Abstract
Per the most recent American Heart Association Cardiac Arrest Guidelines, computed tomography of the head (CTH) is not recommended as part of routine postresuscitation care. The key here is that CTH should not be ordered on every patient, but if there is clinical suspicion for a neurologic etiology for the cardiac arrest then neuroimaging should be obtained. The most devastating neurologic condition that can present with out of hospital cardiac arrest is aneurysmal subarachnoid hemorrhage that accounts for 3–4% of patients presenting with out of hospital cardiac arrest per various estimates (Inamasu et al., 2009). In addition, typical medical management of out of hospital cardiac arrest patients going for cardiac catheterization will include the use of anticoagulation with heparin and targeted temperature management, both of which can significantly increase the risk for a recurrent rupture of an unsecured cerebral aneurysm.
Authored by:
Stephen A. Figueroa, MD
Assistant Professor–Division of Neurocritical Care
The University of Texas Southwestern Medical Center
Dallas, Texas
References
Inamasu J, Miyatake S, Tomioka H, et al. Subbarachnoid haemorrhage as a cause of out of hospital cardiac arrest: a prospective computed tomography study. Resuscitation 2009;80:977–80.
Targeted temperature management (TTM) has become a widely accepted intervention in improving neurologic outcomes after return of spontaneous circulation after cardiac arrest (Avery et al., 2015). Numerous studies have validated the benefits that TTM can have in mitigating postresuscitation syndrome. Implementation of these interventions requires development of a clinical practice protocol and collaboration of an interprofessional team to coordinate the multisystem needs of these patients (Oddo et al., 2006; Kupchik, 2009).
Several teams have published experiences with successful implementation of TTM protocols. Common in these reports are the need to identify stakeholders, develop clinical practice guidelines and order sets, ensure education, and measure outcomes. Patients undergoing TTM are complex and often under the care of multiple specialty services requiring coordination of care. The role of the interprofessional team typically includes physicians from emergency medicine, critical care intensivists, cardiology, neurology, respiratory therapy, pharmacy, clinical nurse educators, and staff nurses.
Initially the TTM team focuses on development of clinical practices to support implementation, selection of equipment, and ensures that all team members have the training needed to provide this intervention. In addition, teams have augmented this process through use of nursing checklists and care bundles to facilitate optimal delivery of TTM care (Walters et al., 2011; Avery et al., 2015; Dixon and Keasling [2014]). Over time the role of the TTM team evolves from development and refinement of guidelines to identification of any quality-of-care issues and tracking of patient outcomes. The TTM committee helps to oversee consistent standardized care for patients. Regularly scheduled team meetings provide an interprofessional forum to review clinical cases and continuously socialize new evidence and improve care processes (Mathiesen et al., 2015).
Authored by:
Claranne Mathiesen, MSN, RN, CNRN, SCRN, FAHA
Director, Medical Operations Neurosciences Service Line
Lehigh Valley Hospital
Allentown, Pennsylvania
References
Avery K, O'Brien M, Daddio Pierce C, Gazarian P. Use of a nursing checklist to facilitate implementation of therapeutic hypothermia after cardiac arrest. Critical Care Nurse 2015;35:29–37.
Dixon M-N, Keasling M. Development of a therapeutic hypothermia protocol implementation for postcardiac arrest STEMI patients. Crit Care Nurs Q 2014;37:377–83.
Kupchik N. Development and implementation of a therapeutic hypothermia protocol. Crit Care Med 2009;37:S279–S284.
Mathiesen C, McPherson D, Ordway C, Smith M. Caring for patients treated with therapeutic hypothermia. Crit Care Nurse 2015;35:e1–e12.
Oddo M, Schaller M-D, Feihl F, Ribordy V, Liaudet L. From evidence to clinical practice: Effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med 2006;34.
Walters E, Morawski K, Dorotta I, Ramsingh D, Lumen K, Bland D, Clem K, Nguyen HB. Implementation of a post-cardiac arrest care bundle including therapeutic hypothermia and hemodynamic optimization in comatose patients with return of spontaneous circulation after out-of-hospital cardiac arrest: A Feasibility Study. Shock 2011;35:360–366.
