SECOND HEART SOUND- PHYSIOLOGY & PATHOPHYSIOLOGY

1. SECOND HEART SOUND- PHYSIOLOGY & PATHOPHYSIOLOGY

2. “Key to auscultation of heart”-Leatham 2 components-first designated as aortic and second as Pulmonary Normally splits into 2 componentsduring inspiration and narrows in expiration Respiratory variation first described by Potain(1866)

3. Physiology Closure of the aortic and pulmonic valves initiates the series of events that produces the second heart sound. The main audible components results from vibrations of the cardiac structures after valve closure. Using high-fidelity, catheter-tipped micro-manometers and echophonocardiography, it has been shown that the aortic and pulmonic valves close silently and that co-aptation of the aortic valve cusps precedes the onset of the second sound by a few milliseconds.

4. The second sound originates from after-vibrations in the cusps and in the walls and blood columns of the great vessels and their respective ventricles. The energy from these oscillations comes from sudden deceleration of retrograde flow of the column of blood in the aorta and pulmonary artery

5. Softer pulmonic sound is confined to pulmonry area Louder aortic sound is heard all over precordium Splitting of second heart sound is normally confined to second left intercostal space

6. Second heart sound • must be separated by more than 20 msec (0.20 sec) in order to be differentiated and heard as two distinct sounds. • Splitting is best identified in the second or third left ICS, since the softer P2 normally is confined to that area, whereas the louder A2 is heard over the entire precordium, including the apex.

7. Why is A2 before P2 ? Both right & left ventricular systole ends at the same time . pulmonary arterial pressure is less than aortic pressure (i.e, pulmonary resistance to forward flow from ventricles is less than aortic resistance pulmonary impedance is less than aortic impedance.){impedance is nothing but resistance}

8. Therefore as pulmonary impedance is less, even after right ventricular systolic contraction blood continues to flow through valve until pulmonary arterial pressure increases more than right ventricle). But as aortic impedance is more ,it stops blood flow through the aortic valve before itself. Due to the above reasons ,Right ventricular ejection begins prior to left ventricular ejection, has a slightly longer duration, and terminates after left ventricular ejection, resulting in P2 normally occurring after A2.

9. Hangout interval Duration of the "hangout interval" is a measure of impedance in the pulmonary artery system. In the highly compliant (low-resistance, high-capacitance) pulmonary vascular bed, the hangout interval may vary from 30 to 120 msec, contributing significantly to the duration of right ventricular ejection.

10. 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 occurance of sound is called HANGOUT interval • Hangout interval is lesser on Aortic (30msec)than Pulmonary side(80msec) • Higher pressure • Less distensibility • Depends on interrelated factors like pressure beyond the valve,dilatation of the artery,distensibility of arterial system,vascular impedance,phase of respiration.

12. In the left side of the heart, because impedance is much greater, the hangout interval between the aorta and left ventricular pressure curves is negligible (less than or equal to 5 msec). The hangout interval therefore correlates closely with impedance of the vascular bed into which blood is being injected. Its duration appears to be inversely related to vascular impedance.

13. Normal physiological splitting during respiration: Alterations in the impedance characteristics of the pulmonary vascular bed and the right-sided hangout interval are responsible for many of the observed changes in splitting of S2. In a normal physiologic setting, inspiration lowers impedance in the pulmonary circuit, prolongs the hangout interval and delays pulmonic valve closure, resulting in audible splitting of A2 and P2.

14. Pulmonic valve closure is earlier, and the A2–P2 interval is separated by less than 30 msec and may sound single to the ear. pulmonary circulation has a much lower impedance than the systemic circulation Flow through the pulmonic valve takes longer than flow through the aortic valve. The inspiratory split widens mainly because of delay in the pulmonic component.

15. Traditional view Inspiratory drop in intrathoracic pressure favored greater venous return to the right ventricle, pooling of blood in the lungs, and decreased return to the left ventricle. On expiration, the reverse occurs

16. The increase in right ventricular volume prolonged right-sided ejection time and delayed P2 Decrease in left ventricular volume reduced left-sided ejection time and caused A2 to occur earlier.

17. The delayed P2 and early A2 associated with inspiration,is an interplay between changes in the pulmonary vascular impedance and changes in systemic and pulmonary venous return. The net effect is that right ventricular ejection is prolonged, left ventricular ejection is shortened, and the A2–P2 interval widens during inspiration.

