Induced Moderate Hypothermia After Cardiac Arrest - American ...

AACN Advanced Critical Care
Volume 20, Number 4, pp.343–355
© 2009, AACN
Induced Moderate Hypothermia
After Cardiac Arrest
Staci McKean, RN, BSN, CCRN
ABSTRACT
The use of induced hypothermia has been
considered for treatment of head injuries
since the 1900s. However, it was not until 2
landmark studies were published in 2002 that
induced hypothermia was considered best
practice for patients after cardiac arrest. In
2005, the American Heart Association included
recommendations in the postresuscitation
support guidelines recommending consideration
of mild hypothermia for unconscious
adult patients with return of spontaneous circulation
following out-of-hospital cardiac
arrest due to ventricular fibrillation. This
article provides an overview on the history
and supportive research for inducing mild
hypothermia after cardiac arrest, the pathophysiology
associated with cerebral ischemia
occurring with hypothermia, nursing management
for this patient population, and the
development of a protocol for induced
hypothermia after cardiac arrest.
Keywords: cardiac arrest, cardiopulmonary
resuscitation, induced hypothermia, therapeutic
hypothermia, ventricular fibrillation
Although only a few clinical trials have looked
directly at the supportive care of the patient
after cardiac arrest, it is evident that postresuscitation
care has the potential to improve outcomes. 1
Even if the patient receives adequate resuscitation
in a timely manner, there may be brain injury
related to reperfusion. 2 Ten percent to 30% of
patients who survive an out-of-hospital cardiac
arrest will have permanent brain damage. 3
Induced mild hypothermia has been studied for
the purpose of reducing the risk of reperfusion
injury to the brain after cardiac arrest. The purpose
of this article is to provide an overview of the
pathophysiology and research that supports the
use of induced mild hypothermia following cardiac
arrest along with nursing considerations for
this patient population. The use and development
of a standardized protocol to care for this patient
population is also discussed.
Historical Overview
The use of induced hypothermia has been considered
for treatment of head injuries since the
1900s. In the 1950s, several studies on canines
and monkeys demonstrated the benefits of
therapeutic hypothermia, which included
decreased cerebral oxygen consumption and
metabolic rates. However, the use of deep or
severe hypothermia, less than 30C, led to
uncontrollable complications such as ventricular
fibrillation (VF). 4 These studies were conducted
prior to the evolution of modern
intensive care units (ICUs). Complications
such as infection and unstable hemodynamics
were too difficult to control without the contemporary
practices used to reduce these risks
today. As a result, the concept of induced
hypothermia as a medical intervention was not
recognized as a therapeutic option. 4–6
Between the 1960s and 1990s, the benefits
of therapeutic hypothermia continued to be
studied in animals. 4 In the 1980s, the use of
Staci McKean is Cardiovascular Nurse Educator, Baylor University
Medical Center, 3500 Gaston Ave, Dallas, TX 75246
(Staci.McKean@baylorhealth.edu).
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hypothermia on dogs after cardiac arrest
demonstrated positive outcomes that included
improved neurological status and survival outcomes.
3 This led the medical community to
explore induced hypothermia following cardiac
arrest once again as a possible intervention
for humans. 4 It was not until 2 landmark
studies were published in 2002 that induced
hypothermia was considered best practice for
patients following cardiac arrest. 2
Supportive Research
Bernard and colleagues 7 compared the use of
induced hypothermia with standard treatment
for patients following VF arrest who remained
comatose after return of spontaneous circulation
(ROSC). Patients were randomly assigned
to hypothermia or normothermia (standard
care). The patients assigned to hypothermia
were cooled to 33C within 2 hours after ROSC
and were kept at that temperature for 12 hours.
Of the 77 patients enrolled in the trial, 49%
treated with hypothermia were discharged
home or to a rehabilitation facility as compared
with 26% of the patients treated with standard
care. 7 The odds ratio for a good outcome with
hypothermia compared with normothermia
was 5.25 when baseline differences in age and
time from collapse to ROSC were considered. 7
The Hypothermia After Cardiac Arrest
Study Group 8 studied patients presenting in the
emergency department with VF or nonperfusing
ventricular tachycardia with ROSC. The
patients randomly selected to receive hypothermia
were cooled and maintained at 32C to
34C for 24 hours. Fifty-five percent of patients
who received hypothermia had a favorable
outcome, indicating that the patient was able
to live independently and work at least part
time. Only 39% of patients who were maintained
at normothermia had similar favorable
outcomes. 8 Mortality at 6 months was 41% in
the hypothermia group as compared with 55%
in those who did not receive hypothermia. 8
Several other studies have shown benefits
related to induced mild hypothermia following
cardiac arrest. Hachimi-Idrissi and colleagues 9
conducted a study inducing hypothermia by
using a helmet device containing a solution of
aqueous glycerol around the head and neck to
cool the patient to 34°C. Patients who had cardiac
arrest from pulseless electrical activity or
asystole of presumed cardiac origin were considered
for this trial. Study results revealed
patients who received hypothermia had a significantly
higher central venous oxygen saturation
and significantly lower arterial lactate
concentrations and oxygen extraction ratio. 9
Another study conducted by Oddo and colleagues
10 included patients who experienced
out-of-hospital cardiac arrest from VF, asystole,
and pulseless electrical activity. A good
outcome, defined as Glasgow–Pittsburgh
Cerebral Performance Category 1 or 2, was
seen in 55.8% of the patients who received
hypothermia treatment as compared with
25.6% treated with standard treatment for
patients with cardiac arrest due to VF. 10
In October 2002, the International Liaison
Committee on Resuscitation (ILCOR) made the
recommendation, based on the above evidence,
that all unconscious adult patients with ROSC
following out-of-hospital cardiac arrest due to
VF should be cooled to 32°C to 34°C for 12 to
24 hours. ILCOR also stated that other
rhythms that cause cardiac arrest and in-hospital
cardiac arrests may benefit from hypothermia.
