1. 1
Therapeutic Hypothermia: A Physiological Analysis of a New
Potential for Post-Cardiac Arrest Care
By
Pedram Matthew Rahmanian, NREMT-B
Research Question:
Why is the induction of therapeutic hypothermia (TH) positive in increasing survival
rates of out-of-hospital cardiac arrest (OHCA) triggered by ventricular fibrillation (VF)?

2. 2
Abstract
This study aims to answer the Research Question: Why is the induction of
therapeutic hypothermia (TH) positive in increasing survival rates of out-of-hospital
cardiac arrest (OHCA) triggered by ventricular fibrillation (VF)?
Annually, nearly 450,000 people in the US and 375,000 people in Europe are
victims of sudden death from cardiac arrest.1
Despite numerous treatment options,
resuscitation success rates to the time of hospital discharge have remained relatively
unchanged throughout the last 50 years.2
While technological advances are increasing the
survivability of cardiac arrest, patients are still not surviving long enough to be
discharged from the hospital.3
The scope of this study focuses on explaining why therapeutic hypothermia is
beneficial for cardiac arrest patients by analyzing the major clinical trials and the
physiology of TH. The scope of this study does not include the use of TH for other
medical conditions except for understanding additional benefits of TH.
Therapeutic Hypothermia has many benefits for cardiac arrest patients and has
been associated with improving the survival rate of cardiac arrest patients. In addition to
increasing survival rates, TH has also been associated with a decrease in neurological
impairment. TH is therefore a beneficial treatment, and has to be implemented as soon as
possible for maximal benefit.
1
Neira, Jorge A., MD, FCCM. “Post-Resuscitation Care Induced Hypothermia to Whom,
How, and When?” (Presentation). World Congress of Cardiology, Buenos Aires,
Argentina, May 18-21, 2008. slide
3
2
Clumpner, Mike and Jim Mobley. “Raising the Dead: Prehospital Hypothermia for
Cardiac Arrest Patients May Improve Neurological Outcome and Survival to Discharge.”
EMS Sep. 2008: 52-60. pg
52
3
Clumpner,
pg
52

3. 3
The earliest stage of the chain of survival in which TH can be successfully
implemented is in the EMS system. However, if the continuum of care cannot be
guaranteed at receiving hospitals, TH should not be started in EMS as an incomplete
treatment would cause harm to the patient. Still, EMS agencies can drive the
implementation of TH by pressuring hospitals and thereby creating a sense of
competition between them that motivates implementation of TH.
Several factors impede the implementation of TH in hospitals. The major factors
inhibiting the implementation of TH are a lack of evidence and concern about the
continuum of care.4
Therefore this article will evaluate the physiology of TH in an effort
to promote the inclusion of TH as part of a general protocol.
Word Count: 332
4
Neumar, Robert W. et al.“Post Cardiac Arrest Syndrome: Epidemiology,
Pathophysiology, Treatment, and Prognostication.” Circulation Cardiovascular Quality
and Outcomes: Journal of the American Heart Association 23 Oct. 2008; 118: 2452-2483
pg
2470

4. 4
Table of Contents
Abstract............................................................................................................................... 2
Introduction......................................................................................................................... 5
The History of Therapeutic Hypothermia........................................................................... 7
ILCOR Recommendations ................................................................................................. 9
A Review of the Trial Evidence.......................................................................................... 9
Reperfusion Injury and the Physiology of Hypothermia .................................................. 12
Conclusion ........................................................................................................................ 19
References......................................................................................................................... 20
Appendix A: Explanation of Terms.................................................................................. 23

