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Critical Care Nurse. 2007;27: 36-42
Copyright © 2007 by the American Association of Critical-Care Nurses.
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Clinical Article
CE Article

Induced Hypothermia for Patients With Cardiac Arrest

Role of a Clinical Nurse Specialist

Teri M. Kozik, RN, MS, CCRN

Teri Kozik is a cardiovascular clinical nurse specialist at Saint Mary’s Regional Medical Center, Reno, Nevada. She currently is working on her doctoral degree through the College of Nursing at the University of Arizona, Tucson, Arizona.

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.

Financial Disclosures
None reported.

This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

  1. Identify the outcome goals for the use of induced hypothermia after cardiac arrest
  2. Describe strategies for developing a protocol for induced hypothermia
  3. Discuss the role of the clinical nurse specialist in the development and implementation of the hypothermia protocol

Corresponding author: Teri M. Kozik, St Mary’s Regional Medical Center, 235 W 6th St, Reno, NV 89503 (e-mail: terikozik{at}yahoo.com or teri.kozik{at}saintmarysreno.com).

Saint Mary’s Regional Medical Center is a Catholic facility in Reno, Nevada, that provides care to many rural communities. The critical care unit had not had a clinical nurse specialist (CNS) or an educator for approximately 2 years before I was hired as a cardiovascular CNS in the fall of 2005. I was hired because there was an opportunity to improve quality measurements and best-practice standards, and increase staff education in the department. In this article, I describe how having a CNS in the department changed practice, facilitated the development of a protocol based on current research, and improved outcomes for patients who had out-of-hospital cardiac arrest.


   Background
Top
 Background
Strategy
 Case Report
 Discussion
 References
 
Patients who have out-of-hospital cardiac arrest historically have had high mortality and morbidity rates.1 More than 90% of these patients die before even reaching the hospital, accounting for more than 300000 deaths each year in the United States alone.1 Widespread cerebral ischemia and edema leading to severe neurological impairment often develop in the patients who do survive after resuscitation.

Studies2–6 have indicated that hyperthermia due to brain injury or ischemia clearly exacerbates the degree of permanent neurological damage after cardiac arrest and contributes to an increased length of stay. Recovery correlates with body temperature. The higher body temperature is after cardiac arrest, the less neurological recovery will be; conversely, the lower body temperature is after cardiac arrest, the better neurological recovery will be.2 In experimental models,3 increased brain temperature and cerebral ischemia increased levels of excito-toxins and oxygen free radicals, leading to unstable cell membranes and an increased number of abnormal electrical depolarizations. With increases as small as 0.5°C, a greater zone of injury and neuronal loss occurred.3

Improving the outcome of patients who survive cardiac arrest requires stopping the ischemic process as quickly as possible and preventing damage from reperfusion.4,5 The results of clinical trials6,7 of induced hypothermia, to a core temperature of 32°C to 34°C for 12 to 24 hours, have suggested that this treatment may be beneficial in reducing the deleterious neurological outcomes in patients who have out-of- hospital cardiac arrest. Hypothermia decreases the metabolic rate by 6% to 7% for every decrease of 1°C in temperature. Because the cerebral metabolic rate for oxygen is the main determinant of cerebral blood flow, inducing hypothermia may improve oxygen supply and reduce oxygen consumption in the ischemic brain.5,6 Hypothermia also decreases intracranial pressure. Although unknown, the exact mechanism is thought to be related to a decrease in blood flow caused by cerebral vasoconstriction.5

Finally, when cerebral perfusion is regained in situations such as the aftermath of cardiac arrest, reperfusion injury occurs as blood flow is restored.7 The increased release of glutamate, an excitatory neuro-transmitter, from presynaptic terminals causes calcium to shift from the extracellular fluid to the intracellular fluid. This shift leads to an accumulation of oxygen free radicals and activates degradative enzymes.7 Advanced Cardiac Life Support guidelines8 now advocate avoiding hyperthermia for all patients after resuscitation and considering induction of hypothermia if a patient is unresponsive but has adequate blood pressure.

