The Hypothermia After Cardiac Arrest Study Group Cooled

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CHILL OUT/ SAVE A BRAIN FOR LATER USE!
Kenny Lawrence, RN Northeastern State
University EBP Symposium April 23,
2010 kenrn_at_sbcglobal.net
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CHILL OUT/ SAVE A BRAIN FOR LATER USE!

• 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/12656
  65152970DS324120HeartStrokeUpdate_2010.pdf

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NEUROLOGICAL STATISTICS

• 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.

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In-Hospital Cardiac Arrests

• 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/downl
  oadable/heart/1236978541670OUT_OF_HOSP.pdf

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Current Research

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

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Learning Objectives

• Discuss pertinent research findings that lead to
  the AHA 2005 guidelines for post resuscitation
  induced hypothermia.
• Analyze the neuro-protective benefits of
  therapeutic hypothermia in the post cardiac
  arrest patient.

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HYPOTHERMIAA HISTORICAL PERSPECTIVE

• Hippocrates advocated packing wounded patients in
  snow and ice to reduce hemorrhage. We dont have
  records of his statistics to know if it worked.

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HYPOTHERMIAA HISTORICAL PERSPECTIVE

• In the 1950s, 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.

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HYPOTHERMIAA HISTORICAL PERSPECTIVE

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

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HYPOTHERMIAA HISTORICAL PERSPECTIVE

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

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Research on Therapeutic Hypothermia

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

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HACA

• The Hypothermia After Cardiac Arrest
• Study Group
• Cooled patients to a target of 33C 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.

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HACA

• 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.

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HACA

• 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.

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Bernard Study

• Cooled patients with the removal of clothing and
  the application of ice packs to the head and
  torso to a target of 33C for 12 hours.
• Population adult survivors of out-of-hospital
  VF arrest. Patients were randomly assigned to
  normothermia or hypothermia treatment groups.

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Bernard Study

• 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.

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Bernard Study

• 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.

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2002 ILCOR

• 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

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2002 ILCOR

• Unconscious adult patients with
• spontaneous circulation after out-of-hospital
• cardiac arrest should be cooled to 32C to
• 34C for 12 to 24 hours when the initial
• rhythm was ventricular fibrillation (VF).
• Such cooling may also be beneficial for other
• rhythms or in-hospital cardiac arrest.

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2005 AHA GUIDELINES FOR POST RESUSCITATION
INDUCED HYPOTHERMIA

• Class I Benefit gtgt Risk (Strongest)
• Class IIa Benefit gt Risk
• Class IIb Benefit gt Risk
• Class III Benefit lt Risk (Harm)

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2005 AHA GUIDELINES FOR POST RESUSCITATION
INDUCED HYPOTHERMIA

• 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

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Post Cardiac Arrest Syndrome

• 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). PostCardiac
  Arrest Syndrome. Circulation, 118, 2452-2483.
  doi 10.1161/CIRCULATIONAHA.108.190652

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Reperfusion Injury

• 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

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Post Cardiac Arrest Brain Injury

• 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.

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Post Cardiac Arrest Brain Injury

• 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.

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MECHANISMS OF NEUROPROTECTION

• CEREBRAL METABOLISM IS DECREASED
• The cerebral metabolic rate is decreased by 6
  to 7 for every 1C 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.

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MECHANISMS OF NEUROPROTECTION

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

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Why Perform Therapeutic Hypothermia

• Mild hypothermia is the only therapy applied in
  the post cardiac arrest setting that has been
  shown to increase survival rates and neurological
  outcomes.
• Source
• ILCOR Consensus Statement. (2008). PostCardiac
  Arrest Syndrome. Circulation, 118, 2452-2483.
  doi 10.1161/CIRCULATIONAHA.108.190652