EM Critical Care

UNDERSTANDING AND CARING FOR

CRITICAL ILLNESS IN EMERGENCY MEDICINE

Practical Aspects Of Postcardiac Volume 3, Number 3

Arrest Therapeutic Hypothermia

Authors

David A. Pearson, MD, FACEP, FAAEM

Assistant Professor, Carolinas Healthcare System; Associate
Residency Program Director, Department of Emergency
Abstract Medicine, Carolinas Medical Center, Charlotte, NC
Alan C. Heffner, MD
Neurologically intact survival following cardiac arrest remains a Director, Medical ICU, Director, ECMO Services Pulmonary
and Critical Care Consultants, Department of Internal
challenge of modern medicine. Internationally, the rate for survival Medicine, Department of Emergency Medicine, Carolinas
of out-of-hospital cardiac arrest has hovered at a disappointingly Medical Center; Clinical Associate Professor, University of
North Carolina School of Medicine, Charlotte, NC
low 6%. Over the past decade, the early postcardiac arrest period
has emerged as a critical window for therapeutic intervention to Peer Reviewers

minimize cerebral injury and improve recovery. Therapeutic hypo- Jon Rittenberger, MD, MS, FACEP
thermia is a cornerstone of this early postresuscitation care. Despite Assistant Professor, Department of Emergency Medicine,
University of Pittsburgh School of Medicine; Attending
accumulating evidence and widespread endorsement, adoption Physician, Emergency Medicine and Post Cardiac Arrest
of therapeutic hypothermia is incomplete. This review focuses on Services, UPMC Presbyterian Hospital, Pittsburgh, PA
overcoming barriers to enable practical application of this life-saving Scott D. Weingart, MD, FCCM
Associate Professor, Department of Emergency Medicine,
treatment. Director, Division of Emergency Department Critical Care,
Icahn School of Medicine at Mount Sinai, New York, NY
Note From The Editor-In-Chief CME Objectives
Readers of EM Critical Care will recall our 2012 issue by Ritten- Upon completion of this article, you should be able to:
berger et al that emphasized the guiding principles of cardiocerebral 1. Describe the indications and contraindications of
resuscitation in the emergency department after cardiac arrest. In therapeutic hypothermia in postcardiac arrest.

