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Post Cardiac Arrest - Adult - Emergency Department/Inpatient

Post Cardiac Arrest - Adult - Emergency Department/Inpatient - Clinical Hub, UW Health Clinical Tool Search, UW Health Clinical Tool Search, Clinical Practice Guidelines, Cardiovascular


1
Post Cardiac Arrest – Adult –
Emergency Department/Inpatient
Clinical Practice Guideline
Note: Active Table of Contents – Click to follow link
EXECUTIVE SUMMARY ........................................................................................................... 3
SCOPE ................................................................................................................................... 4
METHODOLOGY .................................................................................................................... 5
INTRODUCTION ..................................................................................................................... 6
RECOMMENDATIONS ............................................................................................................ 6
Targeted Temperature Management (TTM) ....................................................... 6
Identify and Treat the Etiology of the Arrest ....................................................... 8
Optimize Mechanical Ventilation to Minimize Lung Injury .................................. 9
Reduce the Risk of Multi-organ Injury & Support Organ Function .................... 10
Hemodynamic Support .......................................................................................................... 10
Blood Glucose Control ............................................................................................................ 11
Metabolic Considerations ...................................................................................................... 11
Central Nervous System Support ........................................................................................... 12
Rewarm Slowly ................................................................................................. 12
Prognostication of Neurological Outcome ........................................................ 13
Organ Donation ................................................................................................ 14
TABLE 1. POST-CARDIAC ARREST SYNDROME: PATHOPHYSIOLOGY, CLINICAL
MANIFESTATIONS, AND POTENTIAL TREATMENTS ............................................................... 15
UW HEALTH IMPLEMENTATION ........................................................................................... 16
APPENDIX A. EVIDENCE GRADING SCHEME(S) ...................................................................... 17
UW HEALTH TARGETED TEMPERATURE MANAGEMENT (TTM) COOLING PRODUCTS ............ 19
POST CARDIAC ARREST THERAPEUTIC TARGETED TEMPERATURE MANAGEMENT (TTM) CARE
ALGORITHM ........................................................................................................................ 20
REFERENCES ........................................................................................................................ 21
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2
CPG Authors and Contact:
1DPH���$QQH�0��2¶&RQQRU��0'�- Cardiology
Phone Number: (608) 262-1497
Email address: aoconnor@medicine.wisc.edu
Name: Matthew C. Tattersall, DO - Cardiology
Phone Number: (608) 265-9947
Email address: mtattersall@medicine.wisc.edu
CPG Contact for Changes:
Name: Lindsey Spencer, MS- Center for Clinical Knowledge Management (CCKM)
Phone Number: (608) 890-6403
Email address: lspencer2@uwhealth.org
Coordinating Team Members:
Rama Maganti, MD ± Neurology ± General
Joshua E. Medow, MD- Neurological Surgery ± General
Pierre Kory, MD- Medicine- Pulmonary Medicine
Jeffrey E. Wells, MD- Medicine- Pulmonary
Laura Hammel, MD- Anesthesia- General
Amish Raval, MD- Medicine- Cardiology
Giorgio Gimelli, MD- Medicine- Cardiology
Sarah Ahrens, MD- Medicine- Hospitalists
Haleh VanVliet, MD- Emergency Medicine- General
Michael Safa, MD- Emergency Medicine- General
Stephanie Kraus, MS, RN, CCRN- Cardiology
Jayne McGrath, CNS- Emergency Medicine
Anna Krupp, MS, RN, CCNS, CCRN ± Trauma Life Support (TLC)
Peter Rusch, RT- Respiratory Therapy
Paula Breihan, RT- Respiratory Therapy
Jennifer Lai, PharmD, BCPS- Pharmacy- Inpatient Services
Carin Endres, PharmD- Pharmacy- Drug Policy Program
Jennifer Grice, PharmD, BCPS- Center for Clinical Knowledge Management (CCKM)
Review Individual/Bodies:
Teresa Darcy, MD ± Pathology- General
Committee Approvals/Dates:
Clinical Knowledge Management (CKM) Council (Last Periodic Review: 08/25/2016)
Release Date: August 2016 | Next Review Date: August 2018
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3


Executive Summary
Guideline Overview
This guideline is based on the 2015 AHA Guidelines Update for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care (Part 8: Post-Cardiac Arrest Care)1, the 2010 American
Heart Association (AHA) Guidelines for CPR and Emergency Cardiovascular Care (Part 9: Post
Cardiac Arrest Care)2, and the 2013 AHA Consensus Statement that addresses Strategies for
Improving Survival After In-Hospital Cardiac Arrest in the United States (section highlighting
Post Arrest Care).3

Key Revisions (2016 Periodic Review)
1. Modified inclusion criteria and removed exclusion of patients with suspected non-cardiac
primary etiology for comatose state
2. Added recommendation against routine prehospital cooling.
3. Added reference to the Bedside Shivering Assessment Scale and options to treat shivering.
4. Clarified recommended interventions for patients with STEMI vs. non ST elevation acute
coronary syndromes.
5. Remove recommendation for MAP target of 80-100 mmHg.
6. Added recommendations against prognostication of neurological outcomes prior to 72 hours
after discontinuation of sedation and return to normothermia. Education was also included
regarding delayed awakening.
7. Specific options for neurological assessment were added.

Key Practice Recommendations
1. Routine prehospital cooling of patients after ROSC with rapid infusion of cold intravenous
fluids is NOT recommended.1 (AHA Class III, LOE A)
2. Surface cooling should be initiated immediately following determination that a patient is a
candidate for targeted temperature management (i.e., considerations of exclusion criteria
and non-contrasted computed tomography (CT) of the head has been performed). (UW
Health Class I, LOE B)
3. A non-enhanced CT scan can provide information about structural lesions, stroke, or
intracranial hemorrhage that may have contributed to cardiac arrest. This should be
obtained prior to TTM induction.2,3 (AHA Class I, LOE C-LD)
4. A 12-lead electrocardiogram (ECG) should be obtained as soon as possible after ROSC to
determine whether acute ST segment elevation is present.2 (AHA Class I, LOE B)
5. Aggressive treatment of ST-segment elevation myocardial infarction (STEMI) should begin
as in non±cardiac arrest patients, regardless of coma or induced hypothermia.1,3 (AHA Class
IIa, LOE C-LD)
6. Patients with ventricular fibrillation (VF) or ventricular tachycardia (VT) arrest and shockable
rhythm on presentation should be strongly considered for emergent coronary angiography
due to the benefits demonstrated in the Parisian Registry.4 (UW Health Class IIb, LOE B-NR)
The decision to proceed with coronary angiography should be made with discussion with the
interventional cardiologist, and after weighing the potential risks and benefits of the
procedure.
7. Therapeutic hypothermia (cooled to 32°C to 36°C (AHA Class I, LOE B-R) for at least 24
hours (AHA Class IIa, LOE C-EO))1 for neurologic protection is recommended in the following
patient groups with sudden and unexpected cardiac arrest, that remain comatose (i.e. lack
of meaningful response to verbal commands), and are without exclusion criteria: Return of
spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation (VF)/pulseless
ventricular tachycardia (pVT) arrest1 (AHA Class I, LOE B-R); ROSC after in-hospital cardiac
arrest of any initial rhythm1 (AHA Class I, LOE C-EO); ROSC after out-of-hospital cardiac
arrest non-9)�S97��L�H���³QRQVKRFNDEOH´��1 (AHA Class I, LOE C-EO) The treated goal
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4


