- Second heart sound is widely split because the pulmonary hangout interval* is wide
- Fixed because , the RV stroke volume does not show the normal respiratory changes.
This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .
* Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.
Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )
What is the normal pulmonary hangout interval and systemic hangout interval /
Pulmonary hangout interval is 60-80ms
Aortic hang out interval is 20 ms
Why does it happen ? What does it signify
It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the closed semi lunar valves. This keeps the arterial pressure not only to be sustained little longer but also slightly higher .
This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.
How much of S2 widening is contributed by RBBB in ASD ?
This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )
What happens to S2 when pulmonary arterial hypertension develops in ASD ?
- It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)
- It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.
*Mild PAH usually does not alter the S 2 splitting
Is there any other cause for wide and fixed splitting of second heart sound ?
Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .
Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)
Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?
Guess the answer .It will be posted soon.