Posts Tagged ‘impedence of pulmonary circulation’

  • 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.

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