temperature is a clinical decision left up to the discretion of the treating clinician on a case-
by-case basis, and may be influenced by specific clinical features or the initial temperature
of the patient.1,5 (UW Health Class IIb, LOE C)
8. Rewarming should occur at 0.25º C per hour.2,6 (UW Health Class I, LOE C)
9. The earliest time to prognosticate a poor neurologic outcome in patients not treated with
TTM is 72 hours after cardiac arrest.1 (AHA Class I, LOE B-NR) The time until prognostication
can be even longer than 72 hours after cardiac arrest if the residual effect of sedation or
paralysis confounds the clinical exam.1 (AHA Class IIa, LOE C-LD)
10. Adult patients who progress to brain death after resuscitation from cardiac arrest should be
evaluated for organ donation.1,3 (AHA Class IIb, LOE B-NR)

Companion Documents
1. Post ±Cardiac Arrest Therapeutic Targeted Temperature Management (TTM) Care
Algorithm
2. Post Cardiac Arrest Syndrome: Pathophysiology, Clinical Manifestations, and Potential
Treatments
3. Continuous Infusion Neuromuscular Blocking Agents (NMBAs) ± Adult ± Inpatient Guideline
4. Assessment and Treatment of Pain, Agitation, and Delirium in the Mechanically Ventilated
Intensive Care Unit Patient Guideline
5. Venous Thromboembolism Prophylaxis ± Adult ± Inpatient/Ambulatory Guideline
6. Vasoactive Continuous Infusions in Adult Patients ± Adult ± Inpatient Guideline
7. Wisconsin Insulin Infusion (HIGH DOSE) - Adult- Practice Protocol (ICU ONLY)

External Resources
1. Strategies for Improving Survival After IN-Hospital Cardiac Arrest in the United States:
Consensus Recommendations: A Consensus Statement from the AHA (2013)
http://circ.ahajournal.org/content/127/14/1538

Scope
Disease/Condition(s): Out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest
(IHCA)

Clinical Specialty: Emergency Medicine, Cardiology, Critical Care

Intended Users: Physicians, Advanced Practice Providers, Nurses, Pharmacists

Objective(s): To provide recommendations for the care of OHCA and IHCA patients which
have the potential to improve long-term patient outcomes (e.g., mortality, neurological function).

Target Population: Patients age 18 years and older whom have suffered an out-of-hospital
(OHCA) or in-hospital (IHCA) cardiac arrest.

Interventions and Practices Considered:
ξ Targeted Temperature Management (TTM)
ξ Optimization of hemodynamics and gas exchange
ξ Immediate coronary reperfusion when indicated for restoration of coronary blood flow with
percutaneous coronary intervention
ξ Glycemic control
ξ Neurologic diagnosis, management, and prognostication
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Major Outcomes Considered:
ξ Sudden cardiac death
ξ Survival
ξ Morbidity
ξ Neurological recovery
ξ Quality of life
Methodology
Methods Used to Collect/Select the Evidence:
Electronic database searches (e.g., PUBMED) were conducted by the guideline author(s) and
workgroup members to collect evidence for review. Expert opinion and clinical experience were
also considered during discussions of the evidence.

Methods Used to Formulate the Recommendations:
The workgroup members agreed to adopt recommendations developed by external
organizations and/or arrived at a consensus through discussion of the literature and expert
experience. All recommendations endorsed or developed by the guideline workgroup were
reviewed and approved by other stakeholders or committees (as appropriate).

Methods Used to Assess the Quality of the Evidence/Strength of the Recommendations:
Recommendations developed by external organizations maintained the evidence grade
assigned within the original source document and were adopted for use at UW Health.

Internally developed recommendations, or those adopted from external sources without an
assigned evidence grade, were evaluated by the guideline workgroup using an algorithm
adapted from the Grading of Recommendations Assessment, Development and Evaluation
(GRADE) methodology (see Figure 1 in Appendix A).

Rating Scheme for the Strength of the Evidence/Recommendations:
See Appendix A for the rating scheme(s) used within this document.

Recognition of Potential Health Care Disparities:
Regional disparities in survival after out-of-hospital cardiac arrest exist within North America.7
Early arrest recognition, bystandeU�WUDLQLQJ�LQ�&35�DQG�WKH�XVH�RI�$('��HIILFLHQW�³���´�
activation, and high quality of EMS care are all variables which can improve survival rates.7 King
County in Washington has more than doubled their survival rates for bystander-witnessed
cardiac arrest caused by ventricular fibrillation since 2002 after implementing community
practices, such as increasing the availability of AEDs, mass CPR training to the public, and the
provision of CPR instructions by the 911 dispatcher.

Alternatively, a retrospective analysis of all patients suffering from a cardiac arrest between
2003 to 2012, found that women were less likely to undergo therapeutic procedures (e.g.,
coronary angiography) and targeted temperature management.8 Rates of in-hospital mortality
were also higher in women than men.8 Provider should remain cognizant of these disparities
and provide equal treatment to all patients.

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Introduction
Cardiac arrest results in 300,000 deaths per year in North America. Out-of-hospital cardiac
arrest (OHCA) is a challenging condition with an in-hospital mortality rate of over 50%
worldwide. In-hospital cardiac arrest (IHCA) is estimated to occur at a rate of 6.65 patients per
1,000 adult hospital admissions, with only 18% of patients surviving to discharge and only 6.6%
of patients surviving at 1 year.3

Post cardiac arrest syndrome is sequelae of cardiac arrest with systemic manifestations. The
key components include (1) post-arrest brain injury, (2) post-arrest myocardial dysfunction, (3)
systemic ischemia/reperfusion response, and (4) persistent acute and chronic pathology that
precipitated the event (Table 1).3,9 There is increasing recognition that systematic post-cardiac
arrest care after return of spontaneous circulation (ROSC) can improve the likelihood of survival
with good quality of life.