11 In 2005, the American Heart Association
(AHA) included these recommendations in the
postresuscitation support guidelines. 1
Effects of Cerebral Ischemia and
Induced Hypothermia
The brain has a small amount of oxygen
stores. When cerebral perfusion and oxygen
delivery stop during cardiac arrest, the oxygen
stores are depleted within 20 seconds. 6 If a
patient was connected to continuous electroencephalography
(EEG) during cardiac
arrest, clinicians would see isoelectric lines
after 20 seconds, indicating no brain activity
present. 4 After oxygen is depleted, the brain
turns to anaerobic metabolism to sustain function.
Glucose and adenosine triphosphate levels
are depleted after 5 minutes if return of
blood flow is not achieved. 6 This causes ion
pumps that use adenosine triphosphate to fail,
allowing for electrolyte imbalance, including
potassium, sodium, and calcium, resulting in
cellular edema and cell death. 12
After ROSC, it would be assumed that once
oxygen supply was returned to the brain, cell
death would stop. However, it is believed that
reperfusion initiates chemical processes that
lead to inflammation and continued injury in
the brain. This is known as reperfusion injury.
Reperfusion injury is thought to include the
release of free radicals, nitric oxide, catecholamines,
cytokines, and calcium shifts,
which all lead to mitochondrial damage and
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INDUCED MODERATE HYPOTHERMIA AFTER CARDIAC ARREST
cell death. This process may last as long as 24
to 48 hours. 2,6,12,13 In low perfusion states, the
blood–brain barrier is disrupted, leading to
worsening cerebral edema. 13
The complete benefits of induced hypothermia
are not well understood. The cerebral metabolic
rate is decreased by 6% to 7% for every
1°C decrease in the body temperature. 5 Decreasing
the cerebral metabolic rate decreases cerebral
oxygen consumption. 2 Hypothermia helps
to stabilize the influx of calcium and glutamate
by slowing the neuroexcitatory processes,
thereby reducing the disruptions in the
blood–brain barrier and preventing premature
cell death. 13 Hypothermia is also thought to
decrease many of the chemical reactions that
occur during reperfusion, such as free radical
production. 2 Temperatures less than 35°C lead
to decreased neutrophil and macrophage functions.
This reduces the inflammatory response
that is initiated after ischemia. 13
Hypothermia Methods
Several methods may be used to induce and
maintain hypothermia. The methods may be
classified as noninvasive and invasive.
Noninvasive Induced Hypothermia
Noninvasive methods include traditional
interventions such as using ice packs, fans,
alcohol baths, and cooling blankets not
attached to automatic temperature control
modules. These methods are extremely labor
intensive and require manual control of the
patient’s temperature. The nurse must closely
monitor the patient’s temperature and regulate
the intervention to achieve and maintain the
target temperature. In some instances this may
require staffing to be 1:1. Also, the literature
does not provide strong evidence for best
practice using these methods. No specific
guidelines are available for the noninvasive
induction of hypothermia, such as “place 4 bags
of ice to the axillary and groin areas and when
the patient’s temperature reaches 34.5C
remove one bag.” These methods are based
more on the nurse’s judgment, without any
specific evidence for achieving best outcomes.
A much higher risk of unintentional overcooling
or warming too quickly with these traditional
methods has been shown. Rewarming is
a definite problem with these techniques. It
has also been shown that noninvasive methods
may take a prolonged time to reach the target
temperature or it may not be achieved at all.