5. 5
Introduction
Research Question: Why is the induction of therapeutic hypothermia (TH) positive in
increasing survival rates of out-of-hospital cardiac arrest (OHCA) triggered by
ventricular fibrillation (VF)?
Annually, ~300,000 adults in the United States experience out-of-hospital cardiac
arrest in which the heart stops effectively pumping blood throughout the body.5
Nearly
450,000 people in the US and 375,000 people in Europe are victims of sudden death
annually from cardiac arrest.6
Cardiac Arrest patients today have a variety of treatment regimens available. With
the pharmacological therapy, intra-aortic balloon pumps, state of the art intensive care
units, and extracorporeal membrane oxygenation treatments7
we have today, it seems
apparent that cardiac arrest medical care has progressed tremendously. However, despite
all the treatments available, resuscitation success rates to the time of hospital discharge
has remained relatively unchanged throughout the last 50 years.8
According to the
National Registry of CPR, out of the 19,819 adults and 524 children in 2006 whose hearts
were re-started, in-hospital mortality rates were 67 and 55 percent respectfully.9
While
technological advances increase the survivability of cardiac arrest, patients are not
5
Cooling Therapy for Cardiac Arrest Survivors is as Cost-Effective as Accepted
Treatments for other Conditions. 4 Aug. 2009, American Heart Association. 28
Nov. 2009.
<http://americanheart.mediaroom.com/index.php?s=43&item=795&printable>.
6
Neira,
slide
3
7
Clumpner,
pg
52
8
Clumpner,
pg
52
9
Post-Cardiac Arrest Care Key to Survival. 23 Oct. 2008, American Heart Association.
28 Nov. 2009.
<http://americanheart.mediaroom.com/index.php?s=43&item=554&printable>.

6. 6
surviving long enough to be discharged from the hospital.10
According to University of
Pennsylvania’s Dr. Merchant, “TH is the only post-resuscitation therapy shown to
improve both survival and reduce disability after cardiac arrest.”11
TH thus deserves
further analysis into its potential as part of the Advanced Cardiac Life Support (ACLS)
standard of care for cardiac arrest.
Due to the large proportion of out-of-hospital cardiac arrests, it is in this setting
that the greatest impact could be made by improved treatments. Despite repeated
recommendations by multiple authoritative bodies (ILCOR and the AHA), therapeutic
hypothermia has not been implemented as quickly as was expected. This paper aims to
analyze TH on its evidence and physiological impact in post-cardiac arrest care.
To approach this topic, it is important to have an understanding of the anatomy
and physiology of the heart in its normal state, as well as the hearts reactions during
cardiac arrest.
It is also important to define the terms used in this study, these are found in
Appendix A. Therapeutic hypothermia can be defined as a condition in which the body’s
core temperature is below 35°C. There are three levels of hypothermia, mild (35-32°C),
moderate (32-30°C), and severe (below 30°C).
10
Clumpner,
pg
52
11
Cooling
Therapy
for
Cardiac
Arrest
Survivors
is
as
Cost-­‐Effective
as
Accepted
Treatments
for
other
Conditions.

7. 7
The History of Therapeutic Hypothermia
Therapeutic hypothermia (TH) is not a new concept. The use of inducing
hypothermia has been used for decades with the belief that cooling the body below
normal physiological temperatures protects the brain from ischemic injury.12
Since the
1950s, moderate TH (28-32°C) has successfully been used before cardiac arrest (CA) to
provide this kind of cerebral protection from global ischemia during some open-heart
surgeries.13
Despite successful description of the use of TH after CA during the late
1950s, the practice was abandoned due to uncertainty in the benefits and the difficulty of
its practice.14
Within the past decade, TH after CA has witnessed a renewed level of attention as
several research papers focusing on its use have been published.15
There are only four
trials of mild hypothermia after CA that describe any kind of comparative study; as
treatment could not be blinded, only two of these studies were randomized control trials
(RCT).16
The descriptions of these studies are presented in Table 1. Careful evaluation of
these two trials guided a recommendation in favor of the use of TH.
12
Collins, Tim J. and Peter J. Samworth. “Therapeutic Hypothermia Following Cardiac
Arrest: A Review of the Evidence.” Nursing in Critical Care: British Association
of Critical Care Nurses 2009; 13:144-151. pg
144
13
Nolan, J.P. et al. “Therapeutic Hypothermia After Cardiac Arrest: An Advisory
Statement by the Advanced Life Support Task Force of the International Liaison
Committee on Resuscitation.” Circulation Cardiovascular Quality and Outcomes:
Journal of the American Heart Association 2003; 108: 118-121. pg
118
14
Nolan,
pg
118
15
Collins,
pg
144
16
Foëx, Bernard A. and John Butler. “Therapeutic Hypothermia After Out of Hospital
Cardiac Arrest.” Emergency Medicine Journal 2004; 21:590-591. pg
590