The 2010 and 2015 AHA Post Cardiac Arrest Care Guidelines served as an outline to this
document.1,2 The clinical trials and data in regards to the care of cardiac arrest patient is not as
vigorous as other cardiovascular disease processes (Acute Coronary Syndromes and
Congestive Heart Failure); thus, the guideline workgroup has chosen to include some IIa and IIb
level of evidence recommendations.
Recommendations
Targeted Temperature Management (TTM)

Patient Eligibility
Therapeutic hypothermia (cooled to 32°C to 36°C (AHA Class I, LOE B-R) for at least 24 hours
(AHA Class IIa, LOE C-EO))1 for neurologic protection is recommended in the following patient
groups with sudden and unexpected cardiac arrest, that remain comatose (i.e. lack of
meaningful response to verbal commands), and are without exclusion criteria:
ξ Return of spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation
(VF)/pulseless ventricular tachycardia (pVT) arrest.1 (AHA Class I, LOE B-R)
ξ ROSC after in-hospital cardiac arrest of any initial rhythm.1 (AHA Class I, LOE C-EO)
ξ ROSC after out-of-hospital cardiac arrest non-9)�S97��L�H���³QRQVKRFNDEOH´��1 (AHA Class I,
LOE C-EO)

The treated goal temperature is a clinical decision left up to the discretion of the treating
clinician on a case-by-case basis, and may be influenced by specific clinical features or the
initial temperature of the patient.1,5 (UW Health Class IIb, LOE C) Data from a major RCT suggests
that a higher temperature goal of 36ºC may confer the same neurologic benefit in some
circumstances.10 The TTM trial compared 33ºC to 36ºC and is notable for the high rate of
bystander cardiopulmonary resuscitation (CPR) and for the short emergency medical services
(EMS) transport times in both groups. The higher goal temperature of 36ºC may be more
appropriate for patients that were previously thought to not be candidates for TTM or for whom
lower temperatures convey some risk (e.g., recent trauma, bleeding concerns, or hemodynamic
instability).1 Lower temperatures might be preferred when patients have clinical features which
are worsened by higher temperatures (e.g., seizures, cerebral edema).1

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Active or rapid rewarming should be avoided in comatose patients who spontaneously develop
a mild degree of hypothermia (> 32°C) after resuscitation from cardiac arrest during the first 48
hours after ROSC.1,2 (AHA Class III, LOE C)

Recommended Exclusion Criteria
Targeted temperature management is not recommended for patients who meet the following
exclusion criteria:
ξ > 12 hours since return of spontaneous circulation (ROSC)
ξ Motor component of Glasgow Coma Scale score > 5 (i.e., patient completes purposeful
movement)
ξ Minimal pre-morbid functional status (e.g., advanced dementia, metastatic cancer)
ξ Sepsis as cause of arrest
ξ Do Not Resuscitate (DNR) status
ξ Core body temperature < 30ºC

Note: If intracranial process present, contact Neurosurgery for a decision of the type of cooling
and goal temperature, as these patients were excluded from many of the mild hypothermia post
cardiac arrest clinical trials.10,11

Pregnancy is a unique circumstance in post cardiac arrest care. A pregnancy test should be
performed in all women of childbearing age. (UW Health Class I, LOE A) There are reports of TTM
being used as a successful therapy in pregnant women who have suffered a cardiac arrest.12,13
The decision to use TTM in a pregnant patient should be made in the context of the entire
clinical picture and in consultation with Obstetrics. (UW Health Class IIb, LOE C)

Systemic Cooling
Providers should closely monitor patient core temperature after ROSC.2 (AHA Class I, LOE C) A
tympanic membrane temperature should be assessed immediately following patient
presentation. Two temperature sources should be evaluated (one tympanic, and one either
through an esophageal probe or a urinary probe).2,3 Throughout TTM initiation, maintenance,
and rewarming, temperature should be monitored continuously via esophageal, bladder, or
rectal sources.2

Systemic cooling can occur via two mechanisms (see Appendix B for available equipment):
1. Surface cooling with cooling blankets/ hypothermic wraps
2. Intravascular cooling.

Surface cooling should be initiated immediately following determination that a patient is a
candidate for targeted temperature management (i.e., considerations of exclusion criteria and
non-contrasted computed tomography (CT) of the head has been performed). (UW Health Class
I, LOE B) There is a 20% increase in mortality for every hour of delay in TTM initiation.14
Therefore, early communication with the accepting Critical Care service should occur, allowing
for a decision on cooling method and core temperature goal.
Routine prehospital cooling of patients after ROSC with rapid infusion of cold intravenous fluids
is NOT recommended.1 (AHA Class III, LOE A) However, intravascular cooling may be initiated
upon arrival to the Emergency Department or inpatient admission. A prototype of the catheter
used at UW Health is the Zoll Quattro® catheter. This catheter is both a triple lumen central
venous access for medication and fluid delivery, and also contains heat exchange balloons to
allow for systemic body temperature modification. The Quattro® contains 4 heat exchange
balloons which increases the surface area for cooling and is the longest heat exchange catheter
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PDGH�E\�=ROO�DW����FP��+RZHYHU��LW�LV�LPSHUDWLYH�WR�FRQVLGHU�WKH�SDWLHQW¶V�ERG\�VL]H�LQ�VHOHFWLQJ�
a cooling catheter, as smaller body sizes may not be amendable to Quattro® placement and use
of a shorter catheter may be best. Once the intravascular cooling catheter has been placed
appropriately in the femoral vein, cooling can commence. For additional details, see UWHC
Department Policy 1.42AP.

In the interim while placing the catheter, it is up to the discretion of the clinician as to the
concomitant use of other temporary methods of cooling, such as external ice wraps or cold
saline.

Shivering and Neuromuscular Blockades
The Bedside Shivering Assessment Scale (BSAS) may be performed to objectively document
the degree of shivering. (UW Health Class IIb, LOE C) If shivering poses a barrier to achieving the
goal body temperature, consideration for pharmacologic interventions should be entertained.
(UW Health Class I, LOE B)

Various pharmacologic protocols have been created to mitigate the effects of shivering15-17
Acetaminophen has been shown to lower hypothalmic set point.18,19 (UW Health Class IIa, LOE B)
Buspirone and meperidine can synergistically reduce the shivering threshold as well.20,21 (UW
Health Class IIb, LOE B) Magnesium peripherally vasodialates and improves comfort and cooling
rates during hypothermia.22 (UW Health Class IIb, LOE C) Analagosedation, which is often already
being utilized in cardiac arrest, has the added benefit of aiding in shivering control and therefore
should be optimized. Dexmedetomidine in combination with meperedine or buspirone, have
been shown to reduce shivering threshold.23,24 (UW Health Class IIa, LOE B) Alfentanil, an opioid,
is an option which decreases both the vasoconstrictive and shivering threshold.25 (UW Health
Class IIb, LOE B) Midazolam alone has shown minimal benefit, although midazolam in
combination with ketamine, has shown benefit in controlling shivering. 26 (UW Health Class IIb,
LOE C)

Continuous neuromuscular blockade (NMB) is an option for shivering, however, NMBs may
mask appropriate sedation or seizure, lead to polyneuropathy, interfere with neurologic exam
and additionally, NMBs fail to shut down central shivering mechanisms. Therefore, NMBs
should be utilized after other modalities have been attempted. 16,27,28 (UW Health Class IIa, LOE B)

