supine and passive leg raising No change Elevated JVP

9. Theories of S3 1. Valvular theory 2. Ventricular theory 3 Impact theory BUT, the most popular theory says that S3 originates from either right or left ventricle or their walls . The dynamic interplay between the force of delivery of blood into the ventricle and the ability of the ventricle to accept this flow is an important factor in the genesis of the sound

10. Force of impact and resulting intensity of the of S3 depend primarily on the size of the heart , motion of the heart within the thorax and chest wall configuration (Reddy et al) This explains S3 produced in high output states and conditions with increased end systolic volume secondary to LV dysfunction

11. Diastolic overload states Produced when increased volume of LA blood crosses the mitral valve in early diastole –MR,VSD,PDA In MR, S3 is characteristically early and high frequency simulating opening snap. The development of significant PAH will soften S3. IN RV failure right sided S3 can occur.

12. Left Ventricular Dysfunction S3 characteristic of global LV impairment. Elderly without MR with S3- reduced myocardial contractility. S3- soft Can disappear with improvement of LV function Persists on upright posture.

13. Coronary Artery Disease. S3 in the presence of CAD strongly suggests-major LV asynergy or LV aneurysm S3 gallop – decompensated hypertensive and aortic valve disease Loud S3 – typical of Dilated cardiomyopathy .

14. P ericarditis Early ,loud and high pitched (occurs before the normal s3 Pericardial knock – clicky or snappy Elevated left atrial pressures and a rapid rise of early ventricular diastolic pressure- nondistensible pericardium. In restrictive cardiomyopathy -early S3 with distinct high frequency component can simulate a pericardial knock.

15. S4

16. P hysiology Low frequency Follows left atrial systole Atrial contraction results in abrupt increase in LV end diastolic fiber length Although S4 is an atrial sound , but origin is ventricular. Results from sudden tensing of LV mass , the mitral valve appartus and blood within the ventricle.

17. Hemodynamics

18. Requisites for S4 Healthy atrium in sinus rhythm Non stenotic AV valve Non compliant non dilated LV ( ischaemia , infarction, concentric hypertrophy , restrictive myopathy and acute volume overload )

19. C auses Physiological-Elderly people above 60 years Pathological – All causes of concentric LVH- SHT , aortic stenosis , HOCM , restrictive cardiomyopathies . All causes of concentric RVH- PS,PAH, restrictive cardiomyopathies CAD- ischaemia or infarction Acute regurgitant lesions- AR,MR TR, prolonged PR interval

20. LV Outflow Obstruction Concentric LVH with reduction in ventricular compliance Gradient of atleast 50mmhg across the LV outflow Not applicable for HOCM In presence of severe AS associated with MS , S4 will be masked due to obliteration of pressure gradient across the aortic valve . S4 in AS is better palpable than audible.

21. RV Outflow Obstruction Prominent a wave with JVP > 15 cm RVEDP >12mmhg . RV S4 better heard than LV S4 In severe PS, S4 is relatively long and may simulate pre- systolic murmur of TS Inspiratory increase of S4 is accompanied by decrease / disappearance of ejection click of PS due to RVEDP exceeding pulmonary artery diastolic pressure

22. Coronary Artery Disease Clearly audible and palpable S4 Denotes diastolic dysfunction with LVEDP > 18 mm Hg Commonly seen in MI, ischaemia .

23. Mechanism of absent S4 in rheumatic MR Features Mechanism Chronic MR Dilated compliant LV Associated MS Force of atrial contraction cannot be transmitted to LV Atrial fibrillation Absence of atrial contraction Dilated unhealthy left atrium Atrium incapable of generating enough force

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