The manufacture and implementation of a commercially available esophageal cooling device (ECD) is a more recent development in targeted temperature management. Clinical research regarding the ECD has primarily been published since 2015 (Hegazy et al., 2015). The ECD is a silicone oroesophageal tube consisting of three lumens: two water inflow lumens and a central port that can be used for gastric drainage and suction. The water inflow and outflow lumens allow for closed loop circulation of cold or warm water. The central port allows for gastric drainage and suction (Hegazy at al., 2015). The central port on one manufacturer's third- and fourth-generation ECD has more recently been approved for enteral feedings and medication administration (Attune Medical, 2018). The water inflow and outflow ports attach to established heat transfer exchange units available from other companies that allow for adjustment of the circulating water temperature to a chosen set point with feedback of the patient's temperature from an indwelling urinary catheter or rectal probe to allow automatic adjustment of the water temperature to reach the patient's target temperature, similar to cooling/warming blankets. The ECD affects temperature transfer by conduction through the esophageal mucosa and convection through adjacent large vessel and heart blood flow (Hegazy et al., 2017; Naiman et al., 2018). The ECD has most often been compared with endovascular and surface devices.
Research has been conducted primarily in the cardiac arrest, critically ill neuroscience, surgical, and burn patient populations. Published scientific investigations consist primarily of case studies and small retrospective and prospective studies, consisting of 3–30 participants and one prospective randomized control trial (PRCT). The PRCT used the ECD as an adjunct to another cooling method, intravascular administration of cooled saline, which resulted in an overall decrease in rate of 1.12°C/hour in comatose postcardiac arrest survivors (Markota et al., 2016). Of those studies that report sole use of the ECD, the results were conflicting. Demographics, pathophysiology, differences between baseline temperature and target temperature, uncontrolled shivering, and water flow rate of the heat transfer exchange unit influence efficiency. In febrile patients, the ECD has been found to be comparable or more efficient than an endovascular device and surface cooling with rates of cooling reported as follows: esophageal 0.52°C/hour, intravascular 0.39°C/hour, and surface 0.27°C/hour (Naiman et al., 2016). Goury et al. (2017) reported the rate of cooling in postcardiac arrest patients to be 0.26°C/hour. Hegazy et al. (2017) reported a cooling rate in cardiac arrest survivors to be 0.42°C/hour. The time to target temperature cooling has also varied among studies and patient populations. Time to target temperature across various cooling protocols for postcardiac arrest and burn patients, both febrile and nonfebrile, in Naiman et al. (2018) was achieved at 2.37 hours. Time to target temperature with pyrexic burn patients in Williams et al. (2016) was 2.5 hours. Time to target temperature with cardiac arrest patients in Hegazy et al. (2015) was 3–5 hours in a small case series of three patients and 4 hours 24 minutes with another small cohort of four postcardiac arrest patients (Hegazy et al., 2017). Normothermia was achieved and maintained in subarachnoid and intracerebral hemorrhage patients using the ECD (Khan et al., 2018). In another study consisting primarily of anesthetized surgical patients, the ECD was found to extract less heat than endovascular catheters (Kalasbail et al., 2018).
Postresuscitation evidence-based guidelines do not mandate a specific required time to target temperature but recommend a minimum duration of at least 24 hours (Donnimo et al., 2016). The optimal rate of cooling has not been determined (Goury and Deye, 2017). Rewarming with the ECD has been accomplished at a controlled rate range of 0.2–0.5°C/hour (Markota et al., 2016; Naiman et al., 2016).
Benefits to using the ECD include ease of insertion. The nurse clinician who is skilled at insertion of orogastric tubes can transfer those skills to insertion of the ECD. Time to insertion has been reported to be <5 minutes. Endovascular cooling devices require central venous catheter insertion, a skill reserved for the physician or advanced practice provider who has demonstrated competency. Complications of central venous catheters, including venous thrombosis, central line-associated bloodstream infections, and pneumothorax, are avoided with the ECD (Naiman et al., 2017). Skin and mucosa issues are less of a concern than with the cooling blankets, wrap devices, and adherent pads used with surface cooling. Unlike cooling blankets, cooling wraps, and adherent pads, the ECD allows for full exposure of the body if a procedure is required. Confirmation of placement and location of the ECD is similar to any orogastric tube, with X-ray being most definitive (Naiman et al., 2017). A bite block is needed to prevent compressing the lumens of the ECD that must be repositioned routinely to minimize mouth trauma. The tubing from the ECD to the temperature management unit must be positioned off the skin to minimize injury and shivering (Naiman et al., 2017). Endoscopy or transesophageal echocardiography requires removal of the ECD before the procedure. Concerns regarding esophageal trauma have been stated but rarely reported. The ECD is contraindicated in the presence of esophageal varices or preexisting esophageal trauma (Naiman et al., 2016).
