1    Defibrillation, if available, is indicated to correct ventricular
fibrillation of apparent asystole in extremely hypothermic patients.
Unfortunately, defibrillation attempts are generally unsuccessful when the
core temperature is below 30C (86 F). Could someone explain to me why
defibrillation is unsuccessful in hypothermic victims?

2    I am looking for some information about coagulation disorders in severe
hypothermic patients. Every information is welcome.

3    Can anybody help me to find an algorithm for treatment of hypothermia,
pre-hospital and in the hospital.

Thanks

Bart Vissers

I can't answer your questions myself as I am a student myself. However I
can point you in (Hopefully) the right direction. Check out the homepage of

        Good luck!
        D. Tanstaafl EMT-D
        Vermont

Try searching MedLine at http://www.***.com/

Here's the most recent article (from a different MedLine search
engine).  Several others are in other languages.

ARTICLE TITLE:  The effects of normothermic and hypothermic
cardiopulmonary bypass on defibrillation energy requirements and
transmyocardial impedance. Implications for implantable
cardioverter-defibrillator implantation.
ARTICLE SOURCE:  J Thorac Cardiovasc Surg  (United States), May 1995,
109(5) p981-8
AUTHOR(S):  Martin D; Garcia J; Valeri CR; Khuri SF
AUTHOR'S ADDRESS:  Department of Cardiology, West Roxbury Veterans
Administration Medical Center, MA, USA.
MAJOR SUBJECT HEADING(S):  Defibrillators, Implantable; Electric
Impedance; Heart Arrest, Induced [methods]; Heart [physiology]
MINOR SUBJECT HEADING(S):  Body Temperature; Dogs; Hydrogen-Ion
Concentration; Hypothermia, Induced; Ventricular Fibrillation
[metabolism]
INDEXING CHECK TAG(S):  Animal; Male; Support, Non-U.S. Gov't;
Support, U.S. Gov't, Non-P.H.S.
PUBLICATION TYPE:  JOURNAL ARTICLE
ABSTRACT:  The influence of normothermic and hypothermic
cardiopulmonary bypass on defibrillation energy requirements and
transcardiac impedance is not well characterized. However, this
relationship is of clinical importance during automatic defibrillator
implantation done with concomitant cardiac surgery, and there is
anecdotal information that criteria for successful implantation are
harder to achieve after such operations. We studied the effect of
controlled hypothermia on defibrillation energy requirements and
transcardiac impedance in a canine model of cardiopulmonary bypass in
which 26 animals underwent right atrial and fem{*filter*}arterial
cannulation, as well as continuous hemodynamic and intramyocardial
temperature monitoring. The defibrillation energy requirements were
evaluated at 60-minute intervals with an epicardial patch system, and
transcardiac impedance was measured before and after the multiple
inductions and terminations of ventricular fibrillation. In group 1 (n
= 10) defibrillation energy requirements were evaluated immediately
after initiation of cardiopulmonary bypass at 37 degrees C (T0), after
gradual cooling to 28 degrees C (T1), and after rewarming to 37
degrees C (T2). Group 2 (n = 16) comprised time controls that were
identically instrumented and studied, but maintained at 37 degrees C
throughout. Percent successful defibrillation was plotted against
delivered energy, and the raw data fit by logistic regression. The
energy at which 50% of shocks were successful (E50) was 3.23 +/- 0.89
joules at T0, 5.12 +/- 1.85 joules at T1, and 4.42 +/- 1.22 joules at
T2 in group 1; this was not significantly different from the
corresponding group 2 E50 values, which were 3.11 +/- 1.39 joules,
4.95 +/- 2.47 joules, and 5.59 +/- 3.18 joules, respectively. Both
groups demonstrated a significant increase in E50 during the first
hour of cardiopulmonary bypass (mean increase from T0 to T1 was 1.89
joules in group 1 and 1.84 joules in group 2, p 0.05). Transmyocardial
impedance fell progressively during the group 2 experiments from 73.6
+/- 12.9 omega at the beginning of the T0 shock series to 61.4 +/- 8.9
omega at the end of the T2 shock series. A similar reduction in
transmyocardial impedance was observed during the course of all the
group 1 experiments; however, at the beginning of the T1 shock series
impedance was significantly elevated to 77.4 +/- 12.3 omega (p 0.05
compared with group 2 and with end T0 in group 1). There was no
relationship between defibrillation energy requirements and
transcardiac impedance; there was also no correlation between either
of these parameters and intramyocardial extracellular pH or left
ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 400 WORDS).
MEDLINE INDEXING DATE:  9508
ISSN:  0022-5223
LANGUAGE:  English
UNIQUE NLM IDENTIFIER:  95257617

----------------------------------------
Paul A. Delaney
Georgetown University School of Medicine

Please respond by posting, or by e-mail after
removing the (NoSpam!) from my addess.

According to JAMA's "Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiac Care" special resuscitation situations, there is a
hypothermia algorhythym to follow in just those situations.  If you have
the bound edition it is on page 2245.  This is also the page if you look in
the loose editions.  It will be October 28, 1992. I recently had an
experience with a {*filter*} disorder that can sometimes be attributed to low
temperatures==cold agglutinin syndrome. According to "Current Emergency
Diagnosis and Treatment" by Mary Ho and C E Saunders, the IgM anti-red cell
antibodies tend to jump into action at cold temperatures and lyse the
host's RBC's because it sees them as an invader and thus creates anemia.  I
realize this pertains to cell lysis and not coagulation, but maybe it will
help.  Included the book and article titles in case you wanted to look them
up.  I couldn't find anything else useful for your question in them, but
there they are if you want them.  I'd like to know if you discover anything
else helpful, 'cause I'm kind of curious about that whole defib thing
myself.
Susanne NREMT-P