18. Clinical Significance Normally the aortic closure sound (A2) occurs prior to the pulmonic closure sound (P2), and the interval between the two (splitting) widens on inspiration and narrows on expiration. With quiet respiration, A2 will normally precede P2 by 0.02 to 0.08 second (mean, 0.03 to 0.04 sec) with inspiration. In younger subjects inspiratory splitting averages 0.04 to 0.05 second during quiet respiration.

19. With expiration, A2 and P2 may be superimposed and are rarely split as much as 0.04 second. If the second sound is split by greater than 0.04 second on expiration, it is usually abnormal.

20. Presence of audible splitting during expiration (i.e., the ability to hear two distinct sounds during expiration) is of greater significance at the bedside in identifying underlying cardiac pathology than is the absolute inspiratory increase in the A2–P2 interval.

21. NORMAL SPLIT • 2 components in inspiration,and single in expiration • During inspiration,negative intrathorasic pressure-increased venous return ,increased stroke volume of right ventricle,prolonged RV ejection-P2 is delayed • Inspiratory decrease of venous return to left heart,reduces the LV stroke volume,shortens LV ejection,advancing the A2

22. DETERMINANTS OF NORMAL SPLIT • Pressure difference between 2 circulations • Ejection property of 2 ventricles • Difference in hangout intervals of 2 AV valves • Right and left sided venous return • Intact IAS • Simultaneous onset of electrical impulse to either ventricle

24. LOUDNESS/INTENSITY • A2 relatively loud-hence heard all over precordium • P2 is relatively soft,hence localised to 2nd left intercostal space

25. LOUD A2 • SYSTEMIC HYPERTENSION • ELEVATED PRESSURE BEYOND THE VALVE • DILATED ASCENDING AORTA • ANEURYSM OF ASCENDING AORTA • DILATATION OF VESSEL • AORTIC REGURGITATION • AORTIC ROOT DISEASE • WELL PRESERVED LEAF MOBILITY • INCREASED FLOW ACROSS THE VALVE • DILATED ASCENDING AORTA • CONGENITAL BICUSPID AORTIC VALVE • THICKENED BUT MOBILE AORTIC LEAFLETS

26. LOUD P2 • Graham Steell describes p2 in pulmonary hypertension”…..extreme accentuation of the pulmonary second sound is always present,the closure of semilunar valves being generally perceptible as to the hand placed over the pulmonary area,as a sharp thud……” • An accentuated P2 can be transmitted to mid or lower left sternal edge and,when very loud throughout precordium. • Splitting can be made out in other areas • Pulmonary hypertension,dilated pulmonry trunk(idiopathic,ostium secondum ASD),decreased AP chest dimensions(loss of thorasic kyphosis)

27. LOUD P2 • PULMONARY ARTERIAL HYPERTENSION • HIGHER CLOSING PRESSURE OF VALVE,DILATED PA • LEFT TO RIGHT SHUNTS • INCREASED FLOW ACROSS THE VALVE,INCREASED VALVE EXCURSION • DILATED PA • PAH • HYPERKINETIC CIRCULATORY STATES • INCREASED FLOW ACROSS THE VALVE • DILATED PA INFANTS AND CHILDREN,P2 LOUDER DUE TO HIGHER PULMONARY ARTERIAL PRESSURES

28. DIMINISHED PULMONIC SOUND • DIMINISHED • THICK CHEST WALL • PULMONARY STENOSIS • DYSPLASTIC VALVE • ABSENT • TETROLOGY OF FALLOT • TRANSPOSITION OF GREAT ARTERIES • TRUNCUS ARTERIOSUS • PULMONARY ATRESIA • ABSENT PULMONARY VALVE

29. DIMINISHED PULMONIC SOUND • DIMINISHED • THICK CHEST WALL • PULMONARY STENOSIS • DYSPLASTIC VALVE • ABSENT • TETROLOGY OF FALLOT • TRANSPOSITION OF GREAT ARTERIES • TRUNCUS ARTERIOSUS • PULMONARY ATRESIA • ABSENT PULMONARY VALVE

30. Single semilunar valve may produce multiple sounds rarely as in case of Truncus arteriosus with a quadricuspid valve

31. ABNORMAL SPLITTING OF THE SECOND HEART: (1) single (2) splitting, with normal respiratory variation; (3) splitting without respiratory variation (fixed splitting); and (4) reversed (paradoxical) splitting.

