SECOND HEART SOUND

DR.RAVIKANTH 1ST YR CARDIOLOGY RESIDENT

INTRODUCTION

The second heart sound occurs at the end of the ejection phase

of systole. It is related to the closure of the semilunar valves.

Since there are two semilunar valves, aortic and pulmonary,

there are also two components for the S2, namely the aortic

component (A2)and the pulmonary component (P2)

Mechanism of Formation of S2

Normal s2 The S2 is usually sharper, and shorter in duration compared to S1.

because semilunar valve closures occur at much higher pressures than the A-V valves and the dissipated energy in the columns of blood is much greater.

In normal young one can often hear both components of S2 . The S2 will therefore be heard as a split sound.

The first of the two components is the A2.

The higher resistance to forward flow in the systemic circulation results in earlier acceleration of reverse flow in the aortic root, causing the aortic valve to close earlier.

The pulmonary arterial bed is larger and offers markedly less resistance to forward flow. This will make the tendency to reverse flow occur later and slower compared to the left side.

In addition, the lower pressures achieved by the right ventricle during systole may actually result in a slower rate of relaxation of the right ventricle compared to the left ventricle. For these reasons, the P2 component occurs later.

IntensityAortic Component

The amplitude and intensity of A2 and P2 are directly proportional to the rate of change of the diastolic pressure gradient that develops across the semilunar valves.

The rate of pressure decline in ventricle and level of the diastolic pressure in the great vessels determine the pressure gradient in the root of the great vessels.

Normally, the diastolic pressure gradient in the aorta is greater than that in the pulmonary artery, which explains the normal increased intensity of A2 compared with that of P2

The Increased Intensity Decreased Intensity

The most common cause of the increased intensity of A2 is systemic hypertension. Occasionally, in addition to the increased intensity, a tambour quality of A2 is recognized in systemic hypertension.

Such altered quality of A2 also is appreciated in some patients with aneurysm of the ascending aorta.

The decreased intensity of A2 most frequently occurs from immobility of calcified, sclerosed aortic valves in calcific aortic stenosis.

In aortic regurgitation resulting from fibrosed and retracted aortic valve leaflets, as in syphilitic aortic regurgitation, the aortic component of the S2 also is decreased in intensity

Pulmonic Component

The pulmonic component of the S2 that is, P2 is softer than A2 and is rarely audible at the apex.

Increase in the intensity of P2 indicates pulmonary hypertension, irrespective of its etiology.

When there is increase in its intensity, P2 is also heard at the cardiac apex.

Without pulmonary hypertension, it is uncommon for the P2 to be transmitted to the cardiac apex.

In only approximately 5% of healthy subjects, and only when they are young (<20 years old), can P2 be recorded by phonocardiography over the cardiac apex

A palpable P2 over the left second interspace indicates severe pulmonary hypertension.

When the cardiac apex is occupied by the right ventricle as in patients with large atrial septal defects P2 can be heard at the apex, even when the pulmonary artery pressure is not increased.

Similarly, in patients with primary tricuspid regurgitation without pulmonary hypertension, P2 occasionally is heard at the apex.

In patients with a widely split S2 secondary to right bundle branch block, P2 rarely can be heard at the apex in the absence of pulmonary hypertension.

Decreased intensity of P2 results from a reduction in the pulmonary artery diastolic pressure, as in patients with pulmonary valve stenosis.

Decreased intensity of P2 or absence of P2 may also occur from the loss of the pulmonary valve leaflets or from the congenital absence of the pulmonary valves.

Splitting

In adults, the splitting of S2 during expiratory phase of respiration usually is not appreciated at the bedside, because the degree of splitting usually does not exceed 30 ms.

during inspiration, the splitting is easily appreciated, particularly in the semi recumbent position and even in elderly patients.

splitting of the S2 should be assessed during normal respiration with the diaphragm of the stethoscope over the left second and third interspaces close to the sternal border.

Normally, the aortic component of the S2 (A2) precedes the pulmonic component (P2).

The normal splitting of the S2 primarily results from the differences between pulmonary artery and aortic hangout times .

The left ventricular ejection starts a few milliseconds before the onset of right ventricular ejection because of the earlier onset of left ventricular depolarization ,contributes to the earlier completion of left ventricular ejection.

this earlier completion of left ventricular ejection only accounts for 10 to 15 ms of the degree of splitting of the S2.

Normal Respiratory Variations of A2-P2 Split

The normal respiratory variation is not as prevalent in the elderly as it is in younger patients. because of decreased compliance of the chest wall and great vessels and the relatively increased impedances in both systemic and pulmonary circulation

The hangout time is the interval between the end of ventricular ejection and the closure of the semilunar valves.

The hangout time in the aorta is shorter than that of the pulmonary artery. The hangout time in the pulmonary artery may be as long as 60 to 70 ms; the

hangout time in the aorta may be as short as 15 to 30 ms.

The difference between the pulmonary artery and aortic hangout times determines the degree of splitting of the S2, both in physiologic situations and in many pathologic conditions.

The hangout time also is determined by the compliance of the aorta and the

pulmonary artery.

