Therapeutic Hypothermia

Practice development issues around Induced Therapeutic Hypothermia (ITH) on Cardiac Arrest Patients Contents 1. Introduction 2. Pathophysiological changes during cardiac arrest and return of spontaneous circulation 3. Physiological benefits of therapeutic hypothermia 4. Guideline for induced therapeutic hypothermia after cardiac arrest 5. The UHL guideline’s goal of therapeutic hypothermia 6. Preparation, Monitoring and Supportive therapy 7. Cooling Methods 8. The relative experience 9.
The role of advanced clinical practitioner and multidisciplinary approach 10. Synthesis ————————————————- 11. Conclusion ————————————————- 1. Introduction In UK, there are approximately 50,000 treated cardiac arrests, of which 5-30% of patients survive to leave the hospital every year (Intensive Care Society, 2008). The Majority of these patients have suffered ischemic brain injury, which results in severe disability or ultimately leads to death.
Until recently, there has been no intervention proving a significant reduction in the incidence of brain injury in arrest survivors; however in recent years induced therapeutic hypothermia (ITH) has been used to improve the neurological outcome of comatose patients who had return of spontaneous circulation (ROSC) after resuscitation following sudden cardiac arrest (Holden & Makic 2006). Although it is an evidence-based method, it has its own limitations and complications.

The purpose of this assignment is to look at the current practice in own area, supporting national and international recommendations, review current literature and evidence-based nursing implications in caring for those patients. The physiological benefits of hypothermia, multidisciplinary approach of clinically cooled patients, practice development issues around these patients and scope of advanced nursing practice will also be discussed. 2. Pathophysiological changes during cardiac arrest and return of spontaneous circulation Under ormal circumstances, the brain takes 15% of the cardiac output and consumes 20% of total body oxygen supply (Girolami, Anthony & Froch, 1999). During cardiac arrest the blood supply to the brain decreases or stops, which leads to less or no oxygen supply to the brain causing loss of consciousness. This hypoxic state in the brain can cause depletion of glucose and adenosine triphosphate store (the brain’s source of energy) (Safar, Behringer, Bottiger, et al. 2002).
In hypotensive state or no blood supply state to the brain, membrane depolarize, calcium influxes, glutamate is released leading to acidosis and lipases, proteases, and nucleases are activated contributing to cerebral oedema (Warner 1997, Safar & Behringer 2003). During the spontaneous return of circulation (SROC), further damage to the brain can occur. This is called reperfusion injury which causes series of process involving release of iron, free radicals, nitric oxide, catecholamine, renewed excitatory amino acid and calcium shifts (Warner 1997, Safar & Behringer 2003).
These series of process will result in mitochondrial damage, DNA fragmentation, and cell death (Warner 1997, Safar & Behringer 2003). This process will continue for 3days (Safar & Behringer 2003). This process of injury and subsequent recovery varies depends upon the severity of injury (Girolami et al. 1999). The severity of injury can vary from reversible injury with full recovery to global irreversible injury leading to brain death (Girolami et al. 1999). The severity of injury is dependent on the length of ischemic state and the duration of reduced blood flow (Girlami et al. 1999). 3.
Physiological benefits of therapeutic hypothermia There are several research have been conducted on methods to improve neurological outcome after cardiac arrest including pharmacological approaches, methods to improve cerebral circulation and oxygenation and induced therapeutic hypothermia(Bernard, Gray,Buist et al. 2002). Induced therapeutic hypothermia was used in the treatment of head injury since 1950s. Hypothermia can be divided in to mild (33? C to 35? C), moderate (28? C to32? C), and severe (<28? C) based on core body temperature (Mary Holden, 2006). Studies have indicated that mild to moderate hypothermia (32? C to34?
C) has a neurological protective mechanism within the brain that can improve a patient’s outcome after a sudden cardiac arrest. There are several theories exist on the effect of hypothermia on cerebral tissues and its benefit after cardiac arrest. Jonathan Adler (2011) has described that the possible mechanisms of actions are “decreased temperature reduces cerebral metabolism there by decreases the release of harmful chemicals(glutamate and dopamine which could lead to tissue damage), preservation of blood brain barrier, decreases the cerebral oxygen demand and prevention of cerebral oedema which will reduce the intra cranial pressure”.
