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EM Critical Care
UNDERSTANDING AND CARING FOR
CRITICAL ILLNESS IN EMERGENCY MEDICINE
Postarrest Cardiocerebral
Resuscitation: An EvidenceBased Review
Abstract
Cardiac arrest is a leading cause of death in the United States, resulting in approximately 300,000 deaths per year. Following restoration
of circulation, multiple organ systems demonstrate varying degrees
of injury or failure. This postarrest syndrome demonstrates features
of systemic inflammatory response (the postarrest state has been
likened to a “sepsis-like syndrome”) along with diffuse anoxic injury
to the brain. Aggressive titration of care to optimize cerebral resuscitation improves outcomes. Multiple strategies can be used to prevent secondary neuronal injury, including therapeutic hypothermia,
aggressive revascularization, titrated blood pressure goals, careful
control of ventilator parameters, and monitoring for seizure activity. An in-depth review of the literature to determine the evidence
supporting current postarrest guidelines is presented in this review,
with a primary focus on treatment of the postarrest patient to improve survival and neurologic outcomes.
Volume 2, Number 5
Authors
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
Benjamin S. Abella, MD, MPhil, FACEP
Assistant Professor, Department of Emergency Medicine and
Department of Medicine / Section of Pulmonary Allergy and
Critical Care, University of Pennsylvania School of Medicine;
Clinical Research Director, Center for Resuscitation Science,
Philadelphia, PA
Francis X. Guyette, MD, MS, MPH, FACEP
Assistant Professor of Emergency Medicine, University of
Pittsburgh School of Medicine, Pittsburgh, PA
Peer Reviewers
J. Gordon Boyd, MD, PhD, FRCPC
Neurologist and Critical Care Fellow, Critical Care Medicine,
Kingston General Hospital, Kingston, Ontario, Canada
Benjamin Lawner, DO, EMT-P, FAAEM
Assistant Professor, Department of Emergency Medicine,
University of Maryland School of Medicine; Deputy Medical
Director, Baltimore City Fire Department, Baltimore, MD
Gordon Bryan Young, MD, FRCPC
Professor of Neurology and Critical Care, Western University,
London, Ontario, Canada
CME Objectives
Upon completion of this article, you should be able to:
1.
2.
3.
4.
5.
Describe indications and contraindications for
postresuscitation care.
Describe organ system strategies for optimizing
postresuscitation care.
Describe techniques for optimizing organ system
resuscitation during the postresuscitation phase.
Discuss current controversies in postarrest care.
Summarize the evidence for postresuscitation care.
Prior to beginning this activity, see “CME Information” on the
back page.
Editor-in-Chief
Andy Jagoda, MD, FACEP
Julie Mayglothling, MD
Professor and Chair, Department
Assistant Professor, Department
of Emergency Medicine, Mount
of Emergency Medicine,
Sinai School of Medicine; Medical
Department of Surgery, Division
Lillian L. Emlet, MD, MS, FACEP
Director, Mount Sinai Hospital, New
of Trauma/Critical Care, Virginia
Assistant Professor, Department of
York, NY
Commonwealth University,
Critical Care Medicine, Department
Richmond, VA
of Emergency Medicine, University
of Pittsburgh Medical Center;
William A. Knight, IV, MD
Program Director, EM-CCM
Assistant Professor of Emergency Christopher P. Nickson, MBChB,
Fellowship of the Multidisciplinary
Medicine, Assistant Professor
MClinEpid, FACEM
Associate Editor
Critical Care Training Program,
of Neurosurgery, Emergency
Senior Registrar, Intensive Care
Pittsburgh, PA
Medicine Mid-Level Program
Scott Weingart, MD, FACEP
Unit, Royal Darwin Hospital,
Medical Director, University of
Associate Professor, Department of
Darwin, Australia
Cincinnati College of Medicine,
Emergency Medicine, Mount Sinai Michael A. Gibbs, MD, FACEP
Cincinnati, OH
School of Medicine; Director of
Professor and Chair, Department
Jon Rittenberger, MD, MS, FACEP
Emergency Critical Care, Elmhurst
of Emergency Medicine, Carolinas
Assistant Professor, Department
Hospital Center, New York, NY
Medical Center, University of North Haney Mallemat, MD
of Emergency Medicine,
Carolina School of Medicine,
Assistant Professor, Department
University of Pittsburgh School
Chapel Hill, NC
of Emergency Medicine, University
of Medicine; Attending Physician,
Editorial Board
of Maryland School of Medicine,
Emergency Medicine and Post
Benjamin S. Abella, MD, MPhil,
Baltimore, MD
Robert Green, MD, DABEM,
Cardiac Arrest Services, UPMC
FACEP
Presbyterian Hospital, Pittsburgh,
FRCPC
Assistant Professor, Department
Evie Marcolini, MD, FAAEM
PA
Associate Professor, Department
of Emergency Medicine and
of Anaesthesia, Division of Critical Assistant Professor, Department of
Department of Medicine /
Emergency Medicine and Critical
Care Medicine, Department of
Section of Pulmonary Allergy
Care, Yale School of Medicine,
Emergency Medicine, Dalhousie
and Critical Care, University of
New Haven, CT
University, Halifax, Nova Scotia,
Pennsylvania School of Medicine;
Canada
Clinical Research Director,
Robert T. Arntfield, MD, FRCPC,
FCCP
Assistant Professor, Division
of Critical Care, Division of
Emergency Medicine, Western
University, London, Ontario,
Canada
Center for Resuscitation Science,
Philadelphia, 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
Assistant Professor, Department of
Surgery, Department of Emergency
Medicine, University of New
Mexico Health Science Center,
Albuquerque, NM
Research Editor
Amy Sanghvi, MD
Department of Emergency
Medicine, Mount Sinai School of
Medicine, New York, NY
Case Presentation
You are contacted by one of the paramedics in your
local system regarding a 54-year-old female in cardiac
arrest. The patient experienced a witnessed arrest and
received 5 minutes of bystander CPR prior to the arrival of EMS. She was found to be in ventricular fibrillation and was defibrillated twice, converting her to a
perfusing rhythm. Prior to the second defibrillation,
the patient had a tibial IO line placed and was given 1
mg of epinephrine. Her current vital signs are a pulse
of 110 beats per minute, BP of 110/80 mm Hg, respirations of 6 (assisted with a bag-valve mask), and SpO2
of 92%. She is breathing spontaneously and withdraws
to noxious stimuli but does not follow commands. The
paramedics are 7 minutes from a critical access hospital
with minimal resources and 10 minutes from your tertiary care center with a cardiac catheterization laboratory and a postarrest care team. The paramedics request
orders to address the following questions:
• Should therapeutic hypothermia be initiated upon
hospital arrival or en route to the hospital?