Neuromuscular blocking agents should initially be ordered as boluses, as needed to prevent
shivering, with consideration given to an infusion only if shivering cannot be adequately
controlled with boluses. At UW Health, vecuronium is currently the first line agent if renal and
hepatic functions are normal. (UW Health Class I, LOE B) Atracurium may be used as the first line
agent for post-cardiac arrest patients, due to the high incidence of renal dysfunction in this
patient population. (UW Health Class I, LOE B) Venous thromboembolism (VTE) prophylaxis (UW
Health Class I, LOE A) and scheduled eye lubrication (UW Health Class I, LOE B) are recommended
for patients who receive a neuromuscular blocking agent. For complete recommendations
including dosing, refer to the UW Health Continuous Infusion Neuromuscular Blocking Agents ±
Adult ± Inpatient Guideline.
Identify and Treat the Etiology of the Arrest
Acute coronary syndrome (ACS) is a common cause of cardiac arrest. A 12-lead
electrocardiogram (ECG) should be obtained as soon as possible after ROSC to determine
whether acute ST segment elevation is present.2 (AHA Class I, LOE B)
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In post cardiac arrest patients with arrest due to presumed or known pulmonary embolus,
fibrinolytics may be considered.2 (AHA Class IIb, LOE C)

Patients with ST-segment elevation myocardial infarction (STEMI)
Because it is impossible to determine the final neurological status of comatose patients in the
first hours after ROSC, aggressive treatment of ST-segment elevation myocardial infarction
(STEMI) should begin as in non±cardiac arrest patients, regardless of coma or induced
hypothermia.1,3 (AHA Class IIa, LOE C-LD)

Patients with suspected cardiac etiology
Emergent coronary angiography should be strongly considered for all OHCA patients with
suspected cardiac etiology of arrest and ST elevation on ECG.1 The decision to proceed with
coronary angiography should be made with discussion with the interventional cardiologist, and
after weighing the potential risks and benefits of the procedure. Because of the high incidence
of acute coronary ischemia, consideration of emergent coronary angiography may be
reasonable in select patients (e.g., electrically or hemodynamically unstable) even in the
absence of STEMI.1 (AHA Class IIa, LOE B-NR) Patients with ventricular fibrillation (VF) or
ventricular tachycardia (VT) arrest and shockable rhythm on presentation should be strongly
considered due to the benefits demonstrated in the Parisian Registry.4 (UW Health Class IIb, LOE
B-NR) TTM can be safely combined with primary percutaneous coronary intervention (PCI) after
cardiac arrest caused by acute myocardial infarction (AMI).2,29

Continuous telemetric monitoring should take place to detect and treat arrhythmias.2 (UW Health
Class I, LOE A) Post cardiac arrest myocardial dysfunction is sequelae of OHCA and a
transthoracic echocardiogram should be obtained within 24 hours of presentation; in order
ensure there is no reversible etiology behind the cardiac arrest and to guide ongoing
management.2 (UW Health Class I, LOE A)
Optimize Mechanical Ventilation to Minimize Lung Injury
Pulmonary dysfunction after cardiac arrest is common. Etiologies include hydrostatic pulmonary
edema from left ventricular dysfunction; noncardiogenic edema from inflammatory, infective, or
physical injuries; severe pulmonary atelectasis; or aspiration occurring during cardiac arrest or
resuscitation.2

Hyperoxia was found to be an independent predictor of mortality in the post-cardiac arrest
patient.30 The mechanism is hypothesized to be secondary to oxidative stress and injury. In the
IMPACT registry, patients with hyperoxia, (defined as a PaO2 •����PP�+J��IROORZLQJ�FDUGLDF�
arrest had the highest in-hospital mortality (63%) followed by hypoxia (57%).30

It is important to optimize mechanical ventilation in the post arrest setting to minimize further
pulmonary compromise. The well-established ventilation management strategies for patients at
risk for acute lung injury and adult respiratory distress syndrome (ARDS)31 are also appropriate
strategies in the post cardiac arrest population.
Aggressive ventilator management should be performed to avoid both hypoxia and hyperoxia,
using the following strategies:2
1. To avoid hypoxia in adults with ROSC after cardiac arrest, it is reasonable to use the highest
available oxygen concentration until the arterial oxyhemoglobin saturation or the partial
pressure of arterial oxygen can be measured.1 (AHA Class IIa, LOE C-EO) Titrate oxygen
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10


administration to minimize FiO2 while maintainLQJ�WKH�DUWHULDO�R[\KHPRJORELQ�VDWXUDWLRQ�•�
94%.1 (UW Health Class IIa, LOE C)
Note: Hypothermia can affect the accuracy of the PaO2 measurement by causing changes in
the position of the Hb-O2 dissociative curve. At this time, the UW Health Laboratory does not
adjust for the patient’s body temperature at the time the sample was obtained; therefore the
PaO2 may be artificially elevated. Maintaining the PaCO2 within a normal physiological
range, taking into account any temperature correction, may be reasonable.1 (AHA Class IIb,
LOE B-NR)
2. Routine hyperventilation with hypocapnia should be avoided after ROSC as this may
exacerbate cerebral ischemic injury by excessive cerebral vasoconstriction and may
compromise systemic blood flow via an increase in intrinsic PEEP.2 (AHA Class III, LOE C)
3. Ventilation rate and volume may be titrated to maintain high normal PaCO2 (40-45 mmHg)
while avoiding hemodynamic compromise.2 (AHA Class IIb, LOE C)
4. A chest radiograph should be obtained to ensure proper endotracheal tube placement.2
5. It is reasonable to consider the titrated use of sedation and analgesia in critically ill patients
who require mechanical ventilation or shivering suppression during induced hypothermia
after cardiac arrest.2 (AHA Class IIb, LOE C)
Hypothermia can reduce the clearance of sedatives and analgesics; initiate treatment with
bolus dosing of these agents as needed rather than continuous infusions to facilitate
assessment after normothermia.6 Continuous infusions are recommended for patients
receiving neuromuscular blocking agents (see UW Health Continuous Infusion
Neuromuscular Blocking Agents ± Adult ± Inpatient Guideline).
Reduce the Risk of Multi-organ Injury & Support Organ Function
During the cooling process the patient should have a systemic evaluation to ensure that each
system is maximally supported.
Hemodynamic Support
Hemodynamic instability is common after cardiac arrest.3,32 Death due to multi-organ failure is
associated with a persistently low cardiac index during the first 24 hours after resuscitation.2
Early goal directed hemodynamic optimization is hypothesized to decrease the systemic
inflammatory syndrome and reduce the post cardiac arrest brain injury.33,34

Bleeding Risk
TTM induces coagulative abnormalities which can make the patient more prone to bleeding.2
Therefore, any concern for bleeding should be investigated thoroughly. If no active bleeding is
detected, consider starting venous thromboembolism (VTE) prophylaxis as patients are at an
increased risk for deep venous thrombosis or pulmonary embolism given immobility. (UW Health
Class I, LOE B) For detailed recommendations, refer to the UW Health Venous
Thromboembolism Prophylaxis Guideline.