Hypothermia after cardiac arrest study group (2002) and Bernard et al. (2002) also suggested the same theory. Adler (2011) also states that in the heart, the hypothermia may decrease the area of injury, promote blood reflow to the epicardium, decreases myocardial metabolic demand, and preserve intracellular high-energy phosphate stores. 4. Guideline for induced therapeutic hypothermia after cardiac arrest The University Hospital of Leicester’s (UHL) guideline for ITH (2010) is in cooperated with other ICU care bundle i. e. control of ventilation, Hemodynamic optimisation, blood glucose control and sedation optimisation.
The Guideline did not include all cardiac arrest patients for the treatment of Induced therapeutic hypothermia. The inclusion criteria for ITH (UHL guideline, 2010): * witnessed ventricular fibrillation or nonperfusing ventricular tachycardia * comatose (GCS? 9) within 6 hour of post cardiac arrest, * systolic blood pressure not below 90 mmof Hg on inotropes support * age over 18 years, * an estimated interval of less than 20minutes from the patient’s collapse to the first attempt at resuscitation by emergency medical personnel * mechanically ventilated An interval of no more than 60 minutes from collapse to return of spontaneous circulation (ROSC) Studies have shown that above-mentioned patient’s neurological outcome has improved significantly with ITH. An advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) (2003) has stated that the VF cardiac arrest survivors are the most benefitted from ITH. The effects of ITH on non-cardiac in hospital arrests are unknown therefore; ILCOR does not recommend ITH for those patients.
However, it does suggest that the use of ITH on patients who are comatose after in-hospital arrest with cardiac aetiology may be beneficial. The intensive care society (ICS) (2008) has also advised the same inclusive criteria as ILCOR including other cardiac rhythms and in-hospital cardiac arrest, as studies have shown improvement in their neurological outcome. The Cochrane database systematic review (2009) suggested that the results of their review support ILCOR’s recommendations. The exclusion criteria (UHL guideline, 2010): * major head trauma recent major surgeries * systemic infection/sepsis * patients in coma from other causes * coagulopathy or on anti-coagulant therapy * pregnancy * refractory hypoxemia(SaO2 85% 0n 100% of o2 and IPPV) The ILCOR (2003) strongly advices to avoid ITH on patients with life threatening arrhythmias and severe cardiogenic shocks. It also has some reservations on using ITH on pregnant patients and patients with primary coagulopathy until further data are available. Hypothermia causes mild platelet dysfunction, which will lead to bleeding (Holden & Makic, 2006).
Therefore, ITH is considered as contraindication for patients with coagulopathy or on anti-coagulant treatment. Adler (2011) in his literature review stated that although ITH after pulsless electrical activity (PEA) and in-hospital arrests are not studied fully, it could be used on these patients at the discretion of the treating practitioners. The practitioner should consider the most likely cause of cardiac arrest. He also suggested that the patients who had isolated respiratory arrest & patients with valid do not resuscitate order should not be treated with ITH. . The UHL guideline’s goal of Induced Therapeutic Hypothermia The ultimate goal of the UHL’s guideline (2010) is to return the patient to a state of normal neurological function with a stable cardiac rhythm and normal hemodynamic function. The guideline also advices to achieve a target temperature of 32? -34? C in 4 hours of return of spontaneous circulation, avoid cooling to <32? C. ITH should not be delayed for CT scan, cardiac catheter or other interventions. Maintain therapeutic hypothermia at 32? -34? C for 12-16 hours then passively re-warm at a rate of 0. ? C every hour. If active re-warming is required, stop active re-warming when the temperature reaches 35. 5? to avoid overshoot (UHL guideline, 2010). The ICS (2008) advices to start cooling as soon as possible and continue for 12-24hours period. More evidence is needed to determine the optimum duration of cooling treatment in human beings as the previous studies are conducted on animals. (Adler, 2011). 6. Preparation, Monitoring and Supportive therapy Tracheal intubation is necessary, as ITH is used patients who’s GCS is <8 (UHL guideline, 2010).
