sound is important in diagnosing cardiac lesion. Second heart sound is 120-150
Hz, Coincide with down stroke of carotids.
Generation of second heart sound
deceleration of retrograde blood flow in aorta and pulmonary artery sets
cardiohemic system into vibration leading production of second heart sound It
has two components aortic valve component (A2) and pulmonary valve component
Mechanism of splitting of second
heart sound and Hangout interval
interval is manifestation of impedance of circulation i.e. for pulmonary
circulation impedance is less, hangout interval is more i.e. 30-120 msecs, and
for systemic circulation, impedance is more so hangout interval is less i.e.
5msecs Physiologic splitting of the second heart sound in normal subjects is
due to an inspiratory decrease in impedance, which leads increase of hangout
interval for RV and widening of splitting, while in expiration this impedance
increases so hangout interval decreases for RV so split narrows.
Clinical evaluation of second heart
Palpable second heart sound
second heart sound in pulmonary area means palpable P2, secondary to Pulmonary
artery hypertension. In thin individual second heart sound may be normally
palpable in pulmonary area.
Loud P2 is
diagnosed, if it is heard at apex (normal P2 is not heard in apex) and if P2
component is louder than A2 component in pulmonary area. Cause are PAH and
In case of
ASD due to RV dilatation, P2 may be heard at apex without PAH. However, if P2
is very loud and increase with mild exercise then PAH with ASD can be
secondary to absent pulmonary valve (PR due to PAH, P2 is loud)
placed pulmonary artery (TGA)
This is due
to increased flow, increased pressure and dilatation of root of aorta
Anteriorly placed aorta TGA, TOF
Decreased intensity of A2
and also supra valvular aortic stenosis
3. Soft A2
and loud P2 occurs due to decreased cardiac output and PH secondary to massive
spiting S2 is heard during inspiration and not in expiration.
Ø Wide split
second heart sound heard during both inspiration and expiration.
Ø Fixed wide
spiting is heard in both inspiration and expiration without change with
respiration. Has to be examined in both lying and upright position, with normal
split is heard during expiration and not in inspiration
b. Pulmonary hypertension
c. PAH with RV failure (without RV failure, PAH has narrow
e. Idiopathic dilatation of pulmonary artery
f. Severe biventricular failure
c. Pericardial tamponade (LV filling decreased in inspiration
d. Constrictive pericarditis
e. Restrictive Cardiomyopathy
d. WPW syndrome with LV preexcitation (Type A)
Wide and fixed splitting of S2
1. In ASD
blood coming to RA is does not change with respiration, because inspiratory
increase in Systemic venous flow, is associated decrease in left to right shunt
and expiratory decrease in systemic flow is associated with increase in left to
where Left ventricular stroke volume does not change with inspiration.
4. Acute or
chronic pulmonary embolism
Close splitting or narrow splitting
When A2 -P2
interval is just more than 20msecs than narrow splitting is appreciated. This
is seen in shunt lesion with severe PAH without RV failure.
interval 30msecs. Some congenital heart disease with normal splitting are,
Acynotic CHD like small VSD, mild AS or PS
This can be
secondary absent P2 or secondary to fusion of A2 to P2
d. Most case of tricuspid atresia
e. Inaudible P2 in emphysema, obesity and pericardial
more in expiration or appreciated only in expiration.
AS, Severe AR and large PDA
1. Type 1
:-Single S2 in inspiration and split S2 in expiration
2. Type 2
:-Lesser degree of LV systole prolongation. In inspiration normal A2-P2 order
is maintained with audible splitting, but in expiration this order is reversed
i.e. P2-A2 (confused as fixed splitting) diagnosed by ascultating from
pulmonary area to apex sound that decreases in intensity is P2.
3. Type 3 :-
S2 is heard single because time interval between components of S2 is less than
20msces. P2 precedes A2 in expiration.
In normal persons spltting widens in strain phase of valsalva but in patients with paradoxical splitting it narrows
Labels: Clinical Cardiology, For Doctors