this issue, we will expand on the discussion of the use of therapeutic 2. Describe the most effective strategy to implement
therapeutic hypothermia in your institution.
hypothermia after cardiac arrest and will address a number of the 3. Troubleshoot or prevent common complications of
challenges and logistical considerations for implementing hypother- therapeutic cooling.
mia. More than a decade after the landmark trials by Bernard et al
Prior to beginning this activity, see the back page for faculty
and the Hypothermia After Cardiac Arrest (HACA) Study Group, disclosures and CME accreditation information.
there remain challenges with uptake, implementation, and inclu-
sion/exclusion criteria for therapeutic hypothermia. This issue by
Pearson and Heffner succinctly addresses the spectrum of questions
and complexities that have evolved since therapeutic hypothermias
powerful benefit was demonstrated. Enjoy! - Rob Arntfield
Editor-in-Chief Clinical Research Director, Andy Jagoda, MD, FACEP Julie Mayglothling, MD Emanuel P. Rivers, MD, MPH, IOM
Robert T. Arntfield, MD, FACEP, Center for Resuscitation Science, Professor and Chair, Department Assistant Professor, Department Vice Chairman and Director
FRCPC, FCCP Philadelphia, PA of Emergency Medicine, Icahn of Emergency Medicine, of Research, Department of
Assistant Professor, Division School of Medicine at Mount Sinai; Department of Surgery, Division Emergency Medicine, Senior
of Critical Care, Division of Lillian L. Emlet, MD, MS, FACEP Medical Director, Mount Sinai of Trauma/Critical Care, Virginia Staff Attending, Departments of
Emergency Medicine, Western Assistant Professor, Department of Hospital, New York, NY Commonwealth University, Emergency Medicine and Surgery
University, London, Ontario, Critical Care Medicine, Department Richmond, VA (Surgical Critical Care), Henry
Canada of Emergency Medicine, University William A. Knight, IV, MD, FACEP Ford Hospital; Clinical Professor,
of Pittsburgh Medical Center; Assistant Professor of Emergency Christopher P. Nickson, MBChB, Department of Emergency
Program Director, EM-CCM Medicine, Assistant Professor of MClinEpid, FACEM Medicine and Surgery, Wayne State
Associate Editor Fellowship of the Multidisciplinary Neurosurgery, Medical Director - Senior Registrar, Intensive Care University School of Medicine,
Scott D. Weingart, MD, FCCM Critical Care Training Program, Emergency Medicine Mid-Level Unit, Royal Darwin Hospital, Detroit, MI
Associate Professor, Department Pittsburgh, PA Provider Program, Associate Darwin, Australia
of Emergency Medicine, Director, Medical Director of Neuroscience Isaac Tawil, MD, FCCM
Division of Emergency Department Michael A. Gibbs, MD, FACEP ICU, University of Cincinnati Jon Rittenberger, MD, MS, FACEP Assistant Professor, Department
Critical Care, Icahn School of Professor and Chair, Department College of Medicine, Cincinnati, Assistant Professor, Department of Anesthesia and Critical Care /
Medicine at Mount Sinai, New of Emergency Medicine, Carolinas OH of Emergency Medicine, Department of Emergency Medicine,
York, NY Medical Center, University of North University of Pittsburgh School Director, Neurosciences ICU,
Carolina School of Medicine, Haney Mallemat, MD of Medicine; Attending Physician, University of New Mexico Health
Chapel Hill, NC Assistant Professor, Department Emergency Medicine and Post Science Center, Albuquerque, NM
Editorial Board of Emergency Medicine, University Cardiac Arrest Services, UPMC
Benjamin S. Abella, MD, MPhil, Robert Green, MD, DABEM, of Maryland School of Medicine, Presbyterian Hospital, Pittsburgh,
FACEP Baltimore, MD PA
Research Editor
FRCPC
Assistant Professor, Department Amy Sanghvi, MD
Professor, Department of
of Emergency Medicine and Evie Marcolini, MD, FAAEM Department of Emergency
Anaesthesia, Division of Critical
Department of Medicine / Assistant Professor, Department of Medicine, Icahn School of
Care Medicine, Department of
Section of Pulmonary Allergy Emergency Medicine and Critical Medicine at Mount Sinai, New York,
Emergency Medicine, Dalhousie
and Critical Care, University of Care, Yale School of Medicine, NY
University, Halifax, Nova Scotia,
Pennsylvania School of Medicine; Canada New Haven, CT
Case Presentations
A 63-year-old male experienced a witnessed, out-of-
hospital collapse. The patients wife called 911 and initi-
ated CPR. Ventricular fibrillation was recognized upon
paramedic arrival, but it was resistant to initial biphasic
countershock. ROSC was ultimately achieved 21 min-
utes following cardiac arrest. Hypotension (BP of 92/42
mm Hg, MAP of 59 mm Hg) and persistent coma (GCS
score = 3) are noted upon arrival to the ED. The nurse
asks you if this patient is a candidate for the therapeutic
hypothermia protocol, despite his prolonged downtime.
A short time later, EMS brings in a 39-year-old woman
with a history of asthma who called 911 for shortness of
breath. When EMS arrived, the patient was in severe
respiratory distress. During transport, her respiratory status
worsened, and she became unresponsive. The monitor re-
vealed a bradycardic idioventricular rhythm, and the patient
was noted to be pulseless. ACLS was started by EMS, and
ROSC was achieved following 10 minutes of resuscitation.
The patient remains comatose upon arrival to the ED. The
exam reveals symmetric diffuse expiratory wheezes, and her
chest x-ray is negative for pneumothorax. You continue to
aggressively treat the status asthmaticus and initiate consul-
tation with the critical care team. You consider postcardiac
arrest therapeutic hypothermia, but you wonder whether you
should cool this patient following PEA arrest?
Introduction
Over 300,000 patients per year in the United States
experience sudden cardiac arrest.1 Despite initial
resuscitation, neurological injury sustained dur-
ing cardiac arrest is the leading cause of death and
contributes to the historic survival rate of only 6%
to 8%.1,2 Additionally, 30% of survivors have perma-
nent neurological injury.
Therapeutic hypothermia has emerged as the
only effective intervention to ameliorate anoxic brain
injury and improve neurological outcome.3 Despite
strong evidence and endorsement by the American
Heart Association, therapeutic hypothermia remains
an underutilized modality, with implementation
rates as low as 30% to 40%.4-8
Perceived barriers to implementation of
therapeutic hypothermia include lack of treatment
awareness, premature negative prognostication, and
perceived high workload demands.9,10 Regardless of
the reason, failure to implement this evidence-based
therapy deems its ineffectiveness absolute.
This review focuses on the practical aspects of
implementing therapeutic hypothermia for post-
cardiac arrest patients, regardless of practice locale,
and highlights the key resuscitation adjuncts in
the immediate and early postresuscitation phase
of illness that provide the greatest opportunity to
achieve the goal of neurologically intact survival of
cardiac arrest victims.
EMCC 2013 2
Critical Appraisal Of The Literature
The PubMed database was searched for articles
published from 1950 to August 2012. The terms
used in the search included English publications
containing 1 or more of the following key words:
therapeutic hypothermia, induced hypothermia, car-
diopulmonary resuscitation, and cardiac arrest. This
search revealed over 440 publications. The results
were reviewed, and relevant citations from each
study were searched manually. An Internet search
for practice guidelines and clinical policies identified
the following:
American Heart Association: 2010 International
Consensus on Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care Science
With Treatment Recommendations
Australian Resuscitation Council: Adult Ad-
vanced Life Support Guidelines 2006
Canadian Association of Emergency Physicians,
Critical Care Committee: The Use of Hypother-
mia After Cardiac Arrest
Scandinavian Society of Anesthesiology and
Intensive Care Medicine: Task Force on Scandi-
navian Therapeutic Hypothermia Guidelines,
Clinical Practice Committee
The Hong Kong Society of Critical Care Medi-
cine Position Statement: The Use of Hypother-
mia After Cardiac Arrest
Efficacy Of Therapeutic Cooling
Evidence For Cooling Patients With
Ventricular Tachycardia And Ventricular
Fibrillation
Therapeutic hypothermia is the only neuroprotec-
tive therapy that demonstrates neurological and
survival benefit following cardiac arrest.11-13 A decade
of supportive investigation culminated in comple-
tion of 2 multicenter randomized trials of therapeutic
hypothermia in 2002. Both trials enrolled comatose
survivors of out-of-hospital cardiac arrest with a
first recognized rhythm of ventricular tachycardia
and ventricular fibrillation (VT/VF).11,12 Nonshock-
able rhythms were excluded to avoid experiment
confounding. Both trials showed improved survival
with good neurological outcome. (See Table 1.) The
Hypothermia After Cardiac Arrest (HACA) study
defined a Cerebral Performance Category (CPC) score
of 1 (patient is alert with normal cerebral function) or
2 (patient is alert and has sufficient cerebral function
to live independently and work part time) as a good
neurological outcome. The Bernard study defined
a good outcome as normal or minimal disability
(able to care for self; discharged directly to home). A
powerful treatment impact was demonstrated with 1
survivor, with good neurological outcome achieved
for every 6 patients treated (ie, the number needed
www.ebmedicine.net Volume 3, Number 3
to treat [NNT] was 6).14 Consensus guidelines and
a systematic review endorse the use of cooling in
patients after arrest with an initial rhythm of VT/VF
as a Level IA evidence-based practice.3, 4
A number of institutional observational studies
confirm the feasibility and effectiveness of thera-
peutic hypothermia applied outside of strict re-
search protocols.15-19 Furthermore, these experiences
demonstrate the feasibility of supporting the use of
therapeutic hypothermia in high-risk patients that
were systematically excluded in the controlled trials.
Evidence For Cooling Patients With An
Initial Rhythm Other Than Ventricular
Tachycardia And Ventricular Fibrillation
One challenge to improving outcomes after cardiac
arrest is the epidemiologic trend of patients present-
ing with nonshockable rhythms, which is indepen-
dently associated with worse prognosis.20 Whether
or not patients with nonshockable primary arrest
rhythms (pulseless electrical activity [PEA] and
asystole) are eligible for therapeutic hypothermia
remains controversial. To date, no randomized trials
have focused on therapeutic hypothermia for these
patients. Champions for this group highlight strong
biologic plausibility and irrelevance (to the brain)
of the nonperfusing rhythm that initiated the injury.
Observational evidence regarding therapeutic hypo-
thermia in this patient group is conflicting.21-24
We believe that defining cardiac arrest pa-
tients by primary arrest rhythm is an overly sim-
plistic approach that does little to discriminate
individual patient acuity and physiology. Re-
gardless of the rhythm, once ROSC is achieved,
neurological outcomenot the illness precipitat-
ing cardiac arrestis the primary limitation for
patient recovery and survival. In contrast to the
strict criteria we would expect of clinical trials,
real-world implementation should aim to exclude
fewer potential candidates for cooling, given the
low risk and low cost of this treatment and the
absence of an alternative postarrest treatment
that is proven to improve survival. Multiple
guidelines support application of cooling for all
comatose cardiac arrest victims regardless of the
initial rhythm or arrest precipitant. 4,14 These rec-
ommendations were based primarily on observa-
tional trials showing benefit of cooling following
Table 1. Survival After Cardiac Arrest With
Good Neurological Outcome In Landmark
Trials
Hypothermia Control
HACA12 75/136 (55%) 54/137 (39%)
Bernard et al11 21/43 (49%) 9/34 (26%)
Abbreviation: HACA, Hypothermia After Cardiac Arrest trial.
www.ebmedicine.net Volume 3, Number 3
out-of-hospital cardiac arrest regardless of initial
rhythm. 15-18,25-27 Detractors of such a strategy
point to the absence of a randomized trial sup-
porting use in this group. However, the hetero-
geneity of patient and arrest factors resulting in a
first-identified rhythm of PEA and asystole make
this a challenging subset of patients to study, and
future trials risk the ethical dilemma of random-
izing patients to normothermia in light of our
current evidence.
Many institutions with therapeutic hypother-
mia protocols cool patients regardless of arrest
rhythm. This affords the postarrest patient the best
chance at neurological recovery with minimal risk.
Therapeutic hypothermia represents a cost-effective
resource that should be deemed part of comprehen-
sive postresuscitative cardiac arrest care;28 thus, we
encourage cooling regardless of initial arrest rhythm.
Evidence For Cooling Patients With
Nonprimary Cardiac Events
Death due to brain injury represents the final com-
mon pathway of patients experiencing anoxic or
hypoxic injury, regardless of the inciting event.
Thus, the best available evidence supports ex-
trapolation of therapeutic hypothermia to patients
experiencing nondysrhythmogenic arrest, includ-
ing patients with asphyxia or traumatic nonexsan-
guinating arrest. (See Table 2.) Neuroprotective
cooling should not be withheld due to the lack of
an ideal candidate, as the potential neurologi-
cal benefit of cooling outweighs the potential risk
of hypothermia in these patients. Neurological
recovery is the primary limiting factor to a positive
outcome in most of these circumstances.
Inclusion And Exclusion Criteria For
Therapeutic Cooling
Institutions have slight variations of criteria for
inclusion and exclusion to their postcardiac arrest
care bundle. Our institutions criteria are described
in Tables 3 and 4 (page 4). In this protocol, cardiac
arrest patients are cooled regardless of initial rhythm
or arrest location (inhospital or out-of-hospital).
Patients with severe or terminal illness and those un-
Table 2. Nonprimary Cardiac Events That
May Benefit From Therapeutic Hypothermia
Airway obstruction
Anaphylaxis
Asphyxia
Carbon monoxide poisoning
P
Commotio cordis
.009 Drowning
.046 Drug overdose (ie, narcotics, cocaine) or other toxicological poison-
ings
Hanging/strangulation
3 EMCC 2013
likely to survive the intensive care unit (ICU) based
on comorbid disease (irrespective of cardiac arrest)
are poor candidates for cooling.
The relative contraindications of therapeutic
hypothermia (listed in Table 4) are discussed below.
Age: The sentinel trials focused on adults, but
therapeutic hypothermia also improves cerebral
outcomes following perinatal hypoxia. Although
a gap in the evidence for pediatric patients re-
mains,29,30 selected use in children is endorsed and
widely adopted.4
Pregnancy: Successful therapeutic hypothermia
of pregnant patients, although a rare circumstance,
emphasizes the favorable risk-reward ratio of
therapy in this situation.31-32
Hemodynamic instability: Hemodynamic
instability and postcardiac arrest shock are common.
Postcardiac arrest shock complicates management of
half of all comatose patients and is directly associated
with the length of cardiac arrest. Although patients
in shock were excluded from early trials of therapeu-
tic hypothermia, accumulating evidence supports
the safety and efficacy of therapeutic hypothermia
among patients with serious hemodynamic instabil-
ity, including those requiring catecholamine support
and intra-aortic balloon pump for severe cardiogenic
shock.33 As such, shock is no longer considered a
contraindication to therapeutic hypothermia induc-
tion. New evidence also shows that therapeutic
hypothermia may be associated with a reduced need
for vasopressor and inotropic support in patients with
cardiogenic shock.34,35
Table 3. Inclusion Criteria For Postcardiac
Arrest Therapeutic Hypothermia
ROSC < 60 min after cardiac arrest
Inhospital or out-of-hospital cardiac arrest
Time at induction < 6 h from ROSC
Coma (GCS score 8)
Patient intubated and mechanically ventilated
Abbreviations: GCS, Glasgow Coma Scale; ROSC, return of sponta-
neous circulation.
Table 4. Exclusion Criteria For Postcardiac
Arrest Therapeutic Hypothermia
Absolute Contraindications
Severe terminal illness or Do Not Resuscitate (DNR) / Do Not
Intubate (DNI) order
Relative Contraindications
Age < 18 y
Pregnancy
Hemodynamic instability
Traumatic arrest
Severe systemic infection
Clinical bleeding
EMCC 2013 4
Traumatic arrest: Traumatic arrest is often listed
as a contraindication to cooling due to the concern for
hypothermia-induced coagulopathy in the setting of
life-threatening hemorrhage. However, cardiac arrest
is a frequent precipitant of trauma. A fall or motor
vehicle collision precipitated by cardiac arrest is a
common scenario, so ascertaining historical events
accurately is imperative. Patients who have nonhem-
orrhage-related traumatic hypoxia or arrest should
also be considered for therapeutic hypothermia. Some
centers are utilizing therapeutic hypothermia after
gaining full control of the bleeding source in patients
experiencing traumatic arrest from hemorrhagic
shock; however, little is known about the application
of therapeutic hypothermia in this setting.36
Systemic infection: Hypothermia-associated
immune suppression warrants weighing the
perceived risk and benefit of cooling patients who
have cardiac arrest due to sepsis.37 Acute aspiration
pneumonia should not be considered a contraindi-
cation to hypothermia.