Other care concerns include the potential risk for aspiration or ventilator-associated pneumonia with the ECD in place. If the ECD develops a break in the system, the patient's stomach will be filled with water that could result in vomiting and aspiration, particularly if the central port is not on continuous suction and is being used for medication administration and enteral feeding. Cooling of the esophagus may result in decreased gastrointestinal motility that may also increase the risk of vomiting and aspiration (Hegazy et al., 2017). In addition, enteral feeding, especially continuous, may negatively impact cooling as the tube feeding will be a continuously coursing through the central lumen of the ECD and is warmer than the water entering the ECD from the heat transfer device. Finally, not all medications will be compatible with the coolness of the ECD and may require warm flushes to dilute and deliver to the gastrointestinal tract (Khan et al., 2018).
Less shivering has been reported with the ECD when compared with surface and endovascular cooling. This may be related to its location away from the periphery and lack of contact with the body surface (Naiman et al., 2017). It has been acknowledged that shivering can still occur and patients will require antishivering management but perhaps less sedation and less neuromuscular blockade will be needed. Other antishivering medications and counterwarming may allow for a more complete neurologic assessment and perhaps less time on mechanical ventilation (Khan et al., 2018).
In conclusion, the ECD is effective in cooling, maintaining a target temperature, and warming. Based on current research, it consistently performs better than surface cooling but less efficient than endovascular cooling devices. Insertion of the ECD is less risky than insertion of the intravascular cooling catheter. Sustained injury with the ECD is rare. More research is needed to determine the optimal time to target temperature that may or may not speak to the long-term outcomes utilizing the ECD.
Authored by:
Patricia A. Blissitt, PhD, ARNP-CNS, CCRN, CNRN, SCRN, CCNS, CCM, ACNS-BC
Neuroscience Clinical Nurse Specialist
Harborview Medical Center and Swedish Medical Center and Associate Professor
Clinical Faculty
University of Washington School of Nursing
Seattle, Washington
References
Attune Medical. (2018). ensoETM esophageal temperature management. FAQ. Products. Attune Medical, Chicago, IL. Available at: http://attune-medical.com
Donnimo MW, Andersen LW, Berg KM, Reynolds JC, Nolan JP, Morley PT, Lang E, et al.. Temperature management after cardiac arrest: an advisory statement by the advanced life support task force of the international liaison committee on resuscitation and the American Heart Association emergency cardiovascular care committee and the council on cardiopulmonary critical care, perioperative resuscitation. Resuscitation 2016;98, 97–104.
Goury A, Deye N. Reply letter to: Targeted temperature management using the “esophageal cooling device” after cardiac arrest (the COOL study): A feasibility and safety study. Resuscitation 2017;123:e7–e8.
Goury A, Poirson F, Chaput U, Voicu S, Garcon P, Beeken T, Malissin I, et al. Targeted temperature management using the “esophageal cooling device” after cardiac arrest (the COOL study): a feasibility and safety study. Resuscitation 2017;121:54–61.
Hegazy, AF, Lapierre DM, Butler R, Althenayan E. Temperature control in critically ill patients with a novel esophageal cooling device: a case series. Anesthesiology 2015;15:152.
Hegazy AF, Lapierre DM, Butler R, Martin J, Althenayan E. The esophageal cooling device: a new temperature control tool in the intensivist's arsenal. Heart Lung 2017;46:143–148.
Kalasbail P, Makarova N, Garrett F, Sessler DI. Heating and cooling rates with an esophageal heat exchange system. Anesth Analg 2018;126:1190–1195.
Khan I, Haymore, J, Barnaba B, Armahizer M, Melinosky C, Bautista, MA, Blaber B, et al. Esophageal cooling devices versus other temperature modulation devices of therapeutic normothermia in subarachnoid and intracranial hemorrhage. Ther Hypothermia Temp Manag 2018;8:53–58.
