Shivering Management During. Therapeutic temperature. Modulation: Nurses Perspective

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1 Feature Shivering Management During Therapeutic Temperature Modulation: Nurses Perspective Mary Presciutti, RN, BSN, CCRN, CNRN Mary Kay Bader, RN, MSN, CCNS, CNRN, CCRN Millie Hepburn, RN, PhD(c), ACNS-BC Therapeutic temperature modulation, which incorporates mild hypothermia and maintenance of normothermia, is being used to manage patients resuscitated after cardiac arrest. Methods of modulating temperature include intravenous infusion of cold fluids and surface or endovascular cooling. During this therapy, the shiver response is activated as a defense mechanism in response to an altered set-point temperature and causes metabolic and hemodynamic stress for patients. Recognition of shivering according to objective and subjective assessments is vital for early detection of the condition. Once shivering is detected, treatment is imperative to avoid deleterious effects. The Bedside Shivering Assessment Scale can be used to determine the efficacy of interventions intended to blunt thermoregulatory defenses and can provide continual evaluation of patients responses to the interventions. Nurses knowledge and understanding of the harmful effects of shivering are important to effect care and prevent injury associated with uncontrolled shivering. (Critical Care Nurse. 2012;32[1]:33-42) CEContinuing Education 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. Describe the physiological processes of temperature control 2. Identify subjective and objective measurements for assessment of shivering in patients undergoing therapeutic temperature modulation (TTM) 3. Discuss nursing implications associated with shivering and appropriate interventions to manage shivering during TTM 2012 American Association of Critical- Care Nurses doi: /ccn Therapeutic temperature modulation (TTM), which incorporates mild hypothermia and maintenance of normothermia, is standard treatment after cardiac arrest for comatose patients in whom spontaneous circulation has been reestablished. 1,2 TTM can improve neurological outcome by 49% 3 to 55% 4 in these patients. Implementation of mild hypothermia has 3 distinct phases: induction, maintenance, and rewarming. In the rapid induction phase, a patient s body temperature is decreased to 33ºC. In the maintenance phase, the temperature is kept at this set point. During the rewarming phase, the patient s temperature is slowly increased to 37ºC. Administration of cold intravenous fluids and surface as well as intravascular cooling devices are used to induce mild hypothermia and modulate temperatures safely in a controlled environment. 5-8 Therapeutic mild hypothermia is used in patients who have refractory increased intracranial pressure associated with brain injury and in patients with acute liver failure who are comatose. 9,10 The therapy is also being explored as a treatment in malignant cerebral ischemia related to acute stroke and in refractory vasospasm associated with aneurysmal subarachnoid hemorrhage Cooling strategies are also used to manage refractory fever. 15 Clinicians who provide care to patients undergoing TTM require an understanding of the potential systemic complications associated with manipulating body temperature. CriticalCareNurse Vol 32, No. 1, FEBRUARY

2 One of the most frequent side effects of decreasing and increasing body temperature is shivering, rhythmic tremors of the muscles of the body, which can cause deleterious effects and negate the benefits of TTM. 16 Subjective and objective methods of assessing shivering are vital to detect its presence and provide guidance for interventions and reassessment. In this article, we provide the tools to assess and manage shivering when TTM is used. We describe physiological processes of temperature control, subjective and objective measurements of shivering, interventions to manage shivering, and the application of shivering control in a case study. Neurological Injury Associated With Ischemia Patients in cardiac arrest experience a period of cerebral ischemia and hypoxia. Upon return of circulation, destructive processes occur after the reperfusion and restoration of cerebral blood flow. The initial hypoxic/ischemic injury of the brain creates a cascade of cellular events, including the release of glutamate neurotransmitters, formation of free radicals, impairment of cellular integrity, and mitochondrial dysfunction. 17 These processes lead to cellular death. Hypothermia mediates the physiological changes involved and is thought to mitigate the deleterious effects of ischemiareperfusion injury. 