Mean Arterial Pressure Goals
Following OHCA, cerebral auto regulation is significantly modified, and in some cases absent.
These changes mean that cerebral perfusion pressure becomes even more dependent upon
mean arterial pressure (MAP).35 Because of this relationship, some advocate for higher
allowable MAPs; however there are currently no clinical trials that have addressed the optimal
MAP for patients following OHCA. It should be noted that there is evidence using MAP from 65
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11


mmHg to 100 mmHg.29,36 In the landmark randomized clinical trial that elevated hypothermia
protocol to a level 1 indication it should be noted that the investigators maintained a MAP
between 90-100 mmHg.11 In a randomized controlled clinical trial evaluating levels of
hypothermia, early goal directed hemodynamic optimization was included in the "standard care"
group.37

Avoiding and immediately correcting hypotension (systolic blood pressure < 90 mmHg or MAP <
65 mmHg) during postresuscitation care may be reasonable1 (AHA Class IIb, LOE C-LD) The
clinician should maintain a MAP > 65 mmHg1 (AHA Class IIb, LOE C-LD) and ScvO2 > 70%.2 (AHA
Class I, LOE B)
Continuous arterial blood pressure monitoring should be undertaken with placement of an intra-
arterial catheter to constantly follow these values. Use of central venous oxygen saturation to
guide therapy is reasonable and clinicians can consider further treatment when central venous
oxygenation levels are < 70%.

Hypotension Treatment
Fluid administration in the absence of contraindications is typically the first line treatment of
hypotension.2 (UW Health Class I, LOE A)
Vasodilation may occur from loss of sympathetic tone and from metabolic acidosis. In addition,
the ischemia/reperfusion of cardiac arrest and electric defibrillation both can cause transient
myocardial stunning and dysfunction that can last many hours, but may improve with use of
vasoactive drugs.2 If hypotension is persistent, pharmacotherapeutic agents can be employed.
Vasoactive (e.g., norepinephrine), inotropic (e.g., dobutamine), and inodilator (e.g., milrinone)
agents should be titrated as needed to optimize blood pressure, cardiac output, and systemic
perfusion.2 (AHA Class I, LOE B) There is no evidence supporting one pharmacotherapeutic
agent over another. For detailed recommendations on vasoactive medications, refer to the UW
Health Vasoactive Continuous Infusions in Adult Patients - Adult - Inpatient Guideline.
Blood Glucose Control
The benefit of any specific target glucose range is uncertain in adults with ROSC after cardiac
arrest.1 (AHA Class IIb, LOE B-R) Strategies to target moderate glycemic control (140-180 mg/dL)
may be considered. (UW Health Class IIb, LOE B) Attempts to control glucose concentration within
a lower range (80 to 110 mg/dL [4.4 to 6.1 mmol/L]) should NOT be implemented after cardiac
arrest due to the increased risk of hypoglycemia.2,3 (UW Health Class III, LOE B)
Targeted arterial glucose levels of 140-180 mg/dL or current insulin infusion algorithm goal of
110-150 mg/dL in intensive care unit (ICU) patients are recommended per UW Health
Wisconsin Insulin Infusion Practice Protocol and are supported by an American Association of
Clinical Endocrinologists/American Diabetes Association (AACE/ADA) consensus statement on
inpatient glycemic control.38 These ranges are consistent with the American Heart Association
(AHA) guideline recommendations to target moderate glycemic control in adult patients with
ROSC after cardiac arrest.2,3 (UW Health Class IIb, LOE B)

Hyperglycemia is common2,3 and serial whole blood glucose samples should be obtained (at
least every 6 hours) in conjunction with glucose, POC labs every hour through rewarming. (UW
Health Class IIa, LOE C)
Metabolic Considerations
Following presentation to the hospital (likely via the Emergency Department), the following labs
should be assessed: CBC with differential, magnesium, phosphate, liver function tests (ALT,
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12


AST, albumin), troponin, prothrombin time/INR, PTT, lactate, electrolytes, BUN, calcium, and
creatinine. (UW Health Class IIa, LOE C)

Hypothermia induces many metabolic effects, which need to be carefully monitored throughout
the cooling period. These patients are critically ill with changing volume status. Hypothermia
induces an intracellular shift and diuresis6,39 which will result in low potassium, magnesium, and
phosphate levels which could be a trigger for cardiac arrhythmias or respiratory complications.
Therefore serial electrolyte, calcium, magnesium, BUN, creatinine, and phosphate labs should
be measured at least every 6 hours. Potassium should be replaced to maintain serum levels
within a normal raQJH��PDJQHVLXP�WR�•�����PJ�G/��DQG�SKRVSKDWH�WR�•�����PJ�G/��,W�LV�LPSRUWDQW�
to note that rewarming reverses the potassium flux and increases serum levels39, so repletion
should be held 4 hours before rewarming begins.6 Serial lactate labs2,39 will allow the clinician to
ensure adequate tissue oxygenation and are helpful in modifying vasoactive medications.
Central Nervous System Support
Brain injury is a common cause of morbidity and mortality in post±cardiac arrest patients. Brain
injury is the cause of death in 68% of patients after out-of-hospital cardiac arrest and in 23%
after in-hospital cardiac arrest.40 The pathophysiology of post±cardiac arrest brain injury
involves a complex cascade of molecular events that are triggered by ischemia and reperfusion
and then executed over hours to days after ROSC. Events and conditions in the post±cardiac
arrest period have the potential to exacerbate or attenuate these injury pathways and impact
ultimate outcomes.2

A non-enhanced CT scan can provide information about structural lesions, stroke, or intracranial
hemorrhage that may have contributed to cardiac arrest. This should be obtained prior to TTM
induction.2,3 (AHA Class I, LOE C-LD) An electroencephalogram (EEG) should be performed, with
prompt interpretation as soon as possible, and should be monitored frequently or continuously
in comatose patients after ROSC.1 (AHA Class I, LOE C-LD) Continuous EEG monitoring will
allow for early detection and treatment of seizures which may be masked due to the use of
neuromuscular blockades, and pose a risk of further neurologic injury if not treated. The
Neurology resident on call should be notified of the patient to initiate the continuous EEG
process.

Clinical manifestations of post±cardiac arrest brain injury include coma, seizures, myoclonus,
various degrees of neurocognitive dysfunction (ranging from memory deficits to persistent
vegetative state), and brain death.2,9 The same anticonvulsant regimens for the treatment of
seizures (including myoclonic status epilepticus) used for status epilepticus caused by other
etiologies may be considered after cardiac arrest.1 (AHA Class IIb, LOE C-LD)
Rewarm Slowly
If the patient tolerates TTM to goal temperature for 24 hours, rewarming should subsequently
ensue. It is important that rewarming occurs slowly. While the optimal re-warming rate is not
known, literature suggests rates between 0.2 to 0.5º C/hour.41 Rewarming should occur at 0.25º
C per hour.2,6 (UW Health Class I, LOE C)

Pyrexia Risk
It may be reasonable to actively intervene to prevent and avoid hyperthermia after TTM.1,3 (AHA
Class IIb, LOE C-LD) Rebound hyperthermia is a recognized complication of OHCA. Case series
KDYH�GHPRQVWUDWHG�DQ�DVVRFLDWLRQ�ZLWK�SRRU�VXUYLYDO�DQG�S\UH[LD��•�����ž&���&XUUHQW�JXLGHOLQHV2
recommend intervening to prevent pyrexia; however, there is a lack of randomized controlled
Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
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13


data on methods of treatment (anti-pyretics or cooling techniques). Post rewarming core body
temperature should be maintained at 37º C with surface cooling devices for the next 48
hours. To facilitate this, anti-pyretic pharmacotherapy with acetaminophen may be used in the
absence of hepatic dysfunction. Carefully consider the contribution of nosocomial infectious
processes during this time period.

