Date: 20 Mar 96 00:50:41 EST
From: Mike Darwin <>
Subject: BPI TECH BRIEF #18, Part II

Cryopreservation of CryoCare Patient #C-2150  (continued)
              by Mike Darwin

     Decision to Terminate Life Support 

     At the beginning of December the patient became 
increasingly oxygen dependent and began experiencing a return 
of visual disturbances which were prodromal to his prior 
homonymous hemianopia. He also experienced a return of 
urinary incontinence. The patient expressed justifiable 
concern that the original brain metastases, or another, was 
again beginning to cause problems, or that structures 
adjacent to the tumor were experiencing the un-typical 
delayed death as a result of the high dose radiation to which 
they were exposed. 

     Further, the nausea which had been present since shortly 
after the illness was diagnosed was now more or less constant 
with occasional vomiting. Attempts at pharmacologic control 
of the nausea using hydroxyzine, chlorpromazine, compazine, 
ginger, and tetrahydrocannabinol (THC) were unsuccessful. 

     During the first days of December the patient repeatedly 
contacted BPI and expressed a desire to withdraw from 
palliative oxygen and to abruptly stop steroids and "get it 
over with." He explained that his quality of life was no 
longer acceptable, and that he wished to take action to end 
his life in a legal manner before the quality deteriorated 
further, and especially before he became unable to exercise 
choice in the matter. 

     Unfortunately, while the patient had responded well to 
prompt anti-viral therapy for influenza, two of the team 
members were ill with the flu and with the non-bacterial 
bronchitis which accompanied it. Complicating matters further 
was the illness (again with the flu) of one of the team 
members' two small children. The patient was told that while 
we would respond if he was set upon immediate implementation 
of this course of action, optimum response would best be had 
by delaying a week or so longer in order to give team members 
time to recover and to permit final set-up of equipment in 
the home and last minute preparations to be made. 

     When staff were largely recovered, a window of time was 
agreed for discontinuation of life support. The patient's 
private primary care physician (not involved with BPI) was 
closely involved in this decision, and advised BPI that he 
felt withdrawal of oxygen would result in rapid 
decompensation and cardiovascular collapse. He said he felt 
the patient was making an informed and "rational" choice 
(i.e., he saw no indication of compromising psychiatric 
illness, organic brain disorder, or undue influence). The 
physician commented that he was comfortable with the 
patient's decision since the patient had repeatedly told him 
he would have withdrawn from life support far earlier had it 
not been for his cryopreservation arrangements. The physician 
expressed a willingness to be present when the patient 
discontinued life support and to pronounce legal death. 
Further, the physician ordered that a Hickman catheter be 
implanted in the patient to facilitate administration of pain 
medication (his peripheral veins were "exhausted" from 
repeated sticks and catheter placement). BPI requested that 
the catheter be a large-bore Hickman to facilitate rapid, low 
resistance of transport medications, and the physician agreed 
to this request. 

     During the weekend of 9-10 December the patient's home 
was fully prepared for standby and transport. The Mobile 
Advanced Life Support System (MALSS) was set up in the living 
room and the extracorporeal circuit strung. An operating room 
light was put in place, back tables were set up and 
instrument trays and ancillary supplies were laid out and 
readied. Specialized monitoring equipment for blood 
pressure, cerebral function, pulse oximetry, and acute lab 
collection (blood gases) was also put in place. The CDI 
point-of-care in-line blood gas system was also set up next 
the MALSS and the monitoring cells cut into the arterial and 
venous lines of the extracorporeal circuit to allow for 
continuous acquisition of blood gas data during initial 
bypass-assisted cooling, and during blood washout and 
replacement with 21CMBP-002 flush-store solution. 

     The patient's physician was then consulted about the 
possibility of administering pre-cryopreservation medications 
to reduce the insult from the agonal hypoperfusion/hypoxia 
and post-pronouncement ischemia which would necessarily occur 
prior to mechanical restoration of circulation and breathing 
during transport by BPI. The physician reviewed the 
medications suggested and agreed to prescribe all those 
available in the U.S. and Mexico. The patient had made 
arrangements through an AIDS buyers' club to obtain other 
medications which he believed would be efficacious in helping 
to ameliorate ischemic injury. These were largely drugs 
which 21st Century Medicine animal research had shown to be 
cerebro-protective if given before the ischemic insult. 