• How should the patient’s airway be managed?
• What is the most appropriate destination for this
patient?
Introduction
Cardiac arrest is the third leading cause of death
in the United States, resulting in approximately
300,000 deaths per year.1 Disparate patient outcomes following resuscitation from cardiac arrest
are associated with variability in postarrest care.2
Dedicated postarrest care plans that include aggressive cardiocerebral resuscitation have been
associated with improved outcomes in this population.3-5 Multiple organ systems are affected by
anoxic injury, resulting in the need for aggressive
goal-directed care to prevent secondary neuronal
injury.6 These interventions are organized by organ
system, with a focus on cerebral resuscitation, and
have been compiled in resuscitation guidelines
promulgated by the American Heart Association.7
Individual patients may require some or all of these
interventions. An understanding of the literature
supporting each organ-system intervention and
recommended goals of care is important to provide
the best care to this critically ill population. This
issue of EMCC provides an overview of the current
evidence supporting cardiocerebral resuscitation in
the postarrest patient.
Critical Appraisal Of The Literature
A review of the literature between 1950 and 2011
was completed using Ovid MEDLINE®, PubMed,
Embase, and the Cochrane Database of Systematic
Reviews. Additionally, guidelines from the Ameri-
EMCC © 20122
can Heart Association and American College of
Emergency Physicians were reviewed.
An important consideration to this literature
is that the field of postresuscitation care is rapidly evolving, and there is limited opportunity for
informed-consent trials. Consequently, few randomized controlled trials are available, and much of the
clinical literature is extrapolated from other disease
states such as traumatic brain injury, hypothermic
circulatory support for cardiopulmonary bypass,
status epilepticus, and stroke care. Given the inherent difficulties of studying cardiac arrest, preclinical
data also influence clinical care of this disease. This
review reflects these issues and incorporates a broad
array of evidence sources.
Goals Of Postresuscitation Care
And Therapeutic Hypothermia
Cardiac arrest may be precipitated by many disease
states. Following resuscitation from cardiac arrest,
patients maintain their prearrest comorbidities along
with a global anoxic insult. The degree of injury may
range from mild to devastating. Moreover, different
organ systems demonstrate varying ranges of injury.
This results in heterogeneous physiology during the
postarrest phase. The main focus during the postarrest phase is to prevent secondary injury. The role
of therapeutic hypothermia to optimize neurologic
resuscitation and minimize organ system injury is
described below.
Neurologic Resuscitation
Persistent coma following cardiac arrest is the most
common reason for withdrawal of care in patients
successfully resuscitated from out-of-hospital
cardiac arrest.8,9 Neurologic resuscitation must
therefore be considered a top priority. Currently, the
cornerstone of neurologic resuscitation is the use
of therapeutic hypothermia. One mechanism for
therapeutic hypothermia’s effect is the decrease of
basal metabolic rate and oxygen consumption.10,11
Other hypothesized benefits include a decrease in
free radical production, modulation of inflammatory
response, and a decrease in intracranial pressure.12-14
Therapeutic hypothermia likely exerts its effect
through multiple mechanisms.
Therapeutic Hypothermia Evidence In VF/VT Out-OfHospital Cardiac Arrest
Two randomized controlled studies have demonstrated improved neurologic outcomes in subjects
receiving therapeutic hypothermia after resuscitation from ventricular fibrillation/ventricular tachycardia (VF/VT) out-of-hospital cardiac arrest.
In the first, a European multicenter randomized
controlled trial of postarrest hypothermia, subjects
were randomized to normothermia or treatment
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with therapeutic hypothermia to a goal temperature of 32°C to 34°C for a period of 24 hours. At 6
months, 55% (75/137) of subjects treated with therapeutic hypothermia had a good neurologic outcome,
compared with 39% (54/138) of subjects treated with
normothermia (relative risk [RR] = 1.40; 95% confidence interval [CI], 1.08-1.81). This yields a number
needed to treat of approximately 6; ie, for every 6
patients treated with therapeutic hypothermia, 1
additional patient would experience a good neurologic outcome. Mortality at 6 months was lower in
the therapeutic hypothermia group (41%; 56/137)
than in the normothermia group (55%; 76/138) (RR
= 0.74; 95% CI, 0.58-0.95).15
In the second randomized trial, 77 subjects
received either therapeutic hypothermia for 12 hours
at 32°C or normothermia. The rate of good neurologic outcome on hospital discharge was 49% in
the therapeutic hypothermia group and 26% in the
normothermia group.16
1.37-9.62).22 It is notable that most of the patients
in the study were inhospital arrests and that the
patients receiving therapeutic hypothermia were
more likely to require extracorporeal membrane oxygenation; the higher mortality in the cooled group
may reflect this. The Therapeutic Hypothermia After
Pediatric Cardiac Arrest (THAPCA) trial is an ongoing randomized controlled trial evaluating therapeutic hypothermia in children. It should be noted that
a number of centers currently employ therapeutic
hypothermia after pediatric arrest based on extrapolation from adult studies.
