chill out! - save a brain for later use

Kenny Lawrence, RNNortheastern State UniversityEBP SymposiumApril 23, 2010kenrn@sbcglobal.net

“Each year there are an estimated 295,000 emergency medical services-treated out-of hospital cardiac arrests in the United States.”

Source:American Heart Association. (2010). Heart Disease and Stroke Statistics. Retrieved from: http://americanheart.org/downloadable/heart/1265665152970DS3241%20HeartStrokeUpdate_2010.pdf

“Ten to thirty percent of patients who survive an out-of-hospital cardiac arrest will have permanent brain damage.”

Source:McKean, S. (2009). Induced Moderate Hypothermia After Cardiac Arrest. AACN Advanced Critical Care, 20, 343.

The rates of survival to discharge after in-hospital cardiac arrest are 27% among children and 18% among adults.

Source: American Heart Association. (2009). Out-of-Hospital Cardiac Arrest; Statistical Fact Sheet.

Retrieved from http://www.americanheart.org/downloadable/heart/1236978541670OUT_OF_HOSP.pdf

Therapeutic hypothermia has been shown to provide neuro-protective properties in the post-cardiac arrest victim.

1. Discuss pertinent research findings that lead to the AHA 2005 guidelines for post resuscitation induced hypothermia.

2. Analyze the neuro-protective benefits of therapeutic hypothermia in the post cardiac arrest patient.

Hippocrates advocated packing wounded patients in snow and ice to reduce hemorrhage. We don’t have records of his statistics to know if it worked.

In the 1950’s, hypothermia was utilized for intracranial aneurysm clipping and for cardiac surgery during circulatory arrest. Since this is no longer used, it makes you wonder how effective it was.

In the 1960’s, clinical trials with hypothermia (30 °C or lower) were discontinued because of side effects, uncertain benefits and management problems (BRRR….is that frostbite?).

In the 1980’s, animal studies were conducted that showed benefits using a milder more controlled hypothermia (32-34°C) with fewer side effects.

In 2002 the Bernard and Hypothermia After Cardiac Arrest (HACA) studies were done.

The Hypothermia After Cardiac Arrest Study Group

• Cooled patients to a target of 33°C for 24 hours after cardiac arrest and ROSC using cooling blankets. Ice packs were required in 70% of the patients.

• Population: adult comatose survivors of VF or pulseless VT arrest in the field.

137 patients were cooled (hypothermia group) 138 patients were not (normothermia group).

Neurological status six months after cardiac arrest was the primary measurement in this study.

55% of the patients in the hypothermia group had favorable neurological outcomes six months after cardiac arrest.

39% of the patients in the normothermia group had favorable neurological outcomes six months after cardiac arrest.

Source:Ramsay, P. & Maxwell, R. (2009). Advancements in Cardiopulmonary Resuscitation: Increasing Circulation

and Improving Survival. American Surgeon, 75, 359-362.

Cooled patients with the removal of clothing and the application of ice packs to the head and torso to a target of 33°C for 12 hours.

Population: adult survivors of out-of-hospital VF arrest. Patients were randomly assigned to normothermia or hypothermia treatment groups.

43 patients were cooled (hypothermia group) 34 patients were not (normothermia group).

49% of the hypothermia group survived discharge to home or a rehabilitation facility with favorable neurological outcomes.

26% of the normothermia group survived discharge to home or a rehabilitation facility with favorable neurological outcomes.

Source:Collins, T., & Samworth, P. (2008). Therapeutic hypothermia following cardiac arrest: a

review of the evidence. Nursing In Critical Care, 13, 144-151.

On the basis of the published evidence to date, the Advanced Life Support (ALS) Task Force of the International Liaison Committee on Resuscitation (ILCOR) made the following recommendations in October 2002:

• “Unconscious adult patients withspontaneous circulation after out-of-hospitalcardiac arrest should be cooled to 32°C to34°C for 12 to 24 hours when the initialrhythm was ventricular fibrillation (VF).”

• “Such cooling may also be beneficial for otherrhythms or in-hospital cardiac arrest.”

Class I Benefit >> Risk (Strongest)

Class IIa Benefit > Risk

Class IIb Benefit >= Risk

Class III Benefit < Risk (Harm)

Comatose out-of-hospital adult patient with ROSC after VF:

Class IIa recommendation

In-hospital arrest, other rhythms: Non VF, PEA, Asystole e.g.

Class IIb recommendation

“Post cardiac arrest syndrome is a unique and complex

combination of pathophysiological processes, which

include: post– cardiac arrest brain injury, post–

cardiac arrest myocardial dysfunction and systemic

ischemia/reperfusion response. This state is often

complicated by a fourth component: the unresolved

pathological process that caused the cardiac arrest.”

Source:

ILCOR Consensus Statement. (2008). Post–Cardiac Arrest Syndrome. Circulation, 118, 2452-2483. doi: 10.1161/CIRCULATIONAHA.108.190652

Reperfusion (return of adequate blood flow and oxygen) initiates chemical processes that lead to inflammation and continued injury in the brain.

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 cell death.

This process may last as long as 24 to 48 hours

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.

After oxygen is depleted, the brain turns to anaerobic metabolism to sustain function.

Glucose and adenosine triphosphate (ATP) levels are depleted after 5 minutes if return of blood flow is not achieved. This causes ion pumps that use ATP to fail, allowing for electrolyte imbalances including potassium, sodium, and calcium, resulting in cellular edema and cell death.

CEREBRAL METABOLISM IS DECREASED

“The cerebral metabolic rate is decreased by 6% to 7% for every 1°C decrease in body temperature. Decreasing the cerebral metabolic rate decreases cerebral oxygen consumption.”

Source:Koran, Z. (2009). Therapeutic hypothermia in the postresuscitation patient: the development and

implementation of an evidence-based protocol for the emergency department. Journal Of Trauma Nursing: The Official Journal Of The Society Of Trauma Nurses, 16, 48-57.

INFLAMMATORY AND IMMUNOLOGICAL RESPONSES Hypothermia is also thought to decrease many of

the chemical reactions that occur during reperfusion, such as free radical production

Temperatures less than 35°C lead to decreased neutrophil and macrophage functions. This reduces the inflammatory response that is initiated after ischemia.

“Mild hypothermia is the only therapy applied in the post– cardiac arrest setting that has been shown to increase survival rates and neurological outcomes.”

SourceILCOR Consensus Statement. (2008). Post–Cardiac Arrest Syndrome. Circulation, 118, 2452-2483. doi: 10.1161/CIRCULATIONAHA.108.190652