second heart sound dr shajudeen .k
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SECOND HEART SOUND Dr SHAJUDEEN .K DM Cardiology Resident Calicut Medical college. History. “S2 is the key to auscultation ” : Aubrey Leathem - PowerPoint PPT PresentationTRANSCRIPT
SECOND HEART SOUND
Dr SHAJUDEEN .K DM Cardiology
Resident Calicut Medical
college
History• “S2 is the key to auscultation” : Aubrey
Leathem
• Respiratory variation first described by
Potain (1866)
• Term “Hangout interval” coined by shaver
laboratory.
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
• This causes vibrations in the
cardiohemic system. High frequency
generated from this vibration is the
Second heart sound.
Timing Of S2
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.
Cardiac cycle recorded by high fidelity catheter tipped manometer
Normal values of Hangout intervals
• Pulmonary circulation: 43-86 msec
• Systemic circulation :< 15msec
• ie Pulmonary hangout interval >Systemic
Factors influencing the duration of Hangout interval
• Pressure in the arteries
• Vascular resistance
• Compliance of Vessels
• 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
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))
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.
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.
Normal S2
EXPIRATION(Split < 30msec)
INSPIRATION(Split > 30msec)
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.
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
Clinical Examination Of s2
• At 2nd to 3rd Left ICS preferably with
Diaphram of the stethescope.
• Spliting best apreciated at second
Left intercostal space.
Clinical examination of S2
Two important Points to observe whileexamining for S2 are.
• Splitting of S2
• Intensity of each component of S2
Splitting Of S2
Normal Splitting of S2
EXPIRATION(Split < 30msec)
INSPIRATION(Split > 30msec)
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%).
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
Mechanism of increased split in inspiration
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.
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
Abnormal Splitting Of S2
• Abnormal splitting can be either
absent/inaudible split (single S2) or
presence of audible expiratory splitting
both in supine and upright position
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
Audible expiratory splits
Wide Persistent physiological split
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
Delayed electrical activation of RV
• Complete RBBB
• LV ectopic beat
• LV pacing
Prolonged RV mechanical systole
• Moderate to severe PS with intact IVS
• Right heart failure
• Acute Massive pulmonary embolism
• Anomalous venous connection to RA
Increased Hangout interval
• Mild Pulmonary stenosis
• Idiopathic dilatation of pulmonary
artery
• Normo tensive ASD
• Unexplained audible expiratory
splitting in normal subjects
Shortened LV mechanical systole
• Severe Mitral Regurgitation
• Moderate to Large VSD
Wide fixed splitting
Wide fixed splitting
A2 P2 widely split and split remains fixed ie remains unchanged during respiration or valsalva
• Wide : Due to delay in P2 because of
increased pulmonary vascular
capacitance prolonging the hangout
interval and increased RV ejection
time
• Fixed : As little or no change in RV
filling and stroke volume during
inspiration .so little or no inspiratory
delay occurs to P2
Causes of wide fixed split
• Moderate to Large Ostium Secundum ASD
• Severe right heart failure
Reverse or paradoxical splitting of S2
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
Types of Reversed split
• Type 1 or classic : Only this type is
audible clinically
• Type 2 Detected Phonographically• Type 3
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
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
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
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.)
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
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.
Causes of Reversed spliting
• Due to
Delayed A2 Early P2
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)
Causes of Delayed A2 . . .contiued.
• Decreased Impedance of systemic circulation eg
Post stenotic dilatation
aorta
Chronic severe AR,
PDA.
Early P2
Due to Type B WPW Syndrome
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
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
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
Single S2
Single S2In this there is absent splitting both in inspiration and expiration
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
• 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
INTENSITY OF S2(A2 P2)
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
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.,
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 Coactation of aorta
• Increased flow across the valve
Hyperkinetic States
• Anteriorly placed Aorta
TGA Pulmonary atresia
PTA
Diminished A2
• Occurs due to distortion of aortic leaflet
eg Aortic sclerosis, Calcific AS,
Valvular AR
Aortic atresia(HLHS).
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
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
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
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
S2 in different cardiac conditions
Mitral stenosis
• Mild to Moderate MS without PHTN: Normal
A2 & P2
• Severe MS With PHTN : S2 narrow split P2 Loud
Mitral Regurgitation
• Wide variable split : Severe MR• Wide and Fixed in MR : MR+ ASD• Reverse splitting in MR: MR due to HCM
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
Aortic stenosis
• Reverse split : Due to Delayed A2 in Severe AS
• Single S2 : If A2 is Absent/soft or A2 drowned in the
murmur
Aortic regurgitation
• S2 Split normally split/Reverse split
• A2 loud If AR Due to root dilatation • A2 soft if AR due to Valvular disease.
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
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
S2 in CONGENITAL HEART DISEASE
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.
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.
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
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.
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
BISCUSPID AORTIC VALVE
• In the absence of significant AS or
AR S2 normally split with
accentuated A2
• If significant AS: S2 Reversed split
COA
• Normally splitting S2 with
accentuated A2 due to hypertension
• sometimes reverse split can also
happen
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
S2 in Anomalous pulmonary venous connection
• If Associated ASD : Wide fixed split
• If Atrial septum intact: S2 normal
split with normal respiratory variation
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
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