Second heart sound

1. SECOND HEART SOUND
Dr SHAJUDEEN .K
DM Cardiology
Resident
Calicut Medical
college

3. History
• “S2 is the key to auscultation” : Aubrey
Leathem
• Respiratory variation first described by Potain
(1866)
• Term “Hangout interval” coined by shaver

4. Genesis of S2
• During systole blood flow from LV to Aorta &
RV to PA. Once pressure in the great
vessels becomes more than corresponding
ventricle and hang out interval is over, blood
flow reverses , this retrograde flow is
stopped suddenly by semilunar valves when
the elastic limits of the tensed leaflets are met
during closure of valves

5. • This causes vibrations in the cardiohemic
system. High frequency generated from
this vibration is the Second heart sound.

6. Timing Of S2

7. Hang out interval
• It is the time interval from the crossover of
the pressure between RV and PA or LV and
Aorta during the ejection phase of systole to
the actual closure of the Pulmonary or Aortic
valve respectively.

8. Cardiac cycle recorded by high
fidelity catheter tipped manometer

9. Normal values of Hangout intervals
• Pulmonary circulation: 43-86 msec
• Systemic circulation :< 15msec
• ie Pulmonary hangout interval >Systemic

10. Factors influencing the duration of
Hangout interval
• Pressure in the arteries
• Vascular resistance
• Compliance of Vessels

11. • Aorta is a higher pressure and less
compliant vessel so hangout interval of
aortic is less than the pulmonary side
• Pulmonary circulation is Low pressure ,low
resistance, high capacitance circulation
.So hang out interval more

12. 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

13. 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.

14. 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 do the A-V
valves.

15. Normal S2
EXPIRATION
(Split < 30msec)
INSPIRATION
(Split >
30msec)

16. 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.

17. 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

18. Clinical Examination Of s2
• At 2nd to 3rd Left ICS preferably with
Diaphram of the stethescope.
• Spliting best apreciated at second Left
intercostal space.

19. Clinical examination of S2
Two important Points to observe while
examining for S2 are.
• Splitting of S2
• Intensity of each component of S2

20. Splitting Of S2

21. Normal Splitting of S2
EXPIRATION
(Split < 30msec)
INSPIRATION
(Split >
30msec)

22. Normal splitting of S2
Normal A2 P2 interval
During expiration : < 30 msec
During inspiration : 40-50 ms
Splitting occurs because of delayed P2
(73%)
and early A2 (27%).

23. Factors affecting normal splitting of
S2
• Age :
As age increases split duration decreases. Sing
S2 during both phases of respiration is a norm
finding in subjects with age >40yrs
• Depth of respiration
• Position of body :
In recumbent position prominent splitting
in both phases of respiration is a normal finding

24. Mechanism of increased split in inspiration

25. Recent views regarding inspiratory
widening of split
• Complex interplay of dynamic changes in
pulmonary vascular impedence and
changes in pulmonary and systemic
venous return. Net effect is prolonged RV
ejection and a concomittent decrease in
LV ejection causing widening of split in
inspiration.

26. Decreased pulmonary venous flow
to the left atrium. So LV ejection
time decreases so A2 occurs early
Inspiration causes
more negative
intrathoracic pressure
1) Increased
venous
return
2) Increase
capacitance of
the pulmonary
vessels
Pulmonary hang
out
interval
increases & RV
ejection time
increases
So A2 P2 interval > 30 msec

27. Abnormal Splitting Of S2

28. • Abnormal splitting can be either
absent/inaudible split (single S2) or presence
of audible expiratory splitting both in supine
and upright position

29. Abnormal Splitting of S2 includes
• Persistent physiological split
• Wide fixed split of S2
• Reverse split of S2
• Narrow Physiological split with Loud P2
• No Split : ie Single S2
Expiratory split
interval> 30msec

30. Audible expiratory splits

31. Wide Persistent physiological split

32. Wide physiological splitting
important mechanism
• Delayed P2
Delayed electrical activation of RV
Prolonged RV mechanical systole
Increased Pulmonary Hang out interval
• Early A2
Shortened LV mechanical systole

33. Delayed electrical activation of RV
• Complete RBBB
• LV ectopic beat
• LV pacing

34. Prolonged RV mechanical systole
• Moderate to severe PS with intact
IVS
• Right heart failure
• Acute Massive pulmonary embolism
• Anomalous venous connection to
RA

35. Increased Hangout interval
• Mild Pulmonary stenosis
• Idiopathic dilatation of pulmonary
artery
• Normo tensive ASD
• Unexplained audible expiratory
splitting in normal subjects