Markota A, Fluher J, Kit B, Balazic P, Sinkovic A. The introduction of an esophageal heat transfer device into a therapeutic hypothermia protocol: a prospective evaluation. Am J Med 2016;34:741–749.
Naiman M, Shanley P, Garrett F, Kulstad E. Evaluation of advanced cooling therapy's esophageal cooling device for core temperature control. Expert Rev Med Devices 2016;13:423–433.
Naiman, MI, Gary M, Haymore J, Hegazy AF, Markota A, Badjatia N, Kulstad EB. Esophageal heat transfer for patient temperature control and targeted temperature management. J Vis Exp 2017;129:e56579.
Naiman M, Markota A, Hegazy A, Dingley J, Kulstad E. Retrospective analysis of esophageal heat transfer for active temperature management in post-cardiac arrest, refractory fever, and burn patients. Mil Med 2018;183 (Supplement 1):162–168.
Williams D, Leslie G, Kyriazis D, O'Donovan B, Bowes, J, Dingley J. Use of an esophageal heat exchanger to maintain core temperature during burn excisions and to attenuate pyrexia on the burns intensive care unit. Case Rep Anesthesiol 2016;2016:7306341.
Growing evidence supporting the influence of temperature management on patient outcome demonstrates the importance of understanding temperature measurement devices that may provide reliable data ensuring rapid detection of fever and evaluation of neuroprotection interventions.
Targeted temperature management (TTM) strategies demand the use of a measurement technique that is reliable and closely approximates core temperature. Even if TTM therapies are not being used as a treatment strategy, the importance of temperature monitoring, fever detection, and aggressive intervention may influence outcome in any intensive care unit (ICU) patient. Devices that measure intermittent temperature include temporal artery, tympanic, axillary, and oral thermometry. There are few studies comparing the performance of intermittent devices with continuous devices such as, esophageal, bladder, and rectal thermometry that are more commonly used in the ICU and recommended when targeted temperature strategies are instituted.
Marui et al. (2017) examined the reliability of axillary temperature measurement to approximate core. Axillary thermometry demonstrated more variation from core temperature compared with tympanic measurement. More importantly, researchers discussed the influence of the variation in measurement techniques demonstrated by practitioners and commented on other variations caused by patient factors such as body mass, blood flow to the skin, and basal rate. Lefrant et al. (2003) compared all ICU temperature measurements, including axillary, and found esophageal and bladder to be most representative of core temperature. Axillary was not recommended in the ICU because of large variation in temperature measurement. These variations again were believed to be related to influences of ambient temperature, local blood flow limitations, and sweat. Some clinical practices raise question about reliability of measurements. One such practice describes clinicians adding 0.3°C and 0.5°C to the measured axillary value to approximate core. There is as yet, no evidence supporting this practice (Chacko and Peter, 2018).
Neuroprotection strategies in any ICU must include reliable measurement of temperature. Assessing risk and benefits of fever management strategies include conversation about monitoring that meets patient need. Targeted temperature strategies demand measurement that is reliable and safe. Recently published TTM guidelines (Madden et al., 2017) recommended the use of esophageal temperature measurement followed by bladder measurement to ensure safe management of the patient receiving TTM. Thermometry choice is based on patient need and if an intermittent measurement is appropriate, axillary temperature has limitations in providing reliable results.
Authored by:
Mary M. Guanci, MSN, RN, CNRN, SCRN
Clinical Nurse Specialist, Neuroscience Intensive Care
Massachusetts General Hospital
Boston, Massachusetts
References
Chacko B, Peter J. Temperature monitoring in the intensive care unit. Indian J Respir Care 2018;7:28–32.
Lefrant J, Muller L, et al. Temperature measurement in intensive care patient; comparison of urinary bladder, esophageal, rectal, axillary & inguinal methods vs. pulmonary core method. Intensive care Med 2003;29:414–418.
Madden L, Hill M, et.al. Implementation of targeted temperature management: an evidence-based guideline from the Neurocritical care society. Neurocrit Care 2017;27:468–487.
Marui S, Misawa A, Tanaka Y, Nagashima K. Assessment of axillary temperature for the evaluation of normal body temperature of healthy young adults at rest in a thermoneutral environment. J Physiol Anthropol 2017;36:18.