Blood Pressure Goals
Following resuscitation from cardiac arrest, cerebral
vasoregulation is compromised.23,24 Positron emission tomography studies demonstrate a decrease
in perfusion when the mean arterial blood pressure
(MAP) drops below 80 mm Hg in postarrest patients. Perfusion is restored when the scenario is reversed.25 Thus, many clinicians attempt to achieve a
target MAP of > 80 mm Hg.3-5,26 One theoretical concern is that therapeutic hypothermia may adversely
affect blood pressure. Recent data have shown that
the use of therapeutic hypothermia is not associated
with higher levels of vasopressor use.27
Therapeutic Hypothermia Evidence In Non-VF/VT
Cardiac Arrest
There are no randomized trials of non-VF/VT cardiac arrest patients; however, several observational studies have been conducted. One multicenter
study in 374 patients resuscitated from non-VF/
VT out-of-hospital cardiac arrest demonstrated
better neurologic outcomes in patients treated
with therapeutic hypothermia than in patients
treated with normothermia (odds ratio [OR] 1.84;
95% CI, 1.08-3.13).17 Stated in more practical
terms, the number needed to treat to improve outcomes was 6; ie, by treating 6 postarrest patients
with therapeutic hypothermia, 1 patient will have
benefit (on average). Two other cohort studies
failed to demonstrate a difference between therapeutic hypothermia and normothermia in the nonVF/VT population. In the first, therapeutic hypothermia was induced in 60% (261/437) of non-VF/
VT patients. Therapeutic hypothermia was not
associated with good neurological outcome at hospital discharge (OR 0.71; 95% CI, 0.37-1.36).18 The
second study, of 210 patients, demonstrated no
difference in outcomes between those treated with
therapeutic hypothermia or normothermia.19
Ventilatory Goals
In contrast to cerebral vasoregulation, cerebrovascular responsiveness to partial pressure of carbon
dioxide (PaCO2) remains intact during the postarrest phase.28 Hyperventilation results in cerebral
vasoconstriction and decreased preload to the left
ventricle due to pulmonary vasoconstriction. Hyperventilation may also result in increased intrathoracic
pressure and decreased preload to the right ventricle.29,30 Many patients resuscitated from cardiac
arrest exhibit cardiovascular compromise during
the postarrest period. Thus, hyperventilation may
adversely affect both neurologic and cardiovascular
systems. In many postresuscitation protocols, a goal
is to maintain a PaCO2 of 40 to 45 mm Hg to prevent
vasoconstriction.
Patient Selection
Given that postresuscitation care is geared toward
prevention of secondary neurologic injury, patients
with neurologic injury after resuscitation from
cardiac arrest are candidates for postresuscitation
care. As a practical matter, neurologic injury is
defined as not responding to commands (such as
“Wiggle your toes.” “Squeeze my fingers.”) – ie,
exhibiting a score of < 6 on the motor component of
the Glasgow Come Scale. Patients with preexisting
advanced directives (do not intubate or do not resuscitate orders) are generally excluded. Given the
multiple etiologies of cardiac arrest, the emergency
Therapeutic Hypothermia Evidence In Pediatric
Postarrest
There are a number of studies that support the use
of therapeutic hypothermia in the setting of perinatal hypoxic-ischemic injury,20,21 yet conclusive data
supporting this therapy following pediatric cardiac
arrest are currently lacking. One retrospective trial of
79 pediatric patients treated with either therapeutic
hypothermia or normothermia demonstrated a 3- to
4-fold higher 6-month mortality in patients treated
with therapeutic hypothermia (OR 3.62; 95% CI,
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EMCC © 2012
physician is charged with ruling out major hemorrhage as an etiology; most protocols exclude such
patients from therapeutic hypothermia consideration. Examples include intracranial hemorrhage,
active bleeding, and multisystem trauma. The
original trials excluded pregnancy, hypotension,
and non-VF/VT rhythms of arrest. Patients in each
of these categories have received postresuscitation care, including therapeutic hypothermia, with
varying success.31-33
Practical Considerations
For Postresuscitation Care
Coronary Angiography
Coronary disease remains the most common cause
for cardiac arrest. For patients with cardiac arrest,
an electrocardiogram (ECG) should be obtained
as soon as possible. In patients with ST-segment
elevation myocardial infarction (STEMI) or a new
left bundle branch block (LBBB), emergent catheterization is indicated.6,34,35 In patients without
these findings, emergent catheterization may
be considered in cases of VF/VT as the primary
rhythm of arrest or if the history is suggestive of
acute coronary syndromes (eg, antecedent chest
pain or shortness of breath). The risk of significant
coronary artery disease is large in this population,
regardless of primary rhythm of arrest.34
In a study evaluating 241 postarrest patients,
96 (40%) received coronary angiography. Comatose
patients were less likely to receive coronary angiography. Coronary lesions were found in 69% of these
patients, regardless of primary rhythm of arrest.
After controlling for confounders, patients who
received coronary angiography were more likely to
experience a good neurologic outcome than patients
who did not (OR 2.16; 95% CI, 1.12-4.19).34 However, there was no difference in outcome between
those who received angiography in the first 24 hours
postarrest and those who received later angiographic studies.
A second investigation, of 435 patients receiving coronary angiography immediately following
resuscitation from cardiac arrest, demonstrated
coronary lesions in 96% (128/134) of patients with
STEMI and in 58% (176/301) of patients without
STEMI. Successful angiography was predictive of
survival (OR 2.06; 95% CI, 1.16-3.66).36 Based on
these studies, it is appropriate to consider immediate coronary angiography for ST elevation or a
history suggesting acute coronary syndromes (eg,
chest pain prior to the arrest). Coronary angiography should be considered in patients without
an obvious extracardiac cause, as many patients
will be found to have critical coronary lesions that
warrant treatment.
