Second heart sound

Second heart 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
Sudden 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 (P2)

Mechanism of splitting of second heart sound and Hangout interval
Hangout 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 sound
1. Intensity
2. Respiratory variation
Palpable second heart sound
Palpable 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
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 Eisenmenger syndrome
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 diagnosed.
Soft P2
1. Pulmonary stenosis
2. PR secondary to absent pulmonary valve (PR due to PAH, P2 is loud)
3. TOF
4. Posterior placed pulmonary artery (TGA)

Masking of P2
· Loud A2
· Early opening snap
· Holosystolic murmurs

Increased intensity A2
This is due to increased flow, increased pressure and dilatation of root of aorta
1. Systemic hypertension
2. Coarctation of aorta
3. Ascending aortic aneurysm
4. Anteriorly placed aorta TGA, TOF

Decreased intensity of A2
1. Aortic regurgitation
2. Valvular and also supra valvular aortic stenosis
3. Soft A2 and loud P2 occurs due to decreased cardiac output and PH secondary to massive pulmonary embolism

Ø Normal 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 breathing.
Ø Reverse split is heard during expiration and not in inspiration

Wide splitting of S2
1. Prolonged RV systole
a. Pulmonary stenosis
b. Pulmonary hypertension
c. PAH with RV failure (without RV failure, PAH has narrow splitting)
d. Small ASD
e. Idiopathic dilatation of pulmonary artery
f. Severe biventricular failure
2. Shortened LV systole
a. MR
b. VSD
c. Pericardial tamponade (LV filling decreased in inspiration unlike RV)
d. Constrictive pericarditis
e. Restrictive Cardiomyopathy
f. LA myxoma
3. Electrical cause
b. LV Pacing
c. LV ectopy
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 right shunt.
2. Condition where Left ventricular stroke volume does not change with inspiration.
3. RV failure
4. Acute or chronic pulmonary embolism
4. Severe PH.

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.

Normal splitting
A2-P2 interval 30msecs. Some congenital heart disease with normal splitting are, Acynotic CHD like small VSD, mild AS or PS

Single S2
This can be secondary absent P2 or secondary to fusion of A2 to P2
1. Absent P2
a. Truncus arteriosus
b. Severe TOF
c. Pulmonary atresia
d. Most case of tricuspid atresia
e. Inaudible P2 in emphysema, obesity and pericardial effusion

2. Fusion of A2 and P2
a. Eisenmenger VSD
b. Single ventricle

Paradoxical splitting
Splitting is more in expiration or appreciated only in expiration.
LBBB, Severe 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.
Valsalva manure :-
In normal persons spltting widens in strain phase of valsalva but in patients with paradoxical splitting it narrows

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