Because of these new recommendations, it is important for health-care providers to develop a good understanding of the purpose and the outcomes of inducing hypothermia in patients after cardiac arrest. In addition, because most treatments, including induced hypothermia, have associated complications,9 using the most current research and literature helps practitioners provide the most appropriate and safest care possible.


   Strategy
Top
 Background
 Strategy
Case Report
 Discussion
 References
 
Research on induced hypothermia in patients who have had out-of-hospital cardiac arrest is just now being published in nursing journals. I read a case study10 on induced hypothermia after cardiac arrest that stimulated my interest in the topic. I requested a literature search on recent research on this topic from the medical librarian. Recent publications were selected from prominent peer-reviewed journals.1,3–8 To encourage participation in changing current practice to best practice, I recruited several of the experienced staff members in the critical care unit to read the articles during a 6-week period. The same articles were also distributed to a pharmacist, an emergency department physician, a cardiology medical director, and a pulmonologist/intensivist medical director. Each staff member’s packet of articles included examples of protocols used by other acute care facilities across the United States. The protocols were obtained from hospital Web sites and by professional networking. The articles and protocols were compared, summarized, and discussed informally between each staff member and me.

After the 6 weeks, 3 of the staff nurses, a pharmacist, and I participated in a project to develop a protocol to provide the latest care for patients who had out-of-hospital cardiac arrest, educate healthcare providers about the protocol, and implement the protocol. Meetings, which I coordinated, were informal and were held in the critical care unit when staff worked. I kept notes and comments, and documents were drafted and redistributed to the group as necessary. The medical directors were consulted periodically as necessary.

A protocol was drafted after several weeks. It was reviewed by all involved medical committee sections, and revisions were made. After approximately 3 months of meetings and revisions, the final protocol was approved (see FigureGo).


Figure 1
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  		Figure Physicians’ orders for inducing hypothermia in patients who have out-of-hospital cardiac arrest.

 
Education for those involved (ie, nurses, physicians, pharmacists, and respiratory therapists) was the next step before the protocol could be implemented. A pharmacist, critical care staff involved in the project, and I provided education at staff meetings and at unit-specific in-service training sessions. Posters were developed that showed the new order set and a list of the journal articles used to develop the protocol. All critical care staff received education, because most of the critical and intensive care of patients who would be treated with induced hypothermia would be provided in the critical care unit. Education was also given to physicians and nurses in the emergency department, where the protocol would most often be initiated. During this time, the medical directors presented the final approved protocol to various medical executive committees. In the spring of 2006, the first patient was treated according to the new protocol.


   Case Report
Top
 Background
 Strategy
 Case Report
Discussion
 References
 
SB was a 56-year-old smoker with type 2 diabetes who had had intermittent chest pain for a week. He had no history of cardiac disease and had not sought medical treatment for his chest pain. He was at work on a Friday morning when he suddenly collapsed. When his coworkers realized that he was unconscious and not breathing, they called paramedics. Cardiopulmonary resuscitation was not performed until the paramedics arrived. Resuscitation began approximately 7 minutes after the cardiac arrest. Initial assessment by the paramedics indicated that SB was having ventricular fibrillation. The paramedics performed the standard Advanced Cardiac Life Support procedures, and SB’s first palpable pulse no longer requiring cardiopulmonary resuscitation occurred 17 minutes after the cardiac arrest.

Once SB was transported to the emergency department, the attending physician quickly screened him for inclusion and exclusion criteria for the induced-hypothermia protocol. Because SB’s cardiac arrest had been a witnessed event and his times to treatment and return of spontaneous circulation were well documented, he was a candidate for the protocol. The emergency department staff immediately called me to assist and add support.