Bleeding: Since hypothermia induces coagu-
lopathy, active bleeding is a relative contraindica-
tion. Therapeutic hypothermia induces platelet
dysfunction at temperatures 35C and inhibi-
tion of the coagulation cascade at temperatures
33C.38 Thus, some experts advocate for cooling at a
slightly higher temperature range of 34.5C to 35C
in patients with suspected or active bleeding.39
Additionally, cooling is under investigation to help
treat traumatic and vascular cerebral hemorrhage.
Patients ineligible for therapeutic cooling war-
rant active measures to avoid post-ROSC hyperther-
mia due to its potential to exacerbate brain injury.40
Moderate-to-severe accidental or spontaneous
hypothermia associated with cardiac arrest warrants
rewarming to the goal mild hypothermia tempera-
ture range (32C-34C).
Timing Of Therapeutic Cooling
In addition to the primary ischemic insult during
no-flow and low-flow cardiac arrest, a second insult
of cerebral reperfusion injury evolves over hours
to days.41,42 This window affords an opportunity
for initiating targeted neuroprotective therapies to
mitigate the reperfusion insult and improve neuro-
logical outcome.
Prehospital Cooling
Animal studies demonstrate that cooling that is initi-
ated early results in improved survival and neuro-
logical outcome, while delays negate the beneficial
effect.43-47 The potential benefit of early therapy has
led to prehospital adoption of cooling. This provides
the earliest possible initiation for most patients,
and it is most commonly achieved with ice packs
or cold intravenous (IV) fluids. A prospective study
www.ebmedicine.net Volume 3, Number 3
of 142 patients documented a 20% increased risk of
death for every hour of delay in cooling initiation.48
Additionally, a retrospective study of 172 patients
revealed increased odds of poor neurological out-
come with each 5-minute delay in the initiation of
cooling.49 Garrett et al evaluated 551 patients after
cardiac arrest and showed that prehospital intra-
arrest cooling via 4C normal saline was associated
with improved ROSC (36.5%) when compared to
normothermia resuscitation (26.9%).50
In contrast, 3 prospective randomized trials
showed no difference in neurological outcome be-
tween the prehospital and inhospital cooling groups,
despite the prehospital group reaching the target
temperature more rapidly.51-53
The optimal timing of the initiation of cooling
to maximize benefit remains unclear. However, the
general consensus is that early cooling should be
prioritized as a part of resuscitation.
Cooling In The Emergency Department
It is important to note that prehospital cooling does
not mandate continued therapy, since many prehos-
pital protocols are designed to ensure consistent and
wide implementation. Upon arrival to the emer-
gency department (ED), patients should be individu-
ally evaluated for candidacy for therapeutic hypo-
thermia based on institutional guidelines and the
potential risk and benefit of continued treatment. If a
patient is deemed inappropriate for cooling, gradual
rewarming is advised due to the potential for delete-
rious electrolyte shifts, hemodynamic instability, and
cerebral injury associated with rapid rewarming.54,55
The landmark trials for therapeutic hypother-
mia reached the goal temperature in a mean of 2 to
8 hours.11,12 One approach for treating cardiac arrest
patients with therapeutic cooling would be to achieve
a target temperature of 32C-34C in 6 hours, with the
goal to cool as rapidly as possible. However, cooling
may offer benefit up to 24 hours after cardiac arrest
(and possibly beyond), so delayed initiation of cool-
ing or delays in reaching target temperature does not
necessarily diminish the potential benefit. Given the
potential neurological and cardiac benefit of early
initiation of cooling, we advocate for the earliest pos-
sible induction time. Additionally, cooling should be
considered in all cardiac arrest patients, even in the
setting of delayed induction.
Avoiding Delays
For inhospital arrests (ED or hospital inpatients), sup-
plies to allow rapid initiation cooling (ie, prechilled
4C IV fluids) should be readily available; we recom-
mend maintaining bags of normal saline in refrigera-
tors that are easily accessible to the ED or ICU.
Extensive delays in the initiation of cooling due
to concerns over patient candidacy should be avoid-
ed. Since many commercially available devices have
www.ebmedicine.net Volume 3, Number 3
nonreusable and costly equipment (ie, catheters or
surface pads costing thousands of dollars), cold IV
fluids and ice packs are effective initial measures
while exploring candidacy of individual patients.
Transfer
Postcardiac arrest interventions are time sensitive, so
early initiation of treatment is essential. Facilities that
do not have percutaneous coronary intervention (PCI)
and therapeutic hypothermia capabilities are encour-
aged to initiate therapeutic cooling prior to transfer.
Induction of cooling can be achieved with cold IV flu-
id infusion and surface ice packs applied to the neck,
groin, and axillae. Proactive development of clinical
pathway criteria in conjunction with the development
of protocols for referral to a cardiac arrest center will
help ensure smooth transitions of care.
Techniques For Therapeutic Cooling
Therapeutic cooling is divided into 4 phases. These
include: (1) induction; (2) maintenance; (3) rewarm-
ing; and (4) controlled normothermia. In the ED,
the induction phase of therapeutic cooling will be
the primary focus. This may represent initiation of
the cooling process or continuing the cooling efforts
started by prehospital providers. The maintenance,
rewarming, and controlled normothermia phases
will primarily be done in the ICU, but it is important
to understand the clinical caveats of these phases,
as it may be necessary to maintain or rewarm the
patient in the ED at times.
Cooling Induction
Induction of therapeutic hypothermia with cold
(4C) isotonic fluid is safe, inexpensive, and effec-
tive.56,57 Application of surface ice packs augments
induction and may be required for patients who are
intolerant of volume loading. Two benefits of cold
fluids and ice packs are their low cost and their ease
of use (including in the prehospital setting). The con-
comitant use of cold IV fluids, ice packs, and servo-
controlled automated cooling devices for rapid cool-
ing is helpful. Overshooting the goal temperature
range (< 32C) to a point that it poses significant risk
is rare and should not make the provider hesitate
to be aggressive with cooling measures during the
induction phase.
Reliable core temperature measurement is an
important element for monitoring, and it provides
essential feedback for the servo-controlled automat-
ed cooling systems. Core temperature measurement
should be initiated upon arrival to the ED. Bladder
or esophageal temperature sensors are most com-
monly used for core temperature monitoring. Newer
temperature-sensing Foley catheters do not require
urinary flow; instead, they sense bladder outlet
temperature. However, esophageal temperature
5 EMCC 2013
monitoring is preferred because bladder and rectal
temperature measurements more slowly reflect core
temperature during rapid cooling. Oral or axillary
temperature measurements are not recommended,
as they may not reflect core temperature adequately,
especially when used in patients experiencing rapid
temperature changes.58,59
Sedation and analgesia should be employed for
all comatose postarrest patients in order to attenuate
adrenergic response, hypermetabolism, and shiver-
ing during cooling.60 Adjunctive measures to control
shivering are often employed; these measures are
discussed in the Troubleshooting Therapeutic Cool-
ing section of this article.
Commercially available cooling systems utilize
either external (noninvasive) or internal (endovascu-
lar) devices to complete the induction phase and tran-
sition to the maintenance phase.61 (See Table 5.) There
are important logistical issues to consider regarding
setup and use for both invasive and noninvasive cool-
ing devices, and when compared to each other, nei-
ther is superior with regard to survival or neurologi-
cal outcomes.62-64 New devices continue to emerge for
rapid induction. The RhinoChill (Benechill, Inc., San
Diego, CA) delivers a coolant to the nasopharyngeal
passages, whereas the Thermosuit (Life Recovery
Systems HD, LLC, Kinnelon, NJ) uses cold-water im-
mersion to induce rapid hypothermia.53,65
Cooling Maintenance
Therapeutic cooling for 12 to 24 hours at a goal
temperature of 32C to 34C is recommended based
on the protocols of the landmark trials. The optimal
depth and period of cooling is currently undergo-
ing investigation. Surface cooling with commercially
available water-circulating blankets or gel pads and
intravascular cooling appear to be more effective than
conventional cooling (eg, ice packs and cold fluids)
and air-circulating blankets.66 These new-generation
devices provide automated control to prevent tem-
perature fluctuations and to facilitate slow, controlled
rewarming (< 0.5C/h). There is no clear advantage
between invasive and noninvasive units. Cost is com-
parable among the commercially available surface de-
vices and intravascular cooling devices. Selection of a
cooling strategy should involve the multidisciplinary
team caring for these patients.62,64
Rewarming
Early rewarming prior to completing the hypother-
mia treatment time period is rare. In such cases, slow
controlled rewarming (0.3C/h to 0.5C/h) to a safe
or normal core body temperature is recommended.59
The induction and rewarming phases tend
to be higher-risk periods for the complications of
therapeutic hypothermia, so they require judicious
monitoring for dysrhythmia, potassium shifts,
and hemodynamic instability. Warming-associated
EMCC 2013 6
vasodilation can lead to hypotension, requiring
fluid and/or vasopressor support. Rapid rewarm-
ing causes potassium to move extracellularly, which
risks hyperkalemia.38 However, we caution against
aggressive correction of potassium during rewarm-
ing. Low-dose repletion for potassium < 3.5 mEq/L,
with frequent electrolyte reanalysis, is recom-
mended. Equally important, cerebral injury has been
associated with rapid rewarming and is the basis for
slow, controlled rewarming rates.54,55
Controlled Normothermia
The brain remains vulnerable to heat stress for sev-
eral days following initial injury. Hyperthermia after
warming is common and can lead to neurological de-
terioration. If feasible, keep the cooling device in place
to maintain normothermia after completing cooling.
This fourth phase of controlled normothermia is often
continued for 2 to 3 days after rewarming.
Additional Considerations For
Therapeutic Cooling
Troubleshooting Therapeutic Cooling
The most common challenge during the induction
phase of therapeutic hypothermia is failure to reach
goal temperature in a timely fashion. Unrecognized
shivering plays a significant role. Shivering is often
difficult to discern on examination. Failure to reach
or maintain goal temperature may be an impor-
Table 5. Cooling Methods And Devices
Noninvasive Cooling Devices
Arctic Sun 2000 and 5000 (by CR Bard, formerly Medivance Inc.,
Louisville, CO)
Stryker (formerly Gaymar) Medi-Therm III (Stryker, Orchard Park,
NY)
Phillips InnerCool STx Surface Pad System (Phillips Healthcare,
Andover, MA)
Blanketrol III Body Temperature Regulation System (Cincinnati
Sub-Zero Products, Inc, Cincinnati, OH)
Invasive Cooling Devices
Philips InnerCool RTx Endovascular System, Accutrol catheter
(Phillips Healthcare, Andover, MA)
ZOLL (formerly Alsius) Intravascular Temperature Management
(IVTM) system CoolGard 3000 device & Cool Line, ICY, and
Quattro catheters (ZOLL Medical Corporation, Chelmsford, MA)
Cooling Adjuncts
Ice packs and cold saline (4C normal saline is most commonly
used)
EMCOOLS, refrigerated surface pads (EMCOOLS, Vienna, Austria)
Thermosuit (Life Recovery Systems HD, LLC, Kinnelon, NJ)
RhinoChill intranasal cooling system (Benechill, Inc., San Diego,
CA (At the time of publication, this device was not yet available for
sale in the United States.)
www.ebmedicine.net Volume 3, Number 3
tant clue to subclinical shivering. Persistently low
cooling-unit temperatures required to maintain the
goal temperature is another important clue to ther-
mogenesis due to shivering. Adequate sedation is
paramount to control shivering, especially during
induction. Since hypothermia decreases medica-
tion metabolism and clearance, short-acting agents
such as midazolam (Versed), fentanyl (Abstral,
Actiq, Fentora), dexmedetomidine (Precedex),
remifentanil (Ultiva), and propofol (Diprivan)
are preferred to long-acting agents that may con-
found neurological assessments after rewarming.
Additionally, neuromuscular blockade in the form
of boluses of vecuronium or other nondepolar-
izing paralytic agents are often given routinely at
induction and then, as needed, to control clinical
shivering. These agents halt thermogenesis due
to shivering and facilitate the achievement of goal
temperature. Thereafter, paralytics should only be
used to combat refractory shivering that impacts
maintenance temperature control. IV magnesium
and skin counterwarming (ie, socks and gloves) are
additional adjuncts for shivering control.67
Complications Of Therapeutic Cooling
The unique physiological changes of therapeutic
cooling can occasionally lead to complications. (See
Table 6.) In this section, the hypothermic response
on the cardiovascular, immune, hematologic, meta-
bolic, and endocrine systems will be reviewed.
Sinus bradycardia, typically in the range of 40 to
50 beats/min, is expected, and it indicates that the
patient undergoing therapeutic hypothermia is being
properly managed. If sinus bradycardia is not seen,
inadequate sedation or incomplete hemodynamic
resuscitation may be the cause. Rarely, severe bra-
dycardia resulting in hypoperfusion during cooling
will warrant mild elevation of the target temperature.
Concurrent use of negative chronotropes such as beta
blockers and amiodarone (Cordarone, Pacerone)
should be avoided unless strongly indicated.
Hypothermia suppresses immune system func-
tion; however, increased infection rates and sep-
sis in postarrest patients undergoing therapeutic
Table 6. Potential Adverse Physiologic
Responses And Complications Associated
With Cooling
Coagulopathy and thrombocytopenia
Cold diuresis
Dysrhythmias (sinus bradycardia during cooling is most common)
Electrolyte abnormalities (K, Mg, Phos)
Hypotension (including vasodilation with rewarming
Infection (and masked signs of infection)
Insulin resistance and hyperglycemia
Pancreatitis
Shivering
www.ebmedicine.net Volume 3, Number 3
hypothermia have not been observed.11 Regardless,
postarrest patients have a notable risk of pulmo-
nary infection due to a high incidence of aspira-
tion.68,69 Temperature control obscures fever as a
marker of infection, which has been linked to delay
in antibiotic administration. Thus, early empiric an-
tibiotics are frequently employed for patients with
evidence of aspiration (ie, pulmonary secretions,
radiographic infiltrates). Changes in the water tem-
perature of the cooling bath within the commercial
cooling device can act as a surrogate marker for
fever and should be routinely monitored.
Coagulopathy is a known complication of
therapeutic cooling, but it rarely results in spontane-
ous bleeding. Conventional anticoagulant medica-
tions should be used when indicated.70 Additionally,
thrombolytic therapy for pulmonary embolism and
STEMI should be used when necessary, despite the
anticipated need for cooling. Significant tempera-
ture-related coagulopathy is unusual above 33.5C.
Patients with severe coagulopathy or suspected
bleeding may be preferentially maintained above this
threshold. Additionally, subcutaneous desmopressin
(DDAVP) reverses hypothermia-induced platelet
dysfunction, and it should be considered as a thera-
peutic adjunct for patients with active bleeding.71
Life-threatening bleeding not amenable to surgical
hemostasis warrants rewarming.
Hyperglycemia is common following cardiac
arrest.72 Decreased insulin secretion and sensitivity
occur with hypothermia and may exacerbate hyper-
glycemia. IV insulin infusion is recommended to
maintain moderate glucose control (< 180 mg/dL).73
Complications may also occur due to the cooling
devices used. The use of invasive cooling devices
may result in an increased risk of bleeding, infec-
tion, vascular puncture, and venous thrombosis. In
contrast, surface cooling devices, especially if placed
incorrectly, may lead to skin breakdown. Evidence is
limited with regard to device-specific complications.
Therapeutic cooling may impact lactate pro-
duction and diminish clearance. Serum lactate
is increasingly used as a prognostic marker and
resuscitation endpoint in acute critical illness. The
expected kinetics of lactate in patients undergo-
ing therapeutic cooling following cardiac arrest
remains to be clarified.74,75
Early Postarrest Prognostication
Prognostication of neurological outcome in the ED
remains a challenge. No physician desires a futile
resuscitation; however, premature negative prognos-
tication remains an obstacle to optimal care.76 There
is no evidence to support accurate early neurological
prognostication. Pre-arrest and intra-arrest param-
eters such as duration of arrest, bystander CPR, or
presenting rhythm are unreliable prognosticators
alone or in combination. For reference, the median
7 EMCC 2013
 Clinical Pathway: Adult Patients After Cardiac Arrest
With Return Of Spontaneous Circulation

