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Induced Moderate Hypothermia After Cardiac Arrest - American ...

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MCKEAN<br />

AACN Advanced Critical Care<br />

hypothermia on dogs after cardiac arrest<br />

demonstrated positive outcomes that included<br />

improved neurological status and survival outcomes.<br />

3 This led the medical community to<br />

explore induced hypothermia following cardiac<br />

arrest once again as a possible intervention<br />

for humans. 4 It was not until 2 landmark<br />

studies were published in 2002 that induced<br />

hypothermia was considered best practice for<br />

patients following cardiac arrest. 2<br />

Supportive Research<br />

Bernard and colleagues 7 compared the use of<br />

induced hypothermia with standard treatment<br />

for patients following VF arrest who remained<br />

comatose after return of spontaneous circulation<br />

(ROSC). Patients were randomly assigned<br />

to hypothermia or normothermia (standard<br />

care). The patients assigned to hypothermia<br />

were cooled to 33C within 2 hours after ROSC<br />

and were kept at that temperature for 12 hours.<br />

Of the 77 patients enrolled in the trial, 49%<br />

treated with hypothermia were discharged<br />

home or to a rehabilitation facility as compared<br />

with 26% of the patients treated with standard<br />

care. 7 The odds ratio for a good outcome with<br />

hypothermia compared with normothermia<br />

was 5.25 when baseline differences in age and<br />

time from collapse to ROSC were considered. 7<br />

The <strong>Hypothermia</strong> <strong>After</strong> <strong>Cardiac</strong> <strong>Arrest</strong><br />

Study Group 8 studied patients presenting in the<br />

emergency department with VF or nonperfusing<br />

ventricular tachycardia with ROSC. The<br />

patients randomly selected to receive hypothermia<br />

were cooled and maintained at 32C to<br />

34C for 24 hours. Fifty-five percent of patients<br />

who received hypothermia had a favorable<br />

outcome, indicating that the patient was able<br />

to live independently and work at least part<br />

time. Only 39% of patients who were maintained<br />

at normothermia had similar favorable<br />

outcomes. 8 Mortality at 6 months was 41% in<br />

the hypothermia group as compared with 55%<br />

in those who did not receive hypothermia. 8<br />

Several other studies have shown benefits<br />

related to induced mild hypothermia following<br />

cardiac arrest. Hachimi-Idrissi and colleagues 9<br />

conducted a study inducing hypothermia by<br />

using a helmet device containing a solution of<br />

aqueous glycerol around the head and neck to<br />

cool the patient to 34°C. Patients who had cardiac<br />

arrest from pulseless electrical activity or<br />

asystole of presumed cardiac origin were considered<br />

for this trial. Study results revealed<br />

patients who received hypothermia had a significantly<br />

higher central venous oxygen saturation<br />

and significantly lower arterial lactate<br />

concentrations and oxygen extraction ratio. 9<br />

Another study conducted by Oddo and colleagues<br />

10 included patients who experienced<br />

out-of-hospital cardiac arrest from VF, asystole,<br />

and pulseless electrical activity. A good<br />

outcome, defined as Glasgow–Pittsburgh<br />

Cerebral Performance Category 1 or 2, was<br />

seen in 55.8% of the patients who received<br />

hypothermia treatment as compared with<br />

25.6% treated with standard treatment for<br />

patients with cardiac arrest due to VF. 10<br />

In October 2002, the International Liaison<br />

Committee on Resuscitation (ILCOR) made the<br />

recommendation, based on the above evidence,<br />

that all unconscious adult patients with ROSC<br />

following out-of-hospital cardiac arrest due to<br />

VF should be cooled to 32°C to 34°C for 12 to<br />

24 hours. ILCOR also stated that other<br />

rhythms that cause cardiac arrest and in-hospital<br />

cardiac arrests may benefit from hypothermia.<br />

11 In 2005, the <strong>American</strong> Heart Association<br />

(AHA) included these recommendations in the<br />

postresuscitation support guidelines. 1<br />

Effects of Cerebral Ischemia and<br />

<strong>Induced</strong> <strong>Hypothermia</strong><br />

The brain has a small amount of oxygen<br />

stores. When cerebral perfusion and oxygen<br />

delivery stop during cardiac arrest, the oxygen<br />

stores are depleted within 20 seconds. 6 If a<br />

patient was connected to continuous electroencephalography<br />

(EEG) during cardiac<br />

arrest, clinicians would see isoelectric lines<br />

after 20 seconds, indicating no brain activity<br />

present. 4 <strong>After</strong> oxygen is depleted, the brain<br />

turns to anaerobic metabolism to sustain function.<br />

Glucose and adenosine triphosphate levels<br />

are depleted after 5 minutes if return of<br />

blood flow is not achieved. 6 This causes ion<br />

pumps that use adenosine triphosphate to fail,<br />

allowing for electrolyte imbalance, including<br />

potassium, sodium, and calcium, resulting in<br />

cellular edema and cell death. 12<br />

<strong>After</strong> ROSC, it would be assumed that once<br />

oxygen supply was returned to the brain, cell<br />

death would stop. However, it is believed that<br />

reperfusion initiates chemical processes that<br />

lead to inflammation and continued injury in<br />

the brain. This is known as reperfusion injury.<br />

Reperfusion injury is thought to include the<br />

release of free radicals, nitric oxide, catecholamines,<br />

cytokines, and calcium shifts,<br />

which all lead to mitochondrial damage and<br />

344

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