     The following schedule of pre-cryopreservation 
medication was begun by the patient on 10 December, 1995: 

     Medications for 10 December:

     aspirin, 1.25 grain, p.o., daily 
     ascorbic acid, 1 g t.i.d.
     N-t-butyl-a-phenylnitrone, 500 mg, p.o. with evening meal
     sodium selenite, 1000 mcg selenium p.o.
     co-enzyme Q10, 100 mg p.o. t.i.d. 
     dexamethasone, 4 mg p.o. t.i.d.
     doxycycline, 100 mg p.o. 
     d-alpha tocopherol, 1,000 IU, t.i.d.
     phenytoin (Parke Davis), 100 mg, t.i.d. 
     morphine sulfate by IV pump p.r.n. for pain.
     50 mg thalidomide, p.o. before retiring
     10 mg melatonin, p.o. before retiring

     Medications for 11 December:

     aspirin, 1.25 grain, p.o., daily 
     ascorbic acid, 1 g t.i.d.
     piracetam 800 mg p.o. at 10:00
     N-t-butyl-a-phenylnitrone, 1g mg, p.o. with evening meal
     sodium selenite, 1000 mcg selenium p.o.
     co-enzyme Q10, 100 mg p.o. t.i.d. 
     dexamethasone, 4 mg t.i.d.
     doxycycline, 100 mg, t.i.d. 
     d-alpha tocopherol, 1,000 IU , t.i.d.
     phenytoin (Parke Davis), 100 mg, t.i.d. 
     morphine sulfate by IV pump p.r.n. for pain.
     50 mg thalidomide, p.o. before retiring
     10 mg melatonin, p.o. before retiring

     Patient agreed to take no solid food after 11 December at 2400
since it was his decision to withdraw life support the following

     Medications for 12 December:

     aspirin, 1.25 grain, p.o., daily 
     ascorbic acid, 1 g t.i.d.
     N-t-butyl-a-phenylnitrone, 1 g, p.o. with evening meal
     sodium selenite, 1000 mcg p.o.
     co-enzyme Q10, 100 mg p.o. t.i.d. 
     dexamethasone, 4 mg t.i.d.
     doxycycline, 100 mg , t.i.d. 
     d-alpha tocopherol, 1,000 IU , t.i.d.
     phenytoin (Parke Davis), 100 mg, at 100 and 1600 
     morphine sulfate by IV pump p.r.n. for pain.
     misoprostol, 100 micrograms at 1600
     melatonin, 50 mg, p.o. at 1900 
     prilosec, 20 mg, p.o. at 1900 
     800 mg ibuprofen at 1900
     phenytoin, 500 mg, p.o. at 1900
     Maalox, 60 cc p.o. immediately before discontinuing oxygen.

     The patient obtained on his own, and self-administered 
without assistance at about 2100 through his implanted 
Hickman catheter, 250 cc of Dextran 40 in normal saline 
(Baxter, Irvine, CA) containing 1 mg of Nimodipine (A.G. 
Bayer, Germany), 40,000 IU of sodium heparin and 5 grams of a 
proprietary agent developed by 21st Century Medicine. 
     This latter agent will be hereinafter referred to as 
21CM-006; it was developed to protect against ischemic 
injury, up-regulate the efficacy of anaerobic metabolism, and 
ameliorate V/Q mismatch (where blood flows through 
unventilated area of lung and thus does not get oxygenated) 
and prevent loss off normal vasomotion (where blood delivered 
to the tissues is not distributed to the capillaries properly 
resulting in "shunting" and failure of delivery of oxygen and 
nutrients to the tissues in shock) concurrent with 
discontinuing high flow oxygen support (8-10 LPM by mask with 
reservoir bag: FIO2 was ca. 80-90%). 