EMCC © 20124
Point-Of-Care Ultrasonography
Point-of-care ultrasound can also aid in determining the etiology of the arrest. Focused abdominal
and cardiac ultrasound can evaluate for intraperitoneal blood, determine inferior vena cava size to
guide fluid resuscitation, and provide an estimate of
cardiac function.37,38 Global hypokinesis during the
first day following resuscitation from cardiac arrest
is common.39,40 New focal wall motion abnormality
would suggest acute coronary ischemia and should
prompt consideration for cardiac angiography.
Abnormal right ventricular size or function suggests
pulmonary embolism.
A significant proportion of postarrest patients
require aggressive fluid resuscitation and vasopressor administration. Consequently, many will require
central venous access and arterial access to titrate
vasopressor medications. Central venous access
also permits determination of central venous pressure (CVP) to help guide fluid resuscitation. Several
protocols recommend maintenance of CVP between
8 and 12 mm Hg.3-5,26 Although the evidence supporting the use of CVP monitoring in this setting remains unclear, consensus has grown that maintaining adequate volume is an important consideration.
As mentioned previously, titration of PaCO2
between 40 and 45 mm Hg or an end-tidal carbon
dioxide (ETCO2) of 35 to 40 mm Hg will prevent
hyperventilation and its effect on cerebral vasoconstriction. Determination of PaCO2 is dependent on temperature. Most facilities do not use
the alpha-stat analysis, a method that accounts
for temperature when determining PaCO2. Essentially, when the patient is at goal temperature, the
PaCO2 is 3 to 5 cm H2O lower than what is shown
by traditional arterial blood gas determination. As
a practical matter, many institutions consider this
error to be small enough that temperature correction is not used.
Computed Tomography Of The Brain
Intracranial hemorrhage or early cerebral edema
can be determined by computed tomography of the
brain. In one series, intracranial hemorrhage was
seen in 4% of postarrest patients and was the presumed etiology of the arrest.37 Early cerebral edema
has been associated with poor outcomes in several
studies.41,42
Induction Of Hypothermia
Many methods exist to induce hypothermia, but
they are generally classified as intravascular or
surface approaches. Intravascular methods include
rapid administration of cold (4°C) intravenous
fluids and the placement of an intravascular cooling
catheter. Surface cooling can be accomplished with
a variety of devices, such as evaporative cooling
using application of cool water and fans, ice packs
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in the groin and axillae, surface cooling blankets,
and surface cooling devices over the torso, head, and
legs. Pressure bag infusion of cold intravenous fluids
can reduce core temperature by > 2°C per hour and
may be the most economical method for induction of
hypothermia.
A recent observational study examining neurologic outcome in patients receiving either intravascular or surface cooling showed no difference in time to
achievement of hypothermia or neurologic outcome.43
and limited providers, bag-valve mask ventilation
may be appropriate, while longer transports would
necessitate the use of endotracheal intubation or a
supraglottic airway. Ventilation and oxygenation
should be focused on preventing further insult to the
brain from extremes of oxygen delivery or vasoconstriction. Oxygenation should be managed by
maintaining the oxygen saturation by pulse oximeter (SpO2) > 94% on the lowest fraction of inspired
oxygen (FiO2) possible. Continuous wave-form
ETCO2 should be used to confirm airway placement,
monitor the patient’s perfusion status, and monitor
PaCO2. In the absence of a blood gas, maintaining an
ETCO2 of 35 to 40 mm Hg should ensure adequate
ventilation and prevent cerebral vasoconstriction. In
patients who are unable to respond to verbal commands and who lack evidence of trauma or noncompressible bleeding, the induction of therapeutic
hypothermia should be considered. Simple measures for external cooling, including exposure and
ice packs, may be augmented with infusion of 4°C
saline. Sedation and analgesia may be necessary to
prevent shivering and to facilitate ventilator management. This can be accomplished with short-acting benzodiazepines (such as midazolam [Versed®])
and opiates (such as fentanyl [Sublimaze®]). Use of
these agents will depend on hemodynamic stability
and a protected airway. Ultimately, patients undergoing postarrest care will require transport to a facility capable of continuing hypothermia, providing
critical care services, and (when necessary) emergent
cardiac catheterization.
Prehospital Care
Prehospital Cerebral Resuscitation
Primary data to support prehospital interventions in
postarrest care are limited; however, some principles
can be abstracted from inhospital studies. Each
requires adaptation to the unique challenges of the
prehospital environment. One potential guideline
for prehospital providers is depicted in Figure 1.
In order to ensure adequate cerebral perfusion in
the injured brain, maintenance of an MAP of 80 mm
Hg has been suggested. For simplification in the prehospital environment, a systolic blood pressure goal
of at least 90 mm Hg may be employed. Arrhythmia
management postarrest should be limited to patients
with persistent ectopy or recurrent VF or VT.
Airway management may be deferred until after
return of spontaneous circulation (ROSC) so as not
to interfere with compressions. An appraisal of time
and resources should determine the most appropriate airway intervention. Given a short transport time
Figure 1. Guideline For Prehospital Treatment Of Patients Resuscitated From Cardiac Arrest
ROSC
Assess rhythm and perfusion. If SBP
< 90 mm Hg, initiate vasopressor.
Assess ventilation. Apply
capnograph and maintain ETCO2
of 35-40 mm Hg.
Assess oxygenation. Maintain SpO2
> 94% on lowest FiO2 setting.
Assess level of consciousness. If GCS
score < 8 and no contraindications,
initiate therapeutic hypothermia.
To initiate therapeutic hypothermia,
administer 20 cc/kg of 4°C saline.
Treat shivering or seizure with a
benzodiazepine.
Check glucose.
Assess 12-lead ECG. If STEMI,
administer aspirin and activate the
cardiac lab.
Transport to a cardiac arrest center.
Abbreviations: ECG, electrocardiogram; ETCO2, end-tidal carbon dioxide; FiO2, fraction of inspired oxygen; GCS, Glasgow Coma Scale; ROSC, return of spontaneous circulation; SBP, systolic blood pressure; SpO2, oxygen saturation by pulse oximeter; STEMI, ST-segment elevation myocardial
infarction.