However, these methods are more readily
available at most institutions. The equipment
cost may also be lower although the cost for
the 1:1 nurse–patient ratio may be more. 13,14
Improvements and advances have been
observed in some of the noninvasive methods
that help decrease labor intensity and risks
involved with induced hypothermia. The Arctic
Sun by Medivance (Louisville, CO) (Figure 1)
uses gel pads placed on the patient’s skin to
cover approximately 40% of the patient’s
body. The pads may even be pulled back and
reapplied as many times as needed, allowing
access for patient care. Water circulates
through the pads using a negative pressure system,
which minimizes the risks of leaks as
compared with other devices. The pads and a
patient temperature source, such as a temperature-sensing
urinary catheter, are connected to
a console that automatically adjusts water
temperature to achieve and maintain target
temperature. It also provides a way for controlled
warming to help prevent rebound
hyperthermia. 13,15
Invasive Induced Hypothermia
Invasive methods include use of iced (4°C)
intravenous fluids and the use of intravascular
catheters. A few studies show that use of iced
intravenous fluids may be effective in inducing
hypothermia. 16,17 In a study by Bernard and
colleagues, 16 lactated Ringer solution was
stored in the emergency department blood
refrigerator with a controlled temperature of
4°C until needed. When a patient was identified
for the study, 30 mL/kg of the lactated
Ringer solution was infused over 30 minutes
by using a pressure bag. Ice packs were then
placed to maintain temperature at 33C for
12 hours. 16 Kliegel and colleagues 17 infused
2000 mL of iced lactated Ringer solution
when patients met criteria for their study. As
soon as possible, an intravascular catheter was
placed and connected to a cooling device to
maintain the temperature at 33C for 24
hours. 17 Iced intravenous fluids may help to
induce hypothermia quickly in the emergency
department and has the potential for being
started out in the field by paramedics.
Machines such as the CoolGard 3000 or
the newer version Thermogard XP (Figure 2)
by Alsius (Irvine, CA) use an automatic temperature-control
module similar to that used
by the Arctic Sun. These devices by Alsius use
a closed-loop central venous catheter usually
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Figure 1: Arctic Sun noninvasive automatic temperature control device. Used with permission from
Medivance Corporation.
inserted into the femoral vein. Once the
catheter is connected to the control module,
cold water circulates through the balloons on
the tip of the catheter. The blood is cooled as it
passes by the balloons. Invasive methods such
as the CoolGard 3000 require the placement of a
catheter by a physician credentialed in placing
central venous catheters. This carries the risk of
any central venous catheter, including bleeding,
infection, deep vein thrombosis, vascular puncture,
and pneumothorax, if placed in the chest.
However, patients requiring induced hypothermia
usually will also need a central venous
catheter for other interventions such as medication
administration and frequent blood draws.
The central venous catheter, such as the catheters
that accompany the CoolGard 3000, have 3 ports
that may be used as infusion ports while cooling
or warming the patient. It may continue to be
used as a central venous catheter once the
hypothermia procedure is completed. 13,18
Extensive research has not been conducted
that examines which method produces the best
outcome for the patient. Hoedemaekers and
colleagues 19 compared the use of iced intravenous
fluids followed by ice packs (conventional
cooling); an air-circulating cooling
system that used 1 blanket over the patient; a
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INDUCED MODERATE HYPOTHERMIA AFTER CARDIAC ARREST
Figure 2: Thermogard XP invasive automatic temperature control device. Used with permission from
Alsius Corporation.
water-circulating cooling system that used
blankets placed under and over the patient and
behind the patient’s head; a gel-coated external
cooling device; and an intravascular cooling
system. The last 3 methods were connected
to automatic temperature control modules.
This study found that the methods that used
an automatic temperature control had a significantly
higher speed of cooling. 19 All 3 automatic
temperature control methods were
equally effective in inducing the target temperature.
The intravascular method was significantly
more reliable in maintaining the target
temperature as compared with all other
groups. The target temperature was out of
range 3.2% (4.8%) with the intravascular
catheter compared with 69.8% (37.6%)
with conventional cooling, 50% (35.9%)
with the water-circulating cooling device,
74.1% (40.5%) with the air-circulating
cooling device, and 44.2% (33.7%) with the
gel-coated external cooling system. 19 The
intravascular method group also had no
patients overshoot the target temperature.
One patient who was cooled with conventional
cooling, 3 who were cooled with the
water-circulating device, and 3 who were
cooled with the gel-coated external cooling
device overshot the target temperature by
more than 0.5C. 19 In this study, no adverse
events were noted related to any specific cooling
method. 19
Patient Management and
Nursing Care
As previously discussed, induced moderate
hypothermia following cardiac arrest has been
shown to improve patient outcomes. It, however,
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is beneficial only if the health care team knows
how to care for this patient population. Nursing
care and support is crucial. Patient management
and the vital nursing care needed for this
patient population are described below.
Table 1: The Bedside Shivering
Assessment Scale a
Score
Definition
0 None: no shivering noted on palpation of
the masseter, neck, or chest wall
1 Mild: shivering localized to the neck
and/or thorax only
2 Moderate: shivering involves gross
movement of the upper extremities (in
addition to neck and thorax)
3 Severe: shivering involves gross
movements of the trunk and upper and
lower extremities
a Used with permission from Badjatia et al, “Metabolic Impact of
Shivering During Therapeutic Temperature Modulation: The Bedside
Shivering Assessment Scale,” Stroke, 2008, vol. 39, pp. 3242--3247. 21
Prevention of Shivering
Shivering is a natural body response to
hypothermia. If this natural response is allowed
to occur while inducing hypothermia, there
may be difficulty in achieving the target temperature.