     A final conversation was had with the patient at about 
1900 at which time he was repeatedly advised that he could 
change his mind without any problem to BPI and that he should 
feel no pressure to pursue this course of action. His 
response was: "You don't understand. This is easy. The hard 
thing would be taking one more day of life like this." The 
patient appeared in good spirits and laughed and joked with 
family and team members. He explained that he had accepted 
he was either to die or recover from cryopreservation, and 
that either way he was fully prepared and psychologically 
ready. He had played a card game with family and friends 
that afternoon, and explained that while he was a little 
apprehensive, he intended to take some alprazolam (Xanax) and 
get ready for the journey ahead. 

     Several BPI team members spoke with the patient 
privately and said their good-byes. 

     Cardiopulmonary Arrest 

     At the request of the patient and his family (for 
reasons of intimacy; saying farewells etc., and basic 
privacy) the entire BPI team withdrew to the BPI transport 
vehicle parked outside the patient's apartment. The 
patient's attending and primary care physician remained with 
the patient and the patient's family to supervise withdrawal 
of life support, assure adequate palliation of air hunger and 
discomfort, and promptly pronounce legal death. BPI 
personnel were to be summoned immediately after pronouncement 
by cell phone (four BPI personnel had cell phones!). 

     At approximately 22:50, the patient discontinued oxygen. 
He had taken approximately 3 mg of alprazolam about an hour 
before discontinuing oxygen, and he had access to self-
administered morphine (pump limited boluses) to ease air 

     It was reported that the patient rapidly lost 
consciousness on withdrawal of oxygen and experienced 
cardiopulmonary arrest at 2311 on 12 December, 1995. 

     Transport Phase 1: CPR, Medication, External, Initial 

     Intubation was accomplished at 23:13 by Dr. Harris, and 
"Active Compression-Decompression-High-Impulse CPR" (ACDC-
HICPR), using a custom built Michigan Instruments "Thumper" 
mechanical chest compressor, was initiated at 23:14. A 
standard Ambu ACDC silastic suction cup was used on the 
Thumper to achieve the ACDC component of the ACDC-HICPR. 
Placement of a tympanic temperature probe was achieved 
concurrent with intubation (during securing of the 
endotracheal tube). The initial tympanic temperature reading 
was 36.8 degrees C. 

     Tympanic (eardrum) temperatures were used in this 
patient because it is well established that tympanic 
temperature reflects true brain temperature since the blood 
supply for the eardrum and midrain and cerebral cortex are 
the same. Typmanic temperature is thus a much more reliable 
measure of the temperature of the iorgan we are *most* 
interested in preserving (the brain) than are esophageal or 
rectal temperatures. Further, work with dogs at 21st has 
established a far closer correlation between tympanic 
temperature and actual measured brain temperature (via 
invasive probes) than esophageal or rectal temperatures 

     Family and friends had begun icing the patient at the 
time of pronouncement (legs, abdomen and lower thorax; 
leaving the head unencumbered so that airway management could 
be instituted before icing) and the head, thorax and axilla 
were iced concurrent with the start of cardiopulmonary 

     Simultaneous with the start of external cooling, a 
Darwin rectal thermocouple probe was placed in the descending 
leg of the double barreled colostomy and the 60 cc balloon 
inflated to anchor it in place. A Darwin colonic lavage tube 
with a 60 cc silastic balloon and fenestrated tip was also 
inserted in the stoma of the ascending end of the colostomy, 
and the balloon on the lavage tube was also inflated to 
anchor it into the ascending colon. 

     Immediately thereafter a stab wound was made (using 
sterile technique) through the medial aspect of the right 
external oblique muscle 3 cm to the right of the navel, at 
the level of the iliac crest. The stab wound was rapidly 
extended in depth by blunt dissection with Metzenbaum 
scissors (Mets) until the peritoneum was reached, and a 1 cm 
incision was made in the peritoneum with Mets and a Darwin 
peritoneal lavage tube was inserted and its 60 cc silastic 
balloon rapidly inflated to seal and anchor it in place. 

     Once all lavage tubes were in place the patient's 
ascending, transverse colon, and terminal ileum were 
irrigated with 2 liters of iced Normosol-R, pH 7.4, and the 
peritoneal cavity was irrigated with 4 more liters of this 
solution (Abbott Pharmaceuticals, Chicago, IL). Reservoirs 
connected to the colonic and peritoneal lavage tubes were 
placed on the floor and the lavage fluid was allowed to drain 
into the respective bags by gravity. 

