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 laboratory.

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
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: 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 S 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))

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 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 INSPIRATION (Split < 30msec) (Split > 30msec)
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 (Split < 30msec) INSPIRATION
EXPIRATION
(Split < 30msec)
INSPIRATION
(Split > 30msec)

22. Normal splitting of S2
Normal A2 P2 interval During expiration : < 30 msec During inspiration : 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. Single
S2 during both phases of respiration is a normal
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. 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
Decreased pulmonary venous flow
to the left atrium. So LV ejection
time decreases so A2 occurs early
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 systole

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 expiration
sequence of sound is P2-A2

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
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 predominating

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
3) Transient LBBB

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: Severe 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/Posterior)
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 flow across the valve
Hyperkinetic States
Anteriorly placed Aorta
TGA
Pulmonary atresia
PTA
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
Coactation of aorta

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: Increased flow across the valve
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 area
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 and Fixed in MR : MR+ ASD
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
circulation

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
Paradoxical split occurs if Type B WPW association

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 P2

90. THANK U