Provide positive ventilation support to achieve normocarbia and arterial saturation of 94-98 %( ICS, 2008). Too much oxygen during the initial stages of reperfusion exacerbates neuronal damage through production of free radicals and mitochondrial injury (Richards E. M, Fiskum G. , Rosenthal R. E, et al, 2007). Excessive ventilation can affect cerebral blood flow by decreasing PaCO2 and causes circulatory instability due to high intrathoracic pressure (ACL algorithm, 2011). Sedation and chemical paralysis (if needed) are usually necessary as cooling can be unpleasant experience (UHL Guidelines. 010). Shivering is the natural body’s attempt to maintain temperature homeostasis, which can compromise the hypothermic state as it produces heat interfering cooling process (Adler, 2011). Shivering can increase body’s oxygen demand between 40% and 100%, which can compromise patient’s respiratory status (Holden and Makic, 2006). Monitor pupillary response to light (guidelines). Raise the head of the bed at 30? as neuroprotective mechanism (Adler, 2011). Elevating the head end of the bed will help to prevent aspiration, there by reduce the risk of aspiration pneumonia (Holden and Makic, 2006).
Arterial line is placed for the constant monitoring of blood pressure and for the easy access of arterial blood gases. ECG monitoring is essential as ITH can cause dysrhythmia (most commonly bradcardia) (ICS 2008). Studies have shown that ECG changes including J wave development, VF, Bruguda syndrome & Prinzmetal’s angina can occur when cooling(Pyle, Pierson , Lepman , & Hewett , 2007). If the heart rate <40 more often but there is no hemodynamic instability ITH can be continued (Adler, 2011).
Atrial and ventricular fibrillation are other common side effects of ITH as it has negative choronotrophic effects on pacemaker tissues (Holden and Mackic, 2006). Circulatory instability is quiet common in cardiac arrest patients, therefore inotropes are started to keep mean arterial pressure >80 mmofhg (recommended for cerebral perfusion). Often blood pressure remains elevated during hypothermia due to vasoconstrictive effect. If the patient needed inotropes support, central venous line is also placed (ICS, 2008).
Serum electrolytes are monitored regularly as hypothermia commonly causes hypokalemia, which can be worsen by insulin administration, therefore serum potassium level is maintained between 3. 5 to 4mEq/l (UHL guidelines(2010) & Adler, 2011). Magnesium level is maintained to upper border of normal range because of its role in alleviation of neurological injuries(UHL guideline (2010), Holden & Makic, 2006). Patients are started on sliding scale insulin as studies have proven that ITH can cause hyperglycemia (ICS 2008).
No studies have proven control of serum blood glucose level improves neurological outcome in cardiac arrest patients. Nevertheless, evidence shows that glucose control has reduced hospital mortality in critically ill patients with protected peripheral and central nervous system (Van den Berghe G, Wouters P, Weekers F, et al 2001). Urinary catheterisation to monitor acute fluid balance as cooling causes cold dieresis (Pyle K. , et al 2007). Fluid challenge or resuscitation is given to replace the fluid loss and increase right heart filling pressure (ICS 2008).
Nasogastric tube for free drainage is placed. Feeding is not advisable during cooling and rewarming period due to reduced gut function and paralytic ileus (Adler, 2011). Stress ulcer prophylaxis (intravenous administration of Ranitidine or Omeprazole) is started as part of intensive care bundle (UHL guidelines, 2010). Venous thrombo embolism prophylaxis is started based on the clotting status of the patient (UHL guidelines, 2010). Patient’s prothrombin time, INR and APTT should be monitored closely as hypothermia may impair clotting system (Adler J. 2011).
Continuous temperature monitoring, ideally two sites-core and axilla are advised (UHL guidelines, 2010). Exposing the patient to moderate hypothermia can suppress the immune response and cooling can mask the body’s natural response to infection (i. e. , increased body temperature) (Holden & Makic M. B. 2006). Measures such as regular skin care, frequent change of position, sterile catheter care, and use of ventilator care bundle will help to minimise infection. In spite of all these measures if the patient develops infection, cooling should be stopped (UHL guideline & Holden and Makic, 2006).
The patient is allowed to rewarm. Blood culture is sent and prophylactic antibiotic is started as per unit policy. 7. Cooling Methods According to the guidelines, polar air or arctic sun cooling device is used to cool the patient. In the absence of cooling devices, bedclothes are removed. The patient is covered with single sheet only. Cold air fan, ice packs to head, axillae and groins, cold saline infusion of 20-30mls/kg over30 minutes at 4? c via peripheral line are used to reach target temperature (32? c- 34? c) with in 4hours time period. All the studies and guidelines also suggest the above said methods to cool the patients.