Assess inclusion & exclusion criteria for postcardiac arrest resusci- Perform and document neurological examination.
tation bundle. Consult interventional cardiologist for assessment for coronary
VT / VF arrest (Class I) angiography. (Induction of cooling should be performed concur-
PEA / asystole arrest (Class II) rently with preparation for PCI.)

Goals: Critical care considerations:

Cooling goals: Central venous catheter to assess CVP & ScvO2 (avoid left
Achieve 32C-34C (Class I) in 60 min.
l subclavian catheter, as this may be the preferred site for a pace-
Hemodynamic and ventilatory goals: maker/defibrillator).
Maintain MAP 70 mm Hg (the preferred vasopressor is
l Echocardiogram to assess myocardial function
norepinephrine). Arterial monitoring line
Minimize FiO2 while maintaining oxygen saturation > 95%.
l Glucose control
Maintain PaCO2 38-42 mm Hg.
l Seizure control
Evaluate and address etiology of arrest

Induction: Maintenance:
Infuse cold IV fluids. Goal temperature of 32C-34C.
Administer NS 30 cc/kg IV bolus as tolerated. Continue cooling for 24 h.
Apply ice packs to groin, axilla, and neck. Assess for shivering: short-acting analgesia or sedation (paraly-
Maintain early sedation and paralysis until goal temperature sis if shivering uncontrolled with these measures).
achieved. Assess electrolytes.
Initiate cooling device for 33C. Monitor fluid status: input & output.

