The first heart sound occurs at the onset of ventricular contraction. It is made up of several components: the mitral component (M1), which corresponds to mitral valve closure, is the most important. The tricuspid component (T1) follows M1. In some adults, S1 may be audibly split into M1 and the aortic component (A1). Conditions that increase the rate of ventricular pressure rise, like mitral stenosis, cause a louder M1. Those that delay ventricular contraction, like heart block, cause a softer S1. Abnormally wide splitting suggests electrical delays between the ventricles.

1. First Heart Sound

2. Definition
• Heart sounds are discrete bursts of auditory vibrations of
varying intensity (loudness), frequency (pitch), quality, and
duration .
• All heart sounds are formed when a moving column of blood
comes to a sudden stop or decelerates significantly.
• The intensity of a heart sound will depend on the level of
energy that the moving column of blood has attained.
• The sudden deceleration causes dissipation of energy, which
results in the production of vibrations affecting the
contiguous cardiohemic mass.

3. History
• There are 2 school of thoughts regarding the mechanism of
production of vibration.
• Luisada asserts that onset of isovolumic LV contraction results in
tensing of LV walls, septum and mitral apparatus which produces a
first transient sound and second major audible vibration of S1 is an
ejection component coincident with opening of Aortic valve.
• In contrast, Craige and Leatham have demonstarted convincingly
that first major component of S1(M1) is coincident with maximal
closing excursion of mitral cusps.
• They believed that M1 reflects sudden tensing of closed mitral
valve leaflets which sets the surrounding cardiac structures and
blood into vibration.
• Similarly, they demonstrated T1 as 2nd component of audible S1.

4. • The first heart sound occurs at the onset of ventricular
contraction.
• S1 is relatively wide and is made of many components, which
overlap each other.
• These components are
– Atrial
– Mitral
– Tricuspid
– Aortic

5. Atrial Component
• The energy of the column of blood pushed by the atrial
contraction becomes dissipated as the column decelerates
against the ventricular walls.
• This deceleration is gradual in most normal subjects because
of good compliance and distensibility of the ventricles.
• Therefore, the sound generated by this has a very low
frequency and is not audible.

6. Mitral Component
• This is the most important component of S1.
• It corresponds in timing to the closure of the mitral valve
leaflets.
• However, the mere apposition of the valve leaflets does not
produce the sound.
• The sudden deceleration of the column of blood causes the
mitral component, or M1.
• The energy dissipation causes vibrations of the column of
blood as well as the entire surrounding structures, i.e., the
mitral valve structures and the ventricular wall.

7. Tricuspid Component
• This component is similar in origin to the M1 for similar
cardiac events occur involving the right-sided structures.
• However, these events occur at much lower pressures and
slightly delayed.
• Therefore, the tricuspid component (T1) follows the M1.
• The T1 component tends to be maximally heard over the
sternum and the left sternal border and not usually over the
apex.

8. Aortic Component
• The aortic component (A1) is usually the second component
of audibly split S1 in adults.
• After mitral and tricuspid valve closures, the ventricular
pressure continues to rise during the phase of isovolumic
contraction.
• When the pressure exceeds the aortic and pulmonary
diastolic pressures, the ejection phase begins as the semilunar
valves open.
• The column of blood ejected into the aorta as it hits the aortic
walls decelerates and when the deceleration is significant will
result in an audible sound.

9. Normal S1
• S1 is usually heard loudest at the apex and the lower left
sternal border around the fourth left intercostal space.
• The sound is usually low pitched and longer in duration
compared to the sharper, shorter, and higher-frequency
second heart sound.
• It may be audibly split into two components in some patients
when the separation exceeds at least 20 ms.
• When such a split is heard it could be because of M1-T1 in
children and young adolescents and is usually due to M1-A1 in
the adults.

11. Loud S1
• The higher the dP/dt achieved by the contracting left ventricle
at the time of mitral valve closure (the pressure crossover
point), the louder will be the intensity of the M1.
• Loud S1 may equal or exceed intensity of S2 at base.
• Causes of loud M1
– Short PR
– MV obstruction
– Hyperkinetic states
Causes of loud T1
• Ebstein anomaly
• TV Obstruction
• ASD
• Straight back syndrome

12. S1 in MS
• A loud first heart sound is a hallmark of hemodynamically
significant mitral stenosis.
• Mobile but stiff mitral leaflets produce a loud S1, unless the
leaflets are heavily calcified.
• The loud S1, is due primarily to greater excursion of the
leaflets during closure, since elevated left atrial pressure has
kept the leaflets relatively wide apart.
• In addition, stiff, noncompliant leaflets and chordae tendineae
appear to resonate with increased amplitude.

13. Soft S1
• Decreased intensity of S1, occurs in conditions that cause the
AV valves to close prior to ventricular systole or if there is a
reduction in the rate of intraventricular pressure
development.
• Causes
– First-degree heart block (most common)
– Holosystolic mitral regurgitation
– Ventricular septal defect
– Acute aortic regurgitation
– Myocardial depression

14. S1 in MR/VSD
• The intensity of S1, may be
– decreased or masked by the murmur itself
– the isovolumic period may be absent
– the rate of rise of intraventricular pressure may be blunted
S1 in Aortic Regurgitation
• S1, is most commonly diminished because preclosure of the
mitral valve occurs as a result of the rapid increase in left
ventricular filling pressure .

15. Splitting
• Splitting of the first heart sound into its two audible
components, M1 and T1 , is a normal finding on cardiac
auscultation.
• The M1-T1 interval is normally separated by 20 to 30 msec.
• Wide splitting of the first sound is almost always abnormal.
• The split may be increased to 60 msec in patients with
– Right bundle branch block
– Ebstein's anomaly
– Conditions in which there is electrical delay in activitation of one of
the two ventricles (e .g., ventricular ectopic beats, ventricular
tachycardia, AV block with idioventricular rhythm, and left ventricular
pacing)