8. 8
Table 1: Summary of the Trials
Author and Year Sample Research Methodology Findings Study Limitations
Bernard et al. (1997) 22 adult patients who
remained unconscious
following an initial VF
OHCA. Hypothermic
group was cooled to
33°C for 12 h with
surface cooling and ice
packs. Patients were
then actively rewarmed
over 6 h.
Prospective study
using a historic control
group of 22 patients.
Australian Study.
Good neurological
outcome (GOS 1 or 2)
was found in 11/22 in
hypothermic group
Study was not an RCT or
multicenter.
Prospective study with
small sample size of 22
historic control. A pilot
study for Bernard et al
(2002) RCT.
Yanagawa et al (1998) 28 adult patients in total
who sustained OHCA
and ROSC. 13 selected
for TH of 33-34°C for
48 h. Cooling was
achieved using cooling
blankets. Passively
rewarmed at 1°C/day.
Patients treated with
standard practice and
normothermia.
Prospective study.
Taken from one site in
Japan.
More survivors and
improved neurological
outcome in TH group.
Survivors 7/13 vs. 5/15.
Patients who fully
recovered: 3/13 vs 1/15.
11/13 in TH vs 6/15
control developed
pneumonia as a
complication.
Not an RCT.
Used historic controls
rather than
randomization. Small
scale, single center.
Predominantely male
sample: 76% in TH
compared with even
distribution in control.
The TH group was 6
years younger than
historic control group.
Bernard et al. (2002) 77 patients total, all
remained unconscious
following OHCA. 43
given TH to 33°C for
12 h compared with 34
patients given
normothermia. Cooling
achieved using ice
packs.
RCT. Multicenter
involving 4 hospitals
in Australia.
TH group had good
neurological recovery
with 21/43 vs 9/34 for
normorthermic group.
TH increased survival
with 21/43 vs
normothermia 11/34.
Odd and even day pre-
hospital randomization
that may be difficult to
achieve outside the
controlled hospital
environment. Strict
inclusion criteria, only
involved shockable CAs.
Excluded women below
age 50.
The HACA Study
Group (2002)
275 adult patients in
total who all sustained
OHCA and ROSC. 137
received TH to 32-34°C
for 24 h with an
external cooling device
that consists of a
mattress and cover that
delivers cold air to the
entire body. Following
24 h, passively
remarming commenced
over 8 h.
Multicenter RCT
undertaken in centers
across Europe
55% of TH group had a
good neurological
outcome (CPC 1 or 2)
compared with 39% in
normothermic group. 6-
month mortality was
41% in the TH group
and 55% in the
normothermic group.
The study ended
prematurely because of
funds difficulties. Strict
inclusion criteria causing
a delay in sample
recruitment. However,
largest sample size
related to TH.
GOS, Glasgow Outcome Score; RCT, Randomized Control Trial; ROSC, return of spontaneous circulation; OHCA, out of hospital
cardiac arrest; TH, therapeutic hypothemria
Collins, Tim J. and Peter J. Samworth. “Therapeutic Hypothermia Following Cardiac Arrest: A Review of the Evidence.” Nursing in
Critical Care: British Association of Critical Care Nurses 2009; 13:144-151. pg 146

9. 9
The ILCOR Recommendations
In October of 2002, the Advanced Life Support (ALS) Task Force of the International
Liaison Committee on Resuscitation (ILCOR) recommended that:
• Comatose adult patients with spontaneous circulation after out-of-hospital cardiac
arrest caused by an initial rhythm of Ventricular Fibrillation (VF) should be
cooled to 32°C to 34°C for 12 to 24 hours.
• Such cooling may be beneficial for other rhythms as well, or for in-hospital
cardiac arrest.17
A Review of the Trial Evidence
The earliest of these studies was the preliminary clinical trial by Bernard et al.
(1997), which was the pilot for the future Bernard et al. (2002) RCT.18
Bernard et al.
(1997) performed a study on 22 adult patients who remained comatose after an initial out-
of-hospital VF CA. The TH group was cooled to 33°C using ice packs and maintained in
TH for 12 hours before being actively re-warmed. Neurological outcomes were assessed
using the Glasgow Outcome Score (GOS).
The results of the trial were compared with a historical sample of 22 patients who
did not receive TH after CA.19
The study found that 11 of 22 patients had a good
neurological recovery with a GOS of 1 or 2 compared to 3 of 22 patients in the
normothermia historical control group.20
This showed that TH improved neurological
outcome, however the study was limited due to its use of historic controls, meaning that
17
Christenson, James M., MD, FRCPC. “Hypothermia Recommended After VF Cardiac
Arrest.” Journal Watch Emergency Medicine 13 Aug. 2003.
18
Collins,
pg
147
19
Collins,
pg
147
20
Collins,
pg
147

