SAS
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QUESTIONS

  1. What is wrong with this statement:

    "Subaortic stenosis is believed to be the second most common congenital heart defect."

     
  2. When you think of SAS, what breeds do you think of?
     
  3. What is the difference between "Fixed" SAS & "Dynamic" SAS?
     
  4. Would you expect the murmur of SAS to be systolic or diatolic & why?
     
  5. Why does the murmur of SAS "radiate up the carotids?"
     
  6. Would you expect pulse quality to be weak or bounding in SAS?  Why?
     
  7. How is a diagnosis of SAS confirmed?
     
  8. What are the usual sequellae of SAS?




     

ANSWERS

  1. SAS is believed to be the second most common congenital heart defect except that technically it isn't congenital.  The stenosis, which can be as little as a fibrous ridge or as severe as a narrow tunnel in the left ventricular out flow tract, develops in the first 3 weeks after birth.

    Note: recently it was posted somewhere about a breeder of Newfie's who wanted to screen a litter for the disease.  It was recommended to wait ----------------- weeks.




     
  2. The breeds over-represented are the Newfie, Rott, Boxer & German Shepherd dog.  A heritability has definitely been established in the Newfie though the exact mode has not been worked out.




     
  3. The fixed form is more common.  In fixed SAS, the nature of the stenosis doesn't change.  It is the same old obstruction beat after beat & throughout the course of systole.  In dynamic SAS, the characteristics of the obstuction changes either from beat to beat or during the course of systole.  How can this be?  The interventricular septum and/or anterior leaflet of the mitral valve is flopping up & contributing to the obstruction.  The exact position during systole is different with every "flop."




     
  4. The murmur of SAS is systolic because the turbulence associated with the obstruction occurs during systole.  This should make sense because it is during systole that the heart is dealing with the lesion (trying to pump past it.) On the other side of the stenosis, there's a drop in resistance as "the highway widens" and this is where the turbulence is.




     
  5. The left ventricle must generate some serious pressure to pump a normal volume of blood through that little tiny hole but think what happens on the other side of the hole.  The blood is flying.  It's jamming.  It's supersonic coming through the hole.  And then there's major drop in resistance. The blood hits the aorta with such force that a post-stenotic dilation forms & that's not all.  This blood is jamming  still.  It's rolling.  It's speeding on highway 101.  And this is what you feel radiating up the carotids.

    Or is it that the turbulence is occuring outside the heart (in the aorta) & this is why the murmur radiates.  Most murmurs are from turbulence tucked away & enclosed in the heart.




     
  6. In SAS, pulse quality is poor.  Remember, this doesn't mean blood pressure is low; it means that there is only a small difference between systolic & diastolic pressure.

    (Why is diastolic pressure high?)




     
  7. The "gold standard" involves measuring the pressure in the left ventricle & comparing it to pressure measured in the aorta, both during systole.  This is done using a cardiac catheter & is called looking at "peak to peak" pressures.  It is also rather invasive & doesn't sound like any fun to me.

    SO, now we use Doppler technology.  We can do this because of Bernoulli's equation:

    Pressure gradient= rbc velocity in m/sec  X 4

    And how convenient that Doppler measures RBC velocity. This means we can non-invasively measure pressure gradient & diagnosis this disease.

    Prognosis can be based on pressure gradient.  <30 torr is mild (usually no signs), >70 is very bad.  Of course, not all dogs read the book.




     
  8. Common sequella number one:  SUDDEN DEATH

    (This occurs due to ventricular arrhythmias which occur due to foci of myocardial ischemia)

    Sequella number two:  CHF

    (how?)