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)

• MR
• VSD
• Pericardial tamponade
• LA Myxoma
• Constrictive pericarditis
 Wide split s2 in Cyanotic heart disease
• 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?

• Semilunar valve is expected to close at point of cross over of

ventricular and arterial pressure.

• In reality it is not so

• 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 msec in the

pulmonary vascular bed.
• Hangout interval depends on interrelated factors like :

• pressure beyond the valve

• dilatation of the artery

• distensibility of arterial system

• vascular impedance

• 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 A2-P2
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)

• Pseudo Reverse Split

Only Type I Paradoxic splitting can be detected bedside. Type II and Type
III can be diagnosed only by Phonocardiography .
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
• 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
• 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

• 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

• 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  RAD, RAE, RVCD
Common atrium  RVH, RAD / Superior Axis
Common ventricle  Variable
Truncus  CVH, RVH / LVH
 PBF : No PAH
TOF  RAD, RVH
TOF, Like anomaly  RAD, RVH
PS, Intact IVS + ASD  RV Strain
Tricuspid atresia  LAD, LV dominance
Ebstein’s  RAD, Low Voltage, RVCD
 PBF : PAH
Eisenmenger’s  RAD, RVH
 Phonocardiography
• Single Vs Closed split
• Confirmation P2 or A2
• Reversed Splitting
• For teaching purpose
Thank You