Figure courtesy of Francis X. Guyette, MD and Jon Rittenberger, MD.
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EMCC © 2012
Prehospital Therapeutic Hypothermia
Equipoise exists in the decision to initiate hypothermia in the hospital or in the field. While there are no
definitive data, prehospital hypothermia began with
Bernard et al in their landmark 2002 paper where patients had hypothermia initiated by paramedics who
placed cold packs and exposed the patients’ skin.16
Further studies into prehospital cooling followed
and demonstrated feasibility and safety, culminating
in data suggesting that prehospital initiation of hypothermia leads to goal temperature 3 hours sooner
than cooling initiated in the emergency department
(ED) or intensive care unit (ICU).44-46 None of these
studies were designed to demonstrate a difference in
survival or neurologic outcome. Bernard et al carried
out a subsequent trial in which subjects were allocated to prehospital or hospital cooling based on day of
the month, and no difference in neurologic outcomes
at hospital discharge was demonstrated.47 Nonetheless, many systems have adopted or are in the
process of adopting prehospital therapeutic hypothermia induction as a relatively safe and potentially
useful component of a “system of care” approach to
postresuscitation treatment. Such a prehospital cooling approach would require hospitals to be prepared
to continue cooling in appropriate patients.
Clinical Course In The Emergency
Department
Stabilization
Stability can be short-lived in the postarrest patient,
making vigilance for deterioration essential. Before
presuming a patient to be stable in the ED after
arrest, a number of investigations should be carried out and closely interpreted. After vital signs
are obtained, an ECG to rule out ongoing ischemia,
point-of-care ultrasound to exclude other causes of
arrest (eg, intraperitoneal blood, pericardial effusion,
or abdominal aortic aneurysm), and blood work to
assess metabolic status should be carried out.
Continuous monitoring of the postarrest patient is necessary, as the incidence of re-arrest is
> 35%.48 Episodes of hypotension are also common
and appear to be associated with the duration of
arrest.49 Given these data, central venous access
and arterial line placement are prudent. Placement
of an ETCO2 on the ventilator circuit permits rapid
titration of tidal volume and respiratory rate for an
ETCO2 of 35 mm Hg. A decreasing serum lactate
can be a sign of a successful resuscitation, while
a persistently elevated lactate suggests pursuit of
ongoing ischemia or metabolic abnormality. Correction of acidosis may also improve the effectiveness
of many vasopressors.
EMCC © 20126
Deterioration
As noted previously, re-arrest is not uncommon.
This may be preceded by a decrease in ETCO2, a
dropping blood pressure, or an elevation of serum
lactate. In cases of cardiac ischemia, VF or VT may
be the primary rhythm of re-arrest. Given the high
incidence of coronary artery disease in the postarrest
population, it is reasonable to obtain a repeat ECG
following resuscitation from the re-arrest.34-36
Anticipated Pitfalls
A number of potentially untoward phenomena have
been observed during therapeutic hypothermia
treatment, including bradycardia, hypokalemia, and
QT prolongation. While poorly studied, these 3 effects of cooling are generally considered to be of little clinical consequence. Bradycardia in the setting of
relatively stable hemodynamics, for example, should
not serve as grounds to abort therapeutic hypothermia, and it generally reverses upon rewarming.
Special Circumstances
Hyperoxia
While hypoxia should be avoided, the effect of hyperoxia is less clear. One retrospective cohort of 6326
postarrest patients demonstrated an OR for death of
1.8 (95% CI, 1.5-2.2) in hyperoxic patients.50 Hyperoxia was defined as a PaO2 > 300 mm Hg on the first
arterial blood gas. A larger trial of 12,108 postarrest
patients evaluated the worst arterial blood gas during the first 24 hours after resuscitation and found
no survival difference between hyperoxic (PaO2
> 300 mm Hg) and normoxic (PaO2 of 60-300 mm
Hg) groups.51 Finally, a randomized trial of 28 patients failed to show a difference in survival between
those randomized to 30% or 100% FiO2 during the
first hour postarrest.52 In the context of these trials,
it is reasonable to titrate FiO2 to a pulse oximetry of
> 92%, with the goal of maintaining “normoxia.”
Pregnancy
Two case reports of hypothermia use in pregnant
patients exist. The first is a 35-year-old female who
suffered a witnessed VF out-of-hospital cardiac arrest. She was treated with therapeutic hypothermia.
The mother was discharged with good neurologic
outcome, and the baby demonstrated normal neurodevelopmental testing at birth and 2 months.31 In
the second report, the mother survived with good
neurologic outcome, while the fetus died.32
Coagulopathy
As core temperature decreases below 35°C, the enzymatic process of clotting is inhibited and platelet
function is less effective.53,54 While up to 20% of
patients treated with hypothermia may have some
bleeding, transfusion is rarely required.55 Several
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retrospective cohorts have suggested no difference
in the rate of bleeding between hypothermic and
normothermic postarrest patients.15,16,56 In patients
with active noncompressible bleeding, rewarming
to a core temperature of 35°C reverses hypothermiainduced coagulopathy.57
unknown if longer durations of cooling (> 24 h)
have a larger window of opportunity.
Continuous Electroencephalogram
Monitoring
Recent studies have demonstrated that a significant proportion of postarrest patients develop
seizures during the postarrest phase.63,64 Many of
these seizures are refractory to a single agent, and
outcomes are generally poor.65 Nonetheless, some
patients will experience good neurologic outcomes
despite development of seizures. Similarly, recent
outcomes in certain malignant electroencephalogram patterns classically associated with poor
neurologic outcome (ie, burst suppression) are
better than in prehypothermia-era literature.64 To
date, no trials have specifically evaluated postanoxic seizures; thus, it is unknown if aggressive
treatment or prophylaxis may improve outcomes.
Alternatively, seizures during the postarrest phase
may signify irreversible injury.
