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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MCKEAN 


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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VOLUME 20 • NUMBER 4 • OCTOBER–DECEMBER 2009 

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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MCKEAN 


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 

346



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 

348



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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MCKEAN 


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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MCKEAN 


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



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

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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

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