A literature review by Arrich, Holzer, Mullner Et al (2009) stated that the effective method of cooling the patients to reach the target temperature yet to be studied. It also states that the difference between earlier cooling (pre-hospital) and late cooling (in-hospital) is not yet studied. The target temperature needs to be maintained with in target range for 12-16 hours. Holden and Makic (2006) address that this can be challenging, as the body’s natural reaction is to shiver and warm up. Passive re-warming is started after 12-16 hours of cooling by removing cooling blankets (UHL guidelines, 2010).
ICS (2008) advices to re-warm the patients after 12-24 hours of cooling. The goal is to re-warm the patient 0. 5? c every hour. If passive re-warming delays active re-warming can be started but it should be stopped when the temperature reaches 35. 5? c to avoid rebound hyperthermia as this can cause cerebral oedema. Adler (2011) states the re-warming phase is the crucial period. As body starts to warm up peripheral vasodilatation occurs which leads to hypotension. During rewarming period, intra cellular and intravascular electrolytes shift can occur; therefore, precaution should be taken to avoid hyperkalemia (Adler 2011).
The sedation and paralytic agents are continued until the temperature reaches to 36? c. According to the guidelines, normothermia is achieved in 6hours of time from the time of re-warming. 8. The relative’s experience When looking after critically ill patients especially the cardiac arrest patients, supporting the relatives plays a major part as this is sudden and can put their life on hold, as this is sudden and unexpected. Therefore, supporting, explaining and reassuring them are important. The relatives experience on ‘therapeutic hypothermia on cardiac patients’ is not studied until recently.
The presence of relatives of critically ill patients is crucial as they influence the patient to fight to live and confirm their significance (Engstrom &Soderberg 2007). The presence of relatives can encourage and re-in force their humanity, and sharing their life experience outside the intensive care unit before their illness will help them to fight for the survival(Bergbom & Askwall, 2000). Todres, Fulbrook & Albarran (2000) suggest that the relatives can advocate on behalf of the patient’s interest. The experience in ICU strongly affects relatives.
Their memories are about how warmth the staffs were and how well their loved one’s needs were met with sensitivity and humanity. They also expect time to time update on their loved once condition. A Swedish study conducted by Lof, Sandstrom & Engstrom (2010) shows the unique experience of relatives of those treated with ITH after cardiac arrest. It suggested that the relatives want consolidated information in regular basis. They want to know how the patient will look and feel during ITH, why and how long they will be unconscious and what happens if they sustain brain injuries.
This study went on to advice that the relatives need to be supported in their hope for a realistic outcome of the patient’s condition and opportunity should be given to express their own situation and worries. Supporting the critically ill patient’s relatives is the responsibility of the nurses as they spend more time with them and most of the time this area is overlooked as they are so focused on patients. 9. The role of advanced clinical practitioner and multidisciplinary approach The outcome of the ITH and improvement in patient’s condition are directly related to the standard of care provided.
Therefore, nurse’s understanding of importance of treatment, protocol and physiological changes during cooling and re-warming phases are crucial. It has been observed that the lack of knowledge was compromising patient’s care at times, as the nurses were not informed of ITH and its benefits. Nurses also had lack of knowledge regarding the physiological changes that can occur during cooling and re-warming. They were not aware of the importance of time keeping in achieving the target temperature and maintaining the temperature for set duration and slow re-warming.
At times, the patients were re-warmed too quickly and patients were allowed to become hyperthermic. The physiotherapist’s interventions and nursing care were interfering the cooling phase, which raised the question of multidisciplinary approach and advanced clinical practitioner’s(ACNP) role in implementing ITH effectively. The role of advanced nurse practitioner in critical care setting evolved since 1990s. Shimabukuro (2011) stated that determining the exact role of the ACNP in multidisciplinary ICU team can be challenging, nevertheless the ACNPs can play a greater role in health care education, professional development and research.
A study by Pyle et al (2007) proved multidisciplinary team (team of critical care clinical nurse specialist, emergency department nurse specialist, intensivists, cardiologists& neurology intensivist) approach of ITH protocol development was efficient and successful . Holden and Makic (2006) in their literature review suggested that the knowledge of critical care nurses regarding the benefit of ITH & the physiological changes, which take place during cooling and re-warming phase can make positive impact on patient care and prevent the complications associated with ITH.
This knowledge can only be attained by training and teaching, which can be done by an ACNP by developing educational package. It is also important to evaluate the outcome of the ITH treatment, which is also a role of ACNP. A document by Yarema and Judy (2011) has stated that the role of ACNP are; through attention to holistic patient and family care, including teaching, continuity of care, patient safety and evaluation of care. Kozik (2007) has clearly documented that the role of clinical nurse specialist is to help staff members understand research findings and influence them to apply in practice.
