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2 nd heart sound S2.pptx
1. The Second Heart Sound
Dr. Varshith K
DNB Resident
Department of Cardiology
ASTER MIMS Calicut
2. Definition
The Heart sound produced by sudden deceleration of retrograde flow of
blood column in the aorta and pulmonary artery due to abrupt closure of
the semilunar valves at the onset of ventricular diastole
3. Historical aspects
• In 1832, Rounat demonstrated that the second heart sound results from closure
of semilunar valves.
• 1866, Potain described the physiological splitting of S2 during inspiration.
• 1952, Wood noticed the second sound in PH was single with loud pulmonary
component.
• Leatham in 1964 described S2 as the ‘key to auscultation of the heart’.
• Shaver et al. (1977) coined the term ‘Hangout interval’ and described types of
abnormal split of S2.
4. Genesis of S2
• LV end Systole -----> flow into great vessels complete -----> sudden deceleration of blood
mass towards the semilunar valves--->cessation of forward flow into great vessels---->
coaption of semilunar valves----> abrupt tensing of the closed leaflets and vibration of
LVOT, RVOT and Great vessels
5. Features of S2
Frequency Higher than S1(S1 25-45Hz , S2 50HZ)
Duration 0.11 sec( Shorter than S1 0.14 Sec)
Components of S2 Aortic component (A2) & Pulmonary component
(P2)
Timing of A2 coincides Incisura of Aortic pressure trace
Timing of P2 coincides Incisura of pulmonary artery pressure trace
Normally A2 – P2 interval : During inspiration
During expiration
40-50 msec
<30msec
Normally A2 is earlier and Louder than P2
Normally A2 heard in Aortic area, Pulmonary area , and Apex
Normally P2 heard at pulmonary area only (P2 heard at apex only if PHN Present or If the apex
is formed by RV (eg ASD))
6. Reasons for Higher frequency S2 compared to S1
• The tautness of the semilunar valves more compared to A-V
valves.
• The Greater elastic coefficient of the taut arterial walls that provide
the principal vibrating chambers for the second sound,in
comparison with the much looser, less elastic ventricular chambers
that provide the vibrating system for the first heart sound.
7. Why S2 duration shorter than S1?
• Normally duration of S1 is 0.14 second
and S2 is 0.11 second .
• The reason is that, semilunar valves are more taut than the A-V valves, so
they vibrate for a shorter time than the A-V valves.
8. Hangout interval
• Ventricular pressures fall below arterial pressures by the end of systole
• The semilunar valve is expected to close at the time of pressure cross-
over
• In reality, the actual closure of the valves occurs later due to continued
forward flow of blood
• This gap is referred to as the ‘hangout interval’
9.
10.
11. Factors influencing the duration of Hangout interval
• Impedance or Resistance to forward flow
• Phase of Respiration
• Compliance of Vessels
13. Why P2 Delayed?
• RV systolic ejection last longer than LV ejection even though RV and LV
mechanical systole has same duration
• This occurs due to prolonged hangout interval of pulmonary circulation.
14. Why A2 is earlier and louder than P2
• Due to High Diastolic pressure gradient acoss the
aortic valve
• When compared to pulmonary circulation, LV ejection
time is small as aortic hangout interval is less
15. Components of physiologic Inspiratory split of
S2
Mechanism Relative Contribution
1. ↑ Q-P2 73 %
↑ Pulmonary
hangout interval
45 %
↑ RV ejection time 28 %
2. ↓ Q-A2 interval 27 %
Curtiss et al. Circulation 1975; 51:157
16. Clinical Examination Of S2
• Start at 2nd right ICS , with the Diaphram of the stethoscope
• At 2nd to 3rd Left ICS
• Spliting best apreciated at second Left intercostal space.
17. Dynamic auscultation of normal S2
split
• Widens with inspiration, passive leg raising
• Narrows on standing
• Narrows / abolished during strain phase of valsalva maneuver and
widens during release phase
18. Evaluation of S2
• Audibility of both components
• Intensity
• Normal
• Loud A2 or P2
• Soft A2 or P2
• Split
• Normal
• Wide and variable
• Wide and fixed
• Narrow
• Reversed/ paradoxical
19. Intensity of A2 / P2
• Determined by
• Pressure beyond the valve
• Flow across the valve
• Size of the vessel beyond the valve
• Stenosis or regurgitation of the valve
• Chest wall transmission
20. Accentuated A2 Causes
• Increased size of the vessel
Ascending aorta aneurysm
Root dialatation:
Syphilitic AR
Bicuspid Aortic valve
with post stenotic dilatation
• Incresed pressure in the
vessel beyond the valve
Systemic Hypertension
Coactation of aorta
• Increased flow across the valve
Hyperkinetic States
• Thickened but Mobile aortic leaflets
Congenital bicuspid aortic valve
• Anteriorly placed Aorta
TGA
Pulmonary atresia
21. Diminished A2
• Occurs due to distortion, calcification or fibrosis of aortic leaflet
eg Aortic sclerosis, Calcific AS, Valvular AR
22. Loud P2
• Increased size of the vessel:
Idiopathic dilatation of
pulmonary artery,
ASD
• Incresed pressure in the
vessel beyond the valve:
PHTN
• Increased flow across the valve
Hyperkinetic States
ASD
• Distance From the site of origin of
sound to the chest wall:
Thin Chest wall
Straight Back syndrome
23. Diminished P2
• Thick chest wall: Obesity
• Poor conduction of sound : COPD
• Thickened leaflet and diminished valve mobility
PS & Dysplastic PV
>60 yr old
• Decreased Diastolic Gradient pressure in PA:
PS,Tricuspid atresia
Pulmonary valve is absent - Truncus arteriosus
24. Grading of Pulmonic sound Basics
Normal Pulmonic sound less than A2
Mild, + Equal to A2
Moderate, ++ Louder than A2
Severe, +++ very loud / banging
27. Factors affecting normal splitting of S2
• Age :
As age increases split duration decreases. Single S2 during both phases of respiration is a
normal finding in subjects with age >60yrs in 50%.