Shivering increases metabolic rate and
oxygen consumption. Most protocols use a
combination of sedation and paralytic agents to
prevent shivering especially during induction. 20
Shivering is less likely to occur during the maintenance
and warming phases. The paralytic
may be stopped during the warming phase. 13,20
Patients should be monitored for signs and
symptoms of shivering, including a drop in
mixed venous oxygen saturation, increase in
respiratory rate, facial tensing, static tracing
on the electrocardiogram, and palpation of
muscle fasciculations on the face or chest. 13
The Bedside Shivering Assessment Scale (Table 1)
may be used by nurses to provide a universal
assessment tool for shivering. 21 The nurse must
ensure that analgesia and sedation are optimized
and that the patient is intubated with
the ventilator set to proper parameters to provide
adequate ventilation prior to the start of
the paralytic treatment. A train of 4 should be
established prior to initiation of continuous
paralytics and continued to be monitored for a
goal of 1 out 4. 13,20 It may be difficult to obtain
train of 4 assessments due to peripheral vasoconstriction
during hypothermia. 13 The nurse
might need to rely on clinical indicators such
as overbreathing on the ventilator and spontaneous
movement to know if the paralytic
agent is optimized.
Sedation and analgesic drugs, such as midazolam,
fentanyl, and propofol, have a 30% to
50% decrease in systemic clearance during
hypothermia. For neuromuscular-blocking
agents, such as vecuronium and atracurium,
clearance is decreased 10% for every 1C
below 37C. Their duration of action is also
increased. 20 The least amount of drug should
be used to provide the needed effect. During
hypothermia, the amount of drug required
may be less than what is typically used. 13 The
health care team must be mindful that the
patient may take longer to wake up after treatment.
20 The paralytic and sedation medications
should be stopped as soon as possible
after the completion of induced hypothermia
treatment.
Vital Sign Monitoring
A patient’s normal response to hypothermia is
to increase the heart rate and vasoconstrict in
an attempt to conserve heat. The use of sedation
and paralytic agents prevents this normal
response to hypothermia. Bradycardia and
increased systemic vascular resistance will be
seen in the absence of shivering and with a continued
decrease in temperature. The bradycardia
is usually not hemodynamically significant
and usually refractory to atropine. It is not
always necessary to terminate treatment for
patients who are bradycardic. Blood pressure is
usually maintained without the use of vasopressors
secondary to the increased systemic vascular
resistance. Vasopressors may be used to
maintain systolic blood pressure greater than
90 mm Hg or mean arterial pressure greater
than 60 mm Hg. The patient may be pale, and
peripheral pulses may be difficult to obtain
because of the vasoconstriction. The greatest
risk for hypotension is during the warming
phase secondary to vasodilation. It is critical at
the start of warming that vital signs are monitored
closely. 2,5,20 Ideally, an arterial catheter will
be inserted for continuous blood pressure measurement.
However, if one is not available, then
noninvasive measurements should be obtained
at least every 30 minutes and more often during
induction of warming. 6,20
Continuous electrocardiogram monitoring
is imperative. Dysrhythmias are rare in mild
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hypothermia. The patient is more at risk when
the temperature drops below 32C. Temperatures
below 30C may cause VF and may be
refractory to defibrillation. 6 Prolonged QT
intervals may be noted during cooling and for
several days to weeks after treatment. 5 The
physician should be notified of any change in
rhythm and hemodynamic instability. The
patient must be kept well hydrated during
cooling to help prevent hypotension during
warming when vasodilation occurs. 2,5,6,20
Skin Care
Peripheral vasoconstriction places the patient
at a particularly high risk for skin breakdown.
Extra attention to skin assessment, skin care,
and frequent turning is necessary. The risk
may be slightly increased with the use of surface-cooling
methods such as cooling blankets.
The nurse should be cautious when placing
noninvasive surface cooling devices on fragile
skin and should avoid open skin areas or
wounds. 6,13,15
Fluid and Laboratory Value Monitoring
Fluid and electrolyte imbalances may occur
during hypothermia and during the warming
phase. Cold diuresis occurs during hypothermia
because there is a decrease in the reabsorption
of solute in the ascending limb of the
loop of Henle. Suppression of the antidiuretic
hormone also exists. Fluid status should be
monitored and maintained. 5
Electrolyte shifts may occur from cold diuresis
and from cellular acidosis that may occur during
hypothermia. Electrolytes such as potassium,
magnesium, phosphorus, and calcium should be
monitored and replaced. Hypothermia causes
potassium to shift into the cells and hypokalemia
may occur. 6,13 Risk for hyperkalemia during
warming exists because the potassium shifts
back, out of the cells. 6,13
Potassium replacement should be given
during cooling, to prevent dysrhythmias.
Replacement should be conservative and
possibly discontinued several hours before
warming begins. The patient is at particular
risk for hyperkalemia if the hypokalemia was
overtreated during the cooling phase. The
patient may still require replacement during
the warming phase if the potassium level is
significantly low. 6,13
Hemoconcentration may be noticed during
hypothermia because of the cold diuresis and
fluid shifts from the intravascular space related
to changes in vascular permeability. 5 For every
1C decline in temperature, the hematocrit
increases by approximately 2%. 5
Coagulopathy may occur during hypothermia.