Controversies
Duration And Depth Of Cooling
The optimal duration and depth of cooling is
unknown. Bernard et al cooled subjects to a core
temperature of 32°C for 12 hours, with 49% experiencing good outcome.16 In the Hypothermia After
Cardiac Arrest (HACA) trial, subjects were cooled
for 24 hours to a core temperature of 34°C, with 55%
experiencing good outcomes.15 Animal data suggest that 1 hour of hypothermia is ineffective when
started after return of pulses.58,59 However, shorter
periods of cooling have shown benefit if the animal
was hypothermic when pulses returned. Neonatal
subjects with hypoxic-ischemic encephalopathy have
been cooled for up to 72 hours with good outcomes.
One case series used up to 72 hours of cooling for
severe postarrest brain injury.60 In summary, it
remains unclear whether longer or deeper cooling
would improve outcomes; further work in this area
is warranted. Until such time, the best available
data suggest that 24 hours duration of cooling (from
achievement of target temperature) is reasonable
and appropriate.
Performance Of Cardiac Catheterization
While Cooled
In common practice, cardiologists often express
reluctance to perform catheterization while a patient
is being treated with therapeutic hypothermia. No
data exist to suggest that there are additional risks
from this combination, and many hospitals that
routinely perform hypothermia have a coordinated
approach that includes cardiac catheterization during the process.
Time To Achievement Of Goal Temperature
Disposition
Preclinical data have shown that animals that are
hypothermic when ROSC occurs have excellent
outcomes even with short durations of cooling.59
Short durations of hypothermia are ineffective when
started after return of pulses.58,59 However, longer
durations of hypothermia have shown benefit when
initiated up to 12 hours after return of pulses.61
Clinical data evaluating time to achievement of
goal temperature and outcome are limited. Nielsen
et al reviewed 986 therapeutic hypothermia patients
and found a median time to achievement of goal
temperature (< 34°C) of 260 minutes (interquartile
range, 178-400). The time to goal temperature was
not associated with survival or good outcome.56
Wolff et al evaluated 49 consecutive patients
who received therapeutic hypothermia. Time to
goal temperature was not associated with neurologic outcome, but time to coldest temperature was
associated with neurologic outcome for every hour
delay to achievement of target temperature (OR
0.72; 95% CI, 0.56-0.94).62 The clinical significance
of achievement of coldest temperature is unclear.
These data suggest that there is a window of opportunity to induce and achieve target temperature
that is not longer than 12 hours after ROSC. It is
www.ebmedicine.net • Volume 2, Number 5
All postarrest patients will require ICU monitoring. Cardiac arrest patients are, by definition,
potentially unstable. Even those awake on hospital
arrival frequently experience a brief period of a
lethal arrhythmia and warrant close monitoring.
Some facilities may be unable to provide multidisciplinary postarrest care. In these cases, transfer to
a facility with more extensive postarrest resources
may be the best option.
Additional Considerations To Improve
Cardiac Arrest Outcomes
It is important to note that postarrest care does not
exist in isolation. It is unlikely that postarrest care
alone will substantially improve outcomes from
cardiac arrest; thus, a system of care is necessary to
optimize outcomes. This system includes the prehospital setting, ED, ICU, inpatient ward, and rehabilitation unit. Advanced systems optimize care in each
location in order to improve outcomes.
7
EMCC © 2012
Summary
Must-Do Markers Of Quality Care
Cardiac arrest is a common cause of death and
neurologic injury. A system of care that includes aggressive postresuscitation care is needed to optimize
outcomes in this population. Early, aggressive care
that begins in the ED and includes consideration
for therapeutic hypothermia, evaluation for reversible etiologies or reasons to exclude cooling (such as
hemorrhage), prompt revascularization, and prevention of secondary insults represents the current best
practice for these complex patients.
Interdisciplinary
Case Conclusion
Given the high incidence of coronary artery disease in
patients successfully resuscitated from cardiac arrest, you
order the patient to be transferred to your facility and a
supraglottic airway to be placed by the paramedics. You
find out that the EMS team is not prepared to perform
prehospital cooling, but you prepare to induce therapeutic hypothermia upon her arrival. In the ED, the patient
demonstrated an acute STEMI on ECG. (See Figure 2.)
She was emergently taken to the catheterization laboratory where she received a bare metal stent to the proximal
left anterior descending artery and intra-aortic balloon
pump placement for mechanical support. An endotracheal
tube was placed, and she was cooled for 24 hours and
rewarmed over a period of 16 hours, following the hospital
protocol for therapeutic hypothermia induction, maintenance, and rewarming. She awakened on hospital day 1
following rewarming and was weaned from the balloon
pump on hospital day 4. She returned home on hospital
day 14 and returned to work within 2 months.
Figure 2. Postresuscitation
Electrocardiogram Demonstrating Acute STSegment Elevation Myocardial Infarction
1. Develop a therapeutic hypothermia and postarrest care protocol and plan to perform quality
assurance in this complex patient population.
2. Involve cardiology and critical care staff in the
hospital postarrest care protocol to coordinate
transfer between the ED, the catheterization
laboratory, and/or the ICU.
In The Emergency Department
1. Perform a complete baseline neurologic examination prior to sedation and paralysis (when
possible) to evaluate coma severity.
2. Obtain a rapid ECG to evaluate for STEMI or
new LBBB as the etiology for cardiac arrest.
3. Titrate MAP to > 80 mm Hg to optimize cerebral
perfusion.
4. Titrate ventilation for PaCO2 of 40 to 45 mm Hg
to prevent cerebral vasoconstriction.
5. Consider therapeutic hypothermia and/or
transfer to a facility that is capable of providing
goal-oriented postarrest care, including therapeutic hypothermia and consideration of cardiac
catheterization.
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. Figure courtesy of Jon Rittenberger, MD and Francis X. Guyette, MD.