10. 10
the documented notes used in the comparison were not recorded for the purpose of the
research study.21
Yanagawa et al. (1998) followed the preliminary Bernard et al. study of 1997.
This study, based in Japan, aimed to compare the effects of hypothermia following out of
hospital cardiac arrest. 28 patients were involved; the hypothermia group were cooled to
34°C for 48 hours while the control group was treated per standard practice which did not
include hypothermia.22
The study found that 54% of the hypothermic patients survived
compared to 33% of the normothermic group. Yet, while only 40% of the normal group
developed pneumonia, pneumonia developed in 85% of the hypothermic patients. This
suggests that although TH improves outcome after CA, it also increases the incidence of
pneumonia.23
However, this study was limited in that it was not a RCT, it was based in
one hospital, and it used a historical control group. Furthermore, these factors along with
sex and age differences between the two groups led to a potential for either intentional or
unintentional research bias towards the sampling methods.24
The two randomized controlled trials that served as the basis of the ILCOR
recommendations were the Hypothermia after Cardiac Arrest (HACA) trial and the
Bernard trial.25
The HACA trial was conducted in nine centers across five European
nations while the Bernard Trial was undertaken in four hospitals in Melbourne,
21
Collins,
pg
147
22
Collins,
pg
147
23
Collins,
pg
147
24
Collins,
pg
147
25
“Stock Your Emergency Department with Ice Packs: A Practical Guide to Therapeutic
Hypothermia for Survivors of Cardiac Arrest.” Canadian Medical Association
Journal 13 March 2009; 176:759-762. pg
759

11. 11
Australia.26
The two trials were similar in that they enrolled comatose patients
resuscitated from ventricular fibrillation or pulseless ventricular tachycardia. All patients
received advanced cardiac life support with postresusitation care; all were sedated,
paralyzed to prevent shivering, and ventilated.27
The TH group of both trials were cooled
to 32-34°C within six hours of arrest. The hypothermia protocols of the studies differed
slightly.
In the European study 75 out of the 136 (55%) patients in the hypothermia group
had a favorable neurological outcome and able to live and work independently six
months post arrest compared to 54 of 137 (39%) of the normothermic patients.28
After six
months, death occurred in 41% of the hypothermic group compared to 55% in the
normothermic group.29
The Australian study focused on neurological function at the time of discharge
from the hospital. Of the 43 patients treated with hypothermia, 21 (49%) had good
neurological function, compared to 9 out of 34 (26%) of patients who did not receive
TH.30
A comparison of mortality at discharge presented 51% of TH patients as compared
to 68% of normothermic patients.
Mild hypothermia in both studies was associated with fewer deaths and reduced
disability and was statistically significant.31
The number-needed-to-treat to reduce
26
Nolan,
pg
118
27
“Stock
Your
Emergency
Department
with
Ice
Packs,”
pg
759
28
Nolan,
pg
119
29
Nolan,
pg
119
30
Nolan,
pg
119
31
“Stock
Your
Emergency
Department
with
Ice
Packs,”
pg
759

12. 12
neurological impairment at six months in the HACA trial was 6. 32
The number-needed-
to-treat to achieve one additional survivor to discharge in the Bernard trial was 4.33
Although well designed, both of these trials were limited by their stringent
enrollment criteria. As much as 92% of assessed patients were excluded from the trial.34
Why does therapeutic hypothermia lead to this improved outcome in patients? To
understand this effect, it is important to understand two concepts, reperfusion injury and
the physiology of hypothermia.
Reperfusion Injury and the Physiology of Hypothermia
When cardiac arrest occurs, there is an immediate cession of blood flow to the
brain. As a result, the cerebral tissue becomes ischemic and oxygen levels are depleted.35
Immediately post-resuscitation, there is an excessive increase in cerebral blood flow,
however, for the 90 minutes to 12 hours following this, blood flow is decreased to only
50% of the baseline value (initial level before CA).36
Scientists have known for decades
that cellular oxygen deprivation causes cell damage and can lead to cellular death,
however, due to the work of Dr. Lance Becker of the University of Pennsylvania, we now
have a better understanding of the physiology behind this occurrence.37
When a cell
becomes ischemic, a cycle of three critical reactions occurs within the cell; these cycles
lead to further tissue injury and ischemia even after perfusion returns to baseline values,
32
Christenson.
33
Christenson.
34
Nolan,
pg
119
35
Koran, Zeb. “Therapeutic Hypothermia in the Postresuscitation Patient: The
Development and Implementation of an Evidence-Based Protocol for the
Emergency Department.” Journal of Trauma Nursing Jan-March 2009; 16:48-57.
pg
49
36
Koran,
pg
49
37
Clumpner, pg
53