Platelet counts decrease, and there is an
inhibition of enzyme reactions of both the
intrinsic and extrinsic pathways of the clotting
cascade. 5 Laboratory test values, such as partial
thromboplastin time, prothrombin time,
and international normalized ratio, should be
monitored. Platelets or fresh frozen plasma
should be given only if a clinical concern is
present and not based on the laboratory test
values alone. Studies have shown that there is
not a significant risk of bleeding during
hypothermia. 13,20
Prevention of Infection
Patients receiving induced hypothermia following
cardiac arrest are at high risk for infection
and sepsis. Hypothermia decreases the
number of circulating white blood cells. It also
causes a decreased release of insulin from the
pancreas and causes insulin resistance at the
cellular level. Patients may exhibit refractory
hyperglycemia. Hyperglycemia should be controlled
using insulin treatment with frequent
monitoring, and some patients may even
require a continuous insulin intravenous infusion.
Glucose should be controlled at levels
less than 150 mg/dL. Strict glucose control,
less than 110 mg/dL, has not been shown to
improve outcomes and carries a higher risk of
hypoglycemia. 20 Intravenous fluids that contain
glucose should be avoided. 20
Patients are also at high risk for aspiration
and ventilator-associated pneumonia because
hypothermia causes impairment of ciliary
function reducing airway protective mechanisms.
These patients also tend to require prolonged
ventilation. Wound infections may
have delayed healing as hypothermia decreases
subcutaneous oxygen tension. 5,6,13
Skin care, frequent turning, use of sterile
technique when manipulating catheters, and
use of ventilator bundles will help decrease the
risk of infection. 6 Elevated temperatures related
to infection will be masked by hypothermia, so
other indicators of infection need to be monitored
and considered. Prevention is the key. 13
Rewarming
Guidelines have not been established for how
fast a patient should be warmed. Most recommend
warming the patient at 0.5C to 1C per
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hour. Warming must be done slowly to prevent
complications, such as rebound hyperthermia,
which increases cerebral edema. Other complications
that may occur during warming include
seizures, VF, and hypotension. Fever is common
in the first 48 hours after the completion
of hypothermia treatment. This may be neurologically
mediated, inflammation, or infection
related. The risk of poor neurological outcome
is increased for each degree over 37C reached
in the post–cardiac arrest patient. 5,6,13,20,22
Hyperoxia should be avoided in this patient
population. Research has shown ventilation
with 100% oxygen in the first hour after
experimental cardiac arrest resulted in worse
neurological outcomes. 20 Excessive oxygen
harms postischemic neurons by causing excessive
oxidative stress in the early stages of
reperfusion. 20 Monitor and titrate oxygen
levels by using arterial blood gases and by continuous
saturation monitoring. 20
Quality of care is directly related to outcomes
for this patient population. It is vital that
standard ICU care, such as frequent turning,
oral care, use of ventilator bundles, head of bed
at 30º, strict input and output, sterile technique
when manipulating catheters, glucose level control,
peptic ulcer, and deep vein thrombosis prophylaxis,
be provided for all ICU patients but
especially for this patient population. 6
Protocol Development
The development of a standardized protocol or
order set should be considered before using
induced mild hypothermia following cardiac
arrest. One study indicated that temperature
goals for induced hypothermia could be reliably
achieved when a standardized order set was
used. 23 A protocol should identify the patient
population that is appropriate to receive the
treatment and direct care and assessments. Recommendations
from the AHA and published
research can be utilized to facilitate development
of the protocol. Using examples of order
sets from other institutions may be helpful. If a
particular device is going to be used for cooling,
the company’s experts may also assist in the
development of the order set. The remainder of
this article discusses what should be considered
when developing a protocol for induced
hypothermia following cardiac arrest.
The induced therapeutic mild hypothermia
post–cardiac arrest order set from Baylor University
Medical Center (BUMC) in Dallas,
Texas, is used as an example during this discussion
(Figure 3). A standardized protocol for
inducing mild hypothermia following cardiac
arrest was initiated in 2005. As more research
became available and lessons were learned
during use of the protocol, revisions were
made to reflect the new AHA recommendations
and research. The protocol was also
revised to provide clarity to the health care
team in caring for these patients and answer
questions that were raised with the use of the
initial protocol.
Inclusion and exclusion criteria were developed
based on the 2 studies published by
Bernard 7 and the Hypothermia After Cardiac
Arrest Study Group, 8 the AHA recommendations,
1 ILCOR recommendations, 11 and lessons
learned during use of the initial protocol. The
inclusion and exclusion criteria are detailed in
the protocol to assist the health care team to
identify appropriate patients.
Identification of Appropriate
Patients for Induced Hypothermia
At BUMC, all unconscious, post–cardiac arrest
patients with ROSC whose arrest was believed
to be of cardiac origin are considered for
induced hypothermia. It is an AHA class IIa
recommendation that all unconscious patients
with ROSC after out-of-hospital VF cardiac
arrests receive induced hypothermia. 1 The
AHA also recommends that induced hypothermia
may be beneficial in non-VF arrests for
out-of-hospital or in-hospital arrests. 1 Bernard
et al 7 and the Hypothermia After Cardiac
Arrest Study Group 8 excluded patients who
experienced cardiac arrests of noncardiac etiology,
such as respiratory failure, from their clinical
trials. 7,8,11 Therefore, cardiac arrests of
noncardiac etiology are excluded at BUMC
until future studies are completed.