Rewarming:
Controlled normothermia:
Rewarm approximately 0.5C/h. (Class I)
Keep the cooling device in place for 2 to 3 days after rewarming
Assess electrolytes closely.
to maintain normothermia (37C).
Assess neurological status once at normothermia.

Abbreviations: CVP, central venous pressure; FiO2, fraction of inspired oxygen; IV, intravenous; MAP, mean arterial pressure; NS, normal saline; PaCO2,
partial pressure of carbon dioxide; PEA, pulseless electrical activity; PCI, percutaneous coronary intervention; ScvO2, central venous oxygen satura-
tion; VT/VF, ventricular tachycardia/ventricular fibrillation

Class Of Evidence Definitions

Each action in the clinical pathways section of EM Critical Care receives a score based on the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness
Level of Evidence:
One or more large prospective
studies are present (with rare
exceptions)
High-quality meta-analyses
Study results consistently posi-
tive and compelling
Class II Class III Indeterminate sentatives from the resuscita-
Safe, acceptable May be acceptable Continuing area of research tion councils of ILCOR: How to
Probably useful Possibly useful No recommendations until Develop Evidence-Based Guide-
Considered optional or alterna- further research lines for Emergency Cardiac
Level of Evidence: tive treatments Care: Quality of Evidence and
Generally higher levels of Level of Evidence: Classes of Recommendations;
evidence Level of Evidence: Evidence not available Guidelines for cardiopulmonary
nonrandomized or retrospective Generally lower or intermediate Higher studies in progress resuscitation and emergency
studies: historic, cohort, or case levels of evidence Results inconsistent, contradic- cardiac care. Emergency
control studies Case series, animal studies, tory Cardiac Care Committee and
Less robust randomized con- consensus panels Results not compelling Subcommittees, American Heart
trolled trials Occasionally positive results Association. Part IX. Ensuring
Results consistently positive Significantly modified from: The
Emergency Cardiovascular Care effectiveness of community-wide
Committees of the American emergency cardiac care. JAMA.
Heart Association and repre- 1992;268(16):2289-2295.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patients individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2013 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

EMCC 2013 8 www.ebmedicine.net Volume 3, Number 3

downtime between collapse and ROSC for many of
these patients is > 20 minutes.12 In a recent obser-
vational study of therapeutic hypothermia, 36% of
patients with an arrest interval > 30 minutes expe-
rienced a good neurological outcome.48 Although
advanced age generally worsens prognosis, 30% of
patients > 75 years of age had good neurological out-
come in the same series. The immediate postarrest
neurological examination (including low Glasgow
Coma Scale [GCS] score, poor motor examination,
and absent brainstem reflexes) does not reliably pre-
dict neurological outcome.48 Prediction of prognosis
based on neurological examination becomes more
reliable after at least 72 hours following resuscita-
tion.77 Given these limitations, early neuroprotec-
tive measures should be strongly considered for all
potentially eligible patients.
The Postcardiac Arrest Syndrome
A discussion involving the practical implementation
of therapeutic hypothermia necessitates the contex-
tual background of the postcardiac arrest syndrome.
One cannot simply expect to cool a patient as an
isolated therapy without addressing the multitude
of other resuscitation therapies that define contem-
porary postcardiac care, including acute coronary
interventions and goal-directed critical care. (See the
Clinical Pathway.)
The postcardiac arrest syndrome is a unique
multiorgan condition.78 (See Table 7.) The complex
immunological cascade that ensues from reperfusion
after a transient period of total body ischemia results
in a systemic inflammatory response that mimics
severe sepsis.79,80 Clinically, this is reflected in he-
modynamic instability and early organ dysfunction.
For ease of targeting the unique clinical aspects of
the illness, the International Liaison Committee on
Resuscitation categorizes the syndrome in the fol-
lowing way14:
Postcardiac arrest brain injury
Postcardiac arrest myocardial dysfunction
Systemic ischemia-reperfusion response
Persistent precipitating pathology
By targeting these clinical components of the
postarrest state with a comprehensive resuscitative
protocol, the emergency physician can have the
greatest impact on improving outcomes.
Therapeutic cooling is only one aspect of an ef-
fective, multipronged resuscitative protocol.81,82 The
early postarrest period is an opportunity to address
additional priorities for effective cardiocerebral re-
suscitation. Priorities of the postarrest period include
stabilization of organ perfusion and oxygenation,
identification and treatment of reversible causes
of cardiac arrest, and initiation of neuroprotective
therapy. As such, contemporary emergency care now
emphasizes intensive support during this vulnerable
www.ebmedicine.net Volume 3, Number 3
and modifiable phase of illness. (See Tables 8 and 9
on page 10.) For a detailed review on the postcardiac
arrest syndrome, see the October 2012 issue of EM
Critical Care titled, Postarrest Cardiocerebral Resus-
citation: An Evidence-Based Review.
Reperfusion Therapy For Postcardiac Arrest
Patients
Acute coronary syndromes (ACS) are the most
common cause of sudden cardiac arrest in adults.
The rate of acute coronary occlusion in patients
with ACS is estimated to be 30% to 50%.83,84 Un-
fortunately, clinical history is often limited, and
the electrocardiogram after ROSC can be nondi-
agnostic in discriminating acute coronary occlu-
sion requiring emergent PCI.84 Revascularization
is independently associated with survival and
should be considered for all patients with strongly
suspected acute coronary disease or electrocardio-
gram evidence of ST-segment elevation myocardial
infarction (STEMI).85 PCI is the preferred method of
revascularization and was safely performed con-
current with therapeutic cooling in 2 prospective
observational studies.86,87 With appropriate coor-
dination of cooling and PCI priorities, induction
of hypothermia does not delay cardiac catheteriza-
tion.70 PCI should not be delayed due to an uncer-
tain neurological prognosis.16
Thrombolysis is an acceptable reperfusion strat-
egy for STEMI if PCI is not immediately available.
Thrombolysis is associated with improved survival
and neurological outcome, while the hemorrhagic
risk is comparable to patients not thrombolysed.88
Coadministration with therapeutic cooling does not
appear to increase the risk of significant bleeding.89
Table 7. Postcardiac Arrest Syndrome
Pathophysiology
Acute Myocardial Dysfunction
Acute coronary syndromes
Myocardial stunning
Brain Injury
Anoxic brain insult
Impaired autoregulation
Ischemic reperfusion injury
Persistent Precipitating Pathology
Decompensated cardiomyopathy
Myocardial ischemia
Pulmonary embolism
Systemic Ischemia-Reperfusion Injury
Dysregulated coagulation
Early organ dysfunction
Impaired microvascular function
Inappropriate vasodilation
Systemic inflammatory response syndrome
9 EMCC 2013
Adjunctive aspirin and heparin are recommended
for suspected or confirmed ACS. Withholding acute
beta-blocker and angiotensin-converting enzyme
(ACE)-inhibitor therapy should be considered due
to the potential for hemodynamic deterioration and
shock in postarrest patients.
Based on a similar mechanism as neuroprotec-
tive benefit, cardioprotective effects of hypothermia
are under exploration. Animal models show benefit
with early cooling.90,91 Early trials in noncardiac-ar-
rest patients with STEMI who received hypothermia
prior to PCI showed decreased infarct size, without
significant treatment delay.92
Summary Of Controversies In
Therapeutic Cooling
While therapeutic hypothermia has recognized
value, there remain controversies in regard to
timing and techniques; these issues are summa-
rized below. Additional controversy surrounds the
effectiveness of prehospital cooling and the role of
therapeutic hypothermia in patients experiencing
PEA of asystolic arrests; well-designed prospec-
tive studies with adequate power are needed in
order to resolve these debates.
Devices for cooling: There continues to be
debate over the best way to cool (invasive or non-
invasive). Studies demonstrate improved tempera-
ture control with invasive devices compared to
older generation noninvasive cooling pads.38,59,69
Comparison of newer hydrocolloid gel-pad-based
surface cooling devices and endovascular cooling
devices is limited. What is key to remember is that
the execution of a cooling strategy to ensure that
Table 8. Early Postresuscitation Priorities
patients receive this neuroprotective therapy is
most important.
Rate of cooling: Another challenge involves iden-
tifying the ideal rate of cooling, with several studies
showing that patients who experienced a faster rate
of cooling had a less favorable outcome.93,94 One
hypothesis to explain this is that more severely brain-
injured patients may lose their ability to thermoregu-
late, and, thus, they cool more quickly. However,
Mooney et al found no association between outcomes
and time to goal temperature among 140 postcardiac
arrest patients.48 Nonetheless, given that animal
studies show improved outcomes with faster cooling,
rapid cooling should remain the goal until contradic-
tory evidence is unveiled.43-47
Initiation of cooling: Additionally, the ideal
time to initiate cooling remains controversial. Three
prospective randomized trials showed no difference
between cooling initiated prehospital or inhospital,
despite reaching target temperature more rapidly.51-53
Conversely, Mooney et al found that every hour of
delay in the initiation of cooling led to an increase in
mortality of 20% per hour.48 Another study revealed
increased odds of poor neurological outcome with
each 5-minute delay in initiation of cooling.49
Table 9. Early Hemodynamic Resuscitation
Goals Following Cardiac Arrest
Resuscitation Monitor and Goal Therapy
Priority
1. Preload optimi- Response to fluid Fluids
zation challenge; fluid ther-
apy is guided by:
CVP: 8-12 mm Hg
Echocardiogram:
cardiac function
and IVC variation
Markers of SVV

Provide adequate oxygenation and ventilation. 2. Perfusion MAP 65-100 mm Hg Norepinephrine*

l Avoid hyperventilation (goal PaCO2 of 38-42 mm).* pressure Epinephrine
l Avoid hyperoxia (titrate FiO2 to SpO2 > 95% [or PaO2 > 70 mm Vasopressin
Hg].* 3. Perfusion Global perfusion Dobutamine
Reverse shock and stabilize hemodynamics. optimization markers: Milrinone
Identify and treat reversible cause of cardiac arrest. ScvO2 > 70% IABP
Apply neuroprotective therapies (ie, therapeutic hypothermia). Lactate clearance PRBC transfu-
Correct metabolic disturbances. Clinical perfusion sion
markers:
*The solubility of gases (ie, PaCO2 and PaO2) changes as a function Urine output > 0.5
of temperature.38 At goal temperature, a patients PaCO2 may be up cc/kg/h
to 8 mm Hg lower than reported on the blood gas warmed to normal Peripheral skin
temperature. Unfortunately, the clinical impact of temperature correc- perfusion
tion via pH-stat methodology is unclear. In the absence of clear data,
targeting high-normal PaCO2 may avoid unintended cerebral vasocon- *First-choice vasopressor
striction stemming from arterial hypocapnea. Abbreviations: CVP, central venous pressure; IABP, intra-aortic bal-
loon pump; IVC, inferior vena cava; MAP, mean arterial pressure;
Abbreviations: FiO2, fraction of inspired oxygen; PaCO2, partial ScvO2, central venous oxygenation saturation; IABP, intra-aortic
pressure of carbon dioxide; PaO2, partial pressure of oxygen; SpO2, balloon pump; PRBC, packed red blood cells; SVV, stroke volume
oxygen saturation by pulse oximeter . variation.

