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Wednesday, July 8, 2009

Splitting of Second heart sound

To understand Splitting of S2 better, we should first understand its normal physiology.

Second heart sound:

It has two audible components, the aortic valve closure sound (A2) and the pulmonic valve closure sound (P2), which are normally split on inspiration and virtually single on expiration.

Technique:

It has two audible components, the aortic closure sound (A2) and the pulmonic closure sound (P2), which must be separated by more than 20 msec (0.20 sec) in order to be differentiated and heard as two distinct sounds. It is clinically very important to determine the presence and degree of respiratory splitting and the relative intensities of A2 and P2.

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.

Physiology:

Various research findings suggests that closure of the aortic and pulmonic valves initiates the series of events that produces the second heart sound. The main audible components, however, result 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. The second sound therefore 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 when the elastic limits of the tensed valve leaflets are met. This abrupt deceleration sets the whole cardiohemic system into vibration.

In order to understand splitting of the second heart sound, knowledge of its relationship to the cardiac cycle is essential.

First lets understand why is A2 before P2 ?

1.Both right & left ventricular systole ends at the same time .(ie, systolic muscle contraction of both ventricles ends at same time)

2.pulmonary arterial pressure is less than aortic pressure (i.e, pulmonary resistance to forward flow from ventricles is less than aortic resistance => therefore we can say that pulmonary impedance is less than aortic impedance.){impedance is nothing but resistance}

3.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.

4.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.

A2 and P2 are coincident with the incisura of the aorta and pulmonary artery pressure curves, respectively, and terminate left and right ventricular ejection periods.(incisura reflects closure of valves)

The differences between the aortic and pulmonary artery vascular impedance characteristics are also essential to understanding the effects of respiration on splitting of S2. When the pressure curves of the pulmonary artery and right ventricle are recorded simultaneously, the pulmonary artery curve at the level of the incisura (dicrotic notch) lags behind the right ventricular curve, or "hangs out" after it.

hangout interval

The 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.

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.

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.

On expiration, the reverse occurs: pulmonic valve closure is earlier, and the A2–P2 interval is separated by less than 30 msec and may sound single to the ear. Since the 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.

Traditionally it was believed that an 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. The increase in right ventricular volume prolonged right-sided ejection time and delayed P2; the decrease in left ventricular volume reduced left-sided ejection time and caused A2 to occur earlier. The delayed P2 and early A2 associated with inspiration, however, are best understood as 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.

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. 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.

Therefore, the 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.

ABNORMAL SPLITTING OF THE SECOND HEART:

(1) persistently single;

(2) persistent (audible expiratory) splitting, with normal respiratory variation;

(3) persistent splitting without respiratory variation (fixed splitting); and

(4) reversed (paradoxical) splitting.

splitting s2

(1) 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.
  • In the setting of
    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.
  • Conversely, a single S2 due to inaudibility of the A2 occurs when the aortic valve is immobile (severe calcific aortic stenosis) or atretic (aortic atresia).

(2) persistent (audible expiratory) splitting, with normal respiratory variation;

  • Persistent splitting may be due to a delay in P2, as in cases of simple complete right bundle branch block,or to early timing of the A2, as occasionally occurs in cases of 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.
  • these conditions have wide inspiratory split

(3) fixed splitting;

  • This term applies when the interval between the A2 and P2 is not only wide and persistent but also remains 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.

Reason behind wide splitting:

The wide splitting is caused by a delay in the P2 because a marked decrease in pulmonary vascular impedance prolongs the interval between the descending limbs of the pulmonary arterial and right ventricular pressure pulses (“hangout”), and therefore delays the pulmonary incisura and the P2.

Reason behind fixed splitting:

  • We know that in normal individuals , the amount of pulmonary ejection is more during inspiration compared to that in expiration (since pulmoary impedance decreases during inspiration)
  • In ASD .the amount of blood which passes throught he pulmonary valve ramains the samee in both inspiration& expiration because of Phasic changes in systemic venous return during respiration in patients with atrial septal defect are associated with reciprocal changes in the volume of the left-to-right shunt, minimizing respiratory variations in right ventricular filling. (ie, whenever venous return increases in inspiration, it causes a reciprocal decrease in left to right shunting in atria & whenever venous return decreased as in expiration ,shunting increases =>this maintains equal amount of blood in right ventricle irrespective of inspiration or exoiration)
  • The net effect is the characteristic wide, fixed splitting of the two components of the S2.

(4) reversed (paradoxical) splitting. 

  • This term refers to a reversed sequence of semilunar valve closure, the P2 preceding the A2.
  • Common causes of paradoxical splitting are complete left bundle branch block or a right ventricular pacemaker, both of which are associated with initial activation of the right side of the ventricular septum, and delayed activation of the left ventricle owing to transseptal (right-to-left) depolarization.
  • When the S2 splits paradoxically, its two components separate during exhalation and become
    single (synchronous) during inspiration .
  • Inspiratory synchrony is achieved as the two components fuse because of a delay in the P2, less to earlier timing of the aortic
    component.

  splitting s2

 

Please review this article & if you have any doubts do tell me.

10 comments:

Anonymous said...

Was great, helped me to understand! Thank you!

Anonymous said...

It was splendid,but it will be marvelous if you include the physiological basis of reverse splitting of 2nd heart sound in ASD!!

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Anonymous said...

does systemic hypertention which increases aortic impedence causes wide splitting of s2?

Anonymous said...

thanks! Really helpful!
This website is amazing!

Anonymous said...

excellent!!really understood basic feautures of splitting after reading this page.:-))

Aditya Agarwal said...

Everything is given in the right amount with good explanations..
Quite helpful....good job!

Rameshkumar Thevarajah said...

thank u....

Robert Clark said...

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Anonymous said...

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