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EM Critical Care
UNDERSTANDING AND CARING FOR
CRITICAL ILLNESS IN EMERGENCY MEDICINE
Practical Aspects Of Postcardiac
Arrest Therapeutic Hypothermia
Abstract
Neurologically intact survival following cardiac arrest remains a
challenge of modern medicine. Internationally, the rate for survival
of out-of-hospital cardiac arrest has hovered at a disappointingly
low 6%. Over the past decade, the early postcardiac arrest period
has emerged as a critical window for therapeutic intervention to
minimize cerebral injury and improve recovery. Therapeutic hypothermia is a cornerstone of this early postresuscitation care. Despite
accumulating evidence and widespread endorsement, adoption
of therapeutic hypothermia is incomplete. This review focuses on
overcoming barriers to enable practical application of this life-saving
treatment.
Note From The Editor-In-Chief
Readers of EM Critical Care will recall our 2012 issue by Rittenberger et al that emphasized the guiding principles of cardiocerebral
resuscitation in the emergency department after cardiac arrest. In
this issue, we will expand on the discussion of the use of therapeutic
hypothermia after cardiac arrest and will address a number of the
challenges and logistical considerations for implementing hypothermia. More than a decade after the landmark trials by Bernard et al
and the Hypothermia After Cardiac Arrest (HACA) Study Group,
there remain challenges with uptake, implementation, and inclusion/exclusion criteria for therapeutic hypothermia. This issue by
Pearson and Heffner succinctly addresses the spectrum of questions
and complexities that have evolved since therapeutic hypothermia’s
powerful benefit was demonstrated. Enjoy! - Rob Arntfield
Editor-in-Chief
Robert T. Arntfield, MD, FACEP,
FRCPC, FCCP
Assistant Professor, Division
of Critical Care, Division of
Emergency Medicine, Western
University, London, Ontario,
Canada
Clinical Research Director,
Center for Resuscitation Science,
Philadelphia, PA
Andy Jagoda, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Icahn
School of Medicine at Mount Sinai;
Medical Director, Mount Sinai
Hospital, New York, NY
Lillian L. Emlet, MD, MS, FACEP
Assistant Professor, Department of
Critical Care Medicine, Department
of Emergency Medicine, University William A. Knight, IV, MD, FACEP
of Pittsburgh Medical Center;
Assistant Professor of Emergency
Program Director, EM-CCM
Medicine, Assistant Professor of
Associate Editor
Fellowship of the Multidisciplinary
Neurosurgery, Medical Director Critical Care Training Program,
Emergency Medicine Mid-Level
Scott D. Weingart, MD, FCCM
Pittsburgh, PA
Provider Program, Associate
Associate Professor, Department
Medical Director of Neuroscience
of Emergency Medicine, Director,
ICU, University of Cincinnati
Division of Emergency Department Michael A. Gibbs, MD, FACEP
College of Medicine, Cincinnati,
Critical Care, Icahn School of
Professor and Chair, Department
OH
Medicine at Mount Sinai, New
of Emergency Medicine, Carolinas
York, NY
Medical Center, University of North
Carolina School of Medicine,
Haney Mallemat, MD
Chapel Hill, NC
Assistant Professor, Department
Editorial Board
of Emergency Medicine, University
Benjamin S. Abella, MD, MPhil,
of Maryland School of Medicine,
Robert Green, MD, DABEM,
FACEP
Baltimore, MD
FRCPC
Assistant Professor, Department
Professor, Department of
of Emergency Medicine and
Evie Marcolini, MD, FAAEM
Anaesthesia, Division of Critical
Department of Medicine /
Assistant Professor, Department of
Care Medicine, Department of
Section of Pulmonary Allergy
Emergency Medicine and Critical
Emergency Medicine, Dalhousie
and Critical Care, University of
Care, Yale School of Medicine,
University, Halifax, Nova Scotia,
Pennsylvania School of Medicine;
New Haven, CT
Canada
Volume 3, Number 3
Authors
David A. Pearson, MD, FACEP, FAAEM
Assistant Professor, Carolinas Healthcare System; Associate
Residency Program Director, Department of Emergency
Medicine, Carolinas Medical Center, Charlotte, NC
Alan C. Heffner, MD
Director, Medical ICU, Director, ECMO Services Pulmonary
and Critical Care Consultants, Department of Internal
Medicine, Department of Emergency Medicine, Carolinas
Medical Center; Clinical Associate Professor, University of
North Carolina School of Medicine, Charlotte, NC
Peer Reviewers
Jon Rittenberger, MD, MS, FACEP
Assistant Professor, Department of Emergency Medicine,
University of Pittsburgh School of Medicine; Attending
Physician, Emergency Medicine and Post Cardiac Arrest
Services, UPMC Presbyterian Hospital, Pittsburgh, PA
Scott D. Weingart, MD, FCCM
Associate Professor, Department of Emergency Medicine,
Director, Division of Emergency Department Critical Care,
Icahn School of Medicine at Mount Sinai, New York, NY
CME Objectives
Upon completion of this article, you should be able to:
1.
2.
3.
Describe the indications and contraindications of
therapeutic hypothermia in postcardiac arrest.
Describe the most effective strategy to implement
therapeutic hypothermia in your institution.
Troubleshoot or prevent common complications of
therapeutic cooling.
