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

$7.95
Nursing2015
January 2013 
Volume 43  Number 1
Pages 30 - 36
 
  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) wasn't available. Paramedics responded to the scene, found Mr. S in pulseless ventricular tachycardia (VT), performed rapid defibrillation, ensured continued high-quality CPR, established peripheral venous access, administered I.V. epinephrine, and intubated him. Return of spontaneous circulation (ROSC) occurred after an estimated code time of 16 minutes. He arrived at the ED unresponsive in sinus bradycardia. His medical history includes hypertension and type 2 diabetes.Mr. S may be a candidate for therapeutic hypothermia. Prompt intervention could help to reduce the potential for further neurologic decline. Understanding the link between the pathophysiology of cardiac arrest and the physiology underlying therapeutic hypothermia can facilitate the nursing management of this challenging patient.Each year, nearly 383,000 out-of-hospital sudden cardiac arrests occur, 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) or VT or have a shockable rhythm analyzed by an AED.2Therapeutic hypothermia, a controlled reduction of core body temperature to 89.6[degrees] F to 93.2[degrees] F (32[degrees] C to 34[degrees] C), is used in patients who don't regain consciousness after ROSC following cardiac arrest. How does therapeutic hypothermia help the body? 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

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