13. 13
thus earning the term, reperfusion injury.38
These reactions include the production of
oxygen free radicals (reactive oxygen species), excitatory amino acid release, and
calcium shifts.39
In turn, these lead to mitochondrial damage and apoptosis (programmed
cell death).40
Within the cell, mitochondria use oxygen to produce energy. Once the oxygen is
used, the mitochondrion releases an oxygen free radical. These free radicals are highly
reactive due to an unpaired valence electron.41
The reaction of these radicals triggers a
chemical chain reaction that uses adenosine triphosphate (ATP) and produces lactic
acid.42
The decreased availability of ATP and increased levels of lactic acid – which
cannot be removed with the decreased perfusion – causes muscle death. Under normal
conditions, the body produces antioxidants to counteract the free radicals. However,
during major injury or ischemia, the production of these antioxidants is drastically
reduced and thus the free radicals become a major problem.43
Reperfusion injury causes hypotension, vascular and organ dysfunction, cerebral
edema and apoptosis.44
Hypothermia suppresses many of the chemical reactions
associated with reperfusion injury and thus counteracts some of the negative
physiological effects that result after resuscitation.45
Lowering the core body temperature
38
Clumpner,
pg
54
39
Nolan,
pg
119
40
Nolan,
pg
119
41
Clumpner,
pg
54
42
Clumpner,
pg
54
43
Clumpner,
pg
54
44
Clumpner,
pg
54
45
Nolan,
pg
119

14. 14
decreases the metabolic rate.46
For each 1°C drop in temperature, the cerebral metabolic
rate is decreased 6%-7%.47
This is advantageous because it decreases oxygen demands in
the same cells that are being deprived of oxygen supplies.48
It has been observed that the
negative events (release of free radicals, ion shifts, cell death, etc.) following post-
resuscitation ischemia are slowed down by hypothermia.49
Mild cardiac hypothermia is
the most potent protector of myocardial function.50
Furthermore, approximately 30% of cardiac arrest survivors endure severe brain
damage.51
Three distinct stages of cerebral damage follow anoxic insult: early,
intermediate, and late.52
The early stage starts from the moment of insult and lasts an hour after injury.53
During this stage, the metabolic demands increase while perfusion decreases. Despite a
dramatic loss in supplies, the consumption of oxygen, glucose and ATP continue. 54
Hypothermia works to significantly reduce the metabolic demands on the brain.55
Hypothermia is most beneficial when applied early, within 15 minutes of the onset of
ischemia.56
46
Futterman, Laurie G. and Louis Lemberg. “The Significance of Hypothermia in
Preserving Ischemic Myocardium.” American Journal of Critical Care 2004;
13:79-84. pg
80
47
Koran,
pg
49
48
Futterman,
pg
81
49
Koran,
pg
49
50
Futterman,
pg
79
51
Koran,
pg
49
52
Clumpner,
pg
55
53
Clumpner,
pg
55
54
Clumpner,
pg
55
55
Clumpner,
pg
55
56
Futterman,
pg
81

15. 15
The intermediate stage spans from 1 to 12 hours post resuscitation.57
Excitatory
amino acids and glutamate are released, triggering the ion channels in the brain and
causing a calcium ion rush into the intercellular space.58
This activates cytotoxic cascades
within the cells causing neuronal cell death.59
Increased levels of nitric oxides in the brain
after cardiac arrest can cause vascular dysfunction.60
Hypothermia decreases the release
of excitatory amino acids and glutamate while also decreasing the production of nitric
oxide.61
The late stage is marked from 12-24 hours post resuscitation.62
Markers of this
stage include: cerebral edema, the breakdown of the blood-brain barrier, seizures and
irreversible neuronal death.63
At this point, hypothermia helps by slowing down the
breakdown and decreasing intracranial pressure and cerebral edema.64
In addition to reperfusion injury, patients resuscitated from a ventricular
fibrillation cardiac arrest are at a risk of re-fibrillation.65
A study led by Dr. Kimberley
Boddicker suggests that hypothermia improves defibrillation success and resuscitation
outcomes from VF. In the study, 32 swine were divided into four groups: normothermia
(37°C), mild hypothermia (35°C), moderate hypothermia (33°C) and severe hypothermia
57
Clumpner,
pg
55
58
Clumpner,
pg
55
59Clumpner,
pg
55
60Clumpner,
pg
55
61
Clumpner,
pg
55
62
Clumpner,
pg
55
63
Clumpner,
pg
55
64
Clumpner,
pg
55
65
Boddicker, Kimberly A. et al. “Hypothermia Improves Defibrillation Success and
Resuscitation Outcomes From Ventricular Fibrillation.” Circulation
Cardiovascular Quality and Outcomes: Journal of the American Heart Association
13 Jun. 2005; 111: 3195-3201. pg
3195