Prior to beginning this activity, see the back page for faculty
disclosures and CME accreditation information.
Julie Mayglothling, MD
Assistant Professor, Department
of Emergency Medicine,
Department of Surgery, Division
of Trauma/Critical Care, Virginia
Commonwealth University,
Richmond, VA
Christopher P. Nickson, MBChB,
MClinEpid, FACEM
Senior Registrar, Intensive Care
Unit, Royal Darwin Hospital,
Darwin, Australia
Jon Rittenberger, MD, MS, FACEP
Assistant Professor, Department
of Emergency Medicine,
University of Pittsburgh School
of Medicine; Attending Physician,
Emergency Medicine and Post
Cardiac Arrest Services, UPMC
Presbyterian Hospital, Pittsburgh,
PA
Emanuel P. Rivers, MD, MPH, IOM
Vice Chairman and Director
of Research, Department of
Emergency Medicine, Senior
Staff Attending, Departments of
Emergency Medicine and Surgery
(Surgical Critical Care), Henry
Ford Hospital; Clinical Professor,
Department of Emergency
Medicine and Surgery, Wayne State
University School of Medicine,
Detroit, MI
Isaac Tawil, MD, FCCM
Assistant Professor, Department
of Anesthesia and Critical Care /
Department of Emergency Medicine,
Director, Neurosciences ICU,
University of New Mexico Health
Science Center, Albuquerque, NM
Research Editor
Amy Sanghvi, MD
Department of Emergency
Medicine, Icahn School of
Medicine at Mount Sinai, New York,
NY
Case Presentations
Critical Appraisal Of The Literature
A 63-year-old male experienced a witnessed, out-ofhospital collapse. The patient’s wife called 911 and initiated CPR. Ventricular fibrillation was recognized upon
paramedic arrival, but it was resistant to initial biphasic
countershock. ROSC was ultimately achieved 21 minutes 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 revealed 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 consultation with the critical care team. You consider postcardiac
arrest therapeutic hypothermia, but you wonder whether you
should cool this patient following PEA arrest?
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, cardiopulmonary 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 Advanced Life Support Guidelines 2006
• Canadian Association of Emergency Physicians,
Critical Care Committee: The Use of Hypothermia After Cardiac Arrest
• Scandinavian Society of Anesthesiology and
Intensive Care Medicine: Task Force on Scandinavian Therapeutic Hypothermia Guidelines,
Clinical Practice Committee
• The Hong Kong Society of Critical Care Medicine Position Statement: The Use of Hypothermia After Cardiac Arrest
Introduction
Over 300,000 patients per year in the United States
experience sudden cardiac arrest.1 Despite initial
resuscitation, neurological injury sustained during 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 permanent 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 postcardiac 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 © 20132
Efficacy Of Therapeutic Cooling
Evidence For Cooling Patients With
Ventricular Tachycardia And Ventricular
Fibrillation
Therapeutic hypothermia is the only neuroprotective therapy that demonstrates neurological and
survival benefit following cardiac arrest.11-13 A decade
of supportive investigation culminated in completion 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 Nonshockable 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
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 supporting use in this group. However, the heterogeneity 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 randomizing patients to normothermia in light of our
current evidence.
Many institutions with therapeutic hypothermia 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 comprehensive postresuscitative cardiac arrest care;28 thus, we
encourage cooling regardless of initial arrest rhythm.
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 therapeutic hypothermia applied outside of strict research 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 presenting with nonshockable rhythms, which is independently 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 hypothermia in this patient group is conflicting.21-24
We believe that defining cardiac arrest patients by primary arrest rhythm is an overly simplistic approach that does little to discriminate
individual patient acuity and physiology. Regardless of the rhythm, once ROSC is achieved,
neurological outcome—not the illness precipitating cardiac arrest—is 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 recommendations were based primarily on observational trials showing benefit of cooling following
Evidence For Cooling Patients With
Nonprimary Cardiac Events
Death due to brain injury represents the final common pathway of patients experiencing anoxic or
hypoxic injury, regardless of the inciting event.
Thus, the best available evidence supports extrapolation of therapeutic hypothermia to patients
experiencing nondysrhythmogenic arrest, including patients with asphyxia or traumatic nonexsanguinating arrest. (See Table 2.) Neuroprotective
cooling should not be withheld due to the lack of
an “ideal” candidate, as the potential neurological 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 institution’s 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
Table 1. Survival After Cardiac Arrest With
Good Neurological Outcome In Landmark
Trials
Hypothermia
Control
P
HACA12
75/136 (55%)
54/137 (39%)
.009
Bernard et al11
21/43 (49%)
9/34 (26%)
.046
•
•
•
•
•
•
•
Airway obstruction
Anaphylaxis
Asphyxia
Carbon monoxide poisoning
Commotio cordis
Drowning
Drug overdose (ie, narcotics, cocaine) or other toxicological poisonings
• Hanging/strangulation
Abbreviation: HACA, Hypothermia After Cardiac Arrest trial.
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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 remains,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 therapeutic hypothermia, accumulating evidence supports
the safety and efficacy of therapeutic hypothermia
among patients with serious hemodynamic instability, 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 induction. 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 spontaneous 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 © 20134
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 nonhemorrhage-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 contraindication to hypothermia.