• Depth of respiration
• Position of body :
In recumbent position prominent splitting
in both phases of respiration is a normal finding
28. Causes of Abnormal splitting of S2
• Pressure difference between systemic and pulmonary
circulation
• Difference in ejection times or volumes of RV and LV
• Differential hangout interval
• Delay in electrical activation of either ventricle
• Absent of intact inter-atrial septum
30. Wide split of S2 - Causes
Delayed pulmonic closure (P2)
• Delayed electrical activation of RV
• Complete RBBB
• LV pacing / ectopics
• Prolonged RV mechanical systole
• Acute massive PTE
• PAH with RV failure
• Moderate to severe PS with intact IVS
• Increased pulmonary hangout interval
• Normotensive ASD
• Post operative ASD (70%)
• IDPA
• Mild pulmonic stenosis (post-stenotic dilatation)
31. Early aortic closure (A2)
• Shortened LV mechanical systole (LVET)
• Severe Mitral regurgitation
• VSD
• Cardiac tamponade, constrictive pericarditis
• Early electrical activation of LV
• Type A WPW syndrome
Other causes
• Straight back syndrome, Pectus excavatum
• Idiopathic Audible expiratory splitting (AES) in normal subjects
• Post PA banding
33. Wide Fixed split
Mechanisms
• RV or LV stroke volume remains unchanged with inspiration
• There is a similar degree of alteration in LV/ RV filling with inspiration
• Failure of the RV to augment its stroke volume during inspiration
• RV systole is substantially prolonged
(eg: RBBB with RV failure)
34. • Wide : Due to delay in P2 because of increased pulmonary vascular
capacitance prolonging the hangout interval and increased RV ejection
time
• Fixed : Phasic changes in systemic venous return with respiration are
associated with reciprocal changes in the volume of L to R shunting
35. Causes of wide fixed split
• Moderate to Large Ostium Secundum ASD
• Severe right heart failure
36. Reversed or Paradoxical spliting
• S2 is maximally split on expiration and narrow or fuses on inspiration.
• Directional flow of A2 and P2 during respiratory cycle are reversed from
normal-- Pardoxical splitting
37. Paradoxical Split
Type 1 Type 2 Type 3
increased Q-A2 interval due to
LV mechanical delay
mild delay in Q-A2 and marked
Q-P2 interval
both expiratory and inspiratory
seperation is <20ms
Expiration : prolonged LV
systole makes A2 follow P2 and
is heard in expiration
S2 reverse split is heard S2 is fused in both phases
Inspiration: Q-P2 increases
normally but Q-A2 remains
unchanged
normal split may be heard
38. Differentiation of P2-A2 in reversed Split
• Auscultate from pulmonary area to apex concentrating on the two
components of S2.
• The component which disappears at apex is the pulmonary
component.
39. Clinical recognition of Reversed split of S2
• Trace the two components of S2 to the apex.If the second component of S2 is tracable
up to apex , reverse split present.
(Normally only first component of S2(ie A2) is tracable up to apex, And second component
is heard only at pulmonary area. In reverse split A2 is the second component.)
41. Reversed split of S2 - Causes
• Delayed A2
• Delayed electrical activation of LV
• Complete LBBB
• RV ectopics / pacing
• Prolonged LV mechanical systole
• LVOT obstructions- Valvular AS and HCM
• Hypertensive heart disease, IHD
• Increased systemic hangout interval
• Post-stenotic dilatation of aorta
• PDA
• Early P2
• Type B WPW syndrome
42. Single or Narrow Splitting of S2
In this there is absent splitting both in
inspiration and expiration
43. Mechanism of Persistently
Single S2
Examples
Single semilunar valve present Truncus arteriosus
Atresia/ stenosis of either
semilunar valve
Aortic/ pulmonary atresia/
stenosis
Equal LV/ RV ejection time Eisenmenger complex (VSD),
Single ventricle
Inaudibility of P2 Transposed aorta (d-TGA),
Obesity, emphysema, large PE
Masking of A2 Extremely loud P2
