Transcript heart sounds s2

Second Heart Sound
Key to Auscultation
Dr. I. Sathyamurthy MD, DM, FACC
FRCP (Edin), FRCP (Glas), DSc (Honoris Causa)
Sr. Interventional Cardiologist
Apollo Hospitals, Chennai.
Heart sounds
S2
• Has 2 components
Aortic (A2)
Pulmonary (P2)
• Each coincides with the incisura of its arterial pressure wave
• Inspiratory splitting of S2 – Due to delay in P2
• During inspiration pulmonary arterial incisura moves away from the
descending limb of RV pressure due to increase in capaciitance of
pulmonary vascular bed which delays the P2
• Expiration has the opposite effect.
S2
• A2 louder audible at base, LSB and apex
• P2 softer confined to 2nd LICS
• During expiration A2 and P2 are separated by < 30 ms and are heard
as single sound
• During inspiration the splitting interval widens and A2 & P2 are heard
as two distinct sounds
Abnormal splitting of S2
3 categories
• Wide split
Fixed
Non fixed
• Paradoxically split (Reversed)
• Persistently single
Wide splitting of the second heart sound
Delayed Pulmonic closure
Delayed electrical activation of the right ventricle
Prolonged right ventricular mechanical systole
Decreased impedence of the pulmonary vascular bed (increased “hang
out”)
Early Aortic closure
Shortened LV mechanical systole(LVET)
Wide splitting of s2
Causes of audible expiratory splitting of s2
I. Increased Q - P2 (Prolonged RV systole)
(a) Hemodynamic causes
• PS with intact septum ( A2-P2 delay > 100msec indicates an RV-PA
gdt of 100mmHg when there is no infundibular stenosis )
• Massive Pulmonary embolism
• PAH with RV failure
• Idiopathic dilatation of PA
• ASD
(b) Electrical causes
• Complete RBBB
• PVC of LV origin
• LV pacing
• WPW with LV pre excitation
(II) Decreased Q - A2 Interval (Shortened LV systole)
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MR
VSD
Pericardial tamponade
LA Myxoma
Constrictive pericarditis
Wide split s2 in Cyanotic heart disease
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TAPVC
Single atrium
Ebsteins anamoly of tricuspid valve
ASD Eisenmenger
ASD with left to rt shunt
ASD with PS and right to left shunt at atrial level
• Primary Pulmonary hypertension
Miscellaneous
• Pectus excavatum
• Occasionally normal children
• Straight back syndrome
Fixed S2 split
Interval between A2 & P2 is wide and persistent and
remains unchanged during respiratory cycle
• Hallmark finding of ASD
• Delay in P2 is due to  Pulmonary vascular bed capacitance – and 
Hangout interval (  interval between descending limbs of PA and RV
pressure pulses ) – Split is wide
• No significant respiratory variations in RV filling due to reciprocal
changes in volume of left to right shunt – Split is fixed
What is hangout interval?
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Semilunar valve is expected to close at point of cross over of
ventricular and arterial pressure.
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In reality it is not so
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Time interval from cross over of pressures to actual
occurrence of sound is called HANGOUT interval.
• Just like a rolling ball is stopped by the friction offered by the
ground, the ejection of blood is stopped by the resistance
offered by the pulmonary vasculature
• Since the pulmonary vascular resistance is low compared to the
systemic vascular resistance, it takes some time for the blood
flow from the right ventricle to stop
• This corresponds to the hangout interval.
• On the left side of the heart because impedance is much
greater, the hangout interval between the aorta and
LV
pressure curves is negligible
• Hang out interval may vary from 30 to 120
pulmonary vascular bed.
msec in the
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Hangout interval depends on interrelated factors like :
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pressure beyond the valve
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dilatation of the artery
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distensibility of arterial system
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vascular impedance
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phase of respiration.
