X-Message-Number: 2801
Date: 03 Jun 94 21:18:51 EDT
From: Mike Darwin <>
Subject: SCI.CRYONICS Henson Alcor Case Report

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)  The heart valves are incompetent (i.e., leaky) under static load from
the start of perfusion in either in the presence or the absence of
cryoprotectant.  This is a well known phenomenon in bypass and it is one
of the major reasons why the left ventricle is ALWAYS vented when the
heart is not beating and the ventricle is not opened; otherwise the LV
becomes grossly distended and seriously damaged due to due to
equilibration of pressure (arterial) across the "leaky" aortic valve.
(This is why Jerry Leaf and I routinely vented the LV on whole body
patients.) Normally this leakage is not physiologically significant in the
beating heart because the ventricle is "unloaded" by contracting and
pumping.  Keep in mind these are BIOLOGICAL systems (valves) not
industrial ones and some degree of regurgitation is acceptable under
physiologic conditions.

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.

3) I am at a bit of a disadvantage here in that the Alcor Board has (at
least so far) decided to withold all patient records from me and bar me
from completing the case histories on the patients I cared for while at
Alcor both before I became suspension team leader and after.  As a
consequence I have only limited patient data to draw from.  I would note
that the following is typical:

A neuropatient started out perfusing at a flow rate of 850 cc/min and a
mean arterial pressure (MAP) of 50 mmHg.  During the early period of
glycerolization the MAP dropped to approx. 30 mmHG due to tissue
dehydration (which increases capillary diameter and decreases vascular
resistance).  As glycerol concentration exceeds 1M the arterial pressure
starts to rise.  By the end of perfusion of this patient the MAP is about
50 mmHG and the flow has been decreased to about 450 cc/min. (Case
report A-1049).  A similar pattern is seen in cases A-1068, A-1133,
A-1260, A-1082 and A-1234.  Similarly, the two ACS cases I have done
exhibited a similar (but more pronounced) pattern of MAP increase with
glycerolization since we were perfusing to far higher terminal glycerol
concentrations in these cases: i.e., 6 to 6.5 M vs. 3 to 4 M for
the previously cited Alcor cases.  In fact, terminal MAP on the last ACS
case was 131 mmHg at a flow rate of 950 cc/min up from 62 mmHg and a flow
rate of 1350 cc at the start of cryoprotective perfusion.

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:

a) inject a dye into the perfusate and watch through the burr-hole and
look for cerebral cortical staining with the dye.

b) inject radiopaque or radioactive material and do either angiography or a
brain scan to determine the presence/absence and/or distribution of flow.

c) Perfuse the oxygenator with radioactive Xenon and look at Xenon
distribution/clearance times in the brain.

Please note I am not actively recommending the above (particularly not b
or c), merely noting that these are the only approaches I know of.  I have
used the dye approach with Alcor patients (I developed it) and found it
very useful (I have used both fluroscein green and fluroscein labeled
dextran isothiocyanate and illuminated the cortical surface with UV light
to determine perfusate distribution).

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

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).

Mike Darwin

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