Bleeding: Since hypothermia induces coagulopathy, active bleeding is a relative contraindication. Therapeutic hypothermia induces platelet
dysfunction at temperatures ≤ 35°C and inhibition of the coagulation cascade at temperatures ≤
33°C.38 Thus, some experts advocate for cooling at a
slightly higher temperature range of 34.5°C to 35°C
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 warrant active measures to avoid post-ROSC hyperthermia 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 temperature range (32°C-34°C).
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 neurological outcome.
Prehospital Cooling
Animal studies demonstrate that cooling that is initiated early results in improved survival and neurological 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 outcome with each 5-minute delay in the initiation of
cooling.49 Garrett et al evaluated 551 patients after
cardiac arrest and showed that prehospital intraarrest cooling via 4°C 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 between 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.
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 encouraged to initiate therapeutic cooling prior to transfer.
Induction of cooling can be achieved with cold IV fluid 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
Cooling In The Emergency Department
Therapeutic cooling is divided into 4 phases. These
include: (1) induction; (2) maintenance; (3) rewarming; 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.
It is important to note that prehospital cooling does
not mandate continued therapy, since many prehospital protocols are designed to ensure consistent and
wide implementation. Upon arrival to the emergency department (ED), patients should be individually evaluated for candidacy for therapeutic hypothermia 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 deleterious electrolyte shifts, hemodynamic instability, and
cerebral injury associated with rapid rewarming.54,55
The landmark trials for therapeutic hypothermia 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 32°C-34°C 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 cooling 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 possible induction time. Additionally, cooling should be
considered in all cardiac arrest patients, even in the
setting of delayed induction.
Cooling Induction
Induction of therapeutic hypothermia with cold
(4°C) isotonic fluid is safe, inexpensive, and effective.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 concomitant use of cold IV fluids, ice packs, and servocontrolled automated cooling devices for rapid cooling is helpful. Overshooting the goal temperature
range (< 32°C) 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 automated cooling systems. Core temperature measurement
should be initiated upon arrival to the ED. Bladder
or esophageal temperature sensors are most commonly used for core temperature monitoring. Newer
temperature-sensing Foley catheters do not require
urinary flow; instead, they sense bladder outlet
temperature. However, esophageal temperature
Avoiding Delays
For inhospital arrests (ED or hospital inpatients), supplies to allow rapid initiation cooling (ie, prechilled
4°C IV fluids) should be readily available; we recommend maintaining bags of normal saline in refrigerators that are easily accessible to the ED or ICU.
Extensive delays in the initiation of cooling due
to concerns over patient candidacy should be avoided. Since many commercially available devices have
www.ebmedicine.net • Volume 3, Number 3
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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 shivering during cooling.60 Adjunctive measures to control
shivering are often employed; these measures are
discussed in the Troubleshooting Therapeutic Cooling section of this article.
Commercially available cooling systems utilize
either external (noninvasive) or internal (endovascular) devices to complete the induction phase and transition to the maintenance phase.61 (See Table 5.) There
are important logistical issues to consider regarding
setup and use for both invasive and noninvasive cooling devices, and when compared to each other, neither is superior with regard to survival or neurological 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 immersion to induce rapid hypothermia.53,65
Cooling Maintenance
Therapeutic cooling for 12 to 24 hours at a goal
temperature of 32°C to 34°C is recommended based
on the protocols of the landmark trials. The optimal
depth and period of cooling is currently undergoing 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 temperature fluctuations and to facilitate slow, controlled
rewarming (< 0.5°C/h). There is no clear advantage
between invasive and noninvasive units. Cost is comparable among the commercially available surface devices 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 hypothermia treatment time period is rare. In such cases, slow
controlled rewarming (0.3°C/h to 0.5°C/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 © 20136
vasodilation can lead to hypotension, requiring
fluid and/or vasopressor support. Rapid rewarming causes potassium to move extracellularly, which
risks hyperkalemia.38 However, we caution against
aggressive correction of potassium during rewarming. Low-dose repletion for potassium < 3.5 mEq/L,
with frequent electrolyte reanalysis, is recommended. 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 several days following initial injury. Hyperthermia after
warming is common and can lead to neurological deterioration. 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 (4°C 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
hypothermia have not been observed.11 Regardless,
postarrest patients have a notable risk of pulmonary infection due to a high incidence of aspiration.68,69 Temperature control obscures fever as a
marker of infection, which has been linked to delay
in antibiotic administration. Thus, early empiric antibiotics are frequently employed for patients with
evidence of aspiration (ie, pulmonary secretions,
radiographic infiltrates). Changes in the water temperature 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 spontaneous bleeding. Conventional anticoagulant medications 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 temperature-related coagulopathy is unusual above 33.5°C.
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 therapeutic 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 hyperglycemia. 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, infection, 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 production 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 undergoing therapeutic cooling following cardiac arrest
remains to be clarified.74,75
tant clue to subclinical shivering. Persistently low
cooling-unit temperatures required to maintain the
goal temperature is another important clue to thermogenesis due to shivering. Adequate sedation is
paramount to control shivering, especially during
induction. Since hypothermia decreases medication 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 confound neurological assessments after rewarming.