Following the Hypothermia After Cardiac
Arrest Study Group 8 study design, only those
patients with cardiac arrests that are witnessed
with less than 15 minutes to the first attempt
of resuscitation and ROSC in less than 60 minutes
are considered for this protocol. 8 Patients
who are unable to maintain a systolic blood
pressure of 90 mm Hg despite intravenous
fluids or vasopressors are also not considered
as candidates. 7,8
One of the inclusion criteria on the initial
protocol was coma without a definition. It was
found that the health care team had different
definitions of coma. For this protocol, coma was
defined as “coma suggested by the following:
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Figure 3: Sample order set for induced therapeutic mild hypothermia following cardiac arrest. Used with
permission from Baylor University Medical Center, Dallas, Texas.
unable to follow commands; does not open eyes
to painful stimulus; and Glasgow Coma Scale
score less than or equal to 8.”
Patients with life-threatening arrhythmias
or primary coagulopathy or those who are
pregnant should not receive induced hypothermia
because of the lack of available research. 11
The BUMC protocol excludes patients with a
temperature of 30C or below after ROSC
because the patient is already below the target
temperature of 33C. A further drop in temperature
could lead to life-threatening arrhythmias.
Also, patients with known sepsis are
excluded because of the increased risk of infection
during hypothermia. The team decided to
also exclude patients with a known history of
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terminal illness prior to arrest. Patients who
require thrombolytic therapy are not to be
excluded from treatment. 11
BUMC-Induced
Hypothermia Protocol
The AHA recommends cooling these patients
to 32C to 34C for 12 to 24 hours. 1 This facility
uses devices that automatically control the
temperature. The target temperature for
hypothermia is set at 33C and is maintained at
33C for 18 hours once the target temperature
is achieved. If it takes 4 to 5 hours to reach the
target temperature, then the cooling process
will take approximately 23 to 24 hours as recommended
by the AHA. 1 The patient is then
warmed at 0.5C per hour. The target temperature
for warming is set to 36.5C to avoid poor
neurological outcomes associated with temperatures
above 37C. 20
The goal is to begin induction of hypothermia
and achieve target temperature as soon as
possible after ROSC. However, hypothermia
may still be beneficial if induction is delayed
for 4 to 6 hours after ROSC. 5 The physician
should be notified if the target temperature is
not achieved within a reasonable time.
Bernard and colleagues’ goal of achieving the
target temperature was 2 hours. 7 The median
time to target temperature in the study conducted
by Oddo and colleagues 10 was 5 hours. 10
BUMC decided to consider patients for the
hypothermia protocol when it had been less
than 6 hours since the ROSC, with 4 hours as
the goal to achieve the target temperature once
cooling is started.
Shivering should be considered as a possible
reason for not achieving target temperature
within a reasonable time frame. Sedation and/or
paralytic agents should be considered to help
prevent shivering. The nurse should verify that
both are optimized. 13 If the patient is receiving
dialysis, it should be verified that the blood
warmer is switched off. 20 The physician may
also consider infusing iced sodium chloride to
achieve target temperature more rapidly. 16,17
The patient’s temperature should be monitored
continuously during the entire treatment.
Most automatic temperature control modules
require continuous temperature monitoring of
the patient in adjusting the water temperature
to maintain the target temperature. Studies
have not indicated the best method for monitoring
temperatures continuously. Bladder temperature
is the primary method used at BUMC,
because the patients already require a urinary
catheter for strict input and output monitoring.
The equipment was also already available in the
hospital. However, studies have indicated that
bladder temperatures may be inaccurate when
there is decreased urine output. 24 The nursing
staff members have also found that obtaining
temperature readings with the temperaturesensing
urinary catheter is difficult when the
patient is anuric or has decreased urine output.
As a result, the team decided that rectal temperature
monitoring would be used for these
patients.
The literature indicates different intervals for
how often to monitor vital signs including
blood pressure if an arterial catheter is not present.
We decided to check vital signs every 30
minutes, which is within the recommendations
found in the literature. 5,6 Vital signs assessment
is then performed every 15 minutes for 2 hours
during the warming phase due to the increased
risk of hypotension related to vasodilation.
Recommendations for laboratory tests such
as basic metabolic panel, complete blood cell
count, magnesium, ionic calcium, partial thromboplastin
time, prothrombin time, and international
normalized ratio exist for patients
receiving induced hypothermia. 6 A recommendation
for frequency of serial laboratory studies
could not be found. Laboratory test results
should be obtained to determine baseline values
prior to induction of hypothermia. We choose to
perform the laboratory tests listed above at
induction and then every 6 hours through the
course of treatment. This is to allow time for
treatment between laboratory draws if needed.
Once the patient is normothermic, laboratory
assessments are changed to daily for 48 hours.
Potassium replacement should be considered
in the protocol. Potassium is held for 4
hours prior to the start of warming because of
the risk of hyperkalemia as potassium shifts
out of the cell. 6 The physician is contacted during
this time if the potassium is less than
3.4 mEq/L or if arrhythmias are noted. The
potassium replacement protocol is restarted
once the patient is normothermic.