16. 16
(30°C).66
After hypothermia had been induced, VF was electrically induced. The VF was
left unsupported, meaning no CPR or defibrillation, for eight minutes before shocking
with a biphasic defibrillator, providing successive shocks and CPR as needed until return
of spontaneous circulation (ROSC) or no response for greater than 10 minutes.67
None of the normothermia group achieved ROSC as compared to 3 out of 8 in the
mild TH group, 7 of 8 in the moderate TH group, and 5 of 8 in the severe TH group.68
This beneficial effect was not due to an alteration of the coronary perfusion pressure, as
that factor was kept constant throughout the groups.69
This suggests that a change in the
mechanical, metabolic, or electrophysical properties of the myocardium was responsible
for the improved defibrillation and resuscitative outcome with the use of moderate to
deep hypothermia.
A recent study has shown that for each hour that TH is delayed, the odds of
neurological impairment increase by 30%.70
This factor is the reason why it is essential to
start TH in the pre-hospital setting. EMS thus has a crucial role in affecting the future
survivability success.
As of September 2008, out of the 24,000 EMS agencies in the United States, 100
had already implemented a therapeutic hypothermia protocol.71
Furthermore, in a survey
led by Benjamin Abella, 265 physicians were questioned regarding their use of TH, their
methods used, and/or reasons they have not incorporated TH into their practice. Of these
66
Boddicker,
pg
3195
67
Boddicker,
pg
3195
68
Boddicker,
pg
3195
69
Boddicker,
pg
3195
70
Clumpner,
pg
55
71
Clumpner,
pg
55

17. 17
physicians, 87% said they had not used TH.72
Of the reasons presented for non-use, 49%
felt there were not enough supporting data, 32% cited a lack of incorporation into
advanced cardiac life support (ACLS) protocols, and 28% mentioned that the methods for
cooling were either technically too difficult or too slow.73
EMS is a liaison between out-of-hospital patients and medical centers. Any
treatment or care protocol that is to be started in the field of EMS must not possess a
potential of harm to the patient. If induced hypothermia is lifted prematurely, the patient
might be harmed, therefore, it is crucial that the medical center continue the treatment.74
Hypothermia cannot be implemented in the EMS system if there is no hospital system to
continue the treatment. It is thus important to analyze the factors inhibiting the induction
of TH protocols in both hospitals and EMS systems.
One major setback for the implementation of hypothermia into the standard of
care for both in-hospital and EMS cardiac arrest care is the lack of evidence. It is
important to note that although many studies have been conducted examining the effects
of in-hospital therapeutic hypothermia, few studies have researched the effects of
inducing TH within the pre-hospital setting.75
The National Association of EMS
Physicians believes that the lack of evidence focused on the induction of TH in the pre-
hospital setting precludes the recommendation of the protocol for the standard of care for
72
Abella, Benjamin S. et al. “Induced Hypothermia is Underused After Resuscitation
from Cardiac Arrest: A Current Practical Survey.” Resuscitation Feb. 2005; 64:
181-186.
73
Abella
et
al.
74
“Induced Therapeutic Hypothermia in Resuscitated Cardiac Arrest Patients. Position
Statement Approved by the NAEMSP Board of Directors.” Prehospital
Emergency Care 2008; 12:393-394.
75
Clumpner,
pg
56