Normally, the aorta is much stiffer than the pulmonary artery characteristic that accounts for the shorter hangout time in the aorta than in the pulmonary artery.

The normal inspiratory splitting of the S2 is explained by an increase in the pulmonary hangout time during inspiration that results from an increase in right ventricular stroke volume.

An increase in the right ventricular ejection time after inspiration also contributes to the inspiratory splitting of the S2.

More negative intrathoracic pressure during inspiration is associated with an increased venous return to the right ventricle and an increased right ventricular stroke volume.

During inspiration, A2 occurs slightly earlier because of the slight reduction of left ventricular ejection time associated with a transient, slight reduction of left ventricular stroke volume.

During normal respiration, prolongation of left ventricular ejection time and a delayed A2 usually occur during the expiratory phase, whereas lengthening of the right ventricular ejection time and delay in P2 coincide with the inspiratory phase.

Wide Splitting

In adults, when splitting of the S2 is appreciated during expiration, abnormal wide splitting of the S2 should be suspected.

The inspiratory increase in the degree of splitting of the S2 indicates the presence of physiologic delay in the pulmonary valve closure sound.

The widely split S2 during expiration (with further increase in splitting during inspiration) most frequently occurs in right bundle branch block.

A widely split S2 may be present in Wolff-Parkinson-White syndrome with left ventricular preexcitation.

Left ventricular pacing also produces right bundle branch block types of conduction disturbances and is associated with widely split S2.

The wide splitting of the S2 in conduction disturbances occurs from delayed activation of the right ventricle and consequently delayed completion of right ventricular ejection.

The wide splitting of the S2 may also result from increased resistance of right ventricular ejection, as in patients with pulmonary valve stenosis, infundibular stenosis, supravalvular stenosis, and pulmonary branch stenosis.

If the expiratory splitting of the S2 is approximately 40 to 50 ms, right ventricular systolic

pressure is also 40 to 50 mm Hg.

When the degree of splitting of the S2 exceeds 70 to 80 ms, the right ventricular systolic pressure is extremely high and may exceed 80 mm Hg.

In patients with pulmonary branch stenosis, the intensity of P2 is increased, and, frequently, unilateral or bilateral continuous murmurs are appreciated.

In adults, the most common cause of obvious expiratory splitting of the S2 with increased intensity of P2 is precapillary or postcapillary pulmonary arterial hypertension.

In pulmonary hypertension, although the expiratory splitting is obvious, the degree of splitting is less than that expected from the degree of pulmonary hypertension

Paradoxical Split

recognized when splitting of the S2 during expiration is appreciated. And, during inspiration, the A2 P2 interval shortens, and the S2 may appear single .

The sequence is reversed, with P2 preceding A2 during expiration.

During inspiration, P2 moves toward A2, and the splitting of the interval narrows.

The reversed splitting of the S2 may occur because of a delay in the electrical activation of the left ventricle, which results in a delay in the onset and completion of left ventricular ejection.

The most common cause of reversed splitting of the S2 is left bundle branch block, which is associated with a prolonged electromechanical interval.

Right ventricular ectopic beats and right ventricular pacing produce a delay in the onset of left ventricular contraction and result in reversed splitting of the S2.

The Wolff-Parkinson-White syndrome with right ventricular preexcitation is associated with reversed splitting of the S2.

Reversed splitting of the S2 may occur owing to prolongation of the left ventricular ejection time, resulting from selective increase in the left ventricular forward stroke volume or a marked increase in resistance to left ventricular ejection.

A selective increase in left ventricular forward stroke volume can occur in patients with significant aortic regurgitation or with patent ductus arteriosus with a large left-to-right shunt.

Increased resistance to left ventricular ejection occurs in patients with significant aortic stenosis and obstructive hypertrophic cardiomyopathy.

In patients with aortic stenosis, reversed splitting in the absence of left bundle branch block indicates hemodynamically significant aortic stenosis.

Poststenotic aortic root dilatation is associated with a decrease in the impedance in the

systemic vascular bed; delayed A2 can occur, which may contribute to the reversed splitting of the S2 .

Single Second Heart Sound

Single S2 may result from the absence of either of the two components of the S2 or from the fusion of A2 and P2 without the inspiratory splitting.

The most common cause of an apparently single S2 is the inability to hear the faint pulmonic component because of chronic obstructive lung disease, obesity, or even normal but accentuated respiratory noise.

Another common cause of single S2 is advanced age and most likely occurs because of a decreased inspiratory delay in P2, rather than a delayed A2.

Decreased inspiratory delay of P2 probably results from a decreased right-sided hangout interval related to aging changes in the pulmonary artery compliance.

However, all conditions that can delay A2 may produce a single S2 when the splitting interval becomes less than 30 ms.

In conditions in which one component of the S2 is absent or inaudible (e.g., in patients with severe tetralogy of Fallot, severe pulmonary valve stenosis, severe aortic stenosis, pulmonary atresia, and most cases of tricuspid atresia), S2 is single

CLINICAL ASSESSMENT OF S2S2 is a sharper, crisper sound and can be mimicked by the

syllable “dub.” It marks the end of systole and beginning of diastole.

With normal heart rates, diastole is longer than systole.