The sedation, analgesic, and paralytic protocols
already used in the ICUs were incorporated
into this protocol. These were used to decrease
confusion and reduce the risk of medication
administration errors because there is familiarity
with these protocols. Questions occurred
with use of the initial protocol regarding when
to stop the paralytic and sedation treatments.
352

VOLUME 20 • NUMBER 4 • OCTOBER–DECEMBER 2009
INDUCED MODERATE HYPOTHERMIA AFTER CARDIAC ARREST
Some of the literature suggests discontinuing
the paralytic treatment at the beginning of the
warming phase although no exact guidelines
were found. 13,20 Our protocol requires the paralytic
treatment to be turned off 4 hours after the
warming phase is started. This allows the nurse
to concentrate on the patient’s hemodynamic
status at the beginning of the warming phase,
before changing other parameters.
Because patients receiving induced
hypothermia are at risk for refractory hyperglycemia,
glucose level should be monitored
and treated with sliding-scale insulin. Consider
adding the ability to start an insulin infusion if
a protocol already exists and the blood glucose
level is higher than 150 mg/dL more than 2
times during the hypothermia treatment.
Use of facility-based standardized protocols
that are applicable to induced hypothermia
following cardiac arrest is beneficial. This contributes
to making the process of induced
hypothermia similar to the care of other ICU
patients. Providing a protocol that follows
other current practices and gives detailed
instructions may provide consistent implementation
of induced hypothermia postarrest and
prevent complications from the treatment.
Conclusion
Induced mild hypothermia following cardiac
arrest has been slow to be implemented across
the medical community even with the AHA
recommendations and research that shows the
benefits. 23 The methods for inducing and
maintaining hypothermia are improving, making
it a more feasible treatment option for any
hospital. The development and use of a standardized
protocol can facilitate standardization
of care for this patient population.
Acknowledgment
The author thanks Barbara “Bobbi” Leeper,
MN, RN, CNS, CCRN, FAHA, for being a
wonderful mentor and for her assistance in the
preparation and review of this manuscript.
References
1. American Heart Association. 2005 American Heart Association
Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care, 7.5: postresuscitation
support. Circulation. 2005;112(24)(suppl):IV-84–IV-88.
2. Calver P, Braungardt T, Kupchik N, Jensen A, Cutler C.
The big chill: improving the odds after cardiac arrest.
RN. 2005;68(5):58–62.
3. Safer J, Kochanek P. Therapeutic hypothermia after
cardiac arrest [editorial]. N Engl J Med. 2002;346:
612–613.
4. Varon J, Pilar A. Therapeutic hypothermia: past, present,
and future. Chest. 2008;133(5):1267–1274.
5. Keresztes P, Brick K. Therapeutic hypothermia after cardiac
arrest. Dimens Crit Care Nurs. 2006;25(2):71–76.
6. Cushman L, Warren M, Livesay S. Bringing research to
the bedside: the role of induced hypothermia in cardiac
arrest. Crit Care Nurs Q. 2007;30(2):143–153.
7. Bernard S, Gray T, Buist M, et al. Treatment of comatose
survivors of out-of-hospital cardiac arrest with induced
hypothermia. N Engl J Med. 2002;346:557–563.
8. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic
hypothermia to improve the neurologic outcome
after cardiac arrest. N Engl J Med. 2002;346:549–556.
9. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y,
Huyghens L. Mild hypothermia induced by a helmet
device: a clinical feasibility study. Resuscitation. 2001;51:
275–281.
10. Oddo M, Schaller MD, Feihl F, Ribordy V, Liaudet L. From
evidence to clinical practice: effective implementation of
therapeutic hypothermia to improve patient outcome
after cardiac arrest. Crit Care Med. 2006;34(7):1865–1873.
11. Nolan J, Morley P, Vanden Hoek R, et al. Therapeutic
hypothermia after cardiac arrest: an advisory statement
by the advanced life support task force of the International
Liaison Committee of Resuscitation. Circulation.
2003;108:118–121.
12. Bader MK, Rovzar M, Baumgartner L, Winokur R, Cline
J, Schiffman G. Keeping cool: a case for hypothermia
after cardiopulmonary resuscitation. Am J Crit Care.
2007;16(6):631–635.
13. Holden M, Makic M. Clinically induced hypothermia: why
chill your patient. Adv Crit Care. 2006;17(2):125–132.
14. Merchant R, Abella B, Peberdy M, et al. Therapeutic
hypothermia after cardiac arrest: unintentional overcooling
is common using ice packs and conventional cooling
blankets. Crit Care Med. 2006;34(12)(suppl):S490–S494.
15. Medivance Web site. Arctic Sun ® temperature management
system. http://www.medivance.com/html/products
_arcticgel.htm. Accessed December 31, 2008.
16. Bernard S, Buist M, Monteir O, Smith K. Induced
hypothermia using large volume, ice-cold intravenous
fluid in comatose survivors of out-of-hospital cardiac
arrest: a preliminary report. Resuscitation. 2003;56:9–13.
17. Kliegel A, Losert H, Sterz F, et al. Cold simple intravenous
infusions preceding special endovascular cooling
for faster induction of mild hypothermia after
cardiac arrest: a feasibility study. Resuscitation. 2005;64:
347–351.