36. Shortened LV mechanical systole
• Severe Mitral Regurgitation
• Moderate to Large VSD

37. Wide fixed splitting

38. Wide fixed splitting
A2 P2 widely split and split remains fixed
ie remains unchanged during respiration
or valsalva

39. • Wide : Due to delay in P2 because of
increased pulmonary vascular capacitance
prolonging the hangout interval and
increased RV ejection time

40. • Fixed : As little or no change in RV filling
and stroke volume during inspiration .so
little or no inspiratory delay occurs to P2

41. Causes of wide fixed split
• Moderate to Large Ostium Secundum ASD
• Severe right heart failure

42. Reverse or paradoxical splitting of
S2

43. Reverse or paradoxical splitting
splitting
• S2 Split>30msec during expiration with
reversal of sequence ie P2-A2
• Presence of reverse splitting always indicate
significant underlying Heart disease
• Almost all cases of reversed split are due to
dalayed A2

44. Types of Reversed split
• Type 1 or classic : Only this type is audible
clinically
• Type 2
Detected Phonographically
• Type 3

45. Type 1 Reversed split
No split during inspiration. But splitting during
expiration with reverse sequence due to delay in
A2
It occurs due to delayed LV Electro mechanical

46. Type 2 or Partially Reversed
splitting of S2
Normal Inspiratory splitting But Expiratory
splitting
of S2 with Reverse sequence
• It resemble wide fixed split.But during

47. Type 3 Reversed splitting of S2
ie similar to type 2 but difference is that A2 P2
and P2-A2 seperation is ≤30 ms and so S2 is
heard as a single sound in both phase of
respiration

48. 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
pulonary area.In reverse split A2 is the second
component.)

49. Clinical recognition of Reversed split
of S2
• Valsalva testing
Normally S2 becomes Reversed split S2
becomes
Strain phase Split narrows widens
Release phase widens Splitt narrows

50. 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.

51. Causes of Reversed spliting
• Due to
Delayed A2
Early P2

52. Causes of Delayed A2
• Delayed Electrical
activation of LV
• Complete LBBB
• RV pacing
• RV ectopic beat
• Prolonged LV mechanical
systole
• Complete LBBB
• Severe AS
• Severe HTN (Rarely)
• Chronic ischemic heart d/s
• During episode of angina
pectoris(rarely

53. Causes of Delayed A2 . . .contiued.
• Decreased Impedance of systemic
circulation eg
Post stenotic dilatation aorta
Chronic severe AR,
PDA.

54. Early P2
Due to Type B WPW Syndrome

55. Reversed splitting in LBBB
• In proximal type: Delayed activation of LV
• In peripheral type: There is prolonged
mechanical systole (primarily isovolumic
contraction time increased).
• In most cases of LBBB varying degrees of
both mechanism coexist with one

56. Reversed split in angina pectoris
• It occurs rarely
• Proposed mechanisms are
1) Prolonged isovolumetric
contraction
time of ischemic LV
2) Systemic hypertension
prolonging
LVETime

57. Reverse splitting in HTN
• In HTN Loud A2 with normal split is the
common finding
• Reverse split occurs rarely especially in
acute hypertension . Due to increased LV
ejection & isovolumetric contraction time

58. Single S2

59. Single S2
In this there is absent splitting both in
inspiration and expiration

60. Single S2: Mechanism
• If only one semilunar valve present: eg:
Aortic or Pulmonary atresia,
Persistent truncus arteriosis
• When P2 inaudible: TGA, TOF, Severe PS, PA
• When Delayed A2 coincides with P2: Seve
AS

61. • When early P2 coincides with A2 : Severe
PHTN,
VSD+PHTN
• Any condition producing Paradoxical split with
A2-
P2 interval ≤ 30msec
• A2 sound drowned by murmur of AS/MR/VSD

62. INTENSITY OF S2(A2 P2)

63. Factors influencing the intensity of
S2
• Size of the vessel
• Pressure in the vessel
beyond the valve
• Rate of change of
Diastolic pressure
gradient across the
valve.
• Flow across the
valve
• Position Of
Vessels(Anterior/Po
sterior)
• Valve anatomy

64. S2 intensity relation to the rate of change of
the diastolic pressure gradient that develops
across the valves
It is the driving forces accelerating the
blood mass retrograde into the base of the
great vessels. This pressure gradient is
the result of the level of diastolic pressure
in the great vessel and the rate of
pressure decline in the ventricle.,

65. Accentuted A2 Causes
• Increased size of the vessel
Ascending aorta
aneurysm
Root dialatation:
Syphilitic AR
Ankylosing
Spondylitis
Bicuspid Aortic valve
with post
stenotic
dilatation
• Incresed pressure in the
vessel beyond the valve
Systemic Hypertension
• Increased flow across
the valve
Hyperkinetic States
• Anteriorly placed Aorta
TGA
Pulmonary atresia
PTA

66. Diminished A2
• Occurs due to distortion of aortic leaflet
eg Aortic sclerosis, Calcific AS, Valvular
AR
Aortic atresia(HLHS).