Reverse Splitting of the second heart sound
• Delayed Aortic closure
Delayed electrical activation of the LV
Complete LBBB (Proximal type)
RV paced beat
RV ectopic beats
Prolonged left ventricular mechanical systole
Complete LBBB
LVOT obstruction
Hypertensive heart disease
Arteriosclerotic heart disease
Chronic IHD
Contd,
Decreased impedence of the systemic vascular bed (increased “hang
out”)
Post stenotic dilatation of the aorta secondary to AS or AR
PDA
Early pulmonic closure
Early electrical activation of the RV
WPW syndrome type B
TYPES OF REVERSE SPLIT
Type 1:
Classical reverse split
 During expiration prolonged LV systole causes A2 to follow P2.with
inspiration Q-P2 increased normally but Q-A2 is unchanged or shorten
resulting a single second sound
Type 2:
S2 reversal only in expiration(P2-A2),
normal in inspiration(A2-P2)
 In lesser degrees of Q-A2 delay ,inspiration may still result in normal A2P2 relationship and audible splitting,although s2 reversal occurs in
expiration.
Reversed or parodoxic splitting
Type 3 paradoxical split :S2 single in both phases of respiration
(reverse split not detected by human ear as interval is < 20 msec
both in inspiration and expiration)
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Pseudo Reverse Split
Only Type I Paradoxic splitting can be detected bedside.
Type III can be diagnosed only by Phonocardiography .
Type II and
Aortic Stenosis
Mild
Moderate
Severe
Single S2
• Absence of either component of S2 or fusion of A2P2 without
inspiratory split give rise to single S2
Absent A2
• Severe AS
• Aortic atresia
Absent P2
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Truncus arteriosus
Severe TOF
Severe PS
CHD associated with PS or Pulmonary atresia
contd.,
Fusion of A2 and P2
• Eisenmenger VSD
• Single Ventricle
Inaudibility of P2
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Emphysema
Obesity
Pericardial effusion
Posterior location of PA. Eg.TGA
Pulmonary Stenosis
Single A2
• A2 is the louder component in the pulmonary area and is the only
component heard over the cardiac apex in normal individuals.
Determinant of intensity of A2
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Aortic pressure
Relative proximity of aorta to chest wall
Size of the aortic root
Degree of the opposition of the valve leaflets
Valve mobility
Increased intensity of A2
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Systemic hypertension
Coarctation of Aorta
Ascending Aortic aneurysm
Relative anterior placement of the aorta - TOF,TGA
Decreased intensity of A2
• AR(Lack of apposition of leaflets)
• Valvular & supravalvular AS(Decreased arterial diastolic pressure)
Single P2
Increased intensity of P2
• Normally P2 is not audible at the apex. If P2 is louder than A2 in
2nd LICS or if it is audible at the apex- It is termed loud and
indicates PAH
• In ASD P2 may be audible at the apex in the absence of PAH
because of RV enlargement and RV occupies the apex.
• If P2 is very loud and banging it correlates to approximate mean
PA pressure of > 50mmHg
Single P2
Determinants of intensity of P2
• PA pressure especially the diastolic pressure
• Size of PA
• Degree of apposition of PV leaflets
Loud P2
• Eisenmenger ASD - Wide splitting of S2 with ↑ P2
• Eisenmenger PDA - Narrow splitting of S2 with ↑ P2
• Eisenmenger VSD – S2 is generally single
Soft P2
• Pulmonary stenosis
• TOF(Mild form)
Cyanotic Congenital Heart Disease
Anomaly
P2
ECG
 PBF
CTGA

RAD, RVH
TAPVC
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RAD, RAE, RVCD
Common atrium
Axis
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RVH, RAD / Superior
Common ventricle
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Variable
Truncus
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CVH, RVH / LVH
TOF
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RAD, RVH
TOF, Like anomaly
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RAD, RVH
PS, Intact IVS + ASD
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RV Strain
Tricuspid atresia
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LAD, LV dominance
Ebstein’s
RVCD
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RAD, Low Voltage,
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RAD, RVH
 PBF : No PAH
 PBF : PAH
Eisenmenger’s
Phonocardiography
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Single Vs Closed split
Confirmation P2 or A2
Reversed Splitting
For teaching purpose
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