The first heart sound (S1) signals the onset of left ventricular contraction. It consists of two major audible components - M1 from mitral valve closure and T1 from tricuspid valve closure. The intensity of S1 depends on factors like the PR interval, left ventricular contractility, and the mobility and stiffness of the mitral valve leaflets. A short PR interval, increased LV contractility, or stiff mitral valves can result in a loud S1. Long PR intervals, impaired LV function, or mobile mitral valves produce a softer S1. Abnormal splitting of S1 can occur due to electrical delays or asynchrony of ventricular contraction from conditions like RBBB. The relationship between mitral

1. The First Heart Sound
LUB
Dr. Varun V

2.  “The rubbery mass of the heart muscle which from a physical stand point seems like an
ideal sound deadening substance, apparently gives of no audible vibrations. Its
contraction or filling or even its forceful impact against the chest wall contributes
nothing to the heart sound. The fact that audible vibrations can be obtained from thin
strips of muscle isolated from the ventricle is of no significance, for it is easy to produce
sounds with a thin rubber band but almost impossible with a rubber ball as thick walled
as the heart.”
 William Dock, M.D 1938

3.  The first heart sound signals the onset of left ventricular contraction and consists
of two major audible components (M1 and T1) and two inaudible components.
 The first inaudible low frequency vibrations coincide with the beginning of the LV
contraction and are muscular in origin.
 It is followed by high frequency audible M1 and T1 components, which are
produced due to the closure of mitral and tricuspid valves (William Dock)
 The last inaudible low frequency vibrations coincide with opening of the
semilunar valves with ejection of blood into the aorta and the pulmonary trunk.

4.  However, electrical initiation of LV systole begins 50 to 60 msec before S1 is
heard.
 LV pressure rises above LA pressure well before forward flow across the mitral
valve ceases & valve leaflets have reached their maximally closed position.

5. Mechanism of first major audible vibration of S1

6. Luisada Theory
 Onset of isovolumetric contraction results in prominent tensing of LV walls,
septum and mitral valve apparatus, which produces a sound transient.
 He was against the term M1.

7. Criage and Leatham
 First major component of S1 (M1) is coincident with the maximal closing
excursion of mitral cusps.
 M1 reflects the sudden tensing of the closed mitral leaflets which sets the
surrounding cardiac structures and blood into vibration.

8.  Most, but not all, echophonocardiographic studies indicate that Mitral
valve closure (M1) coincides with first major recordable sound of S1.

9. Mechanism of second major audible vibration of S1

10. Luisada and Shaver Theory
 The second major audible vibration of S1 is an ejection component
coincident with opening of the Aortic valve.

11. Craige and Leatham
 They have obtained echophonocardiograms confirming coincidence of
tricuspid valve closure (T1) with the second component of S1

12.  Most investigators concur that the last recordable component of S1
coincides with onset of ejection into the Aorta.

13. Factors Affecting Intensity of S1

14. PR interval
 Short PR interval results in late Mitral valve closure and a loud S1.
 When PR is short, LV isovolumetric systolic pressure is high at the time of LV-
LA pressure crossover, causing more rapid mitral valve closing motion and
loud S1.
 Maximal intensity of S1 occurs at a PR interval range of 80 to 140 msec.
 PR interval >200 msec results in soft S1 as the Mitral valve has already closed
prior to development of LV pressure.

15. LV Contractility
 The more vigorous the LV contraction, the louder the S1.
 Depressed LV contractilty and a decreased rate of LV pressure
development will result in a decreased intensity of S1.
 Hyper-adrenergic states like excitement, fever or exercise commonly
increases S1 amplitude.
 In general, position of mitral valve leaflets at end-diastole and their closing
velocity are more important than the state of LV contractility.

16. Mitral Leaflets and Left Ventricle
 Mobile but abnormally stiff mitral valve leaflets such as those found in
Mitral Stenosis, produce a loud S1, unless they are severely distorted,
calcified or fibrotic.