Prognostication of Neurological Outcome
Decisions to withdraw life sustaining treatment should not be based on one variable alone, but
based on the integration of clinical scenario (e.g., comorbidities) and several clinical and
diagnostic tests. The earliest time for prognostication using clinical examination in patients
treated with TTM, where sedation and paralysis could be a confounder, may be 72 hours after
discontinuation of sedation and at normothermia.1 (UW Health Class IIb, LOE C-EO) A
retrospective analysis of the Parisian Region OHCA Registry demonstrated that 29% of
comatose survivors of cardiac arrest who recovered consciousness after TTM awoke more than
48 hours after discontinuation of sedation.42 Delayed awakening is more likely to occur in
patients with renal insufficiency on admission, post-resuscitation shock, and older age (> 59
years).42
The earliest time to prognosticate a poor neurologic outcome in patients not treated with TTM is
72 hours after cardiac arrest.1 (AHA Class I, LOE B-NR) The time until prognostication can be
even longer than 72 hours after cardiac arrest if the residual effect of sedation or paralysis
confounds the clinical exam.1 (AHA Class IIa, LOE C-LD)

Neurological Assessments

Clinical Examination
The neurological examination is the most widely studied parameter to predict outcome in
comatose post±cardiac arrest patients. Neurological examination for this purpose can be
reliably undertaken only in the absence of confounding factors (hypotension, seizures,
sedatives, or neuromuscular blockers).2 On the basis of existing studies, no clinical neurological
signs reliably predict poor outcome < 24 hours after cardiac arrest.2,26,27

Among adult patients who are comatose and have not been treated with TTM, the absence of
SXSLOODU\�OLJKW�UHIOH[�•����KRXUV�DIWHU�FDUGLDF�DUUHVW�is a reasonable exam finding with which to
predicted poor neurologic outcome.1 (AHA Class IIa, LOE B-NR) In comatose patients treated with
TTM, the absence of pupillary reflex to light > 72 hours after cardiac arrest is useful to predict
poor neurologic outcome.1 (AHA Class I, LOE B-NR)

The absence of vestibulo-RFXODU�UHIOH[HV�DW�•����KRXUV��)35���������&,����WR������RU�
*ODVJRZ�&RPD�6FDOH��*&6��VFRUH�����DW�•����hours (FPR 0%, 95% CI 0% to 6%) are less
reliable for predicting poor outcome or were studied only in limited numbers of patients. Given
their unacceptable FPR, the findings of either absent motor movements or extensor posturing
should NOT be used alone for predicting a poor neurologic outcome.1 (AHA Class III, LOE B-NR)
Other clinical signs, including the presence of myoclonus, are not recommended for predicting
poor outcome.1-3 (AHA Class III, LOE B-NR) In combination with other diagnostic tests at > 72
hours after cardiac arrest, the presence of status myoclonus during the first 72-120 hours after
cardiac arrest is a reasonable finding to help predict poor neurologic outcomes.1 (AHA Class IIa,
LOE B-NR)


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14


EEG Findings
In comatose patients who are treated with TTM, it may be reasonable to consider persistent
absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent
burst suppression on EEG after rewarming, to predict a poor outcome.1 (AHA Class IIb, LOE B-
NR) Intractable and persistent (more than 72 hours) status epilepticus in the absence of EEG
reactivity to external stimuli may be reasonable to predict poor outcome.1 (AHA Class IIb, LOE B-
NR) In comatose patients not treated with TTM, it may be reasonable to consider the presence
of burst suppression on EEG > 72 hours after cardiac arrest, in combination with other
predictors, to predict a poor neurologic outcome.1 (AHA Class IIb, LOE B-NR) Results obtained
from patients who recently received, or who are receiving a barbiturate, propofol, or sedative at
the time of the EEG, should be interpreted with caution. These agents may impact EEG results
and therefore may not be an accurate indicator of prognosis. The effects of drug induced
alteration of EEG findings are variable and can depend on both medication and patient
characteristics, such as medication elimination half-life and organ dysfunction.

Evoked Potentials
SSEPs are less affected by sedatives or temperature manipulation than the EEG or clinical
examination. In patients who are comatose after resuscitation from cardiac arrest regardless of
treatment with TTM, it is reasonable to consider bilateral absence of the N20 SSEP wave 24-72
hours after cardiac arrest or after rewarming a predictor of poor outcome.1 (AHA Class IIa, LOE B-
NR)

Imaging Tests
In patients who are comatose after resuscitation and not treated with TTM, it may be reasonable
to use the presence of a marked reduction of the GWR on brain CT obtained within 2 hours
after cardiac arrest to predict poor outcome.1 (AHA Class IIb, LOE B-NR) It may be reasonable to
consider extensive restriction of diffusion on brain MRI at 2-6 days after cardiac arrest in
combination with other established predictors to predict a poor neurologic outcome.1 (AHA Class
IIb, LOE B-NR)

Blood Markers
Given the possibility of high FPRs, blood levels of neuron-specific enolase (NSE) and S-110B
should NOT be used alone to predict a poor neurologic outcome.1 (AHA Class III, LOE C-LD)
When performed with other prognostic tests at 72 hours or more after cardiac arrest, it may be
reasonable to consider high serum levels of NSE at 48-72 hours after cardiac arrest to support
the prognosis of a poor neurologic outcome (AHA Class IIb, LOE B-NR), especially if repeated
sampling reveals persistently high values.1 (AHA Class IIb, LOE C-LD)
Organ Donation
Despite maximal support and adequate observation, some patients will be brain-dead after
cardiac arrest. Studies suggest that there is no difference in functional outcomes of organs
transplanted from patients who are brain-dead as a consequence of cardiac arrest when
compared with donors who are brain-dead due to other causes. Adult patients who progress to
brain death after resuscitation from cardiac arrest should be evaluated for organ donation.1,3
(AHA Class IIb, LOE B-NR) For specific procedures (including contact information for the UW
Organ and Tissue Donation team) refer to Policy 4.31.