EMCC 2013 10 www.ebmedicine.net Volume 3, Number 3

 Duration of cooling: Finally, the optimal
duration of cooling has yet to be determined. In
the landmark cooling trials, the period of cooling
once at goal temperature was 12 to 24 hours. Based
on these recommendations, current American
Heart Association guidelines recommend cooling
between 12 to 24 hours;14 however, it is unclear
whether extended periods of cooling offer addi-
tional neuroprotective benefit.
Disposition
The disposition of postcardiac arrest patients de-
pends on whether the facility has comprehensive
postcardiac arrest care capabilities. If your hospital
already has therapeutic hypothermia capability
but does not have a protocol in place, your goal is
aggressive resuscitation that focuses on initiation of
therapeutic hypothermia and hemodynamic optimi-
zation while considering and addressing the pos-
sible causes of the arrest. If your facility has limited
resources or infrequently cares for postcardiac arrest
patients, a transfer protocol that includes cooling
initiation is recommended.
Regionalization Of Postarrest Care
Many obstacles make the comprehensive manage-
ment of a successfully resuscitated cardiac arrest
patient challenging. An important consideration
prior to establishing a hypothermia protocol is to
assess your hospital resources and volume of cardiac
arrest patients. The relative infrequency of applying
the intervention, equipment costs, emergency nurs-
ing resource allocation, and the multidisciplinary
specialized team required all make a postcardiac ar-
rest care bundle difficult to implement effectively.10
Effective management of the unique aspects of the
postcardiac arrest syndrome, beyond therapeutic
hypothermia, must be considered. There exists a
well-defined relationship between increased patient
volume or procedures and improved outcomes for
other complex, time-sensitive disorders. Higher-vol-
ume centers treating patients after cardiac arrest are
associated with improved survival.95 Regional sys-
tems of care have been successfully established for
STEMI, trauma, burns, and stroke, and the rationale
for regional systems of care for postcardiac arrest pa-
tients is analogous to the need for these centers.96,97
The American Heart Association recommends
transporting postarrest patients to a comprehensive
postcardiac arrest treatment system that is capable
of acute coronary interventions, goal-directed critical
care, and therapeutic hypothermia.82
No external certification for designation of a
cardiac arrest center currently exists. These regional
centers should not be restricted to academic medical
centers. Academic and community-receiving hospi-
tals with adequate patient volume, multidisciplinary
www.ebmedicine.net Volume 3, Number 3
care, and resources for postarrest patients will need
to share in this endeavor. Additionally, essential
systems of care include a supportive community,
protocol-driven emergency medical services, and
transferring hospitals.
At present, several prehospital systems (eg,
Charlotte, New York City) prioritize out-of-hos-
pital cardiac arrest patients to designated cardiac
arrest centers despite the availability of more
proximate facilities. The challenge lies when one
considers catchment size and regions with longer
transport times, resource allocation for prehospital
systems with limited ambulances and personnel,
and the fact that not all cardiac arrest patients are
good candidates for aggressive care. In our opin-
ion, the best means to address these challenges is
via predetermined treatment protocols that take
the unique aspects of each prehospital system and
regional resources into consideration. Although
exploration of the ideal regionalized system of
care is just beginning, lengthy critical care trans-
port is safe and feasible.85
Some regions have a transfer-destination hospi-
tal model in order to provide a larger catchment area
with access to comprehensive postarrest care. The
Minneapolis Heart Institute receives patients from a
network of 33 hospitals from a catchment area of 150
miles.48 Another example is our cardiac resuscitation
center, which receives patients from many regional
hospitals within a 100-mile radius via a postcardiac
arrest care pathway known as CODE COOLTM.19
Transferring facilities have a transfer protocol
whereby cooling is initiated with cold fluids and the
patient is subsequently transferred to the cardiac
resuscitation center for resuscitative care, including
therapeutic hypothermia. Table 10 (page 12) shows
the guidelines from the CODE COOLTM poster that
is distributed to all outlying facilities to serve as a
guide to ease the resuscitative and transfer process.
Summary
Therapeutic hypothermia is an effective therapy
to improve chances of neurological recovery af-
ter cardiac arrest. Ensuring broader utilization of
therapeutic cooling is essential to improving out-
comes. Successful execution of therapeutic cooling
must consider the hospitals capabilities as well as
the complexities of the postcardiac arrest syndrome.
Design and implementation of a postcardiac arrest
resuscitation protocol emphasizing hemodynamic
resuscitation, neuroprotective cooling, and critical
care support will enable centers to optimize cerebral
recovery following cardiac arrest.
11 EMCC 2013
 Risk Management Pitfalls For
Therapeutic Hypothermia In The
Emergency Department
1. Delaying initiation of cooling due to exces-
sive imaging. Computed tomography head and
chest imaging is frequently performed to assess
for precipitants of arrest and early brain injury.
Unfortunately, these tests provide uncertain
benefit and frequently delay attention to thera-
peutic cooling. Focused attention to the details
of the patients decompensation and arrest
event, along with simple bedside tests (electro-
cardiogram, echocardiogram, blood analysis),
are frequently sufficient to establish a short
list of differential diagnoses. When cooling is
indicated, imaging should not delay initiation of
cooling.
2. Leaving the patient on 100% FiO2. Too little
oxygen is bad for the brain; however, too much
oxygen may also cause harm. Hyperoxia is as-
sociated with increased mortality in postcardiac
arrest patients.98 Rapidly titrate oxygen to 30%
FiO2 (as tolerated) to maintain oxygen saturation
> 95%.
3. Assuming a poor prognosis. Arrest intervals
> 20 minutes, postarrest GCS score of 3 to 4,
and age > 70 do not equate to a dismal progno-
sis. Recognizing the major limitations to early
prognostication is the first step in avoiding the
therapeutic nihilism that occurs when patients
are excluded from the very treatment that may
improve their outcome.
4. The patient not reaching goal temperature. Oc-
cult shivering is common and frequently thwarts
effective induction to goal temperature. Seda-
tion and paralysis should be routine to assist
in reaching goal temperatureat which point,
most patients can be maintained on sedation
alone. Additionally, supplementing ice packs
and additional boluses of cold IV fluids may be
necessary to ensure rapid induction.
5. Not establishing a postcardiac arrest care plan
and protocol. If your hospital does not have a
predetermined plan for managing postarrest pa-
tients, now is the time to create one. Assess your
current ED and hospital resources and deter-
mine whether your patients can be comprehen-
sively managed or whether they require transfer
to a regional PCI-capable and hypothermia-
capable cardiac resuscitation center for optimal
care. If transfer is preferred, create a transfer
protocol such that cold fluids or ice packs are
readily available for use and cooling is initiated
early. Coordination with an established destina-
tion ensures a smooth transfer of care.
EMCC 2013 12
Case Conclusions
With the prehospital cold fluids continuing to infuse in the
first patient, you note that he fits the demographics (VF/VT
of presumed cardiac origin) and arrest intervals (downtime
of 21 min) of the largest prospective therapeutic hypother-
mia trial; therefore, cooling this patient has Level 1 evi-
dence. Given that your facility does not have PCI or cooling
Table 10. Postcardiac Arrest Resuscitation:
Carolinas Medical Center CODE COOLTM
Transferring Guideline
Inclusion Criteria
Adults (age 18 y)
ROSC within 60 min of arrest
Persistent coma: inability to follow commands and/or GCS score
<9
Exclusion Criteria
Absolute: severe or terminal illness with anticipated nonaggressive
care
Relative: active hemorrhage; systemic infection/sepsis; severe
refractory shock
Resuscitation Priorities
Airway
l Intubation
Breathing
l Avoid hyperventilation (goal PaCO2 of 38-42 mm Hg).
l Avoid hyperoxia (rapidly decrease FiO2 to maintain SpO2 > 95%).
Circulation
Goal MAP is > 70.
l
Anticipate and avoid hypotension.
l
Norepinephrine is the preferred vasopressor.
l
Screen for STEMI using ECG.
l
Cooling Induction
Initiate cooling as soon as possible after ROSC.
Administer refrigerated (4C) NS 30 cc/kg IV bolus as tolerated.
Ice packs to groin, axilla, and neck.
Control shivering with propofol 10 mcg/kg/min.
Paralyze patient with vecuronium 0.1 mg/kg q1h.
Do
Initiate transfer early.
Use paralytics during the induction phase of cooling.
Document the time of arrest, time of ROSC, and neurological
examination.
Do Not
Delay cooling for CT scanning or extensive testing before transfer,
unless clinically indicated.
Abbreviations: ECG, electrocardiogram; FiO2, fraction of inspired
oxygen; GCS, Glasgow Coma Scale; IV, intravenous; MAP, mean
arterial pressure; NS, normal saline; PaCO2, partial pressure of
carbon dioxide; ROSC, return of spontaneous circulation; SpO2,
oxygen saturation by pulse oximeter; STEMI, ST-segment elevation
myocardial infarction.
Used with permission from Carolinas Medical Center.
www.ebmedicine.net Volume 3, Number 3
capability, you initiate the transfer protocol and place ice
packs on the patient. In the meantime, you continue aggres-
sive resuscitation of the patient. After a careful neurological
exam, you confirm nonreactive pupils and a GCS score of
3, and you proceed to sedation with propofol and paralysis
with vecuronium to avoid shivering during the induction
phase. With the blood pressure at 92/42 mm Hg (MAP of
59 mm Hg), you continue fluid resuscitation concurrently
with initiation and titration of norepinephrine to reach a
MAP > 70 mm Hg to ensure appropriate brain perfusion.
Next, you titrate the FiO2 for goal SpO2 of 95% to avoid
hyperoxia-related injury. You ask for an arterial blood gas
to ensure that the PaCO2 is in the target range of 38 to 42
mm Hg. Shortly thereafter, the patient is transported to the
cardiac arrest center.
For your patient with PEA due to a respiratory arrest
secondary to status asthmaticus, you acknowledge the
Level II evidence that exists for therapeutic hypothermia.
You activate your postarrest resuscitative bundle and
begin cooling the patient with 30 cc/kg of 4C normal
saline. The patient has cooling pads placed, ice packs ap-
plied, and sedation administered. An hour into cooling,
her temperature remains > 35C. You realize that unrec-
ognized shivering may be the cause, so you paralyze her
with vecuronium. An hour later, she is at goal tempera-
ture. The patient is subsequently transferred to the ICU of
the nearest cardiac arrest receiving hospital and completes
24 hours of therapeutic hypothermia at 33C via protocol.
She is then rewarmed slowly over 10 hours. On day 3
postarrest, her sedatives are weaned and she ultimately
awakens. Her CPC score is 1, which equates to a good
neurological outcome. Several days later, she is ready for
discharge. She is discharged directly to home with appro-
priate asthma management.
References
Evidence-based medicine requires a critical ap-
praisal of the literature based upon study methodol-
ogy and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study, will be included in bold type following
the reference, where available. In addition, the most
informative references cited in this paper, as deter-
mined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
1. Nichol G, Thomas E, Callaway CW, et al. Regional
variation in out-of-hospital cardiac arrest incidence and
outcome. JAMA. 2008;300(12):1423-1431. (Prospective
observational; 20,520 patients)
2. Sasson C, Rogers MA, Dahl J, et al. Predictors of sur-
vival from out-of-hospital cardiac arrest: a systematic
review and meta-analysis. Circ Cardiovasc Qual Outcomes.
2010;3(1):63-81. (Meta-analysis)
www.ebmedicine.net Volume 3, Number 3
3. Walters JH, Morley PT, Nolan JP. The role of hypother-
mia in post-cardiac arrest patients with return of spon-
taneous circulation: a systematic review. Resuscitation.
2011;82(5):508-516. (Review)
4. Hazinski MF, Nolan JP, Billi JE, et al. Part 1: Executive sum-
mary: 2010 international consensus on cardiopulmonary
resuscitation and emergency cardiovascular care science
with treatment recommendations. Circulation. 2010;122(16
Suppl 2):S250-S275. (Consensus statement)
5. Abella BS, Rhee JW, Huang KN, et al. Induced hypother-
mia is underused after resuscitation from cardiac arrest: a
current practice survey. Resuscitation. 2005;64(2):181-186.
(Survey)
6. Merchant RM, Soar J, Skrifvars MB, et al. Therapeutic hy-
pothermia utilization among physicians after resuscitation
from cardiac arrest. Crit Care Med. 2006;34(7):1935-1940.
(Survey)
7. Laver SR, Padkin A, Atalla A, et al. Therapeutic hy-
pothermia after cardiac arrest: a survey of practice in
intensive care units in the United Kingdom. Anaesthesia.
2006;61(9):873-877. (Survey)
8. Brooks SC, Morrison LJ. Implementation of therapeutic hy-
pothermia guidelines for post-cardiac arrest syndrome at a
glacial pace: seeking guidance from the knowledge transla-
tion literature. Resuscitation. 2008;77(3):286-292. (Review)
9. Bigham BL, Dainty KN, Scales DC, et al. Predictors of
adopting therapeutic hypothermia for post-cardiac arrest
patients among Canadian emergency and critical care
physicians. Resuscitation. 2010;81(1):20-24. (Survey)
10. Toma A, Bensimon CM, Dainty KN, et al. Perceived bar-
riers to therapeutic hypothermia for patients resuscitated
from cardiac arrest: a qualitative study of emergency
department and critical care workers. Crit Care Med.
2010;38(2):504-509. (Questionnaire)
11.* Bernard SA, Gray TW, Buist MD, et al. Treatment of
comatose survivors of out-of-hospital cardiac arrest with
induced hypothermia. N Engl J Med. 2002;346(8):557-563.
(Prospective randomized controlled; 77 patients)
12.* Hypothermia after Cardiac Arrest Study Group. Mild
therapeutic hypothermia to improve the neurologic out-
come after cardiac arrest. N Engl J Med. 2002;346(8):549-556.
(Prospective randomized controlled; 273 patients)
13. Arrich J, Holzer M, Herkner H, et al. Hypothermia for neu-
roprotection in adults after cardiopulmonary resuscitation.
Cochrane Database Syst Rev. 2009;(4):CD004128. (Review)
14.* Nolan JP, Neumar RW, Adrie C, et al. Post-cardiac arrest
syndrome: epidemiology, pathophysiology, treatment, and
prognostication. A scientific statement from the Interna-
tional Liaison Committee on Resuscitation; the Ameri-
can Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and
Anesthesia; the Council on Cardiopulmonary, Periopera-
tive, and Critical Care; the Council on Clinical Cardiology;
the Council on Stroke. Resuscitation. 2008;79(3):350-379.
(Consensus statement)
15. Oddo M, Schaller MD, Feihl F, et al. From evidence to
clinical practice: effective implementation of therapeutic
hypothermia to improve patient outcome after cardiac
arrest. Crit Care Med. 2006;34(7):1865-1873. (Retrospective
cohort; 109 patients)
16. Sunde K, Pytte M, Jacobsen D, et al. Implementation of
a standardised treatment protocol for post resuscitation
care after out-of-hospital cardiac arrest. Resuscitation.
2007;73(1):29-39. (Prospective interventional; 199 patients)
17. Storm C, Schefold JC, Kerner T, et al. Prehospital cooling
with hypothermia caps (PreCoCa): a feasibility study. Clin
Res Cardiol. 2008;97(10):768-772. (Prospective interven-
tional; 20 patients)
18. Polderman KH. Induced hypothermia and fever control for
prevention and treatment of neurological injuries. Lancet.
13 EMCC 2013
 2008;371(9628):1955-1969. (Review)
19. Heffner AC, Pearson DA, Nussbaum ML, et al. Region-
alization of post-cardiac arrest care: implementation of a
cardiac resuscitation center. Am Heart J. 2012;164(4):493-
501. (Prospective observational; 220 patients)
20. Teodorescu C, Reinier K, Dervan C, et al. Factors associ-
ated with pulseless electric activity versus ventricular
fibrillation: the Oregon sudden unexpected death study.
Circulation. 2010;122(21):2116-2122. (Retrospective; 1277
patients)
21. Testori C, Sterz F, Behringer W, et al. Mild therapeutic
hypothermia is associated with favourable outcome in
patients after cardiac arrest with non-shockable rhythms.
Resuscitation. 2011;82(9):1162-1167. (Retrospective cohort;
374 patients)
22. Kim YM, Yim HW, Jeong SH, et al. Does therapeutic hy-
pothermia benefit adult cardiac arrest patients presenting
with non-shockable initial rhythms?: a systematic review
and meta-analysis of randomized and non-randomized
studies. Resuscitation. 2012;83(2):188-196. (Systematic
review)
23. Pfeifer R, Jung C, Purle S, et al. Survival does not improve
when therapeutic hypothermia is added to post-cardiac ar-
rest care. Resuscitation. 2011;82(9):1168-1173. (Retrospective
review; 210 patients)
24. Henry TD, Sharkey SW, Burke MN, et al. A regional system
to provide timely access to percutaneous coronary inter-
vention for ST-elevation myocardial infarction. Circulation.
2007;116(7):721-728. (Prospective observational; 1345
patients)
25. Bernard SA, Jones BM, Horne MK. Clinical trial of induced
hypothermia in comatose survivors of out-of-hospital car-
diac arrest. Ann Emerg Med. 1997;30(2):146-153. (Prospec-