EMCC © 20128
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JAMA. 2008;24(12):1423-1431. (Prospective observational
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3.* Sunde K, Pytte M, Jacobsen D, et al. Implementation of
a standardized treatment protocol for post resuscitation
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survivors of cardiac arrest. Resuscitation. 2008;79(2):198-204.
(Retrospective review; 241 patients)
5. Gaieski DF, Band RA, Abella BS, et al. Early goal-directed
www.ebmedicine.net • Volume 2, Number 5
hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation. 2009;80(4):418-424. (Case control; 20 cases)
6.* Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest
syndrome: epidemiology, pathophysiology, treatment and
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7.* Peberdy MA, Callaway CW, Neumar RW, et al. Part 9:
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when therapeutic hypothermia is added to post-cardiac arrest care. Resuscitation. 2011;82(9):1168-1173. (Retrospective
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21. Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicenter randomized trial. Lancet. 2005;365(9460):663670. (Randomized controlled trial; 234 subjects)
22. Doherty DR, Parshuarm CS, Gaboury I, et al. Hypothermia therapy after pediatric cardiac arrest. Circulation.
2009;119(11):1492-1500. (Retrospective study; 79 patients)
23. Nishizawa H, Kudoh I. Cerebral autoregulation is impaired
in patients resuscitated after cardiac arrest. Acta Anaesthesiol
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of cerebral blood flow in patients resuscitated from cardiac
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arrest. Stroke. 2001;32(1):128-132. (Case series; 18 patients, 6
volunteers)
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and metabolism in resuscitated patients with severe posthypoxic encephalopathy. J Neurol Sci. 2003;210(1-2):23-30.
(Case series; 8 patients)
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Huynh N, Kloke J, Gu C, et al. The effect of hypothermia
“dose” on vasopressor requirements and outcome after cardiac arrest. Resuscitation. 2012 Jun 26. [Epub ahead of print].
(Retrospective review; 361 comatose postarrest patients)
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during mild hypothermia after cardiac arrest. Crit Care Med.
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Buunk G, van der Hoeven JG, Meinders AE. Cerebrovascular
reactivity in comatose patients resuscitated from a cardiac
arrest. Stroke. 1997;28(8):1569-1573. (Observational study; 10
patients)
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resuscitation. Circulation. 2004;109(16):1960-1965. (Observational study; 13 subjects)
Rittenberger JC, Kelly E, Jang D, et al. Successful outcome
utilizing hypothermia after cardiac arrest in pregnancy:
a case report. Crit Care Med. 2008;36(4):1354-1356. (Case
report)
Wible EF, Kass JS, Lopez GA. A report of fetal demise during
therapeutic hypothermia after cardiac arrest. Neurocrit Care.
2010;13(2):239-242. (Case report)
Hovdenes J, Laake JH, Aaberge L, et al. Therapeutic
hypothermia after out-of-hospital cardiac arrest: experiences with patients treated with percutaneous coronary
intervention and cardiogenic shock. Acta Anaesthesiol Scand.
2007;51(2):137-142. (Retrospective review; 50 cardiac arrest
patients, 23 of which received intra-aortic balloon counterpulsation support)
Reynolds JC, Callaway CW, El Khoudary SR, et al. Coronary
angiography predicts improved outcome following cardiac
arrest: propensity-adjusted analysis. J Intensive Care Med.
2009;24(3):179-186. (Retrospective review; 241 patients)
Spaudling CM, Joly LM, Rosernberg A, et al. Immediate
coronary angiography in survivors of out-of-hospital cardiac
arrest. N Engl J Med. 1997;336(23):1629-1633. (Retrospective
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Dumas F, Cariou A, Manzo-Silberman S, et al. Immediate
percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest. Circulation.
2010;3(3):200-207. (Retrospective review; 435 patients)
Jones AE, Tayal VS, Sullivan DM, et al. Randomized,
controlled trial of immediate versus delayed goal-directed
ultrasound to identify the cause of nontraumatic hypotension in emergency department patients. Crit Care Med.
2004;32(8):1703-1708. (Randomized controlled trial; 184
subjects)
Moore CL, Copel JA. Point-of-care ultrasonography. N Engl J
Med. 2011;364(8):749-757. (Review article)
Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial
dysfunction in survivors of out-of-hospital cardiac arrest.
J Am Coll Cardiol. 2002;40(12):2110-2116. (Retrospective
review; 73 patients)
Ruiz-Bailén M, Aguayo de Hoyos E, Ruiz-Navarro S, et al.
Reversible myocardial dysfunction after cardiopulmonary
resuscitation. Resuscitation. 2005;66(2):175-181. (Case series;
29 patients)
Metter RB, Rittenberger JC, Guyette FX, et al. Association
between a quantitative CT scan measure of brain edema and
outcome after cardiac arrest. Resuscitation. 2011;82(9):11801185. (Retrospective review; 240 patients)
EMCC © 2012
42. Torbey MT, Selim M, Knorr J, et al. Quantitative analysis
of the loss of distinction between gray and white matter in
comatose patients after cardiac arrest. Stroke. 2000;31(9):21632167. (Retrospective review; 25 patients)
43. Tømte Ø, Drægni 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.
(Retrospective review; 167 patients)
44. Virkkunen I, Yli-Hankala A, Silfvast T. Induction of
therapeutic hypothermia after cardiac arrest in prehospital
patients using ice-cold Ringer’s solution: a pilot study. Resuscitation. 2004;62(3):299-302. (Case series; 13 patients)
45. Kim F, Olsufka M, Longstreth WT, et al. Pilot randomized
clinical trial of prehospital induction of mild hypothermia in
out-of-hospital cardiac arrest patients with a rapid infusion
of 4 degrees C normal saline. Circulation. 2007;115(24):30643070. (Randomized controlled trial; 125 subjects)
46. Kamarainen A, Virkkunen I, Tenhunen J, et al. Prehospital
therapeutic hypothermia for comatose survivors of cardiac
arrest: a randomized controlled trial. Acta Anaesthesiol Scand.