     The first pulse oximetry and end-tidal CO2 readings were 
obtained at 23:16 and were 95% and 5% respectively. Wave form 
acquisition on the pulse oximeter was excellent and the pulse 
rate of 80 per minute correlated exactly with the action of 
the Thumper. At 23:19 the patient's tympanic and descending 
colon temperatures had declined to 29.8 degrees C. By 23:20 
the descending colon temperature had rebounded to 34 degrees 
C. At 23:21 the peritoneum was lavaged with 2 additional 
liters of iced Normosol. At 23:22 the tympanic temperature 
was 28.7 degrees C and the descending colon temperature was 
28.6 degrees C. Oxygen saturation at that time was 93%, and 
End tidal CO2 (EtCO2) was 4%. 

     Administration of Transport Medications began at 23:12 
and was as follows: 

     Epinephrine 12.6 mg, 23:12, IV push (given to support 
blood pressure during CPR). 

     The drug 21CM-005 3.15 g, IV push, 23:16, (This drug is 
a proprietary compound given to inhibit lactic acidosis and 
increase the efficacy of anaerobic metabolism). 3.15 g of 
21CM-005 contains approximately 40 mEq of potassium, an 
amount sufficient to preclude restoration of spontaneous 
cardiac activity. 

     Soporate (21CM-004) 6.30 g IV push, 23:12 (Soporate is a 
proprietary compound given to inhibit excito-toxicity in a 
class of brain receptors found to be critical in mediating 
cerebral re-perfusion injury in dogs following 12+ minutes of 
global cerebral ischemia using a cardiac arrest model. The 
drug also acts as a general anesthetic preventing patient's 
from regaining consciousness during cardiopulmonary support.) 

     21CM-005 6.30 g IV push, 23:12 (see above for 
explanation of the pharmacology of this agent). 

     Oxynil (21CM-003) 630 mg IV push, 23:13 (Oxynil is a 
proprietary agent which has been shown to ameliorate brain 
ischemia in dogs by its free radical trapping ability. It is 
useful primarily as an adjunct and potentiator of other 
antioxidant medications). 

     21CM-002 100 ml; 50 ml IV push, 50 ml over ca. 10 
minutes. Push dose given at 23:15, infusion completed at 
23:28. (21CM-002 is a cremophor emulsion (micellized) 
mixture of two proprietary antioxidants which rapidly cross 
the blood brain barrier. One of these antioxidants crosses 
mitochondrial membranes rapidly and prevents failure of high 
energy metabolism in neuron and glial cells following re-
perfusion after global ischemic injury in dogs of 12+ minutes 

     Deferoxamine 2g was added to the mannitol infusion (126 
g mannitol as 20% solution in water). Mannitol infusion was 
begun at 23:32 and concluded at 23:40. 

     Exiquell (21CM-005) 315 mg IV push. (Exiquell is a 
proprietary agent used to inhibit the quaint-quisqualate 
receptor system which is a significant source of excito-
toxicity following global cerebral ischemia in the dog.) 

     THAM (tromethamine) 15.75 g in 250 cc (50 cc IV push), 
with the balance by IV infusion, 23:18 

     Mannitol (see Deferoxamine above). 

     Pavulon (pancuronium bromide) 2 mg, 23:16, to inhibit 
shivering and prevent return of spontaneous respiration. 

     Methylprednisolone 1 g IV infusion over a minimum of 5 
minutes, begun 23:16, ended, 23:20. 

     Cipro IV (ciprofloxacin; antibiotic causing no cold 
agglutination) 400 mg IV infusion given slowly between 23:16 
and 23:30. 

     Dextran 40 (Gentran) in 10% saline, 500 cc. 

     Administration of all transport medications to this 
patient was completed at 23:40. 

