Second Heart Sound in Congenital Heart Disease

1. Second Heart Sound in Congenital Heart Disease R J Manjuran Prof & HOD of Cardiology Director, Pushpagiri Heart Institute Thiruvalla 689101

2. Heart sounds • Heart sounds correspond to important events in cardiac cycle • S1 corresponds to beginning of systole • S2 corresponds to beginning of diastole • S3 corresponds to end of rapid filling phase • S4 corresponds to end of atrial systole

4. Second heart sound evaluation is the most important assessment in physical diagnosis of congenital heart disease.

5. Normal Second Heart Sound (S2) • Mechanism – The S2 is due to vibration of cardiac structures and great vessels due to sudden cessation of blood flow at the end of systole. This correspond S2 to the coaptation of semilunar valves. Second Heart Sound Components – The S2 has two components * Aortic component (A2) * Pulmonary component (P2). Most investigators have documented that A2 and P2 correspond to Aortic and Pulmonary valve closure respectively.

6. Respiratory variation In normal individuals both components of S2 occur together during expiration while during inspiration A2 and P2 are separated (normal inspiratory splitting). The mechanisms of inspiratory splitting are: • Increased hang out interval of P2 • Increased venous return to right side of heart causes longer right ventricular ejection time. • Decrease in venous return to left side of heart results in shorter left ventricular ejection time. Increased hang out interval is the most important cause of delayed P2 during inspiration.

9. Clinical evaluation of S2 • Intensity • Relative to each component • Absolute increase • Respiratory variation

11. Abnormalities of S2 in Congenital Heart Disease • Intensity of S2 • Palpable S2 → Palpable S2 in pulmonary area indicate palpable pulmonary component and is due to pulmonary arterial hypertension (PAH) eg. Eisenmenger syndrome. Caution – In very thin chest walled individuals sometimes P2 is palpable without PAH.

12. Loud P2 - Indicate PAH – eg. Eisenmenger Syndrome. Normally P2 is not audible at apex. However, audible P2 at apex indicate PAH or ASD. In ASD, apex may be formed by right ventricle and in that situation P2 is audible at apex. • Soft P2 → P2 can be soft because the sound is feeble as in valvular pulmonary stenosis or the pulmonary artery is posterior and hence P2 is not well conducted to the chest as in Transposition of great arteries. In mild form of Tetralogy of Fallot sometimes a feeble P2 is audible.

13. Loud A2 Loud A2 in congenital heart disease is due to • augmented aortic closure as in coarctation of aorta, the aorta is anteriorly placed as in Transposition of Great Arteries, Tetralogy of Fallot (TOF) especially, severe TOF, when the aorta is large and relatively anterior. • abrupt closing motion of a pliable domed stenosed aortic Valve. Soft A2 Can occur in congenital Aortic stenosis due to distortion of Aortic leaflet. A2 is soft in congenital aortic regurgitation.

14. Splitting of S2 • Normal splitting - Normal splitting of S2 is heard in mild acyanotic congenital heart lesions like small ventricular septal defect (VSD) mild aortic stenosis., or mild pulmonary stenosis.

15. Wide variable split –In this, the S2 is split during inspiration and expiration, but the split widens during inspiration. This type of split of S2 can be present in moderate to severe pulmnonary stenosis, Ebstein’s anomaly, severe mitral regurgitation, moderate to large VSD and small atrial septal defect (ASD). • Wide fixed split -The S2 split is fixed during expiration and inspiration. This is a feature of moderate to large Atrial septal defect. Diagnosis of fixed splitting of S2 must be made during normal breating both in lying and upright positions.

16. Close splitting Normal splitting of S2 is appreciated when the interval between A2and P2 is more than 20 msec. However, in PAH even when the split is equal to 20 msec the split is appreciated. This is what is meant by close splitting. Patients of shunt lesion with PAH can have close splitting of S2.

17. Single S2 – The S2 split is not appreciated during expiration or inspiration. This is because both the P2 and S2 occur together as in Eisenmenger VSD or the A2 is heard loud and the P2 very feeble and hence a single S2 is appreciated as in TOF or the pulmonary artery is posterior and aorta is anterior resulting in easily audible loud A2 and poorly transmitted P2 as in Transposition of great arteries or when there is only a single great vessel as in Truncus Arteriosus. Conditions which can came paradoxical split may present as single S2 if the movement of P2 is such that the A2 – P2 interval during inspiration and P2 – A2 interval during expiration is equal to or less than 20 msec.

18. Paradoxical split The S2 split is appreciated during expiration and during inspiration the split shortens or becomes a single S2. This can occur in congenital severe AS, severe AR or large patent ductus arteriosus. The paradoxical splitting can have the following patterns.

19. Type I - Single S2 during inspiration and split S2 during expiriation. This is the classic paradoxical split. Expiration Inspiration S1 P2 A2 S1 P2A2

20. Type II - There will be normal split A2 – P2 during inspiration while during expiration also the split is appreciated(P2-A2). This can masquerade as fixed split of S2 Expiration Inspiration S1 P2 A2 S1 A2 P2

21. Type III -In this, the P2 – A2 patterns occurs during expriation and A2 – P2 patterns during inspiration. However the separation of sounds both during inspiration and expriation is less than 20 msec and this results in a single S2. Expiration Inspiration S1 P2A2 S1 A2P2

22. Paradoxical split and Valsalva maneuver * In strain phase: Paradoxically split S2 widens Normally split S2 narrows * In release phase: Paradoxically split S2 narrows Normally split S2 widens

23. Summary The evaluation of S2 is the most important single clinical assessment in the diagnosis of congenital heart disease.

24. Thank you