2009;53(7):900-907. (Randomized controlled trial; 37 subjects)
47. Bernard SA, Smith K, Cameron P, et al. Induction of
therapeutic hypothermia by paramedics after resuscitation
from out-of-hospital ventricular fibrillation cardiac arrest: a
randomized controlled trial. Circulation. 2010;122(7):737-742.
(Randomized controlled trial; 234 subjects)
48. Salcido DD, Stephenson AM, Condle JP, et al. Incidence of
rearrest after return of spontaneous circulation in out-of-hospital cardiac arrest. Prehosp Emerg Care. 2010;14(4):413-418.
(Retrospective review; 1199 patients)
49. Menegazzi JJ, Ramos R, Wang HE, et al. Post-resuscitation
hemodynamics and relationship to the duration of ventricular fibrillation. Resuscitation. 2008;78(3):355-358. (Animal
study)
50. 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):21652171. (Retrospective review; 6326 patients)
51. Bellomo R, Bailey M, Eastwood GM, et al. Arterial hyperoxia
and in-hospital mortality after resuscitation from cardiac arrest. Crit Care. 2011;15(2):R90. (Retrospective review; 12,108
patients)
52. Kuisma M, Boyd J, Voipio V, et al. Comparison of 30 and the
100% inspired oxygen concentrations during early postresuscitation period: a randomized controlled pilot study.
Resuscitation. 2006;69(2):199-206. (Randomized controlled
trial; 60 subjects)
53. Michelson AD, MacGregor H, Barnard MR, et al. Reversible
inhibition of human platelet activation by hypothermia in
vivo and in vitro. Thromb Haemost. 1994;71(5):633-640. (Volunteer study)
54. Reed RL, Bracey AW Jr, Hudson JD, et al. Hypothermia and
blood coagulation: dissociation between enzyme activity and
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55. Jarrah S, Dziodzio J, Lord C, et al. Surface cooling after
cardiac arrest: effectiveness, skin safety, and adverse events
in routine clinical practice. Neurocrit Care. 2011;14(3):382-388.
(Retrospective review; 69 patients)
56. Nielsen N, Hovdenes J, Nilsson F, et al. Outcome, timing and
adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest. Acta Anaesthesiol Scand. 2009;53(7):926934. (Retrospective review; 986 patients)
57. Valeri CR, Feingold H, Cassidy G, et al. Hypothermiainduced reversible platelet dysfunction. Ann Surg.
1987;205(2):175-181. (Animal study)
58. 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, ran-
EMCC © 201210
59. 60. 61. 62. 63. 64. 65.
domized study. Crit Care Med. 1993;21(9):1348-1358. (Animal
study; 22 dogs)
Zhao D, Abella BS, Beiser DG, et al. Intra-arrest cooling with
delayed reperfusion yields higher survival than earlier normothermic resuscitation in a mouse model of cardiac arrest.
Resuscitation. 2008;77(2):242-249. (Animal study; 45 rats)
Nagao K, Kikushima K, Watanabe K, et al. Early induction
of hypothermia during cardiac arrest improves neurological outcomes in patients with out-of-hospital cardiac arrest
who undergo emergency cardiopulmonary bypass and
percutaneous coronary intervention. Circ J. 2010;74(1):77-85.
(Retrospective review; 171 patients)
Coimbra C, Wieloch T. Moderate hypothermia mitigates
neuronal damage in the rat brain when initiated several
hours following transient cerebral ischemia. Acta Neuropathol. 1994;87(4):325-331. (Animal study; 20 rats)
Wolff B, Machill K, Schumacher D, et al. Early achievement
of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest. Int J Cardiol. 2009;133(2):223-228.
(Retrospective review; 49 patients)
Abend NS, Topjian A, Ichord R, et al. Electroencephalographic monitoring during hypothermia after pediatric
car44. Salcido DD, Stephenson AM, Condle JP, et al.
Incidence of rearrest after return of spontaneous circulation in out-of-hospital cardiac arrest. Prehosp Emerg Care.
2010;14(4):413-418. (Retrospective review; 1199 patients)
Rittenberger JC, Popescu A, Guyette FX, Callaway CW.
Frequency and timing of nonconvulsive status epilepticus in
comatose post-cardiac arrest subjects treated with hypothermia. Neurocrit Care. 2012;16(1):114-122. (Retrospective
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CME Questions
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1. The most common reason for withdrawal of
care in patients successfully resuscitated from
out-of-hospital cardiac arrest is:
a. Persistent coma
b. Heart failure
c. Renal failure requiring dialysis
d. Overwhelming sepsis
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2. Randomized controlled trials have shown
improved neurologic benefit for therapeutic
hypothermia in:
a. Pulseless electrical activity
b. Asystole
c. VF/VT
d. Sepsis
e. A, B, and C
3. Regarding therapeutic hypothermia in the
pediatric population:
a. Studies have shown definite benefit.
b. Studies have shown definite harm.
c. One retrospective study showed a lower 6-month mortality in pediatric patients treated with therapeutic hypothermia.
d. Many centers employ therapeutic hypothermia in pediatric patients based on data extrapolated from adult populations.
4. The suggested MAP that should be maintained
after cardiac arrest is stated as:
a. > 110 mm Hg
b. > 100 mm Hg
c. > 90 mm Hg
d. > 80 mm Hg
e. > 65 mm Hg
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a. Of those with a STEMI, only a minority
were found to have coronary lesions.
b. A significant percentage were found to have coronary lesions, regardless of the primary rhythm of arrest.
c. Coronary angiography should not be considered in those without VF/VT arrest.
d. Emergent cardiac catheterization is not indicated in patients with new LBBB.
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6. Regarding methods to achieve core body temperature in induction of hypothermia, which of
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d. Intravascular cooling is more effective when performed early, and surface cooling is more effective when performed later.
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EMCC © 201212
www.ebmedicine.net • Volume 2, Number 5