32. Persistently single When S2 remains single throughout the respiratory cycle, one component is absent or the two components are persistently synchronous. The most common cause of a single S2 is inaudibility of the P2 in older adults with increased anteroposterior chest dimensions.

33. congenital heart disease, a single S2 due to absence of the pulmonary component is a feature of pulmonary atresia, severe pulmonary valve stenosis, dysplastic pulmonary valve, or complete transposition of the great arteries. single S2 due to inaudibility of the A2 occurs when the aortic valve is immobile (severe calcific aortic stenosis) or atretic (aortic atresia).

34. Persistant (audible expiratory) splitting, with normal respiratory variation Persistent splitting may be due to a delay in P2, as in complete right bundle branch block early timing of the A2, mitral regurgitation(since early emptying of left ventricle –> early closure of Aortic valve). Normal directional changes in the interval of the split (greater with inspiration, lesser with exhalation) in the presence of persistent audibility of both components defines the split as persistent but not fixed.

35. Fixed splitting Interval between the A2 and P2 is not only wide and persistent but also unchanged during the respiratory cycle. Fixed splitting is an auscultatory hallmark of atrial septal defect(ASD). A2 and P2 are widely separated during exhalation and exhibit little or no change in the degree of splitting during inspiration. Mechanism RA,LA act as common venous reservoir Inspiration-decresed left to right shunt,transient right to left shunt Balance out changes in ventricular filling in different phases of respiration

38. Reversed (paradoxical) splitting Maximally split on expiration and narrows or fuses on inspiration A2 occurs after P2

39. TYPES OF REVERSE SPLIT Type 1:Two components are close together in inspiration-single second sound in inspiration Type 2:S2 reversal only in expiration,normal in inspiration Type 3:S2 single in both phases of respiration

40. REVERSE SPLITTING OF SECOND HEART SOUND • DELAYED ELECTRICAL ACTIVATION OF LV LBBB RV PACING RV ECTOPY PROLONGED LV SYSTOLE SEVERE AS SEVERE SYSTEMIC HYPERTENSION ACUTE MYOCARDIAL INFARCTION CARDIOMYOPATHY INCEREASED HANGOUT INTERVAL ON AORTIC SIDE ANEURYSM OF ASCENDING AORTA EARLY PULMONIC CLOSURE TYPE B WPW SYNDROME(EARLY ACTIVATION OF RV)

41. REVERSE SPLITTING OF SECOND HEART SOUND • DELAYED ELECTRICAL ACTIVATION OF LV LBBB RV PACING RV ECTOPY PROLONGED LV SYSTOLE SEVERE AS SEVERE SYSTEMIC HYPERTENSION ACUTE MYOCARDIAL INFARCTION CARDIOMYOPATHY INCEREASED HANGOUT INTERVAL ON AORTIC SIDE ANEURYSM OF ASCENDING AORTA EARLY PULMONIC CLOSURE TYPE B WPW SYNDROME(EARLY ACTIVATION OF RV)

42. SINGLE SECOND SOUND • TRUNCUS ARTERIOSUS • PULMONARY ATRESIA • TRANSPOSITION OF GREAT VESSELS • AS • PS • PULMONARY ARTERY HYPERTENSION

43. CAUSES OF WIDE SPLIT SECOND HEART SOUND • PROLONGED RV EJECTION • PS • SEVERE PAH • ACUTE PE • ASD • RV FAILURE • DELAYED ELECTRICAL IMPULSE TO RV • RBBB • LV PACING • LV ECTOPY • INCREASED HANGOUT INTERVAL • ASD • IDIOPATHIC DILATATION OF PULMONARY ARTERY

44. EARLIER COMPLETION OF LV EJECTION • SEVERE MR • IMPAIRED DIASTOLIC FILLING • RESTRICTIVE CARDIOMYOPATHY • HYPERTROPHIC DISORDERS OF MYOCARDIUM • CONSTRICTIVE PERICARDITIS

45. SINGLE SECOND SOUND IN CONGENITAL HEART DISEASE • TOF -ABSENT P2 due to PS • D-TGA- INAUDIBLE P2-POSTERIOR PLACEMENT • L-TGA- ” • DORV- “

46. SINGLE VENTRICLE “ TRICUSPID ATRESIA-absent P2 due to PS TRUNCUS ARTERIOSUS-only one semi lunar valve

47. S2 in Eisenmenger syndrome ASD-wide and fixed split VSD-single loud P2 PDA-close split,normal inspiratory split

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