Additionally, neuromuscular blockade in the form
of boluses of vecuronium or other nondepolarizing 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, metabolic, 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 bradycardia 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 function; however, increased infection rates and sepsis in postarrest patients undergoing therapeutic
Table 6. Potential Adverse Physiologic
Responses And Complications Associated
With Cooling
•
•
•
•
•
•
•
•
•
Early Postarrest Prognostication
Prognostication of neurological outcome in the ED
remains a challenge. No physician desires a futile
resuscitation; however, premature negative prognostication remains an obstacle to optimal care.76 There
is no evidence to support accurate early neurological
prognostication. Pre-arrest and intra-arrest parameters such as duration of arrest, bystander CPR, or
presenting rhythm are unreliable prognosticators
alone or in combination. For reference, the median
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
7
EMCC © 2013
Clinical Pathway: Adult Patients After Cardiac Arrest
With Return Of Spontaneous Circulation
Assess inclusion & exclusion criteria for postcardiac arrest resuscitation bundle.
• VT / VF arrest (Class I)
• PEA / asystole arrest (Class II)
• Perform and document neurological examination.
• Consult interventional cardiologist for assessment for coronary
angiography. (Induction of cooling should be performed concurrently with preparation for PCI.)
Goals:
• Cooling goals:
Achieve 32°C-34°C (Class I) in 60 min.
• Hemodynamic and ventilatory goals:
Maintain MAP ≥ 70 mm Hg (the preferred vasopressor is
norepinephrine).
Minimize FiO2 while maintaining oxygen saturation > 95%.
Maintain PaCO2 38-42 mm Hg.
Critical care considerations:
• Central venous catheter to assess CVP & ScvO2 (avoid left
subclavian catheter, as this may be the preferred site for a pacemaker/defibrillator).
• Echocardiogram to assess myocardial function
• Arterial monitoring line
• Glucose control
• Seizure control
• Evaluate and address etiology of arrest
Induction:
• Infuse cold IV fluids.
• Administer NS 30 cc/kg IV bolus as tolerated.
• Apply ice packs to groin, axilla, and neck.
• Maintain early sedation and paralysis until goal temperature
achieved.
• Initiate cooling device for 33°C.
Maintenance:
• Goal temperature of 32°C-34°C.
• Continue cooling for 24 h.
• Assess for shivering: short-acting analgesia or sedation (paralysis if shivering uncontrolled with these measures).
• Assess electrolytes.
• Monitor fluid status: input & output.
Controlled normothermia:
• Keep the cooling device in place for 2 to 3 days after rewarming
to maintain normothermia (37°C).
Rewarming:
• Rewarm approximately 0.5°C/h. (Class I)
• Assess electrolytes closely.
• Assess neurological status once at normothermia.
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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 saturation; 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 positive and compelling
Class II
• Safe, acceptable
• Probably useful
Level of Evidence:
• Generally higher levels of
evidence
• nonrandomized or retrospective
studies: historic, cohort, or case
control studies
• Less robust randomized controlled trials
• Results consistently positive
Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative treatments
Level of Evidence:
• Generally lower or intermediate
levels of evidence
• Case series, animal studies, consensus panels
• Occasionally positive results
Indeterminate
• Continuing area of research
• No recommendations until
further research
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling
Significantly modified from: The
Emergency Cardiovascular Care
Committees of the American
Heart Association and repre-
sentatives from the resuscitation councils of ILCOR: How to
Develop Evidence-Based Guidelines for Emergency Cardiac
Care: Quality of Evidence and
Classes of Recommendations;
Guidelines for cardiopulmonary
resuscitation and emergency
cardiac care. Emergency
Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA.
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 patient’s 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
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 Resuscitation: An Evidence-Based Review.”
downtime between collapse and ROSC for many of
these patients is > 20 minutes.12 In a recent observational study of therapeutic hypothermia, 36% of
patients with an arrest interval > 30 minutes experienced a good neurological outcome.48 Although
advanced age generally worsens prognosis, 30% of
patients > 75 years of age had good neurological outcome 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 predict neurological outcome.48 Prediction of prognosis
based on neurological examination becomes more
reliable after at least 72 hours following resuscitation.77 Given these limitations, early neuroprotective measures should be strongly considered for all
potentially eligible patients.
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 Unfortunately, clinical history is often limited, and
the electrocardiogram after ROSC can be nondiagnostic in discriminating acute coronary occlusion requiring emergent PCI.84 Revascularization
is independently associated with survival and
should be considered for all patients with strongly
suspected acute coronary disease or electrocardiogram evidence of ST-segment elevation myocardial
infarction (STEMI).85 PCI is the preferred method of
revascularization and was safely performed concurrent with therapeutic cooling in 2 prospective
observational studies.86,87 With appropriate coordination of cooling and PCI priorities, induction
of hypothermia does not delay cardiac catheterization.70 PCI should not be delayed due to an uncertain neurological prognosis.16
Thrombolysis is an acceptable reperfusion strategy 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
The Postcardiac Arrest Syndrome
A discussion involving the practical implementation
of therapeutic hypothermia necessitates the contextual 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 contemporary 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 hemodynamic 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 following way14:
• Postcardiac arrest brain injury
• Postcardiac arrest myocardial dysfunction
• Systemic ischemia-reperfusion response
• Persistent precipitating pathology
Table 7. Postcardiac Arrest Syndrome
Pathophysiology
Acute Myocardial Dysfunction
• Acute coronary syndromes
• Myocardial stunning
Brain Injury
• Anoxic brain insult
• Impaired autoregulation
• Ischemic reperfusion injury
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 effective, multipronged resuscitative protocol.81,82 The
early postarrest period is an opportunity to address
additional priorities for effective cardiocerebral resuscitation. 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
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 neuroprotective benefit, cardioprotective effects of hypothermia
are under exploration. Animal models show benefit
with early cooling.90,91 Early trials in noncardiac-arrest 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 summarized below. Additional controversy surrounds the
effectiveness of prehospital cooling and the role of
therapeutic hypothermia in patients experiencing
PEA of asystolic arrests; well-designed prospective 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 noninvasive). Studies demonstrate improved temperature 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
patients receive this neuroprotective therapy is
most important.
