Therapeutic Hypothermia

NUR 437 Nursing Research: The Beneficial Effects of Therapeutic Hypothermia

According the statistics from the American Heart Association (2012), when electrical impulses to the heart suddenly become uncoordinated, causing the immediate cessation of the heart to function, this is considered a cardiac arrest. Cardiac arrest that occurs outside of the hospital has an incidence of 359,400 with a survival rate of 9.5 % (American Heart Association (AHA), 2012). In absence circulation, neurological injury occurs from the lack of oxygen delivered to the brain (Deckard & Ebright, 2011). This disruption of oxygen can cause a cascade of events that include hypoxia, cellular death, the activation of the inflammatory response, and cerebral edema. The continuation

Therapeutic hypothermia has been an identified intervention that will slow the inflammation process and improve neurological outcomes for patients experiencing out of hospital cardiac arrest (Bernard et al., 2010). Therapeutic hypothermia is defined as the controlled induction of reducing a patient’s core body temperature below 34° C while managing the body’s compensatory mechanism by prevent shivering (So, 2010). The integrity of the process is the accurate measurement of the core body temperature, which can be obtained if the probe is place in the central venous, bladder, rectal, or esophageal (So, 2010). Therapeutic hypothermia occurs in the following phases: induction, maintenance, and rewarming (Deckard & Ebright, 2011). The induction phase begins when a health care professional lowers the patient’s core temperature to the target temperature. (Deckard & Ebright, 2011). Cooling methods include a combination of external cooling methods such as, surface cooling with ice packs and cooling blankets, as well as internal cooling methods such as, catheter-based technologies for the infusion of cold fluids (Mooney et al., 2011). During the induction phase it is important for the nurse to pay close attention to the patient’s blood pressure and fluid balance, as

(2014), collected data for the control group using historical data for 37 adult patients hospitalized at the same center from 2009 to 2011. Whereas the group that received the intervention was collected on 28 adult patients treated from 2011 to 2013. Inclusion into the study required a systolic blood pressure above 80 mm HG, cardiac arrest time and recruitment time of less than four hours, initial Glasgow Coma Scale (GCS) of < 8, and an age older than 18. Exclusion criteria included active bleeding, unconsciousness prior to the cardiac arrest, presence of any disease that diminished normal life expectancy, and an initial body temperature of less than 30°C. The study monitored temperature using an esophageal temperature probe with a target temperature set at 33°C. The maintenance phase lasted for 36 hours. During the rewarming phase the core temperature was increased 0.01°C per hour. Cognitive function was assessed using the Cerebral Performance Categories (CPC) scale and Glasgow Coma Scale. Assessments were performed by a qualified neurologist. For the intervention group, the assessment was immediately after the complication of the intervention and the discontinuation of sedation and analgesia medications. The control group was assessed after the cessation of anesthetic administration. A CPC score of 1 or 2 and a GCS of 13 or above were associated with a favorable neurological outcome. All participants scored a favorable