18. Alsius. Intravascular temperature management: products.
http://www.alsius.com/products. Accessed December
31, 2008.
19. Hoedemaekers C, Ezzahti M, Gerritsen A, et al. Comparison
of different cooling methods to induce and maintain
normo- and hypothermia in ICU patients: a prospective
intervention study. Crit Care. 2007;11:R91.
20. Peberdy M, Torbey M. Hypothermia after cardiac arrest:
clinical perspective on monitoring, treatment and
prognostication. Presented lecture online via Inquisit.
http://www.inquist.org/education/category.asp?catalog
%5Fname=Learning%200n%20Demand&category
%5Fname=Board+of+Registered+Nursing+%2D+State
+of+California&Page=4.
21. Badjatia N, Strongilis E, Gordon E, et al. Metabolic
impact of shivering during therapeutic temperature
modulation: the Bedside Shivering Assessment Scale.
Stroke. 2008;39:3242–3247.
22. Farley A, McLafferty E. Nursing management of the
patient with hypothermia. Nurs Stand. 2008;22(17):43–46.
23. Kilgannon J, Roberts B, Stauss M, et al. Use of a standardized
order set for achieving target temperature in
the implementation of therapeutic hypothermia after
cardiac arrest: a feasibility study. Acad Emerg Med. 2008;
15(6):499–505.
24. Bartlett E. Temperature measurement: why and how in
intensive care. Intensive Crit Care Nurs. 1996;12:50–54.
353

AACN
ADVANCED CRITICAL CARE
Test writer: Teresa Wavra, RN, MSN, CNS, CCRN
Sharon A. Hoier, RN, BSN, CEN, MICN
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Category: A, Synergy CERP A
Passing score: 8 correct (73%)
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Induced Moderate Hypothermia After Cardiac Arrest
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CE Test Questions
Induced Moderate Hypothermia After Cardiac Arrest
Objectives:
Upon completion of this article, the reader will be able to:
1. Review pathophysiology of decreased perfusion and reperfusion injury following a cardiac arrest.
2. Examine research on mild hypothermia.
3. Describe nursing management of patients receiving mild hypothermia after cardiac arrest.
4. Identify candidates for mild hypothermia following cardiac arrest using inclusion and exclusion criteria.
1. After return of spontaneous circulation, which of the following
leads to mitochondrial damage and cell death?
a. Release of serotonin
b. Release of free radicals, catecholamines, and cytokines
c. Increase in blood pressure
d. Sodium shifts
2. Noninvasive methods of induction of hypothermia such
as using a cooling blanket not attached to automatic
temperature control module, ice packs, fans, and
alcohols baths can result in which of the following?
a. Higher risk of unintentional overcooling or warming too
quickly
b. Decreased labor intensity
c. Reaching the target temperature the quickest every time
d. Use of evidence-based practice proven to improve outcomes
3. What percentage of the patient's skin is approximately
covered when using Medivance gel pads?
a. 80% b. 30%
c. 40% d. 100%
4. In the Hoedemaekers study, which of the following
methods did not overshoot target temperature?
a. Iced intravenous fluids followed by ice packs
b. Gel-coated external cooling device
c. Water-circulating cooling system that used blankets placed
under and over the patient
d. Intravascular cooling system
5. What signs and symptoms of shivering should be
monitored?
a. Improvement in venous oxygen saturation
b. Decrease in respiratory rate
c. Palpation of muscle fasciculation on the face or chest
d. Development of paronychia
6. During hypothermia, what is the percentage of decrease
in systemic clearance of sedating and analgesic drugs?
a. 30 to 50% clearance b. 40 to 60% clearance
c. 10% clearance d. 5% clearance
7. How does the body attempt to conserve heat during
hypothermia?
a. Increased heart rate and vasoconstriction
b. Increased heart rate and vasodilation
c. Decreased heart rate and decreased respiratory rate
d. Vasodilation and increased urine output
8. What are the causes of cold diuresis?
a. Suppression of antidiuretic hormone and an increase in the
reabsorption of solutes
b. Increase in the reabsorption of solute
c. Increase in antidiuretic hormone
d. Suppression of antidiuretic hormone and a decrease in the
reabsorption of solutes in the loop of Henle
9. What puts the patient at risk for hyperkalemia?
a. Overcooling
b. Over treatment of hypokalemia during the cooling phase
c. Under treatment of hypokalemia during cooling
d. Cold diuresis
10. How can the use of 100% oxygen during the first hour
following cardiac arrest harm the patient?
a. Increased risk for arrhythmias
b. Oxidative stress to the postischemic neurons
c. Harms the cerebrum during reperfusion
d. Decreases renal function during reperfusion
11. Which of the following patients are candidates for
induction of hypothermia after cardiac arrest?
a. Patient has return of spontaneous circulation and is awake
and alert
b. Witnessed cardiac arrest with return of spontaneous circulation
and down time of less than 15 minutes
c. Patient with life threatening arrhythmias
d. Pregnant patient has return of spontaneous circulation in
less then 60 minutes
355