Rate of cooling: Another challenge involves identifying 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 braininjured patients may lose their ability to thermoregulate, 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 contradictory 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
Priority
Monitor and Goal
Therapy
1. Preload optimization
Response to fluid
challenge; fluid therapy is guided by:
• CVP: 8-12 mm Hg
• Echocardiogram:
cardiac function
and IVC variation
• Markers of SVV
Fluids
2. Perfusion
pressure
MAP 65-100 mm Hg
• Norepinephrine*
• Epinephrine
• Vasopressin
3. Perfusion
optimization
Global perfusion
markers:
• ScvO2 > 70%
• Lactate clearance
Clinical perfusion
markers:
• Urine output > 0.5
cc/kg/h
• Peripheral skin
perfusion
•
•
•
•
Table 8. Early Postresuscitation Priorities
• Provide adequate oxygenation and ventilation.
Avoid hyperventilation (goal PaCO2 of 38-42 mm).*
Avoid hyperoxia (titrate FiO2 to SpO2 > 95% [or PaO2 > 70 mm
Hg].*
• Reverse shock and stabilize hemodynamics.
• Identify and treat reversible cause of cardiac arrest.
• Apply neuroprotective therapies (ie, therapeutic hypothermia).
• Correct metabolic disturbances.
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*The solubility of gases (ie, PaCO2 and PaO2) changes as a function
of temperature.38 At goal temperature, a patient’s PaCO2 may be up
to 8 mm Hg lower than reported on the blood gas warmed to normal
temperature. Unfortunately, the clinical impact of temperature correction via pH-stat methodology is unclear. In the absence of clear data,
targeting high-normal PaCO2 may avoid unintended cerebral vasoconstriction stemming from arterial hypocapnea.
Abbreviations: FiO2, fraction of inspired oxygen; PaCO2, partial
pressure of carbon dioxide; PaO2, partial pressure of oxygen; SpO2,
oxygen saturation by pulse oximeter .
EMCC © 201310
Dobutamine
Milrinone
IABP
PRBC transfusion
*First-choice vasopressor
Abbreviations: CVP, central venous pressure; IABP, intra-aortic balloon pump; IVC, inferior vena cava; MAP, mean arterial pressure;
ScvO2, central venous oxygenation saturation; IABP, intra-aortic
balloon pump; PRBC, packed red blood cells; SVV, stroke volume
variation.
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 additional neuroprotective benefit.
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-hospital 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 opinion, 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 transport is safe and feasible.85
Some regions have a transfer-destination hospital 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.
Disposition
The disposition of postcardiac arrest patients depends 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 optimization while considering and addressing the possible 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 management 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 nursing resource allocation, and the multidisciplinary
specialized team required all make a postcardiac arrest 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-volume centers treating patients after cardiac arrest are
associated with improved survival.95 Regional systems of care have been successfully established for
STEMI, trauma, burns, and stroke, and the rationale
for regional systems of care for postcardiac arrest patients 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 hospitals with adequate patient volume, multidisciplinary
www.ebmedicine.net • Volume 3, Number 3
Summary
Therapeutic hypothermia is an effective therapy
to improve chances of neurological recovery after cardiac arrest. Ensuring broader utilization of
therapeutic cooling is essential to improving outcomes. Successful execution of therapeutic cooling
must consider the hospital’s 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 excessive 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 therapeutic cooling. Focused attention to the details
of the patient’s decompensation and arrest
event, along with simple bedside tests (electrocardiogram, 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 associated 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 prognosis. 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. Occult shivering is common and frequently thwarts
effective induction to goal temperature. Sedation and paralysis should be routine to assist
in reaching goal temperature—at 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 patients, now is the time to create one. Assess your
current ED and hospital resources and determine whether your patients can be comprehensively managed or whether they require transfer
to a regional PCI-capable and hypothermiacapable 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 destination ensures a smooth transfer of care.
EMCC © 201312
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 hypothermia trial; therefore, cooling this patient has Level 1 evidence. 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
Intubation
• Breathing
Avoid hyperventilation (goal PaCO2 of 38-42 mm Hg).
Avoid hyperoxia (rapidly decrease FiO2 to maintain SpO2 > 95%).
• Circulation
Goal MAP is > 70.
Anticipate and avoid hypotension.
Norepinephrine is the preferred vasopressor.
Screen for STEMI using ECG.
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Cooling Induction
• Initiate cooling as soon as possible after ROSC.