     The first blood sample for gases, chemistries and 
electrolytes could not be collected until after the 
conclusion of medication administration. A central venous 
sample was collected via the patient's Hickman line at 23:50 
on 13 December and yielded the following results: 


Tympanic Temperature: 25.7 degrees C, Descending Colon 
Temperature 19.0 degrees C 

     pH	7.34	7.35 (mean)
     pCO2	52.4 mmHg	45-55
     pO2	37.0 mmHg	40-50
     O2 Sat	89%	70-75
     BUN	15.0 mg/dl	7-25
     Creatinine	1.1 mg/dl	0.7-1.4
     Sodium	120 mEq/l	135-146
     Potassium	5.5 mEq/l	3.5-5.3
     Chloride	82 mEq/l	95-108
     Magnesium	1.7 mEq/l	1.2-2.0
     Calcium	7.2 mg/dl	8.5-10.3
     Phosphorus	7.8 mg/dl	2.4-4.5
     Protein, Total	5.8 g/dl	6.0-8.5 
     Glucose	251 mg/dl	70-125
     Bilirubin,Total	0.8 mg/dl	0.0-1.3
     Alk Phosphatase	76 U/L	20-125
     LDH, Total	227 U/L	0-250
     GGT	58 U/L	0-65
     AST	101 U/L	0-42
     ALT	69 U/L	0-48
     Uric Acid	0.5 mg/dl	4.0-8.5
     Iron, Total	138 mcg/dl	25-170
     Iron Binding Capacity	748 mcg/dl	200-450
     % Saturation	18	12-57
     HCT	26%	41-50

     The next central venous blood sample collected during CPR at 0020
on 13 December, yielded the following results:

     Tympanic Temperature: 23.0 degrees C, Descending Colon 
Temperature13.8 degrees C 

     pH	7.115	7.35 (mean)
     pCO2	27.8 mmHg	45-55
     pO2	35.1 mmHg	40-50
     O2 Sat	88%	70-75
     BUN	17.0 mg/dl	7-25
     Creatinine	1.1 mg/dl	0.7-1.4
     Sodium	132 mEq/l	135-146
     Potassium	4.3 mEq/l	3.5-5.3
     Chloride	91 mEq/l	95-108
     Magnesium	1.8 mEq/l	1.2-2.0
     Calcium	7.8 mg/dl	8.5-10.3
     Phosphorus	9.9 mg/dl	2.4-4.5
     Protein, Total	3.4 g/dl	6.0-8.5
     Glucose	300 mg/dl	70-125
     Bilirubin, Total	1.1 mg/dl	0.0-1.3
     Alkaline Phosphatase	92 U/L	20-125
     LDH, Total	376U/L	0-250
     GGT	69 U/L	0-65
     AST	182 U/L	0-42
     ALT	126 U/L	0-48
     Uric Acid	0.5 mg/dl	4.0-8.5
     Iron, Total	177 mcg/dl	25-170
     Iron Binding Capacity	779 mcg/dl	200-450
     % Saturation	18	12-57
     HCT	26	41-50

     At 0050 another central venous sample was collected from the
Hickman catheter and revealed the following results:

     Tympanic Temperature: 21. degrees C, Descending Colon 
Temperature 9.9 degrees C 

     pH	7.087	7.35 (mean)
     pCO2	25.2 mmHg	45-55
     pO2	39.2 mmHg	40-50
     O2 Sat	91%	70-75
     BUN	17.0 mg/dl	7-25
     Creatinine	1.0 mg/dl	0.7-1.4
     Sodium	134 mEq/l	135-146
     Potassium	4.9 mEq/l	3.5-5.3
     Chloride	91 mEq/l	95-108
     Magnesium	1.9 mEq/l	1.2-2.0
     Calcium	7.9 mg/dl	8.5-10.3
     Phosphorus	10.6 mg/dl	2.4-4.5
     Protein, Total	3.5 g/dl	6.0-8.5
     Glucose	308 mg/dl	70-125
     Bilirubin, Total	1.1 mg/dl	0.0-1.3
     Alkaline Phosphatase	91 U/L	20-125
     LDH, Total	366 U/L	0-250
     GGT	69 U/L	0-65
     AST	204 U/L	0-42
     ALT	140 U/L	0-48
     Uric Acid	0.5 mg/dl	4.0-8.5
     Iron, Total	179 mcg/dl	25-170
     Iron Binding Capacity	778 mcg/dl	200-450
     % Saturation	23	12-57
     HCT	26	41-50

     The final central venous sample taken during CPR was at 
01:20 on 13 December and yielded the following results: 