Ice packs to the armpits and groin were started 20 minutes after SB’s arrival in the emergency department to start the cooling procedure as quickly as possible. An indwelling urinary catheter with a temperature probe was inserted to monitor core temperature as accurately as possible while hypothermia was induced and maintained. SB was intubated, and ventilatory support was started. He did not initiate any spontaneous breaths. He was given a bolus of vecuronium to cause paralysis and prevent shivering, which would make achieving a hypothermic state difficult. He was given midazolam for sedation in case he had any awareness of the induced paralysis. He was unresponsive, his pupils were 2.5 to 3 mm in diameter and reacted sluggishly to light, and his score on the Glasgow Coma Scale was 3/15. At the time of admission, he had sinus tachycardia with frequent runs of ventricular tachycardia. An amiodarone infusion was started, and aspirin was administered rectally for potential acute coronary syndrome, although a 12-lead electrocardiogram showed non-specific changes.

SB was transported to the critical care unit after approximately 1 hour in the emergency department. The nurses in the unit had 2 full-length body-surface-cooling ice blankets precooling. One was on the bed and the other was placed on the top surface of SB once he arrived. Continuous vecuronium and midazolam infusions were started soon after his arrival.

SB’s family members, who were at the bedside, were informed about the hypothermia procedure. They were told that although the goal of this therapy was to improve neurological function, SB’s prognosis for a full recovery was grim because of the extended period before he received cardiopulmonary resuscitation and because he had remained pulseless for so long. On the basis of their experience with outcomes of previous patients in a condition similar to SB’s and their lack of practice with this new protocol, the staff members were skeptical.

A target hypothermic temperature of 33.2°C was achieved 6 hours after SB’s arrival at the hospital and was maintained until rewarming started 22 hours later. The goal had been to achieve the target temperature in a shorter time, because in the randomized trials used as models for the protocol, target temperatures were achieved in 2 to 4 hours.6,7 The physician made the decision to start rewarming 2 hours earlier than the written protocol called for (24 hours) because SB appeared to be waking up and was requiring more sedation. The level of sedation or consciousness was measured by using a bispectral index monitor, which continually analyzes a patient’s electroencephalogram during general anesthesia or sedation to assess the patient’s hypnotic state. SB stayed clinically stable during the hypothermic state.

Six hours after rewarming started, SB had a core temperature of 36.0°C and the vecuronium was discontinued. Two hours later, he started to respond to pain, although his score on the Glasgow Coma Scale remained about 5/15 to 6/15. The following morning, after approximately 12 hours of normothermia, SB started to awaken. He opened his eyes to verbal and tactile stimuli. He slowly improved, and by day 5 was extu-bated and was following simple commands. Ventilator-associated pneumonia had developed, but was successfully treated with antibiotics. On day 6, SB’s score on the Glasgow Coma Scale was 15/15, and he was transferred to the telemetry unit, where speech and occupational therapy were started to improve his overall weakness and slow speech.

During SB’s hospitalization, his troponin I enzyme level peaked at 1.5 ng/mL (1.5 µg/L). On day 10, cardiac catheterization revealed a critical occlusion of the left anterior descending artery that was subsequently stented. The ejection fraction was approximately 35%. On day 11, the results of a neurological examination indicated that SB had "no neurological deficits." He was discharged home to his family’s care on day 12. By the fall of 2006, he returned to work.


   Discussion
Top
 Background
 Strategy
 Case Report
 Discussion
References
 
Evidence-based practice is a common goal of staff in hospitals, but obtaining and using the knowledge to carry out such practice can often be challenging. The public continues to demand quality health-care and outcomes. With the inception of the Internet, consumers have access to statistics on hospitals’ and physicians’ outcome data. Using research to provide the best care possible has become an important aspect of healthcare.