• Administer refrigerated (4°C) 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 aggressive 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 4°C normal
saline. The patient has cooling pads placed, ice packs applied, and sedation administered. An hour into cooling,
her temperature remains > 35°C. You realize that unrecognized shivering may be the cause, so you paralyze her
with vecuronium. An hour later, she is at goal temperature. The patient is subsequently transferred to the ICU of
the nearest cardiac arrest receiving hospital and completes
24 hours of therapeutic hypothermia at 33°C 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 appropriate asthma management.
3. Walters JH, Morley PT, Nolan JP. The role of hypothermia in post-cardiac arrest patients with return of spontaneous circulation: a systematic review. Resuscitation.
2011;82(5):508-516. (Review)
4. Hazinski MF, Nolan JP, Billi JE, et al. Part 1: Executive summary: 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 hypothermia 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 hypothermia 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 hypothermia 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 hypothermia guidelines for post-cardiac arrest syndrome at a
glacial pace: seeking guidance from the knowledge translation 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 barriers 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 outcome 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 neuroprotection 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 International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and
Anesthesia; the Council on Cardiopulmonary, Perioperative, 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 interventional; 20 patients)
18. Polderman KH. Induced hypothermia and fever control for
prevention and treatment of neurological injuries. Lancet.
References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology 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 determined 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 survival 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
13
EMCC © 2013
2008;371(9628):1955-1969. (Review)
19. Heffner AC, Pearson DA, Nussbaum ML, et al. Regionalization of post-cardiac arrest care: implementation of a
cardiac resuscitation center. Am Heart J. 2012;164(4):493501. (Prospective observational; 220 patients)
20. Teodorescu C, Reinier K, Dervan C, et al. Factors associated 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 hypothermia 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 arrest 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 intervention 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 cardiac arrest. Ann Emerg Med. 1997;30(2):146-153. (Prospective nonrandomized interventional; 44 patients)
26. Busch M, Soreide E, Lossius HM, et al. Rapid implementation of therapeutic hypothermia in comatose out-ofhospital 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 hypothermia 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-effectiveness of therapeutic hypothermia after cardiac arrest. Circ
Cardiovasc Qual Outcomes. 2009;2(5):421-428. (Cost-effectiveness analysis)
29. Jacobs S, Hunt R, Tarnow-Mordi W, et al. Cooling for newborns 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. (Metaanalysis)
31. Rittenberger JC, Kelly E, Jang D, et al. Successful outcome
utilizing hypothermia after cardiac arrest in pregnancy:
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32. Wible EF, Kass JS, Lopez GA. A report of fetal demise during therapeutic hypothermia after cardiac arrest. Neurocrit
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33. Hovdenes J, Laake JH, Aaberge L, et al. Therapeutic hypothermia after out-of-hospital cardiac arrest: experiences
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2007;51(2):137-142. (Prospective descriptive; 50 patients)
34. Zobel C, Adler C, Kranz A, et al. Mild therapeutic hypothermia in cardiogenic shock syndrome. Crit Care Med.
EMCC © 201314
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
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36. McGrane S, Maziad J, Netterville JL, et al. Therapeutic hypothermia after exsanguination. Anesth Analg. 2012;115(2):
343-345. (Case report)
37. Todd MM, Hindman BJ, Clarke WR, et al. Mild intraoperative hypothermia during surgery for intracranial
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randomized controlled; 1001 patients)
38. Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med.
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39. Rittenberger JC, Polderman KH, Smith WS, et al. Emergency 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. (Retrospective; 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. Reperfusion accelerates acute neuronal death induced by simulated 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 window 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 cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs. Crit Care Med. 1991;19(3):379389. (Animal model)
47. Boddicker KA, Zhang Y, Zimmerman MB, et al. Hypothermia improves defibrillation success and resuscitation outcomes from ventricular fibrillation. Circulation.
2005;111(24):3195-3201. (Animal model)
48. Mooney MR, Unger BT, Boland LL, et al. Therapeutic hypothermia 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 variation in temperature management on cerebral performance
category scores in patients who received therapeutic hypothermia post cardiac arrest. Resuscitation. 2012;83(7):829834. (Retrospective review; 172 patients)
50. Garrett JS, Studnek JR, Blackwell T, et al. The association 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 patients)
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):737742. (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 prehospital 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. (Prospective randomized; 200 patients)
54. Suehiro E, Povlishock JT. Exacerbation of traumatically
induced axonal injury by rapid posthypothermic rewarming 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 hypothermia followed by slow rewarming protects the cerebral microcirculation. J Neurotrauma. 2003;20(4):381-390. (Animal
study)
56. Bernard SA, Buist M, Monteiro O, et al. Induced hypothermia 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. (Prospective 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 temperature 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):12561264. (Review)
60. Badjatia N, Strongilis E, Gordon E, et al. Metabolic impact
of shivering during therapeutic temperature modulation: 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 hypothermia 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. Resuscitation. 2010;81(4):388-392. (Prospective observational; 24
patients)
66. Hoedemaekers CW, Ezzahti M, Gerritsen A, et al. Comparison 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):18931897. (Prospective observational; 50 patients)
www.ebmedicine.net • Volume 3, Number 3
68. Gajic O, Festic E, Afessa B. Infectious complications in survivors 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. Resuscitation. 2010;81(4):398-403. (Prospective observational;
90 patients)
71. Ng KF, Cheung CW, Lee Y, Leung SW. Low-dose desmopressin improves hypothermia-induced impairment of
primary haemostasis in healthy volunteers. Anaesthesia.