Patients who do not have ROSC after resuscitation efforts or who would otherwise have
termination of efforts may be considered candidates for kidney or liver donation in settings
where programs exist.1 (AHA Class IIb, LOE B-NR)
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15


Table 1. Post-Cardiac Arrest Syndrome: Pathophysiology, Clinical
Manifestations, and Potential Treatments

Syndrome Pathophysiology Clinical
Manifestation
Potential Treatments
Post±cardiac arrest
brain injury
‡�,PSDLUHG�FHUHEURYDVFXODU�
autoregulation
‡�&HUHEUDO�HGHPD��OLPLWHG�
‡�3RVWLVFKHPLF�
neurodegeneration
‡�&RPD
‡6HL]XUHV
‡�0\RFORQXV
‡�&RJQLWLYH�
dysfunction
‡�3HUVLVWHQW�YHJHWDWLYH�
state
‡�6HFRQGDU\�
parkinsonism
‡�&RUWLFDO�VWURNH
‡�%UDLQ�GHDWK
‡�7KHUDSHXWLF�K\SRWKHUPLD
‡�(DUO\�KHPRG\Qamic
optimization
‡�$LUZD\�SURWHFWLRQ�DQG�
mechanical ventilation
‡�6HL]XUH�FRQWURO
‡�&RQWUROOHG�UHR[\JHQDWLRQ�
(SaO2 94%±96%)
‡�6XSSRUWLYH�FDUH
Post±cardiac arrest
myocardial
dysfunction
‡�*OREDO�K\SRNLQHVLV�
(myocardial stunning)
‡�$&6
‡�5HGXFHG�FDUGLDF�
output
‡�+\SRWHQVLRQ
‡�'\VUK\WKPLDV
‡�&DUGLRYDVFXODU�
collapse
‡�(DUO\�UHYDVFXODUL]DWLRQ�RI�
AMI
‡�(DUO\�KHPRG\QDPLF�
optimization
‡�,QWUDYHQRXV�IOXLG
‡�,QRWURSHV
‡�,$%3
‡�/9$'
‡�(&02
Systemic
ischemia/reperfusion
response
‡�6\VWHPLF�LQIODPPDWRU\�
response syndrome
‡�,PSDLUHG�YDVRUHJXODWLRQ
‡�,QFUHDVHG�FRDJXODWLRQ
‡�$GUHQDO�VXSSUHVVLRQ
‡�,PSDLUHG�WLVVXH�R[\JHQ�
delivery and utilization
‡�,PSDLUHG�UHVLVWDQFH�WR�
infection
‡�2QJRLQJ�WLVVXH�
hypoxia/ischemia
‡�+\SRWHQVLRQ
‡�&DUGLRYDVFXODU�
collapse
‡�3\UH[LD��IHYHU)
‡�+\SHUJO\FHPLD
‡�0XOWL-organ failure
‡�,QIHFWLRQ
‡�(DUO\�KHPRG\QDPLF�
optimization
‡�,9�IOXLG
‡�9DVRSUHVVRUV
‡�+LJK-volume
hemofiltration
‡�7HPSHUDWXUH�FRQWURO
‡�*OXFRVH�FRQWURO
‡�$QWLELRWLFV�IRU�GRFXPHQWHG�
infection
Persistent
precipitating
pathology
‡ Cardiovascular disease
(AMI/ACS,
cardiomyopathy)
‡�3XOPRQDU\�GLVHDVH�
(COPD, asthma)
‡�&16�GLVHDVH��&9$�
‡�7KURPERHPEROLF�GLVHDVH�
(PE)
‡�7R[LFRORJLFDO��RYHUGRVH��
poisoning)
‡�,QIHFWLRQ��VHSVLV��
pneumonia)
‡�+\SRYROHPLD�
(hemorrhage, dehydration)
‡�6SHFLILF�to cause but
complicated by
concomitant PCAS
‡�'LVHDVH-specific
interventions guided by
patient condition and
concomitant PCAS
ACS indicates acute coronary syndrome; AMI, acute myocardial infarction; CNS, central nervous system; COPD, chronic obstructive
pulmonary disease; CVA, cerebrovascular accident; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon
pump; IV, intravenous; LVAD, left ventricular assist device; PCAS, post±cardiac arrest syndrome; and PE, pulmonary embolism.

Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 08/2016CCKM@uwhealth.org

16


UW Health Implementation
Potential Benefits:
ξ Reduced mortality
ξ Decreased hospital stay

Potential Harms: No apparent identifiable harms.

Pertinent UW Health Policies & Procedures
1. UWHC Department Policy 1.42AP - Intravascular Cooling Catheter System - Thermogard
XP (Adult & Pediatric)
2. UWHC Departmental Policy 4.02 - Hypo/Hyperthermia Blankets, Use of
3. UW Health Clinical Policy 2.1.2 ± Admission and Discharge of Patients to and from the
Cardiac Intensive Care Unit
4. UWHC Clinical Policy 4.31- Organ & Tissue Donation

Patient Resources
1. Health Facts For You #6583 What to Expect after Cardiac Arrest
2. Health Facts For You #5784- Organ Donation
3. Health Information- Cardiac Arrest

Guideline Metrics:
1. Evaluation of overall patient survival rate
2. Retrospective assessment of whether goal core temperature was achieved within 6 hours
following initiation of TTM
3. Number of patients targeted core temperatures of 33°C vs. 36°C
4. Average length of inpatient hospitalization stay
5. Percent of patients receiving TTM and post arrest care with significant neurologic recovery

Implementation Plan/Clinical Tools
1. Guideline will be posted on uConnect in a dedicated location for Clinical Practice Guidelines.
2. Release of the guideline will be advertised in the Physician/APP Briefing newsletter.
3. Content and hyperlinks within clinical tools, documents, or Health Link related to the
guideline recommendations (such as the following) will be reviewed for consistency and
modified as appropriate.

Order Sets
IP ± Post Cardiac Arrest Hypothermia ± Adult ± Intensive Care ± Admission [701]
IP ± Comprehensive Donation After Cardiac Death (DCD) ± Adult ± Intensive Care ±
Supplemental [3627]

Disclaimer
Clinical practice guidelines assist clinicians by providing a framework for the evaluation and
treatment of patients. This guideline outlines the preferred approach for most patients. It is not
LQWHQGHG�WR�UHSODFH�D�FOLQLFLDQ¶V�MXGJPHQW�RU�WR�HVWDEOLVK�D�SURWRFRO�IRU�DOO�SDWLHQWV��,W�LV�
understood that some patients will not fit the clinical condition contemplated by a guideline and
that a guideline will rarely establish the only appropriate approach to a problem.

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17


Appendix A. Evidence Grading Scheme(s)

Figure 1. 2010 AHA Grading Scheme















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18


Figure 2. 2015 AHA Grading Scheme

Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 08/2016CCKM@uwhealth.org

19



UW Health Targeted Temperature Management (TTM) Cooling Products
Note: No single cooling method has proven to be optimal2,41 and no formal comparative cost analyses have been completed.
Method Equipment Type & Name Obtain From:
Intravascular
Cooling
Thermogard machine by Zoll (formerly Coolgard) TLC, F4M5, F8/4 Sign equipment out from home unit
Intravascular
Catheters
Quattro

(4 balloon heat exchange catheter)- 9.3 Fr, 45 cm
Central Services
³&DWKHWHU�IHPRUDO��&RROJDUG��WUSO�OXPHQ´
Item # 4008876
Note: Some units may stock this item on unit
Cool Line

(2 balloon heat exchange catheter)-9.3 Fr, 22cm
Central Services
³&DWKHWHU�VXEFODYLDQ��&RROJDUG��WUSO�OXPHQ´
Item# 4008559
Note: Some units may stock this item on unit
Tubing

Central Services
³.LW�start-XS�&RROJDUG�PDFKLQH´
Item# 4008558
Note: Some units may stock this item on unit
Surface
Temperature
Regulation*


Hyper/Hypothermia machines by Gaymar (bought by Stryker) Central Services
³+\SHU�K\SRWKHUPLD�PDFKLQH´
Cooling Wraps
Central Services
³9HVW�K\SHU�K\SRWKHUPLD�ODUJH���´- ��´�FKHVW´
Item# 4013572
³9HVW�K\SHU�K\SRWKHUPLD�VP�PHG���´- ��´�FKHVW´
Item# 4013571
Note: Some units may stock this item on unit
Cooling Blanket
Central Services
³%ODQNHW�K\SHU�K\SRWKHUPLD���´�[���´´
Item# 4004226
Note: Some units may stock this item on unit
* Surface temperature regulation methods may be used in conjunction with one another.