The position of CNS was originated in the 1900s and has evolved to an advanced practice role.11 The role of a CNS has 5 domains: practitioner, researcher, consultant, leader/administrator, and educator/mentor.12 Within these domains, the practice standard of a CNS is to help staff members understand research findings and apply the findings to practice. These specialists consult and support nurses in professional development.13 By doing so, CNSs play a key role in providing quality patient care, improving outcomes for patients, reducing hospital costs, and engaging staff to use research to improve and support practice.14 Involving and educating staff nurses and helping them develop research-based care and protocols empower the nurses to become best practice change agents. This opportunity encourages a stronger clinical practice by keeping staff current with ongoing research, providing up-to-date care based on research findings before the findings become standard practice, and promoting recognition in nursing excellence.

The hypothermia protocol was so successful at Saint Mary’s that staff members are starting to think "hypothermia" the minute anyone has a cardiac arrest in the hospital as well as outside the hospital. Use of the protocol has caused such an increased awareness that staff members are asking for chart audits of patients for whom the protocol is not used. This protocol has encouraged staff members to think beyond published research and has created an excitement to learn and apply research to patients in the staff members’ unit.

Since the successful case of SB, staff nurses in the critical care unit are becoming more involved in projects and research of their own through use of the nursing research committee and the medical librarian. Currently, staff members in the critical care and emergency departments are evaluating different cooling devices to induce hypothermia in less than the 6 hours required in SB’s case.

The CNS at this medical center played an important role in this particular project and case. Educating staff and empowering them to use research are examples of raising the bar for nursing care and improving patient outcomes at Saint Mary’s.


   Acknowledgments
 
Special thanks to Donna Alexander, medical librarian, and the supportive and outstanding critical care unit staff. Their trust, expertise, and compassion are responsible for the quality outcomes accomplished at Saint Mary’s.


   References
Top
 Background
 Strategy
 Case Report
 Discussion
 References
 

  1. Abella BS, Rhee JW, Huang KN, Vanden Hoek TL, Becker LB. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation. 2005;64(2):181–186.[Medline]
  2. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med. 2001;161(16):2007–2012.[Abstract/Free Full Text]
  3. Diringer MN, Reaven NL, Funk SE, Uman GC. Elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. Crit Care Med. 2004;32;1489–1495.[Medline]
  4. Holzer M, Bernard SA, Hachimi-Idrissi S, Roine RO, Sterz F, Mullner M. Hypothermia for neuroprotection after cardiac arrest: systematic review and individual patient data meta-analysis. Crit Care Med. 2005; 33:414–418.[Medline]
  5. Bernard SA, Buist M. Induced hypothermia in critical care medicine: a review. Crit Care Med. 2003;31:2041–2051.[Medline]
  6. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549–556.[Abstract/Free Full Text]
  7. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557–63.[Abstract/Free Full Text]
  8. American Heart Association. Highlights of the 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Curr Emerg Cardiovasc Care. 2005–2006;16(4):1–27.
  9. Polderman KH. Application of therapeutic hypothermia in the intensive care unit. Opportunities and pitfalls of a promising treatment modality, part 2: practical aspects and side effects. Intensive Care Med. 2004;30(5):757–769.[Medline]
  10. Calver P, Braungardt T, Kupchik N, Jensen A, Cutler C. The big chill: improving the odds after cardiac arrest. RN. 2005;68(5):58–62.[Medline]
  11. Holmes SB. Advanced practice nursing role: clinical nurse specialist. Orthop Nurs. 1998; 17(6):61–64.[Medline]
  12. Stark SW. The effects of master’s degree education on the role choices, role flexibility, and practice settings of clinical nurse specialists and nurse practitioners. J Nurs Educ. 2006;45(1):7–15.[Medline]
  13. Clinical Nurse Specialist Interest Group. Standards of practice. http://www.rnao.org/. Accessed July 23, 2007.
  14. Benedict L, Robinson K, Holder C. Clinical nurse specialist practice within the Acute Care for Elders interdisciplinary team model. Clin Nurse Spec. 2006;20(5):248–252.[Medline]




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