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To: techdiver@opal.com
Subject: bubble trapping, (was Australian O2 protcol.)
From: shelps@ac*.ma*.ad*.ed*.au* (Prime Rat)
Cc: ddoolett@ac*.ma*.ad*.ed*.au*
Date: Tue, 20 Dec 1994 15:44:34 +1030
I lost the thread here a bit so I'll be "brief" and maybe provide more 
detail if requested.  These topics appear from time to time on Techdiver and 
I don't want to bore the old timers with the same old stuff. 

>>Well, you don't like my hypothesis - can you come up with an 
>>alternative one or do you discount the anecdotal observations it 
>>attempted to address?
>I forget what these anecdotal observations were.  I was just pointing out 
>that aterial bubble trapping is an old theory that is neither established as 
>fact or particularly likely to be the case. 

Blocking of brain arterioles or capillaries by bubbles produced during 
decompression or directly injected into the arterial circulation is only 
seen when the heart stops beating, ie (as is well known) after death.  If we 
perform a craniotomy on a rabbit and produce intra-artial bubbling by 
decompression or direct injection of air into the arterial circulation the 
bubbles are seen to pass though the artioles and disappear.  They can in 
fact, be detected in the saggital sinus (using ultrasonic Doppler) exiting 
the brain vascular bed.  Conclusion?  Bubbles do not block the capillaries.  
Brain blood flow is not affected for at least 2 hours after this type of 
injury.  Small doses of air produce a progressive loss of brain function 
(flow and function remain coupled), larger doses of air produce a sudden and 
profound cessation of brain function (flow and function are uncoupled).  

>>#This is not so.  There is little (or no?, comments Prime Ra?) evidence that 
>>#bubbles trap in the arterial circulation.  One workers calculations suggest 
>>#that the bubble, which would be tubular in shape, would need to extend 
>>#through three generations of arteries before they would trap.

And then they only do so temporarily and in any event collateral 
vascularisation means that blood flow is not affected.  We know the 
secondary effects of intravascular bubbling are the important ones because 
if we modify them (remove the white cells or make them slippery) the effects 
of cerebral arterial air embolism on brain blood flow and brain function can 
be largely prevented.

>>Firstly, if bubbles were to lodge at all I would imagine them to do so 
>>in arterioles/capillaries: I didn't mean to imply they could get 
>>trapped in the arteries themselves. If this trapping can't happen, 
>>then how does the lung normally trap the so-called "silent bubbles" 
>>present in the pulmonary artery?
>The pulmonary arterial pressure is much lower than the systemic arterial 
>pressure.

Althought the lungs also have an enormous surfcae area and will filter a 
certain amount of any intravascular gas load, they can fill up.  The cycle 
of compression-decompression (ascent-descent) will also cause some of air 
trapped in lungs to escape back into the arterial circulation.

>>Secondly, lack of evidence don't always mean something ain't true.

What does it mean then?  That more experiments need to be done?

>>#Bubbles are a problem if untrapped, they activate the  complement and kinin 
>>#systems and damage the blood vessel endothelium.
>>That's why I said simplistically, and I didn't suggest that bubble 
>>trapping was the only factor involved.
>>Were your assertion correct, then why would arterial bubbles be 
>>considered more of a problem (PFO and the like) than venous ones per 
>>se?  Are the complement and kinin systems only activated on the 
>>passage of bubbles through capillaries? 

Complement and kinin systems can be activated by shaking blood in a test 
tube.  To see the effect of exposing blood to a gas interface, just cut 
yourself.  Bubbles inside the circulation initiate many of these clotting 
processes.

>I suspect these systems are activated by venous bubbles (the first to form) 
>and this accounts for the 'flu' like symptoms of mild DCI.

So consider the possible spectrum; 

- bubbles form in the venous before the arterial circulation because 
  it is at a lower pressure (bubbles formation in the arterial circulation
  has been observed during normal decompressions)

- bubbles then activate components of the complement and clotting cascade

- these (soluble) intermediary compounds arrive in the artial circulation

- some bubbles arrive in the arterial circulation, either because of a 
  patent foramen ovale, lung dysfunction, patent ductus arterious or 
  they simply form there

- bubbles bouncing along the vascular lumen irritate the endothelial cells

- damaged endothelium collected some of these clotting factors (some of 
  them actually live in the endothelial cells

Outcome depend on the interaction of these (and a whole bunch of other) things.

- none of this stuff affects your central nervous system because the dose 
  is too small.  You do you dive and you feel great ("silent bubbles")

- your central nervous system is partially affected.  You do you dive, 
  but you feel a bit more stuffed than usual. ("not so silent bubbles")

- your central nervous system is affected in a big way.  You do
  your dive and you now have mild but recognisable symptoms of DCI.
  Conservative treatment works.  You take up diving again some weeks later.
  ("noisy bubbles")

- your central nervous system is affected in a major way.  You do
  your dive and you now have serious DCI with neurological symptoms.
  Conservative treatment doesn't work.  Aggressive and multiple hyperbaric
  oxygen treatment is indicated.  After a couple of weeks of this you are
  better but the treating doctor says "no more diving". ("very loud bubbles")

- your central nervous system is wrecked.  You die. ("positively
  deafening bubbles")

Each of these conditions has been modelled using experimental animals and 
even sometimes (believe it or not) human beings.

/rat

ps Buy the book "Pathophysiological basis of cerebral arterial gas 
   embolism (DCI)" [AUD$250 from the Dept.Anaesthesia, University of 
   Adelaide] and get the latest on scientific research into decompression
   illness.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
shelps@ac*.ma*.ad*.ed*.au*|Stephen Helps PhD            Ack!  ___/|
FAX   (08)232-3283             |Anaesthesia & Intensive Care       \O.o|
Voice (08)224-5495             |University of Adelaide            =(___)=
                               |ADELAIDE, 5005, South Australia      U
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
"It's not denial. I'm just very selective about what I accept as reality."
                                         --- Calvin ("Calvin and Hobbes")
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

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