2011;66(11):999-1005. (Prospective randomized; 52 patients)
72. Beiser DG, Carr GE, Edelson DP, et al. Derangements in
blood glucose following initial resuscitation from in-hospital cardiac arrest: a report from the national registry of cardiopulmonary resuscitation. Resuscitation. 2009;80(6):624630. (Retrospective review; 17,800 patients)
73. Padkin A. Glucose control after cardiac arrest. Resuscitation. 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 randomized; 22 patients)
75. Starodub R, Abella BS, Grossestreuer AV, et al. Association of serum lactate and survival outcomes in patients
undergoing therapeutic hypothermia after cardiac arrest.
Resuscitation. 2013 Feb 8. [Epub ahead of print] (Retrospective; 199 patients)
76. Hemphill JC III, White DB. Clinical nihilism in neuroemergencies. 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 cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American 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 cardiopulmonary resuscitation after cardiac arrest as a “sepsislike” syndrome. Circulation. 2002;106(5):562-568. (Prospective; 107 patients)
80. Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease 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 outof-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. (Prospective 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 emergency 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 cardiac arrest. N Engl J Med. 1997;336(23):1629-1633. (Prospective observational; 84 patients)
84.* Garot P, Lefevre T, Eltchaninoff H, et al. Six-month
outcome of emergency percutaneous coronary intervention in resuscitated patients after cardiac arrest compli-
15
EMCC © 2013
cating ST-elevation myocardial infarction. Circulation.
2007;115(11):1354-1362. (Prospective observational; 186
patients)
85. Hartke A, Mumma BE, Rittenberger JC, et al. Incidence of
re-arrest and critical events during prolonged transport of
post-cardiac arrest patients. Resuscitation. 2010;81(8):938942. (Retrospective; 248 patients)
86. Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic
hypothermia in patients after out-of-hospital cardiac arrest
due to acute ST-segment elevation myocardial infarction
undergoing immediate percutaneous coronary intervention. Crit Care Med. 2008;36(6):1780-1786. (Prospective
observational; 33 patients)
87. Knafelj R, Radsel P, Ploj T, et al. Primary percutaneous
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 patients)
88. Richling N, Herkner H, Holzer M, et al. Thrombolytic
therapy vs primary percutaneous intervention after ventricular 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
hypothermia after cardiac arrest and the risk of bleeding
in patients with acute myocardial infarction. Int J Cardiol.
2009;132(3):387-391. (Prospective observational; 62 patients)
90. Shao ZH, Chang WT, Chan KC, et al. Hypothermiainduced cardioprotection using extended ischemia and
early reperfusion cooling. Am J Physiol Heart Circ Physiol.
2007;292(4):H1995-H2003. (Bench research)
91. Yannopoulos D, Zviman M, Castro V, et al. Intra-cardiopulmonary resuscitation hypothermia with and without
volume loading in an ischemic model of cardiac arrest.
Circulation. 2009;120(14):1426-1435. (Animal model)
92. Gotberg M, Olivecrona GK, Koul S, et al. A pilot study
of rapid cooling by cold saline and endovascular cooling
before reperfusion in patients with ST-elevation myocardial infarction. Circ Cardiovasc Interv. 2010;3(5):400-407.
(Prospective randomized; 20 patients)
93. Haugk M, Testori C, Sterz F, et al. Relationship between
time to target temperature and outcome in patients treated
with therapeutic hypothermia after cardiac arrest. Crit
Care. 2011;15(2):R101. (Retrospective cohort; 588 patients)
94. Italian Cooling Experience (ICE) Study Group. Early-versus late-initiation of therapeutic hypothermia after cardiac
arrest: preliminary observations from the experience of 17
Italian intensive care units. Resuscitation. 2012;83(7):823828. (Prospective observational cohort study; 122 patients)
95. Carr BG, Kahn JM, Merchant RM, et al Inter-hospital
variability in post-cardiac arrest mortality. Resuscitation.
2009;80(1):30-34. (Retrospective; 4674 patients)
96.* Nichol G, Aufderheide TP, Eigel B, et al. Regional systems
of care for out-of-hospital cardiac arrest: a policy statement from the American Heart Association. Circulation.
2010;121(5):709-729. (Policy statement)
97. Lick CJ, Aufderheide TP, Niskanen RA, et al. Take Heart
America: A comprehensive, community-wide, systemsbased approach to the treatment of cardiac arrest. Crit Care
Med. 2011;39(1):26-33. (Prospective observational)
98. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation
from cardiac arrest and in-hospital mortality. JAMA.
2010;303(21):2165-2171. (Multicenter cohort; 6326 patients)
EMCC © 201316
CME Questions
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www.ebmedicine.net/C0613
1. Which of the following statements is currently
true about therapeutic hypothermia for VT/VF
arrest?
a. The practice is performed often but has no known benefit.
b. It is endorsed by consensus guidelines, but implementation remains a challenge at some centers.
c. The practice has a prohibitively large number needed to treat.
d. It is not as effective as cooling a PEA/
asystolic arrest.
2. Regarding patients that are candidates for
therapeutic hypothermia:
a. PEA arrest is an absolute exclusion criteria.
b. Asystolic arrest is an absolute exclusion criteria.
c. Severe terminal illness is an exclusion criteria.
d. ROSC < 5 minutes after arrest is an exclusion criteria.