17. How to listen to S1?

18. Timing
 S1 should be timed simultaneously with palpation of the carotid pulse or
apical impulse.
 S1 immediately precedes the palpable carotid arterial upstroke.
 It will appear to initiate the outward LV thrust of apex beat.

19. Characteristics
 S1 is of medium to high frequency.
 Usually lower pitched than S2.
 S1 splitting is better detected medial to the apex or at the left lower
sternal border.
 T1 is usually softer at the apex and louder at the lower left sternal border.

20.  S1 is usually not prominent at the base.
 Splitting of S1 is best detected in expiration.
 T1 more prominent with inspiration.
 When apparent splitting of S1 is heard at the base, one should suspect
presence of an ejection sound or early mid-systolic click.

21. Ejection Click vs. Split S1
 Ejection click is usually more intense than T1.
 Ejection click is better hear at the base.
 Aortic click is best heard at the apex.
 Pulmonic ejection click will vary with respiration if caused by pulmonic
stenosis.

22. S1 vs. S4
 S4 is usually audible at the apex mostly in left lateral position.
 S4 is not heard in left lower sternal border where splitting is best detected.
 S4 may vary in intensity with respiration.

23. Abnormalities of S1

24. Increased intensity of S1
 Short PR interval such as in WPW and Lown-Ganong-Levine syndrome.
 It may equal or exceed the intensity of S2 at the base.
 Loud S1 is often associated with a hypertrophied, non-compliant left
ventricle, because of elevated LVEDP that causes a late and abrupt
acceleration of mitral valve closure.
 Mitral valve prolapse with early or holosystolic prolapse, S1 may be very
loud.

26.  Mechanism of loud S1 is in Mitral Stenosis.
 Persistently elevated LA pressure in late diastole allows ventricular pressure to
rise considerably higher than normal during isovolumetric systole.
 A wide closing excursion of mitral valve leaflets, which are held open deep
within the left ventricle during late diastole, resulting in delayed M1 and may
follow T1.
 The stiff, noncompliant leaflet and chordal tissue probably resonate with an
increased sound amplitude.

27.  Left Atrial Myxoma
 S1 may be loud and delayed due to obstructing tumor which results in
elevated LA pressure as it keeps the mitral valve cusps apart in late diastole.

28. Decreased intensity of S1
 Long PR interval
 Audible reduction in S1 amplitude occurs at PR intervals > 0.16sec.
 S1 is markedly attenuated with a PR > 0.20sec.
 Impaired LV function with depressed rate of rise of isovolumetric pressure.
Thus S1 is soft in AR, MR and CCF.
 Cardiomyopathy, Myocarditis, Myxedema, Ventricular aneurysm – reduced
myocardial contractility hence soft S1.

29.  In acute AR a markedly elevated LVEDP results in premature closure of Mitral
Valve, thus reducing the intensity of S1
 S1 intensity is usually decreased in LBBB, in part because of reduced LV
contractility and in part because of the delay in onset of LV contraction.
 M1 may follow T1 in patients with LBBB

31. Abnormal Splitting of S1
 Wide splitting of S1 can result from an electrical delay in ventricular activation
which results in asynchrony of contraction.
 RBBB, PVC with RBBB configuration and LV pacing have been associated with
prominent splitting of S1.
 In acute MI LV pre-ejection time may be prolonged which may result in
splitting of S1.

32.  Prominent splitting of S1 is common in Ebstein’s anomaly – the delayed closing
of septal leaflet of the tricuspid valve produces a loud and early systolic closing
sound.
 Tricuspid valve closure sound is exaggerated in patients with ASD.

34. Variable S1
 Whenever the relationship between the position of mitral valve leaflets
and LV pressure rise is inconstant, the intensity as well as spitting interval
of S1 will vary.
 Thus 2nd or 3rd degree heart block and AV dissociation will result in S1 of
variable intensity.

36. Thank You!