17 Cerebral resuscitation with mild therapeutic hypothermia, defined as a temperature range of 32ºC to 34ºC, 18 had its origins in research completed in the 1950s. 4 Difficulties in implementing therapeutic hypothermia in the clinical setting at that time created major barriers, a situation that led to the near abandonment of this intervention until recently. Today, therapeutic mild hypothermia has experienced a renaissance due to the beneficial findings in studies in animals and in small, preliminary trials in humans during the 1990s. In 2 landmark studies, 3,4 survivors of cardiac arrest had decreased mortality and improved neurological outcomes after mild hypothermia. Subsequently, the International Liaison Committee on Resuscitation 2 and the American Heart Association 1 included therapeutic hypothermia as a recommendation for care of comatose patients who have survived cardiac arrest. Induced mild hypothermia has myriad side effects that warrant treatment in a controlled environment. Patients are admitted to the intensive care unit (ICU) because of Authors Mary Presciutti is a staff nurse in the neurological intensive care unit at New York Presbyterian Hospital, New York, New York. Mary Kay Bader is a neurological critical care clinical nurse specialist at Mission Hospital, Mission Viejo, California. Millie Hepburn is a neuroscience clinical nurse specialist at New York University Langone Medical Center, New York, New York. Corresponding author: Mary Presciutti, RN, BSN, CCRN, CNRN, 3300 Netherland Ave, 2J, Riverdale, NY ( lanipres@yahoo.com). To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA Phone, (800) or (949) (ext 532); fax, (949) ; , reprints@aacn.org. the complexity and acuity of their cases. The main aspects of care are keeping hemodynamic status stable, maintaining adequate oxygenation and perfusion, monitoring fluids and electrolyte derangements, delivering safe and controlled cooling and rewarming, and managing shivering. The goals are to minimize the injury associated with cardiac arrest by reducing the destructive molecular changes in the brain that lead to neuronal damage or death and to optimize neurological outcome. Physiological Processes of Thermoregulation Thermoregulation consists of a complicated network of central and peripheral sensors as well as pathways to maintain core body temperature The preoptic region of the hypothalamus has temperature-sensitive, temperature-insensitive, and effector neurons. Effector neurons are further classified as heat-loss or heatproduction neurons. Activation and inhibition of these neurons are the foundation of the model of set-point temperature; these neurons are thought to be responsible for the ability of the body to regulate its temperature and adapt to changes, thereby maintaining homeostasis. 20 Normally, core temperature is tightly regulated within a narrow range of 36ºC to 37ºC. 22 Sensory receptors on the skin, peripheral tissues, and organs are constantly sensing differences in body temperature. Afferent input from these changes in local body temperature is centrally integrated within the preoptic region of the hypothalamus. Alterations in the set-point temperature activate both behavioral and 34 CriticalCareNurse Vol 32, No. 1, FEBRUARY

3 physiological responses to maintain homeostasis. 23 Examples of behavioral responses include wearing heavy clothing in cold weather and turning on air conditioning during warm weather. This natural adaptive capacity allows humans to live in different environments. Behavioral responses are not expressed in comatose and sedated patients. Activation of warm-sensitive neurons in the preoptic area of the hypothalamus results in an increase in their firing rate. 19,20 This increase signals heat-loss effector neurons to produce vasomotor responses such as vasodilatation of blood vessels and sweating. These physiological mechanisms allow heat to escape through evaporation, thus cooling down the body. Vasodilatation of blood vessels increases blood flow, promoting heat loss via convection and conduction processes. On the other hand, a decrease in the firing of warm-sensitive neurons in the hypothalamus during cooling allows cold-sensitive neurons to increase their firing rates and stimulate heat production. 19,20 Heat retention responses are activated, including nonshivering thermogenesis, stimulation of metabolic hormones, and activation of vasomotor responses, resulting in vasoconstriction and shivering. 