3. Why is traumatic active bleeding a contraindication for therapeutic hypothermia for VT/VF
arrest?
a. Patients that are cooled cannot get transfusions.
b. Patients that are hypotensive should not be cooled.
c. Patients with a sympathetic surge are at greater risk for shivering.
d. There is a concern that hypothermia will induce coagulopathy.
www.ebmedicine.net • Volume 3, Number 3
4. The authors suggest cooling for ____ at a goal
temperature of ____ .
a. 6 to 12 hours, 34°C to 38°C
b. 12 to 24 hours, 34°C to 36°C
c. 12 to 24 hours, 32°C to 34°C
d. 24 to 48 hours, 34°C to 38°C
e. 24 to 48 hours, 32°C to 34°C
Coming Soon In EMCC
Ventilator Management
In The Intubated Emergency
Department Patient
5. The rewarming phase increases the patient’s
risk for which of the following?
a. Hypertension and hypokalemia
b. Hypertension and hyperkalemia
c. Hypotension and hypokalemia
d. Hypotension and hyperkalemia
AUTHORS:
SAMANTHA L. WOOD, MD
Assistant Professor of Emergency Medicine, Tufts
University School of Medicine, Boston, MA; Attending
Physician, Department of Emergency Medicine, Maine
Medical Center, Portland, ME
6. Which of the following statements is true
regarding patients with cardiac arrest and signs
of a STEMI?
a. Therapeutic hypothermia is not advised.
b. Therapeutic hypothermia should be undertaken after PCI.
c. Priority should be given to hypothermia; PCI is not indicated.
d. Therapeutic hypothermia has been safely performed along with PCI in 2 studies.
e. A patient who receives thrombolytic therapy should not be cooled because they have a significantly higher risk of bleeding.
THOMAS VAN DER KLOOT, MD
Assistant Clinical Professor of Medicine, Tufts
University School of Medicine, Boston, MA; Director,
Medical Critical Care, Maine Medical Center; Medical
Director, MaineHealth Vital Network, Portland, ME
Emergent airway management is one of the defining
skills of the practice of emergency medicine.
Emergency physicians must be comfortable
with the initial intubation and stabilization of
these patients as well as with ongoing ventilator
management during the patient’s stay in the
emergency department. A retrospective review of
a large national data set found that patients who
require mechanical ventilation represent only 0.23%
of emergency department visits, but they have an
inhospital mortality rate of 24%. The same study
found that 75% of mechanically ventilated patients
spent >2 hours in the emergency department,
and 25% were there for >5 hours. Retrospective
studies have found that an emergency department
boarding time of >2 hours before transfer to the
ICU is associated with increased ventilator days
and hospital length of stay, and boarding time of
>6 hours is associated with increased mortality.
Close attention to the optimal management of
mechanically ventilated patients in the emergency
department may help improve outcomes.
7. What is the most common dysrhythmia encountered during cooling?
a. Third-degree block
b. Atrial fibrillation
c. VF
d. Sinus tachycardia
e. Sinus bradycardia
8. Strategies that can be used to avoid postcardiac
arrest syndromes include:
a. Avoiding hyperventilation with a goal PaCO2 of 45 to 50 mm Hg
b. Avoiding hyperoxia by not allowing SpO2 to exceed 90%
c. Allowing hypotension at a MAP between 40 to 50 mm Hg, as this is cardioprotective
d. Correcting metabolic disturbances
Upon completion of this article, you should be able to:
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
Gastrointestinal Bleeding
April 2013
3
Therapeutic Uses Of Hypertonic Saline In The Critically
Ill Emergency Department Patient
February 2013
3 (trauma)
Critical Care Of Severe Thermal Burn Injury
December 2012
3 (trauma)
Postarrest Cardiocerebral Resuscitation: An EvidenceBased Review
October 2012
3
Air Transport Of The Critically Ill Emergency Department
Patient
August 2012
3
Supportive Management Of Critical Illness In The
Pregnant Patient
June 2012
3
Emergency Management Of Coagulopathy In Acute
Intracranial Hemorrhage
April 2012
3 (stroke)
Emergency Ultrasound In Patients With Respiratory
Distress
February 2012
3
Complications Of Acute Coronary Syndromes
December 2011
3
High-Risk Scenarios In Blunt Trauma: An EvidenceBased Approach
October 2011
3 (trauma)
Noninvasive Ventilation: Update On Uses For The
Critically Ill Patient
August 2011
3
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
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Your recommendation to your hospitalist colleagues would be much appreciated! And it’s easy to
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EMCC © 2013
Erratum
CME Information
In the “Emergency Ultrasound In Patients With
Respiratory Distress” article in EM Critical Care Vol. 2,
No. 1, an incorrect version of Figure 18D, Subxiphoid
was published. The “LA” appearing on the bottom
right-hand side of liver should have been labeled
“LV.” The correct version of this image appears below
and on our website at www.ebmedicine.net/EMCC.
We regret any confusion this may have caused.
Date of Original Release: June 1, 2013. Date of most recent review: May 1,
2013. Termination date: June 1, 2016.
Accreditation: EB Medicine is accredited by the Accreditation Council for
Continuing Medical Education (ACCME) to provide continuing medical
education for physicians. This activity has been planned and implemented
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www.ebmedicine.net • Volume 3, Number 3