As patients are cooled for therapeutic hypothermia, sedation and analgesia are started to mitigate pain, agitation, and delirium. The guidelines on care after cardiac arrest suggest that intermittent or continuous analgesia and sedation may be used (Peberdy et al., 2010). Although they do not recommend a particular agent, the use of anxiolytics and opioids to allow for the successful implementation of therapeutic hypothermia are recommended with a lower level of evidence (LOE; Class IIb, LOE C). Depending on the institutional protocol and characteristics of individual patients, neuromuscular blockade may also be initiated for shivering. Shivering should be avoided as it can increase body temperature and can delay the attainment of temperature goals (Callaway et al., 2015).
A systematic literature review was conducted that examined analgesia and sedation regimens used during therapeutic hypothermia between 1997 and 2009 (Chamorro et al., 2010). Continuous infusions of midazolam and propofol were the most common sedatives used, with fentanyl and morphine being the most common analgesics. Neuromuscular blocking agents were used frequently to prevent and/or treat shivering (Chamorro et al., 2010).
Although many institutions use deeper levels of sedation, a study investigated the use of moderate-dose sedation in patients undergoing therapeutic hypothermia (May et al., 2015). In this study, 166 patients received moderate-dose sedation and analgesia and were excluded for continuous infusions of neuromuscular blockade. Fentanyl and propofol were used most frequently, with median doses of 25 μg/hour and 20 μg/kg/minute, respectively (May et al., 2015). The authors conclude that a strategy of moderate-dose analgesia and sedation is well-tolerated and effective.
Although no specific agents are recommended in the guidelines, clinicians can use pharmacokinetic and dynamic characteristics to choose ideal agents. When compared with morphine, fentanyl does not have an active metabolite nor causes as much hypotension and is also easily titratable. When considering sedatives, continuous infusion benzodiazepines have fallen out of favor as general sedative agents because of the association with delirium. In addition, midazolam has an active metabolite that can accumulate, especially in patients with renal dysfunction. Propofol is easily titratable, does not have an active metabolite, and is not associated with tachyphylaxis as is midazolam.
As institutions develop protocols for therapeutic hypothermia, care should be taken to include options for analgesia, sedation, and delirium. Fentanyl and propofol remain common options, although further research is needed as to the optimal dose and choice of sedative and analgesic agents.
Authored by:
Leslie A. Hamilton, PharmD, FCCP, FCCM, BCPS, BCCCP
Associate Professor of Clinical Pharmacy and Translational Science
University of Tennessee Health Science Center College of Pharmacy
Knoxville, Tennessee
References
Callaway CW, Donnino MW, Fink EL, et al. 2015 American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2015;132:S465–S482.
Chamorro C, Borrallo JM, Romera MA, et al. Anesthesia and analgesia protocol during therapeutic hypothermia after cardiac arrest: a systematic review. Anesth Analg 2010;110:1328–1335.
May TL, Seder DB, Fraser GL, et al. Moderate-dose sedation and analgesia during targeted temperature management after cardiac arrest. Neurocrit Care 2015;22:105–111.
Peberdy MA, Callaway CW, Neumar RW, et al. American Heart Association Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122:S768–S786.
To best examine this question, one needs to understand the effect of cardiac arrest and return of spontaneous circulation (ROSC) on the brain. It has been determined through multiple animal studies and human studies that after ROSC, cerebral hypoperfusion develops within hours and can last hours to days. Specifically, in humans, Sundgreen et al. (2001) found that after ROSC, cerebral autoregulation is either absent or shifted to the right, meaning a higher mean arterial pressure (MAP) is necessitated to maintain a constant cerebral blood flow because of impaired autoregulation.
What exactly is this magical number for blood pressure to ensure adequate cerebral perfusion? To date, there have been no interventional studies targeting blood pressure in isolation (Callaway et al., 2015). Several observational studies have shown blood pressure augmentation, even if achieved with vasopressors, improves outcomes (Beylin et al., 2013). Bundles of care that address postarrest have been studied, but we cannot isolate the blood pressure effect. These studies overall have framed the American Heart Association (AHA) 2015 recommendation that “avoiding and immediately correcting hypotension (systolic blood pressure less than 90 mm Hg, MAP less than 65 mm Hg) during post-resuscitation care may be reasonable (Class IIb, LOE C-LD)” (Callaway et al., 2015; S467). Another professional resource to mention is the Neurocritical Care Society's (NCS) Emergency Neurological Life Support algorithm for targeted temperature management after cardiac arrest (Elmer and Polderman, 2017). This guideline recommends MAPs greater than 80, ensuring there is adequate perfusion to minimize cerebral hypoperfusion.