18. 18
all EMS patients resuscitated from CA.76
In addition, Dr. G. C. Fisher has argued that a
lack of thorough detail reports in the two major foundational studies allowed for the
clinically skeptic to claim the trials invalid and therefore resist using TH.77
To overcome
this factor, either additional research must be conducted, or the current evidence could be
accepted. The European Resuscitation Council serves as an example as it stated that pre-
hospital hypothermia is “safe” and effective even if there is a lack of experience.”78
Since the induction of TH in a pre-hospital control group is ethically unjustifiable79
, EMS
focused trials are difficult, and thus more reliance is placed on the current evidence.
Major factors inhibiting the implementation of TH include: the lack of evidence,
cost, concern about the continuum of care, the induction methodology, uncertainty of
adverse effects, time, and resources. In addition, personal barriers such as the
unawareness and resistance to change of many individuals may be a significant inhibiting
factor.80
An in-depth analysis of these factors is presented in the article, “Therapeutic
Hypothermia: An Analysis of the Factors Inhibiting the Implementation of a General
Protocol.”
76
“Induced
Therapeutic
Hypothermia
in
Resuscitated
Cardiac
Arrest
Patients.”
77
Fisher, G.C. “Hypothermia After Cardiac Arrest: Feasible but is it Therapeutic?”
Anaesthesia: The Association of Anaesthetists of Great Britain and Ireland 2008;
63:885-886.
pg
885
78
Clumpner,
pg
56
79
Clumpner,
pg
56
80
Neumar, Robert W. et al.“Post Cardiac Arrest Syndrome: Epidemiology,
Pathophysiology, Treatment, and Prognostication.” Circulation Cardiovascular
Quality and Outcomes: Journal of the American Heart Association 23 Oct. 2008;
118: 2452-2483 pg
2470

19. 19
Conclusion
Therapeutic Hypothermia has many benefits for cardiac arrest patients and has
been associated with improving the survival rate of cardiac arrest patients. In addition to
increasing survival rates, TH has also been associated with a decrease in neurological
impairment. “TH is the only post-resuscitation therapy shown to improve both survival
and reduce disability after cardiac arrest.”81
TH is therefore a beneficial treatment, and
should be implemented as soon as possible, thus within the EMS system. However, if the
continuum of care cannot be guaranteed at receiving hospitals, TH cannot be started in
EMS as an incomplete treatment would cause harm to the patient. Despite several
recommendations by ILCOR and the AHA, Several factors are inhibiting the
implementation of TH in most medical centers and thus among EMS agencies. An in-
depth analysis of these factors is presented in the article, “Therapeutic Hypothermia: An
Analysis of the Factors Inhibiting the Implementation of a General Protocol.”
81
Cooling Therapy for Cardiac Arrest Survivors is as Cost-Effective as Accepted
Treatments for other Conditions

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Appendix A
Explanation of Terms
• Myocardial Infarction (MI)- heart attack, the term "myocardial infarction" focuses
on the myocardium (the heart muscle) and the changes that occur in it due to the
sudden deprivation of circulating blood. The main change is necrosis (death) of
myocardial tissue.
• Cardiac Attack- heart attack
• Cardiac Arrest- A primary cardiac disorder that results in sudden loss of cardiac
output and a resultant loss of end-organ perfusion resulting in death unless the
primary cardiac disorder is corrected.
• Heart Rhythms
o Normal Sinus Rhythm
Normal beating of the heart.
o Ventricular Fibrillation (VF)-

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Arrhythmia in which uncoordinated contractions of the myocardium
causes the ventricles to tremble rather than contact properly.
o Ventricular Tachycardia (VT)
Arrhythmia that consists of rapid ventricular contractions that deter the
circulation ability by decreasing the refill time of the ventricles, thus
decreasing the volume of blood pumped.
o Pulseless Electrical Activity (PEA)
A clinical condition characterized by unresponsiveness and lack of
palpable pulse in the presence of organized cardiac electrical activity.
o Asystole
Cardiac standstill with no cardiac output and no ventricular depolarization;
it eventually occurs in all dying patients.
• Induced Hypothermia –

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The lowering of a patient’s core body temperature.
• Standard of Care –
A diagnostic and treatment process that a clinician should follow for a certain
type of patient, illness, or clinical circumstance
• Emergency Medical Services (EMS)-
The organized systems with set protocols for responding to, providing definitive
care, and transport of patients in the event of an out-of-hospital medical or
traumatic emergency.
• Comatose-
A state of unconsciousness.
• Return of Spontaneous Circulation (ROSC)-
A palpable pulse that is present after clinically documented asystole.