Acute Care Advisor: Improving outcomes with therapeutic hypothermia
Linda Bucher PhD, RN, CEN, CNE
Rolma Buruschkin BSN, RN
Dina M. Kenyon BS, RN
Kelley Stenton RN
Susan Treseder BSN, RN

$3.95
The Nurse Practitioner: The American Journal of Primary Health Care
January 2013 
Volume 38  Number 1
Pages 49 - 52
 
  PDF Version Available!

ABSTRACT
Mr. S, 57, experienced a foreign body airway obstruction and subsequent cardiac arrest while eating lunch at work. His coworkers called 911 and began CPR; an automated external defibrillator (AED) was not available. Paramedics responded to the scene and found Mr. S in pulseless ventricular tachycardia (VT). They performed rapid defibrillation, ensured continued high-quality CPR, and established peripheral venous access. He was given epinephrine and intubated. Return of spontaneous circulation (ROSC) occurred after an estimated code time of 16 minutes. He arrived at the ED unresponsive and in a sinus bradycardia. His medical history includes hypertension and type 2 diabetes.Mr. S may be a candidate for therapeutic hypothermia and will need quick intervention to avoid possible or further neurologic decline.Each year, there are nearly 383,000 out-of-hospital sudden cardiac arrests and 88% of these occur at home.1 Only about 33% of those who experience an emergency medical services (EMS)-treated out-of-hospital cardiac arrest report symptoms within 1 hour of arrest. Fewer than 25% of EMS-treated out-of-hospital cardiac arrest victims have an initial rhythm of ventricular fibrillation (VF), VT, or are shockable by an AED.2Therapeutic hypothermia is a controlled reduction of the core body temperature to 32[degrees] C to 34[degrees] C (89.6[degrees] F to 93.2[degrees] F) and is used in patients who have not regained consciousness after ROSC following cardiac arrest. Cardiac arrest can result in global ischemia, direct cell damage, and cerebral edema, leading to a high rate of cerebral ischemia. Hypoxic brain injury directly results in neuronal damage and cerebral edema. The earliest rationale for the effects of hypothermia as a neuroprotectant was based on the slowing of cellular metabolism that resulted from a drop in body temperature. For every 1[degrees] C (1.8[degrees] F) drop in body temperature, cellular metabolism slows by 5% to 7%.3 Consequently, hypothermia protects

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