Reference: UW Health Post Cardiac Arrest ± Adult ± ED/Inpatient Guideline
Copyright © 201� University of Wisconsin Hospital s and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 08/2016CCKM@uwhealth.org

Post Cardiac Arrest Algorithm- Adult – Emergency Dept/Inpatient
R
E
W
A
R
M
I
N
G
M
A
I
N
T
E
N
A
N
C
E
I
N
I
T
I
A
T
I
O
N
Presentation of
Post Cardiac
Arrest
Does patient
meet exclusion
criteria?
Proceed with
standard of care
(Outside scope of
guidance document)
1. IV bolus normal saline (2 L)
2. Initiate Surface Cooling (Initial goal temp.: 36°C)
3. Obtain:
ξ Non-contrasted head CT (if trauma/collapse)
ξ 12-Lead ECG
ξ Urgent echocardiogram
ξ Troponin
ξ Vital signs (including temperature at 2 sources)
STEMI?*
No
ACS or other
suspected cardiac
etiology?
Admit patient to
Critical Care Unit
Admit patient to
Cardiac Cath Lab
Admit patient to
CCU
Exclusion Criteria:
1. > 12 hours since ROSC
2. Motor component of Glasgow Coma Scale score > 5 (i.e., purposeful movement)
3. Minimal pre-morbid cognitive status (i.e., advanced dementia, metastatic cancer)
4. Sepsis as cause of arrest
5. DNR status
6. Core body temperature < 30°C
Continue Targeted
Temp Management
(TTM)?
Decision by Accepting Critical
Care Team
*Set goal core
temperature: 33°C
*Set goal core
temperature: 36°C
Goal
temperature
achieved within
2 hours?
Continue Surface
Cooling
Initiate
Intravascular
Cooling
Yes
No
ξ Arterial line placement
ξ EEG (continuous) and neurological assessment
ξ Wean FiO2 aggressively
ξ Maintain oxyhemoglobin > 94%
ξ Monitor ScVO2 > 70%. If < 70% consider PRBC, inotropic agents
ξ Moderate glucose control (140-180 mg/dL)
ξ Measure temperature continuously from 2 sources
ξ Consider neuromuscular blockade if shivering
ξ Draw electrolytes, BUN, creatinine, magnesium, phosphate,
calcium, lactate labs (at least every 6 hours)
MAP > 65 mmHg
achieved?
MAP < 65 mmHg
ξ IV fluids first
ξ Consider vasoactive
medications
MAP > 100 mmHg
ξ Consider IV nitroglycerin
No
Increase core temperature
by 0.25-0.5°C/hr to 37°C
Maintain goal core
temperature for
24 hours
Maintain core
temperature of
37°C for 48 hours
Continue care as appropriate by Critical Care team
Prognosticate neurological assessment after patient
warm for 72 hours
Note: If difficulty maintaining core temperature at 37°C or
rewarming faster than 0.5 °C/hr, consider:
ξ Continuation of intravascular or surface cooling
ξ Scheduled acetaminophen, if no significant liver disease
Last revised: 08/2016
UW Health Post Cardiac Arrest Clinical Practice Guideline
Yes
No No
Yes
Yes
Yes
No
Yes
Due to the severity of illness in post cardiac arrest patients, consider consulting Palliative Care.
If patient is pregnant, consult Obstertrics.
Goal Temperature
Goal core temperature of 32-36°C (AHA Class I, LOE B-R) for at least 24 hours (AHA Class IIa, LOE C-EO).
Evidence (2013) suggests 36°C may be an appropriate goal temperature, particularly in patients
not previously thought to be candidates for TTM (e.g., recent trauma, bleeding concerns, or
hemodynamic instability) or those unable to tolerate 33°C goal temperature.
Once the decision is made to proceed with TTM, the goal temperature is determined by the
accepting critical care team. This decision is made after careful and timely review of the clinical
GDWD�DQG�SDWLHQW�IDFWRUV�WKDW�DUH�DYDLODEOH�WR�WKH�WHDP�DW�WKH�WLPH�RI�WKH�SDWLHQW¶V�DGPLVVLRQ.
*Contact Interventional Cardiology. VF/VT arrest and shockable rhythm should be strongly considered for
emergent coronary angiography.
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21


References
1. Callaway CW, Donnino MW, Fink EL, et al. Part 8: Post-Cardiac Arrest Care: 2015
American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. Nov 2015;132(18 Suppl 2):S465-482.
2. 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. Nov 2010;122(18 Suppl 3):S768-786.
3. Morrison LJ, Neumar RW, Zimmerman JL, et al. Strategies for improving survival after
in-hospital cardiac arrest in the United States: 2013 consensus recommendations: a
consensus statement from the American Heart Association. Circulation. Apr
2013;127(14):1538-1563.
4. Dumas F, Bougouin W, Geri G, et al. Emergency Percutaneous Coronary Intervention in
Post±Cardiac Arrest Patients Without ST-Segment Elevation PatternInsights From the
PROCAT II Registry. JACC: Cardiovascular Interventions. 2016;9(10):1011-1018.
5. Jacobs I, Nadkarni V. Targeted temperature management following cardiac arrest An
update. 2013; http://www.ilcor.org/data/TTM-ILCOR-update-Dec-2013.pdf. Accessed
April 3, 2014.
6. Scirica BM. Therapeutic hypothermia after cardiac arrest. Circulation. Jan
2013;127(2):244-250.
7. Wang HE, Devlin SM, Sears GK, et al. Regional variations in early and late survival after
out-of-hospital cardiac arrest. Resuscitation. Nov 2012;83(11):1343-1348.
8. Kim LK, Looser P, Swaminathan RV, et al. Sex-Based Disparities in Incidence,
Treatment, and Outcomes of Cardiac Arrest in the United States, 2003-2012. J Am
Heart Assoc. Jun 2016;5(6).
9. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,
pathophysiology, treatment, and prognostication. A consensus statement from the
International Liaison Committee on Resuscitation (American Heart Association,
Australian and New Zealand Council on Resuscitation, European Resuscitation Council,
Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation
Council of Asia, and the Resuscitation Council of Southern Africa); 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; and the Stroke Council. Circulation. Dec
2008;118(23):2452-2483.
10. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C
versus 36°C after cardiac arrest. N Engl J Med. Dec 2013;369(23):2197-2206.
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. Feb 2002;346(8):557-
563.
12. Chauhan A, Musunuru H, Donnino M, McCurdy MT, Chauhan V, Walsh M. The use of
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Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 08/2016CCKM@uwhealth.org