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Archive for the ‘Clinical cardiology -Cyanosis’ Category

Can we close an  ASD in a  25 year old women  severe  pulmonary hypertension ?
Volumes of literature has been written  on the subject.Dedicated cath studies  have been done with multiple parameters .
Still , there is a lingering doubt !
Here is  a  3 minute  practical solution  based on 5 easily available parameters. (* Also referred to as  unscientific  in medical parlance !)
1.  O2 saturation
2. Pulmonary artery diastolic and pulse pressure
3. RV function,
4 .Systemic pressure
5. Functional class
  • If O2 saturation is > 90 % consistently  there is likely to be significant  left to right shunt  .Closure is to strongly considered
  • If 02  saturation is near 95 % there is absolutely no contraindication at any level of PVR.
  • Systolic pulmonary artery pressure derived by TR jet is least useful index.Pulmonary artery diastolic pressure reflects true vascular  reactivity of the pulmonary  circulation.A wide swinging pulmonary arterial pulse indicates dynamism in circulation and hence operablity.
  • If pulmonary artery  pulse pressure is  wide (>50)  , or PA diastolic BP is < 30 one can safely presume irreversible damage to pulmonary vasculature has not occurred and these patients would  benefit  from surgical closure .
  • RV  function should be assessed carefully in every patient.This is as important as PVR .Significant RV dysfunction is an absolute contraindication.
  • Never close the shunt in patients who is in class 4  symptoms.
  • Never close a shunt if the systemic blood pressure is low( 90mmhg)
  • Some believe  PDA may be closed at any given PVR , while  worst outcomes occur with ASD as supra-systemic pulmonary pressure is possible.
Always monitor these patients meticulously especially  in the initial days following surgery  for deterioration .Most patients will do well if they cross the first 30 days. The RV  learns to adopts with  new  pulmonary hemodynamics !

 

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All left to right shunts are  acyanotic heart disease to begin with. Cyanosis appears if there is progressive PHT and reversal of shunt .We know this happens late in ASD.(third decade)

It is important to remember some of the  patients  with large ASD  can show significant desaturation without severe pulmonary HT.  This should not be mistaken for Eisenmenger reaction.

How ?

In  any large ASD ,

  • IVC blood can stream into LA by hitting preferentially the lower part of IAS.( It is the old fetal route that heart does not forget  and indulges whenever the  local hemo-dynamics permits !)
  • During straining , (Valsalva and equivalents)  right atrial pressure can exceed LA and small amount of shunts occur across RA.
  • ASD is often (15%) associated with systemic venous anomaly. The common one is persistent LSVC.  LSVC  is usually connected to coronary sinus . If it has a communication with LA (Un-roofed CS) , there can be significant cyanosis .
  • Further , a large ASD can act as a single atrium and considerable mixing happens and cyanosis results.

Finally ,two conditions should always be considered

  • ASD if associated with VPS auguments R-L shunt .
  • TAPVC can be mistaken for Eisenmengerisation of  ASD in bedside which presents as clinical signs of ASD + Cyanosis

* It is useful to recall ,even PFOs can shunt right to left at times of extreme RA pressures like during PEEP ventilation and orthostatic  deoxia in sick ICU patients are reported (If PFO can shunt R-L , why not huge ASD ?)

Final message

Cyanosis  in ASD is not always  an ominous sign .There are few important causes other than Eisenmenger. Though it  occurs intermittently , persistent mild desaturation is also possible.

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