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.

S 2 A2 louder audible at base, LSB and apex P2 softer confined to 2 nd 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 s 2 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 s 2 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 2 nd 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

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) Single P2

AnomalyP2 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 Cyanotic Congenital Heart Disease

Phonocardiography Single Vs Closed split Confirmation P2 or A2 Reversed Splitting For teaching purpose

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