X-Message-Number: 2807
Date: 7 Jun 94 08:28:27 GMT
From:
Subject: SCI.CRYONICS Presure fall at end.
I had no idea that such a minor point would result in so much reply.
(I was hoping someone might comment on the new aorta blocking method.)
Mike Darwin writes:
.Keith Henson notes in his recent commentary on the last Alcor perfusion:
.<<We were very near our target when perfusion was terminated by loss of
.arterial pressure. This is something we have seen before. Since
.there was no jump in perfusate loss it was almost certainly due to
.heart valves starting to leak as they were deformed by glycerol
.dehydration--something we have seen in a number of suspensions.>>
.Without being in any way recriminatory or negative I wish to simply point
.out that this observation is not correct and does not represent either my
.experiences with or without Jerry Leaf in caring for either Alcor or
.non-Alcor patients.
.I would make the following points:
.1)
[discussion of heart valves and procedure during bypass--no
disagreement.]
.2) Contrary to Keith's statement that loss of arterial pressure is routine
.or common during the tail-end of cryoprotective perfusion, the REVERSE is
.the case; mean arterial (and central venous) pressures RISE as glycerol
.concentration increases near the end of the CPA ramp. This happens due to
.the fact that the viscosity of the perfusate increases as the glycerol
.concentration rises (and as the temperature is sometimes reduced
.concomitantly to minimize toxcicity, further increasing viscosity). The
.increased viscosity means increased resistance to flow which in turn means
.increased pressure. This is usually compensated for by the perfusuionist
.manually DECREASING the arterial flow rate.
I agree with the last points. In fact, we had adjusted the flow rate
2-3 times to keep the pressure in bounds as the viscosity built up.
(high concentration glycerol approaches the viscosity of honey!)
3)
[typical patient data presented--again no disagreement with the data
or conclusions on these patients.]
Mike, I don't have the patient records at hand either, but I remember
at least one other Alcor high molar case (I think it was the one you
missed the tail end of the perfusion because of another case) where we
had the terminal fall in MAP and concluded it was due to glycerol
deforming the heart valves. I definitely remember one other with
Jerry Leaf where we lost pressure at the end, but I think that one was
due to leakage we could no longer control around the cannula insert
points. (The tissue got so stiff with glycerol it would no longer
seal.)
There are other possible reasons for the pressure to fall, but given
the observed state, I considered this one the most likely. It was not
a point I felt the need to investigate because we were right at the
end of perfusion anyway (and wanted to start the patient cooling
ASAP).
.Failure of the brain to swell is NOT indicative of continuing cerebral
.perfusion. The only ways I know of to assess whether brain perfusion is
.continuing is to do one of the following:
Agreed. But serious swelling IS indicative of cutting off cerebral
perfusion (as happened when Jerry Leaf was suspended). That we did
not get. I hear that the same high ramp method for an ischemically
injured patient worked well for you the following week. Re your
point,
.a) inject a dye into the perfusate and watch through the burr-hole and
.look for cerebral cortical staining with the dye.
I was there the first time you did it, and it worked great! But it
only tells about the flow under the burr-hole, unless you have enough
brain shrinkage to look at a wider area with a fiberscope.
Your b) and c) [deleted] methods should work better. However, I am
not aware of a lot you can do in real time if you find there are
some areas of the brain which are not getting perfused. (Correct me
if I am wrong.) I certainly would not have been surprised to find
serious regional blockage--given the history of the patient. On the
other hand, there was other indirect evidence of good washout. The
glycerolized skin was very smooth, indicating even *skin* circulation,
and few blocking clots.
(There is considerable room for debate on how much *research* you
should try to get out of each patient, and how much an organization
can afford and still keep the cost of suspensions within reason. *I*
won't get involved in this on cryonet, but there is truly no limit as
to how much can be spent for research!)
.The sudden loss of arterial pressure during cryoprotective is NOT a normal
.course of affairs and in my opinion represents a serious (and in this
.case) unexplained compromise of the intergrity of either the arterial leg
.(i.e., high pressure side) of the circulatoruy system/perfusion circuit.
.I have perfused MANY rabbits, dogs, cats and humans to high terminal
.glycerol concentrations (3-7+ M) and have never observed this
.phenomenon.
*IF* the pressure loss had happened at an earlier point in the
perfusion, we would have had to find the cause for it--and fix if
possible. My assumption of valve leakage due to dehydration was
because there was no loss of recirculating volume. I would be open to
other causes, but again, we were right at the cutoff point, and there
was no reason to delay getting the patient into cooldown.
.Finally, I urge that the current embargo on patient raw data be ended and
.that such data be made available to all who request it (with appropriate
.steps taken to protect patient confidentiality). BPI intends to follow
.this policy and will shortly be posting the technical case historires/raw
.data on all three of the patients it has treated to date (one case report
.has been ready for several weeks and will be posted shortly).
I appreciate your doing this. Eventually someone will have to do an
analysis of the suspensions to date, and, even though the data is
*very* noisy, try to draw some conclusions about how to improve
suspension practice.
Keith Henson
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