     Tympanic Temperature: 19.3. C, Descending Colon 
Temperature 7.5 degrees C 

     pH	7.047	7.35 (mean)
     pCO2	23.7 mmHg	45-55
     pO2	110.4mmHg	40-50
     O2 Sat	98.1%	70-75
     BUN	17.0 mg/dl	7-25
     Creatinine	1.0 mg/dl	0.7-1.4
     Sodium	133 mEq/l	135-146
     Potassium	5.7mEq/l	3.5-5.3
     Chloride	92 mEq/l	95-108
     Magnesium	1.9 mEq/l	1.2-2.0
     Calcium	7.9 mg/dl	8.5-10.3
     Phosphorus	11.3 mg/dl	2.4-4.5
     Protein, Total	3.5 g/dl	6.0-8.5
     Glucose	364 mg/dl	70-125
     Bilirubin, Total	1.2 mg/dl	0.0-1.3
     Alkaline Phosphatase	92 U/L	20-125
     LDH, Total	380 U/L	0-250
     GGT	69 U/L	0-65
     AST	214 U/L	0-42
     ALT	148 U/L	0-48
     Uric Acid	0.5 mg/dl	4.0-8.5
     Iron, Total	178 mcg/dl	25-170
     Iron Binding Capacity	777 mcg/dl	200-450
     % Saturation	23	12-57
     HCT	22	41-50

     Intermim Interpretation and Comment On Cooling 

     From the laboratory and temperature data above, several 
important conclusions can be drawn, particularly when taken 
in the context of the protocol used in this case, in 
comparison with results obtained in two previous cases which 
compare with this one closely (Alcor patient A-1260, and ACS 
patient 9577). 

     Direct comparisons of many of the parameters in these two cases is
not possible owning to absence of data in the previous cases. For
instance, in patient A-1260 no temperature data was acquired until
32 minutes after cardiac arrest. Thus, a direct comparison between
cooling rates during (say) the critical first 10 minutes post
arrest is not possible here. However, comparisons can still be
made where data does exist at corresponding intervals.

     These three patients are of particular interest to compare because
they match each other closely in sex, weight, fat 
distribution, and body surface areas, and they are of 
reasonably close ages. All patients were cooled at a minimum 
using a portable ice bath and ice-water circulating 
pump/distribution assembly (two with identical equipment). 
All patients had cooling and CPR begun within 2-4 minutes of 
cardiopulmonary arrest, and all were promptly medicated using 
the specified protocol. It is also important to note that all 
patients died of illnesses, two of AIDS and one of 
disseminated cancer, which left them cachectic and which 
involved compromise to multiple organ systems. One notable 
difference was the prolonged agonal course of ACS-9577 
compared to the other two patients, and the poor response to 
cardiopulmonary support this patient exhibited, probably as a 
result of the antemortem ischemic injury and pulmonary 

     Data from one other patient, A-1049, a 32.8 kg severely wasted
patient who arrested from dehydration secondary to end-stage 
adenocarcinoma of the lung, is also relevant. This patient is 
included since her mass and fat content/distribution and 
response to cardiopulmonary support were the most favorable 
of any patient cryopreserved by comparable methods available 
to this author. This patient thus serves as "best-case" for 
the efficacy of previously used methods of cooling, 
medication and CPR. 

     The number of asterisks after the case number indicates 
the overall score, from zero to ****, for response to 
cardiopulmonary support as evaluated by EtCO2, skin-color, 
femoral pulse, and other parameters when available. 

     A critical determining factor in how well a patient will 
cool during transport in addition to surface area, mass and 
fat quantity and distribution (fat is a good insulator) is 
the adequacy of blood circulation. Warm blood being delivered 
to the surface of the body and to structures with good 
surface to volume ratios that facilitate good exchange (such 
as fingers, toes, arms, and legs) will clearly be superior in 
patients with good cardiac output. The patient's antemortem 
condition will be a major factor in determining how well s/he 
will respond to CPR. However, also of great importance is the 
use of highly efficient means of CPR and the use of drugs 
which prevent shunting of blood away from tissues that need 
it, and which prevent shunting of blood through parts of the 
lung which are fluid filled or not able to exchabfe oxygen. 
No doubt part, but by no means all of the superior cooling 
results observed in this patient were as a result of better 
perfusion during CPR. 