If the jugular contour is normal and visible in the patient, then the S2 can be noted to coincide with the systolic descent or the x′ descent  of the jugular pulse.

The x′ descent  is noted to fall onto the S2.

When assessing the S2, one needs to pay attention to the

-intensity.

-the nature of the individual components.

-variation with respiration.

Trying to pose a series of questions and answer them in a systematic manner is a useful bedside method to adapt:

The A2 is equally loud at the left ventricular apex as it is in the second right intercostal space, and it may occasionally be loudest at the apex.

A2 is never palpably loud unless significant systemic hypertension is present.

The intensity of theA2 does not vary with respiration.

P2, is never heard normally beyond the second and third left interspace.

when heard over the lower sternal border region and/or to the xiphoid region

would indicate either a louder intensity P2 as in pulmonary hypertension or that the right ventricle is enlarged because of a volume-overload state.

the P2 is not usually audible at the normal apex area, which is usually formed by the

left ventricle.

P2 often can be noted to increase in intensity with inspiration.

The increased volume in the right side presumably provides a greater right ventricular stroke volume, distending the pulmonary root to a greater degree.

A palpable P2 in the second left intercostal space usually indicates pulmonary hypertension, correlates to a pulmonary systolic pressure of at least 75mmHg.

Grade III A2 and grade III P2 fusing on expiration may occasionally become palpable. If this happens, the S2 palpability will be restricted to expiration.

S2 were palpable throughout inspiration and expiration in the second left intercostal space, it would definitely indicate pulmonary hypertension.

The exception,when an A2 may be actually palpable at the second left interspace, is transposition of the great vessels (whether congenitally corrected or not) where the aortic root is anterior, superior, and leftward

In young, thin adults, adolescents, and children, because of the thinner chest wall the P2 may be normally audible over a larger area.

These patients will tend to have an easily audible split of the S2, which

is sometimes wide.

When examined in the erect position, the respiratory variations become maximal .

In patients older than 60 yr it is unusual to hear a good split of S2 because of poor chest wall compliance as well as age-related increases in the pulmonary impedance.

Therefore, split S2 in the elderly is often abnormal and deserves clarification

Second Heart Sound In CCHD

Sequence Identification

In the normal, A2 precedes P2.

While A2 is heard over the apex, P2 is usually not heard at the normal apex, which is formed by the left ventricle.

If one auscultates over the second or third left intercostal space and hears a split S2 and then quickly changes over to apex with the rhythm of the split S2 in mind, one may be able to detect which of the two components is dropped or not heard at the apex.

If the first of the two components is dropped at the apex, then the sequence will have to be P2 A2.

If the second component of the split is dropped, then the sequence will be A2-P2. These conclusions stem from the fact that the normal P2 is the one that is not heard at the apex.

Mechanism Disease

Only one semilunar valve is present Truncus arteriosus

One of semilnar valve is atretic Pulmonary atresiaAortic atresia

Posterior location of pulmonary valve

TGA

Severe stenosis of one semilunar valve

AS or PS

Mechanisms And causes Of Single Second Sound

Mechanism Causes

Prolonged RV ejection Moderate to severe PSSevere PAH

Acute pul embolism ASD Severe RVF

Delayed electrical impulse to RV RBBBLV pacingLV ectopy

Increase in hangout interval Idiopathic dilation of pul arteryASD

Earlier completion of LV ejection Severe MR

Impaired diastolic filling Restrictive cardiomyopathyHCM

Constrictive pericarditis

Mechanisms and causes of wide split second heart sound

Mechanism Causes

Defect in interatrial septum allowing free communication between to atria

ASD

RVF failing to increase the stroke volume from the increased venous

return

All causes of wide split with associated severe RVF

Mehanisms And Causes Of Fixed Split

Mechanism Causes

Delayed electrical activation of LV LBBBRV pacingRV ectopy

Prolonged LV mechanical systole Sever ASSevere Hypertension

Acute MISevere ARLarge PDA

Increase of hangout interval on aortic side

Aneurysm of ascending aortaPost stenotic dilation in AS

Early pulmonary closure Severe TRWPW syndrome right lateral pathway

Mechanism And Causes Of Reversed Splitting

Causes Mechanism

Systemic hypertension Elevated pressure beyond valveDilated ascending aorta

Aneurysm of ascending aorta Dilatation of vessel

AR Aortic root diseaseDilated ascending aorta

Congenital bicuspid aortic valve

Thickened but mobile aortic leaflets

Causes And Mechanism Of Loud A2

MECHANISM CAUSES

High pulmonary arterial pressure Normal in infants and children

Proximity of pulmonary artery to steth Adults with chest deformity or thin chest

Higher closing pressure of valveDilated PA

PAH

Increased flow across valve with exagerrated valve excursion

Dilated PAPAH

L R shunts

Increased flow across valve with exagerrated valve excursion

Dilated PA

Hyperkinetic circulatory states

Loud P2

Causes Of Diminished P2

Second Heart Sound In ASD

Second Heart Sound In VSD

Second Heart Sound In PDA

Second Heart Sound In PS

Second Heart Sound In Eisenmingers