In conclusion, there is no single study that directs the ideal blood pressure after cardiac arrest. We know that after arrest the brain undergoes a period of hypoperfusion, with avoiding hypotension being critical. The American Heart Association postcardiac arrest guidelines recommend avoiding and correcting hypotension (Callaway et al., 2015). The Neurocritical Care Society (NCS) specifies that the goal MAP should be greater than 80 mm Hg (Elmer and Polderman, 2017). As an expert clinician, you will have to evaluate individual patient characteristics (e.g., cardiac function after arrest) to determine the most appropriate goal blood pressure to ensure cerebral perfusion.
Authored by:
Liz Fox, MSN, AG-ACNP, ACNS, CCRN, FAHA
Neurocritical Care–Advanced Practice Provider
Stanford Health Care
Palo Alto, California
References
Beylin ME, Perman SM, Abella BS, Leary M, Shofer FS, Grossestreuer AV, et al. Higher mean arterial pressure with or without vasoactive agents is associated with increased survival and better neurological outcomes in comatose survivors of cardiac arrest. Intensive Care Med 2013;39:1981–1988.
Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM, Zimmerman JL. Part 8: post-cardiac arrest care: 2015 American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2015;132(suppl 2):S465–S482.
Elmer J, Polderman KH. Emergency neurological life support: resuscitation following cardiac arrest. Neurocritical Care 2017;27(Suppl 1):134–143.
Sundgreen C, Larsen FS, Herzog TM, Knudsen GM, Boesgaard S, Aldershvile J. Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest. Stroke 2001;32:128–32.
Mild therapeutic hypothermia (TH) has been shown to improve neurologic outcome in patients experiencing cardiac arrest after return of spontaneous circulation (ROSC). Optimal timing or therapeutic window for initiating mild TH has not been clearly defined but current consensus is to initiate cooling as soon as possible (Bernard et al., 2002; Hypothermia After Cardiac Arrest Study Group, 2002; Che et al., 2011). One animal study indicated that TH can be initiated within 4 hours of ROSC with improved mortality and neurologic outcomes (Che et al., 2011).
For a patient who has had an out-of-hospital or emergency department (ED) arrest, the emergency department physician will assess the inclusion and exclusion criteria and initiate intravenous cool saline 30 mL/kg to start the cooling process. In our facility the final decision and the order for TH for both in-hospital arrest and out-of-hospital arrest is the responsibility of the pulmonary critical care intensivist who will continue to manage the patient in the critical care.
When a cardiac arrest (Code Blue) is called for either in-hospital or out-of hospital arrests our Rapid Response Team (RRT) nurse and cardiac intensive care unit (CICU) charge nurse respond to the code. The RRT and CICU charge nurses are educated on the TH clinical guidelines and can assist in preparing the patient for TH. As we do external cooling we have to stock the urinary catheter with temperature probe in the ED. When ROSC is achieved and the decision has been made to initiate TH, the urinary catheter with the temperature probe is inserted. If there is any delay to transfer the patient to critical care, the pads are brought down from CICU and put on the patient in the ED. TH is started in the ED with the assistance of the RRT nurse and the CICU sends a nurse down as soon as possible to manage the patient in the ED until the critical care bed is available. If the patient is a ST-Elevation Myocardial Infarction (STEMI) we quickly transfer the patient for a computed tomography (CT) examination before cardiac catheterization. The cooling pads are applied while removing from the CT table and the cooling machine is brought directly to catheterization laboratory. The CICU nurse attaches the cooling machine in the catheterization room and stays with the patient during the procedure to manage the TH.
Authored by:
Teresa Wavra, RN, MSN, CCRN
Cardiovascular CNS
Mission Hospital
Mission Viejo, California
References
Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–563.
Che D, Li L, Kpil CM, Lie Z, Guo W, Neumar RW. Impact of therapeutic hypotherma onset and duration on survival, neurologic function, and neurodegeneration after cardiac arrest. Crit Care Med 2011;39:1423–1430.
Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest [published correction appears in N Engl J Med 2002;346:1756]. N Engl J Med 2002;346:549–556.
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