     As can be seen from the table above, patient C-2150, the 
subject of this report, cooled at a rate of approximately 1 
degree C/min during the first ten minutes post arrest, and at 
a rate of 0.56 degrees C/min for the entire 30 minute period 
after arrest. This is a rate twice that of a patient with 
roughly half his mass and with far less subcutaneous fat 
during the first 10 minutes post arrest, and twice that at 30 
minutes post arrest. It is also interesting to note that the 
30-minute post arrest cooling rates of all three other 
patients are well below 0.5 degrees C/min., and are in close 
agreement (0.24 and 0.21) for the two patients whose mass, 
fat distribution and surface area most closely approximate 
those of this patient. 

     We believe that this patient experienced such superior 
rates of cooling--indeed, rates achieveable in a patient of 
his surface area only with extracorporeal (blood/body core) 
cooling--because of the following factors: 

     * Superior perfusion  due (blood circulation) during CPR 
as a result of: 
     a) cardiac arrest in the absence of a long period of 
agonal shock. 
     b)pre-arrest medication which reduced cold 
agglutination, prevented loss of 
     c) normal vasmotion and adequate control and 
distribution of blood flow. 
     d) greatly improved cardiac out, mean arterial pressure 
(MAP) and decreased venous pressure as a result of ACDC-HICPR 
     e) improved oxygenation due to ventilation with each 
compression upstroke using ACDC-CPR 
     f) in hibition of oulmonary edema as a result of lower 
central venous pressures and better mitral valve function as 
a result of ACDC-HICPR 

     *Superior cooling due to the use of colonic and 
peritoneal lavage with ice cold solution in addition to 
external cooling using the portable ice bath (PIB) and a 
circulating water system to pump ice cold water over the 
patient's body. 

     The use of these modalaties and the cooling rates 
achievable with them was established in dog lab. Further, 
other cooling approaches such as the use of ice-slush lavages 
in stomach, inaddition to the colon and peritoneum, and the 
addition of liquid ventilation (using perfluburon chilled to 
0-2 degrees C) or subzero jet gas ventilation, are currently 
under investigation (and patent) and may provide for cooling 
rates approach 1.5 to 2.0 degrees C per minute if added to 
the modalities used in this patient. 
     Administration of all transport medications to this 
parient was completed at 2340. 

     Transport Phase 2: Initiation of Extracorporeal Support 
and Total Body Washout 

     Surgery to raise the right femoral artery and vein was begun at
23:30 following standard prep of the right groin with Betadine
scrub/solution, and creation of a sterile field with sterile muslin
towels and disposable drapes. Two femoral arteries of 3-5 mm in
diameter were rapidly located and a pressure line was placed in one
at 23:55 (initial pressure measured was MAP 47 mmHg). 

     However, despite extensive further dissection of the right groin no
femoral vein could be located. Dissection along the tissue plane
of the femoral arteries failed to reveal the femoral vein (although
the sciatic nerve was identified) and the femoral arteries appeared
to bifurcate within the abdomen. (Subsequent autopsy disclosed that
the patient had no femoral vein and a right iliac artery that
bifurcated into two femoral vessels at the terminus of the
abdominal aorta). Several small veins (3-5 mm in diameter) were
located and one of these opened to determine feasibility of cannula
placement for venous return. While this was deemed not possible,
it was noted that the venous blood was free-flowing and arterial
red in color, indicating adequate oxygen delivery to the patient
(the patient's tympanic temperature at that time was 
approximately 23 degrees C, colonic temperature 14.5 degrees 

     By 00:15 a decision had been made to abandon the right groin wound
and proceed with surgery to raise the left femoral artery and vein. 
Prep of the left groin was made at 00:21 and the femoral artery and
femoral artery and vein were rapidly identified. The femoral vein
was cannulated with a Biomedicus Carmeda-coated, 21 Fr. x 50 cm
venous cannula (#34284).