The document also stated that these specialist nurses support nurses, in professional development, thereby they play an important role in providing high standard evidence based care, improve outcome of care, reducing the hospital cost and encouraging staff to use research to improve and support practice. It also suggested that this kind of evidence-base care providing, allow the nurses to become the best practice change agent. This case study based article has proven that the multidisciplinary approach involving clinical nurse specialist, intensivists, cardiologists and staff nurses, helped the ITH rotocol to be delivered successfully. 10. Synthesis The effects of ITH on cardiac arrest patients are researched since 1990s. Arrich Et al (2009) in their literature review they have concluded that ITH after cardiac arrest has prevented major brain damage and the mortality after six months was less. Before then in October 2002, ILCOR made the recommendation, from the previous evidence, that all the unconscious patients who had ROSC following VF/VT arrest outside the hospital should be treated with ITH.
It also recommended including other rhythms that causes cardiac arrest and in-hospital cardiac arrest patients could also be considered for ITH. In 2005, the American Heart Association included ITH treatment recommendation in the post cardiac arrest treatment support. Obtaining and implementing evidence-based knowledge can be challenging. NICE guideline (2007) stated that while implementing new guidelines we might encounter barriers such as awareness and knowledge of health professionals, skills to implement the guidelines, motivation and acceptance.
These barriers can be overcome by providing educational materials, educational interactive meetings, educational outreach visits and reminder system. This NICE guideline also suggested that a nominated opinion leader can positively influence the team and it is the best way of disseminating the information. Timely auditing and feed backing along with educational meeting is essential for the successful implementation of the guidelines (NICE guideline, 2007).
It is necessary to identify the barriers, which can affect the implementation of ITH protocol and the methods to overcome those barriers are crucial for the desired outcome. With the influence of the internet, consumers can access the statistical data of a hospitals and physicians’ outcome of the treatment, and up to date development of current treatment options. Therefore, it is important to use current research to provide best care possible. ITH has been proven as evidenced based care for the cardiac arrest patients who had spontaneous return of circulation to improve their neurological out-come.
Powell (2003) stated that the well-defined strategies are important for a care pathway or clinical guidelines to succeed. The article suggested that the current literature review supporting the change, and involving the health professionals in promoting the guidelines is important to disseminate and implement the guidelines. Feeding back the results to the practitioners who are involved in implementing the guidelines is essential for the sustainability (Powell, 2003). Studies have proven that this can be achieved by advanced clinical practice.
The current UHL‘s guidelines on ITH is facility based and follows other current practices therefore it doesn’t need any modifications. Nevertheless, it needs advanced clinical practice for its success and sustainability. 11. Conclusion In conclusion, induced therapeutic hypothermia is an evidence-based care, which is used to improve the neurological outcome of the patients who had return of spontaneous circulation after cardiac arrest. However, it does have its own limitations and complications.
The enhanced staff knowledge and multidisciplinary approach are the key factors to deliver the ITH protocol lucratively and improve the patient’s condition predominantly. Involving advanced clinical practice aspects such as protocol development, enhanced literature review, educating the staff, evaluating the outcome of the treatment and feeding back the outcome to the staff are essential for the sustainability of the protocol. There are limited evidence regarding when to cool the patients, what methods to use and how long cooling should take place.