tive nonrandomized interventional; 44 patients)
26. Busch M, Soreide E, Lossius HM, et al. Rapid implemen-
tation of therapeutic hypothermia in comatose out-of-
hospital cardiac arrest survivors. Acta Anaesthesiol Scand.
2006;50(10):1277-1283. (Prospective interventional; 27
patients)
27. Don CW, Longstreth WT Jr, Maynard C, et al. Active
surface cooling protocol to induce mild therapeutic hypo-
thermia after out-of-hospital cardiac arrest: a retrospective
before-and-after comparison in a single hospital. Crit Care
Med. 2009;37(12):3062-3069. (Retrospective; 491 patients)
28. Merchant RM, Becker LB, Abella BS, et al. Cost-effective-
ness of therapeutic hypothermia after cardiac arrest. Circ
Cardiovasc Qual Outcomes. 2009;2(5):421-428. (Cost-effec-
tiveness analysis)
29. Jacobs S, Hunt R, Tarnow-Mordi W, et al. Cooling for new-
borns with hypoxic ischaemic encephalopathy. Cochrane
Database Syst Rev. 2007;(4):CD003311. (Review)
30. Edwards AD, Brocklehurst P, Gunn AJ, et al. Neurological
outcomes at 18 months of age after moderate hypothermia
for perinatal hypoxic ischaemic encephalopathy: synthesis
and meta-analysis of trial data. BMJ. 2010;340:c363. (Meta-
analysis)
31. Rittenberger JC, Kelly E, Jang D, et al. Successful outcome
utilizing hypothermia after cardiac arrest in pregnancy:
a case report. Crit Care Med. 2008;36(4):1354-1356. (Retro-
spective; 272 patients)
32. Wible EF, Kass JS, Lopez GA. A report of fetal demise dur-
ing therapeutic hypothermia after cardiac arrest. Neurocrit
Care. 2010;13(2):239-242. (Case report)
33. Hovdenes J, Laake JH, Aaberge L, et al. Therapeutic hy-
pothermia after out-of-hospital cardiac arrest: experiences
with patients treated with percutaneous coronary inter-
vention and cardiogenic shock. Acta Anaesthesiol Scand.
2007;51(2):137-142. (Prospective descriptive; 50 patients)
34. Zobel C, Adler C, Kranz A, et al. Mild therapeutic hypo-
thermia in cardiogenic shock syndrome. Crit Care Med.
EMCC 2013 14
2012;40(6):1715-1723. (Case-control study; 20 patients)
35. Huynh N, Klocke J, Gu C, et al. The effect of hypothermia
dose on vasopressor requirements and outcome after
cardiac arrest. Resuscitation. 2013;84(2):189-193. (Retrospec-
tive review; 361 patients)
36. McGrane S, Maziad J, Netterville JL, et al. Therapeutic hy-
pothermia after exsanguination. Anesth Analg. 2012;115(2):
343-345. (Case report)
37. Todd MM, Hindman BJ, Clarke WR, et al. Mild intra-
operative hypothermia during surgery for intracranial
aneurysm. N Engl J Med. 2005;352(2):135-145. (Prospective
randomized controlled; 1001 patients)
38. Polderman KH. Mechanisms of action, physiological ef-
fects, and complications of hypothermia. Crit Care Med.
2009;37(7 Suppl):S186-S202. (Review)
39. Rittenberger JC, Polderman KH, Smith WS, et al. Emergen-
cy neurological life support: resuscitation following cardiac
arrest. Neurocrit Care. 2012;17 Suppl 1:S21-S28. (Review
article)
40. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after
cardiac arrest is associated with an unfavorable neurologic
outcome. Arch Intern Med. 2001;161(16):2007-2012. (Retro-
spective; 151 patients)
41. Neumar RW. Molecular mechanisms of ischemic neuronal
injury. Ann Emerg Med. 2000;36(5):483-506. (Review)
42. Li D, Shao Z, Vanden Hoek TL, Brorson JR. et al. Reperfu-
sion accelerates acute neuronal death induced by simu-
lated ischemia. Exp Neurol. 2007;206(2):280-287. (Bench
research)
43. Kuboyama K, Safar P, Radovsky A, et al. Delay in cooling
negates the beneficial effect of mild resuscitative cerebral
hypothermia after cardiac arrest in dogs: a prospective
randomized study. Crit Care Med. 1993;21(9):1348-1358.
(Animal model)
44. Nozari A, Safar P, Stezoski SW, et al. Critical time win-
dow for intra-arrest cooling with cold saline flush in a
dog model of cardiopulmonary resuscitation. Circulation.
2006;113(23):2690-2696. (Animal model)
45. Abella BS, Zhao D, Alvarado J, et al. Intra-arrest cooling
improves outcomes in a murine cardiac arrest model.
Circulation. 2004;109(22):2786-2791. (Animal model)
46. Sterz F, Safar P, Tisherman S, et al. Mild hypothermic car-
diopulmonary resuscitation improves outcome after pro-
longed cardiac arrest in dogs. Crit Care Med. 1991;19(3):379-
389. (Animal model)
47. Boddicker KA, Zhang Y, Zimmerman MB, et al. Hypo-
thermia improves defibrillation success and resuscita-
tion outcomes from ventricular fibrillation. Circulation.
2005;111(24):3195-3201. (Animal model)
48. Mooney MR, Unger BT, Boland LL, et al. Therapeutic hy-
pothermia after out-of-hospital cardiac arrest: evaluation of
a regional system to increase access to cooling. Circulation.
2011;124(2):206-214. (Prospective descriptive study; 140
patients)
49. Sendelbach S, Hearst MO, Johnson PJ, et al. Effects of vari-
ation in temperature management on cerebral performance
category scores in patients who received therapeutic hy-
pothermia post cardiac arrest. Resuscitation. 2012;83(7):829-
834. (Retrospective review; 172 patients)
50. Garrett JS, Studnek JR, Blackwell T, et al. The associa-
tion between intra-arrest therapeutic hypothermia and
return of spontaneous circulation among individuals
experiencing out of hospital cardiac arrest. Resuscitation.
2011;82(1):21-25. (Retrospective observational; 551 pa-
tients)
51. Bernard SA, Smith K, Cameron P et al. Induction of
therapeutic hypothermia by paramedics after resuscitation
from out-of-hospital ventricular fibrillation cardiac arrest:
a randomized controlled trial. Circulation. 2010;122(7):737-
742. (Prospective randomized controlled clinical study;
www.ebmedicine.net Volume 3, Number 3
 234 patients)
52. Bernard SA, Smith K, Cameron P, et al. Induction of pre-
hospital therapeutic hypothermia after resuscitation from
nonventricular fibrillation cardiac arrest*. Crit Care Med.
2012;40(3):747-753. (Prospective randomized controlled
clinical study; 163 patients)
53. Castren M, Nordberg P, Svensson L, et al. Intra-arrest
transnasal evaporative cooling: a randomized, prehospital,
multicenter study (PRINCE: Pre-ROSC IntraNasal Cooling
Effectiveness). Circulation. 2010;122(7):729-736. (Prospec-
tive randomized; 200 patients)
54. Suehiro E, Povlishock JT. Exacerbation of traumatically
induced axonal injury by rapid posthypothermic rewarm-
ing and attenuation of axonal change by cyclosporin A. J
Neurosurg. 2001;94(3):493-498. (Animal study)
55. Suehiro E, Ueda Y, Wei EP, et al. Posttraumatic hypother-
mia followed by slow rewarming protects the cerebral mi-
crocirculation. J Neurotrauma. 2003;20(4):381-390. (Animal
study)
56. Bernard SA, Buist M, Monteiro O, et al. Induced hypo-
thermia using large volume, ice-cold intravenous fluid
in comatose survivors of out-of-hospital cardiac arrest: a
preliminary report. Resuscitation. 2003;56(1):9-13. (Prospec-
tive interventional; 22 patients)
57. Polderman KH, Rijnsburger ER, Peerdeman SM, et al.
Induction of hypothermia in patients with various types
of neurologic injury with use of large volumes of ice-cold
intravenous fluid. Crit Care Med. 2005;33(12):2744-2751.
(Prospective interventional; 134 patients)
58. Weingart S, Mayer S, Polderman K. Rectal probe tempera-
ture lag during rapid saline induction of hypothermia
after resuscitation from cardiac arrest. Resuscitation. 2009;
80(7):837-878. (Case report)
59. Holzer M. Targeted temperature management for comatose
survivors of cardiac arrest. N Engl J Med. 2010;363(13):1256-
1264. (Review)
60. Badjatia N, Strongilis E, Gordon E, et al. Metabolic impact
of shivering during therapeutic temperature modula-
tion: the Bedside Shivering Assessment Scale. Stroke.
2008;39(12):3242-3247. (Prospective observational; 50
patients)
61. Seder DB, Van der Kloot TE. Methods of cooling: practical
aspects of therapeutic temperature management. Crit Care
Med. 2009;37(7 Suppl):S211-S222. (Review)
62. Tomte O, Draegni T, Mangschau A, et al. A comparison of
intravascular and surface cooling techniques in comatose
cardiac arrest survivors. Crit Care Med. 2011;39(3):443-449.
(Prospective observational; 167 patients)
63. Haugk M, Krizanac D, Stratil P, et al. Comparison of
surface cooling and invasive cooling for rapid induction
of mild therapeutic hypothermia in pigs--effectiveness of
two different devices. Resuscitation. 2010;81(12):1704-1708.
(Animal model)
64. Gillies MA, Pratt R, Whiteley C, et al. Therapeutic hypo-
thermia after cardiac arrest: a retrospective comparison of
surface and endovascular cooling techniques. Resuscitation.
2010;81(9):1117-1122. (Retrospective cohort; 83 patients)
65. Howes D, Ohley W, Dorian P, et al. Rapid induction of
therapeutic hypothermia using convective-immersion
surface cooling: safety, efficacy and outcomes. Resuscita-
tion. 2010;81(4):388-392. (Prospective observational; 24
patients)
66. Hoedemaekers CW, Ezzahti M, Gerritsen A, et al. Com-
parison of cooling methods to induce and maintain
normo- and hypothermia in intensive care unit patients: a
prospective intervention study. Crit Care. 2007;11(4):R91.
(Prospective observational; 50 patients)
67. Badjatia N, Strongilis E, Prescutti M, et al. Metabolic
benefits of surface counter warming during therapeutic
temperature modulation. Crit Care Med. 2009;37(6):1893-
1897. (Prospective observational; 50 patients)
www.ebmedicine.net Volume 3, Number 3
68. Gajic O, Festic E, Afessa B. Infectious complications in sur-
vivors of cardiac arrest admitted to the medical intensive
care unit. Resuscitation. 2004;60(1):65-69. (Retrospective
cohort; 56 patients)
69. Perbet S, Mongardon N, Dumas F, et al. Early-onset
pneumonia after cardiac arrest: characteristics, risk factors
and influence on prognosis. Am J Respir Crit Care Med.
2011;184(9):1048-1054. (Retrospective cohort; 641 patients)
70. Batista LM, Lima FO, Januzzi JL Jr, et al. Feasibility and
safety of combined percutaneous coronary intervention
and therapeutic hypothermia following cardiac arrest. Re-
suscitation. 2010;81(4):398-403. (Prospective observational;
90 patients)
71. Ng KF, Cheung CW, Lee Y, Leung SW. Low-dose desmo-
pressin improves hypothermia-induced impairment of
primary haemostasis in healthy volunteers. Anaesthesia.
2011;66(11):999-1005. (Prospective randomized; 52 pa-
tients)
72. Beiser DG, Carr GE, Edelson DP, et al. Derangements in
blood glucose following initial resuscitation from in-hospi-
tal cardiac arrest: a report from the national registry of car-
diopulmonary resuscitation. Resuscitation. 2009;80(6):624-
630. (Retrospective review; 17,800 patients)
73. Padkin A. Glucose control after cardiac arrest. Resuscita-
tion. 2009;80(6):611-612. (Editorial)
74. Stayer SA, Steven JM, Nicolson SC, et al. The metabolic
effects of surface cooling neonates prior to cardiac surgery.
Anesth Analg. 1994;79(5):834-839. (Prospective random-
ized; 22 patients)
75. Starodub R, Abella BS, Grossestreuer AV, et al. Associa-
tion of serum lactate and survival outcomes in patients
undergoing therapeutic hypothermia after cardiac arrest.
Resuscitation. 2013 Feb 8. [Epub ahead of print] (Retrospec-
tive; 199 patients)
76. Hemphill JC III, White DB. Clinical nihilism in neuro-
emergencies. Emerg Med Clin North Am. 2009;27(1):27-viii.
(Review)
77. Wijdicks EF, Hijdra A, Young GB, et al. Practice parameter:
prediction of outcome in comatose survivors after cardio-
pulmonary resuscitation (an evidence-based review): re-
port of the Quality Standards Subcommittee of the Ameri-
can Academy of Neurology. Neurology. 2006;67(2):203-210.
(Practice guidelines)
78. Negovsky VA. Postresuscitation disease. Crit Care Med.
1988;16(10):942-946. (Review)
79. Adrie C, dib-Conquy M, Laurent I, et al. Successful cardio-
pulmonary resuscitation after cardiac arrest as a sepsis-
like syndrome. Circulation. 2002;106(5):562-568. (Prospec-
tive; 107 patients)
80. Adrie C, Laurent I, Monchi M, et al. Postresuscitation dis-
ease after cardiac arrest: a sepsis-like syndrome? Curr Opin
Crit Care. 2004;10(3):208-212. (Review)
81. Hinchey PR, Myers JB, Lewis R, et al. Improved out-
of-hospital cardiac arrest survival after the sequential
implementation of 2005 AHA guidelines for compressions,
ventilations, and induced hypothermia: the Wake County
experience. Ann Emerg Med. 2010;56(4):348-357. (Prospec-
tive observational; 1365 patients)
82. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9:
post-cardiac arrest care: 2010 American Heart Association
guidelines for cardiopulmonary resuscitation and emer-
gency cardiovascular care. Circulation. 2010;122(18 Suppl
3):S768-S786. (Practice guidelines)
83. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate
coronary angiography in survivors of out-of-hospital car-
diac arrest. N Engl J Med. 1997;336(23):1629-1633. (Prospec-
tive observational; 84 patients)
84.* Garot P, Lefevre T, Eltchaninoff H, et al. Six-month
outcome of emergency percutaneous coronary interven-
tion in resuscitated patients after cardiac arrest compli-
15 EMCC 2013
 cating ST-elevation myocardial infarction. Circulation. CME Questions
2007;115(11):1354-1362. (Prospective observational; 186
patients)
85. Hartke A, Mumma BE, Rittenberger JC, et al. Incidence of Take This Test Online!
re-arrest and critical events during prolonged transport of
post-cardiac arrest patients. Resuscitation. 2010;81(8):938-
942. (Retrospective; 248 patients) Current subscribers can receive CME credit
86. Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic absolutely free by completing the following test.
hypothermia in patients after out-of-hospital cardiac arrest This issue includes 3 AMA PRA Category 1 CreditsTM.
due to acute ST-segment elevation myocardial infarction Online testing is now available for current and
undergoing immediate percutaneous coronary interven- Take This Test Online!
archived issues. To receive your free CME credits for
tion. Crit Care Med. 2008;36(6):1780-1786. (Prospective
observational; 33 patients) this issue, scan the QR code below or visit
87. Knafelj R, Radsel P, Ploj T, et al. Primary percutaneous www.ebmedicine.net/C0613
coronary intervention and mild induced hypothermia
in comatose survivors of ventricular fibrillation with
ST-elevation acute myocardial infarction. Resuscitation.
2007;74(2):227-234. (Prospective observational; 72 pa-
tients)
88. Richling N, Herkner H, Holzer M, et al. Thrombolytic
therapy vs primary percutaneous intervention after ven-
tricular fibrillation cardiac arrest due to acute ST-segment
elevation myocardial infarction and its effect on outcome.
Am J Emerg Med. 2007;25(5):545-550. (Retrospective; 147
patients)
89. Schefold JC, Storm C, Joerres A, et al. Mild therapeutic 1. Which of the following statements is currently
hypothermia after cardiac arrest and the risk of bleeding true about therapeutic hypothermia for VT/VF
in patients with acute myocardial infarction. Int J Cardiol. arrest?
2009;132(3):387-391. (Prospective observational; 62 pa-
a. The practice is performed often but has no
tients)
90. Shao ZH, Chang WT, Chan KC, et al. Hypothermia- known benefit.
induced cardioprotection using extended ischemia and b. It is endorsed by consensus guidelines, but
early reperfusion cooling. Am J Physiol Heart Circ Physiol. implementation remains a challenge at
2007;292(4):H1995-H2003. (Bench research) some centers.
91. Yannopoulos D, Zviman M, Castro V, et al. Intra-cardio-
c. The practice has a prohibitively large
pulmonary resuscitation hypothermia with and without
volume loading in an ischemic model of cardiac arrest. number needed to treat.
Circulation. 2009;120(14):1426-1435. (Animal model) d. It is not as effective as cooling a PEA/
92. Gotberg M, Olivecrona GK, Koul S, et al. A pilot study asystolic arrest.
of rapid cooling by cold saline and endovascular cooling
before reperfusion in patients with ST-elevation myocar-
2. Regarding patients that are candidates for
dial infarction. Circ Cardiovasc Interv. 2010;3(5):400-407.
(Prospective randomized; 20 patients) therapeutic hypothermia:
93. Haugk M, Testori C, Sterz F, et al. Relationship between a. PEA arrest is an absolute exclusion criteria.
time to target temperature and outcome in patients treated b. Asystolic arrest is an absolute exclusion
with therapeutic hypothermia after cardiac arrest. Crit criteria.
Care. 2011;15(2):R101. (Retrospective cohort; 588 patients)
c. Severe terminal illness is an exclusion
94. Italian Cooling Experience (ICE) Study Group. Early-ver-
sus late-initiation of therapeutic hypothermia after cardiac criteria.
arrest: preliminary observations from the experience of 17 d. ROSC < 5 minutes after arrest is an
Italian intensive care units. Resuscitation. 2012;83(7):823- exclusion criteria.
828. (Prospective observational cohort study; 122 pa-
tients)
3. Why is traumatic active bleeding a contraindi-
95. Carr BG, Kahn JM, Merchant RM, et al Inter-hospital
variability in post-cardiac arrest mortality. Resuscitation. cation for therapeutic hypothermia for VT/VF
2009;80(1):30-34. (Retrospective; 4674 patients) arrest?
96.* Nichol G, Aufderheide TP, Eigel B, et al. Regional systems a. Patients that are cooled cannot get
of care for out-of-hospital cardiac arrest: a policy state- transfusions.
ment from the American Heart Association. Circulation.
b. Patients that are hypotensive should not be
2010;121(5):709-729. (Policy statement)
97. Lick CJ, Aufderheide TP, Niskanen RA, et al. Take Heart cooled.
America: A comprehensive, community-wide, systems- c. Patients with a sympathetic surge are at
based approach to the treatment of cardiac arrest. Crit Care greater risk for shivering.
Med. 2011;39(1):26-33. (Prospective observational) d. There is a concern that hypothermia will
98. Kilgannon JH, Jones AE, Shapiro NI, et al. Associa-
induce coagulopathy.
tion between arterial hyperoxia following resuscitation
from cardiac arrest and in-hospital mortality. JAMA.
2010;303(21):2165-2171. (Multicenter cohort; 6326 patients)