     However, a further complication occurred in that the femoral artery
was invaded with malignancy; apparently between the tunica media
vasorum and the intima of the vessel. The vessel also was
moderately atherosclerotic (soft yellow atheroma). This
complicated arterial cannulation and required extensive further
dissection of the groin to avoid a dissecting aneurysm of the
entire arterial tree secondary to cannula placement.

     Thumper support was discontinued at 01:07 at a tympanic 
temperature of 20.2 degrees C and a colonic temperature of 
8.4 degrees C. MAP had dropped to 35 mmHg at this time, and 
it was felt that further Thumper support was not productive. 

     Both cannulae were in place by 01:18 and closed circuit
femoral-femoral bypass was begun at about 01:18, using a prime
consisting of 750 cc Dextran 40 in Normal saline, 1500 cc of
Normosol-R pH 7.4, 500 cc 20% mannitol in water, and 50 cc (1
mEq/cc) of sodium bicarbonate solution. At 01:21 a "popping sound"
was heard, and the polycarbonate housing of the Sarns 9444 Turbo
oxygenator was noted to have developed a leak at the joint between
the two halves of the housing. This occurred at a pressure of 260
mmHg, well below the 760 mmHg pressure this unit is rated for.

     The problem (popping sound) was noted at exactly 01:20 and the pump
was shut down and lines were clamped at 01:21. The circuit was
carefully inspected for air from the oxygenator through the filter
and up to the patient, and none was noted. The oxygenator was
changed out of the circuit and replaced with a fresh one and the
bypass line was used to prime the new oxygenator and debubble the
circuit. Bypass was resumed uneventfully at 01:33, 12 minutes
later. Closed circuit bypass was continued at a MAP of 45 mmHg and
flow rate of 2-3 liters per minute (LPM).

     When the patient's tympanic temperature reached 
approximately 16 degrees C (colonic , 6.2 degrees C) the 
patient was progressively hemodiluted with 10 liters of 
Viaspan using 2 liters of open circuit flush at a MAP of 45-
50 mmHg. At the conclusion of the Viaspan flushes, the 
patient was flushed with 10 liters of 5% (v/v) glycerol in 
21CM-BPI-002 base perfusate. Glycerol-containing flush was 
introduced slowly in two liter aliquots. Flushing with 5% 
glycerol began at 01:42 and was followed by flushing with 10 
liters of 10% w/v glycerol perfused in the same fashion. 
Flushing with 2 liter aliquots of 10% w/v glycerol was 
completed at 02:35. Flushing proceeded more slowly than 
normal due to partial cold and chemical-induced rupture of 
both plastic bags containing the flush solution, with leakage 
which required a great deal of effort to contain. 

     At 02:02 the tympanic probe was replaced with a frontal sinus probe
to facilitate movement of the patient at the conclusion of bypass. 
It is interesting to note that frontal sinus and tympanic 
temperatures agreed to within 0.2 degrees C. Frontal sinus 
temperature at the conclusion of flushing/glycerolization was 
5.5 degrees C, colonic, 1.6 degrees C. 

     Following the conclusion of total body washout and phase I
glycerolization, the patient was disconnected from the
extracorporeal circuit with care taken to avoid introduction 
of air into either the arterial or venous cannula (the 
cannulae were cross-connected with a short length of 3/8" x 
3/32" bypass tubing which was filled with perfusate and 
carefully purged of air before the occluding clamps on the 
cannulae were removed). 

     The patient was then removed from the PIB of the MALSS and placed
in a more easily transportable PIB for transfer to the BPI/21CM
facility for cryoprotective perfusion. Originally it had been
planned that the patient would be moved with extracorporeal 
support on the MALSS continuing. However, the patient 
occupied a second story apartment with a stairway that became 
extremely slick and hazardous during what was the first (and 
unexpected) rain of the Los Angeles basin's winter season. 
For the safety of the patient and the personnel, a decision 
was made not to attempt to transport the 600 pound-plus 
MALSS, with the patient in it, down the stairs in heavy rain. 

     The patient was transported by BPI ambulance from 
Huntington Beach to Rancho Cucamonga, CA starting at 
approximately 0350.  Driving conditions were very poor with 
heavy rain and an earlier than usual morning rush hour 
traffic beginning by the time the freeway was reached at 
0400.  The patient arrived at the facility at 0545 on 13 

End of PART II