Nevertheless, studies have proven that it improves the neurological outcome of the cardiac arrest patients with minimal complications that can be treated easily. Hence, ILCOR (2003), ICS (2008) and ACLS algorithms (2011) have recommended ITH as post cardiac arrest care. The care and support of relatives are also important in delivering therapeutic hypothermia. Reference Acls-algorithms. com/post-cardiac-arrest-care 2011 (accessed on 18th November 2011) Adler J. (2011), Therapeutic Hypothermia (on line), Available at: http://emedicine. edscape. com/article/812407-overview (accessed 15th November 2011). Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) (2003), an advisory statement: Therapeutic hypothermia after cardiac arrest, Circulation; 108:pp118-121 Arrich J. , Holzer M. , Herkner H. & Mullner M. (2009) Hypothermia for Neuroprotection in Adults after Cardio Pulmonary Resuscitation, Cochrane Database Of Systematic Reviews, Issue 4. Art. No:CD004128 DOI:10. 1002/15651858. CD004128. pub2 Bergbom I. & Askwell A. 2000) The nearest and the dearest: a lifeline for ICU patients, Intensive and Critical care Nursing 16(6), pp. 384-395. Bernard S. A. , Gray T. W. , Buist M. D. , Jones B. M. , Silvester W. , Gutteridge G. & Smith K. (2002) Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia, The New England Journal of Medicine 346(8), pp. 557-563 Engstrom A. & Sodenberg S (2007) Receiving power through Confirmation: The Meaning of Close Relatives for people who have been critically ill, Journal of Advanced Nursing 59 (6), pp. 569-576 Girolami U. D. Anthony D. C. & Frosch M. P. (1999), The Central Nervous System, In Robbins Pathologic Basis of Disease, 6th edition, Philadelphia: W. B. Saunders Co, pp1293-1357 Holden M. & Makic M. B. (2006) Clinically Induced Hypothermia. AACN Advanced Critical Care 17(2): pp. 125-132. Hypothermia after Cardiac Arrest Study Group (2002) Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest, The New England Journal of Medicine 346(8), pp. 549-556 Kozik T. M. (2007) Induced Hypothermia for Patients with Cardiac Arrest: Role of a Clinical Nurse Specialist.
Critical Care Nurse 27, pp. 36-42 Lof S. , Sandstrom A. & Engstrom A. (2010) Patients treated with therapeutic hypothermia after cardiac arrest: Relatives Experience. Journal of Advanced Nursing 66(8), pp. 1760-1768 NICE Guideline (2007) How to change practice, N1924, ISBN 1-84629-565-3, Online Available at: http://www. nice. org. uk (accessed on 3rd November 2011) Powell. C. V. E (2003) How to implement change in clinical practice Paediatric Respiratory Reviews 4, pp 340-346, Online Available at: www. sciencedirect. com (accessed on 20th November 2011) Pyle K. , Pierson G. Lepman D. & Hewett M. (2007) Keeping Cardiac Arrest Patients Alive with Therapeutic Hypothermia: How to develop a successful protocol. American nurse today (2) 7: pp. 32-36 Reperfusion after global ischemia decreases hippocampal energy metabolism. Stroke 38: pp. 1578-1584 Richards E. M. , Fiskum G. , Rosenthal R. E, Hopkins I. & McKenna M. C. (2007) Hyperoxic Safar P. & Behringer W. (2003) Cerebral Resuscitation from cardiac arrest, In Textbook of Neurointensive care (Layon a. j. , Gabrielli A. & Friedman W. A. , Eds), Philadelphia: W. B. Saunders Co, pp. 457-498.
Safar P. , Behringer W. , Bottiger B. W. & Sterz F. (2002) Cerebral Resuscitation potentials for cardiac arrest, Critical Care Medicine 30(4), s140-s144 Shimabukuro D. (2011) Acute Care Nurse Practitioners in an Academic Multidisciplinary ICU: Good, Bad, and Not So Ugly, ICU Director 2:28 (on line) Available at http://icu. sagepub. com/content/2/1-2/28 accessed on 17th November 2011 The Intensive Care Society(2008), Standards for the management of Patients After cardiac Arrest, Standards and guidelines, Standards Documents (online), Available at: http//www. ics. ac. k/intensive_care_professional_management of patient’s aftercardiacarrest (accessed on 16th november2011) Todres L. , Fullbrook P. & Albarran J. (2000) on the receiving end: a hermeneutic-phenomenological analysis of a patient’s struggle to cope while going through intensive care. Nursing in Critical Care 5(6), pp. 277-287. University Hospital Leicester Adult Intensive Care Unit (2010) Guideline for Induced Therapeutic Hypothermia after Cardiac Arrest (unpublished) Van den Berghe G, Wouters P, Weekers F, et al. (2001) Intensive insulin therapy in the critically ill patients.
New England Journal of Medicine 345: pp. 1359-1367 Warner D. S. (1997) Effects of anaesthetic agents and temperature on injured brain. In Textbook of Neuroanesthesia with Neurosurgical and Neuroscience prospective (Albin M. S. , Ed), McGraw-Hill, New York, pp. 595-611 Yarema T. C. & Judy J. A. (2011) Participation of an Acute Care Nurse Practitioner Group in a Medical-Surgical Intensive Care Unit: One Hospital’s Perspective, ICU Director 2:25 (on line) Available at: http://icu. sagepub. com/content/2/1-2/25 accessed on 17th November 2011

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