EMCC 2013 16 www.ebmedicine.net Volume 3, Number 3

4. The authors suggest cooling for ____ at a goal
temperature of ____ .
a. 6 to 12 hours, 34C to 38C Coming Soon In EMCC
b. 12 to 24 hours, 34C to 36C
c. 12 to 24 hours, 32C to 34C
d. 24 to 48 hours, 34C to 38C Ventilator Management
e. 24 to 48 hours, 32C to 34C In The Intubated Emergency
5. The rewarming phase increases the patients
Department Patient
risk for which of the following?
a. Hypertension and hypokalemia AUTHORS:
b. Hypertension and hyperkalemia SAMANTHA L. WOOD, MD
c. Hypotension and hypokalemia Assistant Professor of Emergency Medicine, Tufts
d. Hypotension and hyperkalemia University School of Medicine, Boston, MA; Attending
Physician, Department of Emergency Medicine, Maine
6. Which of the following statements is true
Medical Center, Portland, ME
regarding patients with cardiac arrest and signs
of a STEMI? THOMAS VAN DER KLOOT, MD
a. Therapeutic hypothermia is not advised. Assistant Clinical Professor of Medicine, Tufts
b. Therapeutic hypothermia should be University School of Medicine, Boston, MA; Director,
undertaken after PCI. Medical Critical Care, Maine Medical Center; Medical
c. Priority should be given to hypothermia; Director, MaineHealth Vital Network, Portland, ME
PCI is not indicated.
d. Therapeutic hypothermia has been safely Emergent airway management is one of the defining
performed along with PCI in 2 studies. skills of the practice of emergency medicine.
e. A patient who receives thrombolytic therapy Emergency physicians must be comfortable
should not be cooled because they have a with the initial intubation and stabilization of
significantly higher risk of bleeding. these patients as well as with ongoing ventilator
management during the patients stay in the
7. What is the most common dysrhythmia en- emergency department. A retrospective review of
countered during cooling? a large national data set found that patients who
a. Third-degree block require mechanical ventilation represent only 0.23%
b. Atrial fibrillation of emergency department visits, but they have an
c. VF inhospital mortality rate of 24%. The same study
d. Sinus tachycardia found that 75% of mechanically ventilated patients
e. Sinus bradycardia spent >2 hours in the emergency department,
and 25% were there for >5 hours. Retrospective
8. Strategies that can be used to avoid postcardiac studies have found that an emergency department
arrest syndromes include: boarding time of >2 hours before transfer to the
a. Avoiding hyperventilation with a goal ICU is associated with increased ventilator days
PaCO2 of 45 to 50 mm Hg and hospital length of stay, and boarding time of
b. Avoiding hyperoxia by not allowing SpO2 >6 hours is associated with increased mortality.
to exceed 90% Close attention to the optimal management of
c. Allowing hypotension at a MAP mechanically ventilated patients in the emergency
between 40 to 50 mm Hg, as this is department may help improve outcomes.
cardioprotective Upon completion of this article, you should be able to:
d. Correcting metabolic disturbances
1. Summarize the data behind low-tidal-volume
ventilation, and describe which patients should
and should not receive such therapy.
2. Describe treatment approaches for a crashing
intubated patient, a patient with urgent
ventilation or oxygenation difficulty, and a patient
with ventilator dyssynchrony.
3. Cite situations in which patients may be
extubated in the ED.

www.ebmedicine.net Volume 3, Number 3 17 EMCC 2013

The EM Critical Care Archives
Title Publication Date # Of Free CME Credits

Resuscitation Of The Patient With Massive Upper April 2013 3

Gastrointestinal Bleeding

Therapeutic Uses Of Hypertonic Saline In The Critically February 2013 3 (trauma)

Ill Emergency Department Patient

Critical Care Of Severe Thermal Burn Injury December 2012 3 (trauma)

Postarrest Cardiocerebral Resuscitation: An Evidence- October 2012 3

Based Review

Air Transport Of The Critically Ill Emergency Department August 2012 3

Patient

Supportive Management Of Critical Illness In The June 2012 3

Pregnant Patient

Emergency Management Of Coagulopathy In Acute April 2012 3 (stroke)

Intracranial Hemorrhage

Emergency Ultrasound In Patients With Respiratory February 2012 3

Distress

Complications Of Acute Coronary Syndromes December 2011 3

High-Risk Scenarios In Blunt Trauma: An Evidence- October 2011 3 (trauma)

Based Approach

Noninvasive Ventilation: Update On Uses For The August 2011 3

Critically Ill Patient

Respiratory Monitoring In The Emergency Department June 2011 3

To view these articles, go to www.ebmedicine.net/EMCC

EMCC 2013 18 www.ebmedicine.net Volume 3, Number 3

 Introducing

A New Educational Resource

For Your Hospitalist Colleagues
OmniaCore has a similar format as EM Critical Care:
In-depth, single-topic reviews
Evidence-based summaries
Extensively researched recommendations
Unbiased approach
Available in print and online including a mobile-
optimized website
Approved for up to 48 AMA PRA Category 1 CreditsTM
per year
Published by EB Medicine, just like EM Critical Care

There is no other publication like this for hospitalists, and

thats why were asking you to help us spread the word.

OmniaCore In Hospital Medicine:

Is the only single-topic, evidence-based, monthly
journal that is written by hospitalists for hospitalists
Can be immediately applied to inpatient care
Empowers hospitalists with concise articles that are pertinent to their practice
Provides practice pearls, risk-management pitfalls, clinical pathways, and evidence-based
recommendations
Enables hospitalists to objectively assess the evidence base
Propels educational and mentoring capabilities
Your recommendation to your hospitalist colleagues would be much appreciated! And its easy to
recommend OmniaCore. Simply give your hospitalist colleagues the postcard that was mailed with this
issue (let us know if you need extras), tell them to visit www.OmniaCore.com/subscribe, or ask them to
call 1-800-249-5770.

Coupon Code: emccoffer (a $50 savings off the regular price of $347!)

www.ebmedicine.net Volume 3, Number 3 19 EMCC 2013

Erratum CME Information
Date of Original Release: June 1, 2013. Date of most recent review: May 1,
In the Emergency Ultrasound In Patients With 2013. Termination date: June 1, 2016.
Respiratory Distress article in EM Critical Care Vol. 2, Accreditation: EB Medicine is accredited by the Accreditation Council for
No. 1, an incorrect version of Figure 18D, Subxiphoid Continuing Medical Education (ACCME) to provide continuing medical
was published. The LA appearing on the bottom education for physicians. This activity has been planned and implemented
in accordance with the Essential Areas and Policies of the ACCME.
right-hand side of liver should have been labeled Credit Designation: EB Medicine designates this enduring material for a
LV. The correct version of this image appears below maximum of 3 AMA PRA Category 1 Credits. Physicians should claim only
and on our website at www.ebmedicine.net/EMCC. the credit commensurate with the extent of their participation in the activity.
We regret any confusion this may have caused. AOA Accreditation: EMCC is eligible for up to 18 American Osteopathic
Association Category 2A or 2B credit hours per year.
Needs Assessment: The need for this educational activity was
determined by a survey of medical staff, including the editorial board of
this publication; review of morbidity and mortality data from the CDC,
AHA, NCHS, and ACEP; and evaluation of prior activities for emergency
physicians.
Target Audience: This enduring material is designed for emergency
medicine physicians, physician assistants, nurse practitioners, and
residents as well as intensivists and hospitalists.
Goals: Upon completion of this article, you should be able to: (1)
demonstrate medical decision-making based on the strongest clinical
evidence; (2) cost-effectively diagnose and treat the most critical ED
presentations; and (3) describe the most common medicolegal pitfalls for
each topic covered.
RV Discussion of Investigational Information: As part of the newsletter,
faculty may be presenting investigational information about pharmaceutical
LV products that is outside Food and Drug Administration-approved labeling.
Information presented as part of this activity is intended solely as
continuing medical education and is not intended to promote off-label use
of any pharmaceutical product.
Faculty Disclosure: It is the policy of EB Medicine to ensure objectivity,
balance, independence, transparency, and scientific rigor in all CME-
sponsored educational activities. All faculty participating in the planning

EMCC Has Gone Mobile!
You can now view all EMCC content on your iPhone or
Android smartphone. Simply visit www.ebmedicine.net from
your mobile device, and youll automatically be directed to
our mobile site.
On our mobile site, you can:
View all issues of EMCC since inception, including issues
on NIV, blunt trauma, ACS, and more
Take CME tests for all issues thats over 20 AMA
Category 1 CreditsTM!
View your CME records, including scores, dates of
completion, and certificates
Comment on EMCCs Whats Your Diagnosis blog, by
visiting www.ebmedicine.net/emccblog
Renew your subscription or purchase additional content
Check out our mobile site, and give us your feedback!
Simply click the link at the bottom of the mobile site to
complete a short survey to tell us what features youd like
us to add or change.
or implementation of a sponsored activity are expected to disclose to the
audience any relevant financial relationships and to assist in resolving any
conflict of interest that may arise from the relationship. In compliance with
all ACCME Essentials, Standards, and Guidelines, all faculty for this CME
activity were asked to complete a full disclosure statement. The information
received is as follows: Dr. Pearson, Dr. Rittenberger, Dr. Weingart, Dr.
Sanghvi, Dr. Arntfield, and their related parties reported no significant
financial interest or other relationship with the manufacturer(s) of any
commercial product(s) discussed in this educational presentation. Dr.
Heffner reported a relevant financial interest in Medivance, Inc. in the
form of honoraria for lectures, papers, or teaching.
Commercial Support: This issue of EMCC did not receive any commercial
support.
Earning Credit: Two Convenient Methods: (1) Go online to
www.ebmedicine.net/CME and click on the title of this article.
(2) Mail or fax the CME Answer And Evaluation Form with your
December issue to EB Medicine.
Hardware/Software Requirements: You will need a Macintosh or PC to
access the online archived articles and CME testing.
Additional Policies: For additional policies, including our statement of conflict
of interest, source of funding, statement of informed consent, and statement
of human and animal rights, visit www.ebmedicine.net/policies.

CEO & Publisher: Stephanie Williford Managing Editor: Dorothy Whisenhunt Scientific Content Editor: Kelli Miller, ELS Assistant Editor: Kay LeGree
Director of Member Services: Liz Alvarez Member Services Representative: Kiana Collier
Marketing Manager: Robin Williford Senior Marketing Specialist: Angela Hammond

EB Medicine EMCC Subscription Information:

Phone: 1-800-249-5770 or 1-678-366-7933
Fax: 1-770-500-1316 6 print issues per year, 18 AMA PRA Category 1 CreditsTM,
5550 Triangle Parkway, Suite 150, Norcross, GA 30092 and full online access to searchable archives
E-mail: ebm@ebmedicine.net and additional CME: $299
Website: www.ebmedicine.net (Call 1-800-249-5770 or go to
www.ebmedicine.net/EMCCinfo to order)
To write a letter to the editor, please email:
arntfieldmd@ebmedicine.net

EM Critical Care (EMCC) (ISSN Print: 2162-3031, ISSN Online: 2162-3074, ACID-FREE) is published 6 times per year by EB Medicine (5550 Triangle Parkway, Suite 150, Norcross, GA 30092).
Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is
intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The
materials contained herein are not intended to establish policy, procedure, or standard of care. EM Critical Care and EMCC are trademarks of EB Medicine. Copyright 2013 EB Medicine. All
rights reserved. No part of this publication may be reproduced in any format without written consent of EB Medicine. This publication is intended for the use of the individual subscriber only
and may not be copied in whole or part or redistributed in any way without the publishers prior written permission -- including reproduction for educational purposes or for internal distribution
within a hospital, library, group practice, or other entity.

EMCC 2013 20 www.ebmedicine.net Volume 3, Number 3