67. 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

68. Grading Of Loud P2
• Grade 1: P2= A2
• Grade 2: P2>A2 Localised to Pulmonary are
• Grade 3: P2>A2 But heard Beyond the
pulmonary artery

69. Relation Between P2 intensity and
Pulmonary pressure
Pulmonary
Systolic
pressure
Mean
pulmonary
pressure
Grade 1 Mild PHTN 30-49 mm of Hg 21-34 mm of
Hg
Grade 2 Moderate PHTN 50-75 mm of Hg 35-50mm of Hg
Grade 3 Severe PHTN > 75mm of Hg > 50 mm of Hg

70. Diminished P2
• Thick chest wall: Obesity
• Poor conduction of sound : COPD
• Thickened leaflet and diminished valve mobility
PS & Dysplastic PV
TOF
>60 yr old
• Decreased Diastolic Gradient pressure in PA:
PS,Tricuspid atresia

71. S2 in different cardiac conditions

72. Mitral stenosis
• Mild to Moderate MS without PHTN:
Normal A2 &
P2
• Severe MS With PHTN : S2 narrow split P2
Loud

73. Mitral Regurgitation
• Wide variable split : Severe MR
• Wide and Fixed in MR :
MR+ ASD
• Reverse splitting in MR:
MR due to HCM

74. P2 in Mitral regurgitation
• In MR with giant Left atrial enlargement
.P2 is more prominent even with slight
increase in pulmonary hypertension.It is
due to the enlarged LA displaces the
pulmonary artery anteriorly closer to the
chest wall

75. Aortic stenosis
• Reverse split : Due to Delayed A2 in Severe AS
• Single S2 : If A2 is Absent/soft or A2 drowned in
the
murmur

76. Aortic regurgitation
• S2 Split normally split/Reverse split
• A2 loud If AR
Due to root dilatation
• A2 soft if AR due to Valvular disease.

77. Pulmonary hypertension
• Spectrum of the width of splitting can
happen in PHTN depending on the
selective prolongation of RV systole.
• In PHTN hangout interval will always be
narrow

78. Spliting of S2 in PHTN
• Narrow physiological split with Loud P2
• Wide variable splitting of S2 with Loud P2
• Fixed splitting in PHTN due
1) If RV failure: Due to inability of
compromised RV to accept the
augmented venous return associated
with inspiration
• 2) Altered vascular impedence in
pulmonary

79. S2 in CONGENITAL HEART
DISEASE

80. ASD
• Wide fixed split with loud p2 in absence of
PHTN
is the hallmark of ASD
P2 Loud because Dilated P2 is close to the
chest wall.

81. Fixed split in ASD Mechanism:
• Fixed : Inspiratory augmentation of
systemic venous return produces less Left
to Right shunt and it causes delayed A2.
And expiratory decrease in systemic
venous return causes increased Left to
right shunt producing early A2.

82. VSD
• Small VSD : Normal S2 split with
normal
intensity P2
• Moderate VSD: Normal split with
moderate
accentuation of P2
• Large VSD : Wide variable Split with
Loud P2
• VSD with PS physiology :Single Loud S2

83. PDA
• Small PDA : Normal S2 split and normal
intensity P2 but S2 masked
by
continous murmur
• Large PDA: Normal S2 split with
accentuated
P2. Occationally paradoxical
splitting can be seen.

84. Pulmonary stenosis
• Mild PS: Normal S2 Split with decreased
intensity P2
• Moderate – Severe PS: Wide Variable Split
With Diminished
P2
• Severe PS : P2 absent
• Dysplastic pulmonary valve : P2 can be
normal or inaudible depending severity of
stenosis

85. BISCUSPID AORTIC VALVE
• In the absence of significant AS or AR S2
normally split with accentuated A2
• If significant AS: S2 Reversed split

86. COA
• Normally splitting S2 with accentuated A2
due to hypertension
• sometimes reverse split can also happen

87. S2 in Ebsteins anomaly
• S2 is often single because pulmonary closure is
inaudible due to low pressure in pulmonary trunk
• Wide splitting of S2 can happen if complete
RBBB

88. S2 in Anomalous pulmonary venous
connection
• If Associated ASD : Wide fixed split
• If Atrial septum intact: S2 normal split with
normal respiratory variation

89. S2 in Eissenmenger syndrome
• ASD Eissenmenger syndrome: S2 narrow
fixed
split
• VSD Eisenmenger syndrome: Single Loud
P2
• PDA Eisenmenger syndrome:
Closely split S2 with Loud