19 Temperatureinsensitive neurons are thought to mediate input through a feedback system from both the warm-sensitive neurons and the cold-sensitive neurons, thus regulating temperature through synaptic excitation or inhibition of these neurons. 20 Pyrogens associated with the release of cytokines cross the blood-brain barrier, causing pertubations of set-point temperature. 20 Endotoxins produced by an infectious process release endogenous pyrogens, such as interleukin 1, which in turn stimulate the release of prostaglandin E. These substances act on a region near the preoptic region of the hypothalamus and reduce the firing of warmsensitive neurons. Because heat-loss responses are lost, the set point is moved upward. In addition, the cold-sensitive neurons increase their firing, leading to heat retention. 20 The vasoconstriction that results in heat retention is due to arteriovenous shunts in the body. These shunts are special connections or anastomoses between arterioles and veins. 22 Located in the extremities in the fingers and toes, their primary function is to shunt blood away as body temperature decreases a few tenths of a degree to a temperature less than the set point of 37ºC, creating a reduction in blood flow to the arms and legs. This reduction lowers the temperature in the extremities. Heat created by deep organs in the trunk and cranium stays inside these organs, and the temperature in these areas is usually 2ºC to 4ºC higher than that in the peripheral compartment. 22 Heat flows toward the body parts that have lower temperatures, creating a thermoregulatory vasomotion phenomenon and the transfer of heat from the core when needed. 22 When the skin receives continuous sensations of cold, motor neurons are stimulated, creating a shiver response in the muscles of the body. This motor response begins in the trunk and spreads to the extremities in an attempt to generate heat. The shivering mechanism is activated when body temperature decreases to approximately 1ºC less than the threshold temperature for vasoconstriction. 22 The ABCs of Shivering Shivering activated during cold stimulation 24 is a natural physiological response to an altered hypothalamic set point. 19 As body temperature decreases to less than the set point of 36ºC to 37ºC, efferent signals cross the median forebrain bundle, which terminates in the hypothalamus, communicate downward to the reticulospinal neurons in the lower part of the brain stem, and activate shivering. Patients with lesions within this efferent pathway lack a shivering response. 24,25 Shivering is an involuntary, rhythmic tremor of skeletal muscle groups that consists of oscillatory movement. 22 Early experiments 24 revealed that a mild shivering reaction can be elicited within minutes and can progress to severe shivering, involving generalized movement of all muscle groups. Shivering typically increases the basal metabolic rate to a value 2 to 5 times greater than the normal rate. 23,26 Shivering is associated with increased expenditure of energy, consumption of oxygen, and production of carbon dioxide. 16 It also is associated with activation of hemodynamic changes in vital signs, including increases in heart rate, blood pressure, respiratory rate, and intracranial pressure. In addition, shivering may retard the cooling process as heat is transferred from the core to the periphery. 22 Furthermore, shivering can lead to cerebral metabolic stress. 17 By increasing the work of muscles, shivering can increase a patient s postoperative pain by stressing and CriticalCareNurse Vol 32, No. 1, FEBRUARY

4 stretching the muscles near incisions. 27 After cardiac surgery, shivering can elicit a hyperdynamic response manifested by tachycardia, elevated cardiac indices, and low mixed venous oxygen level. 28 In elderly patients, the shivering response occurs at a much lower core temperature than in younger patients, a situation that places the former at a greater risk for complications. 29 Predictors of shivering include being male and having low serum levels of magnesium. 30 Bedside Assessment of Shivering Because the deleterious effects of shivering further compromise already vulnerable patients, detection of shivering is an important bedside activity during TTM. Assessments of shivering include both subjective and objective methods. Subjective reports of shivering by patients can be documented, but the intensity of the shivering should be quantified. Methods to objectively measure the onset and severity of shivering include observation of piloerection (erection of hair on the skin of the arms and legs), tactile confirmation of a vibration in the mandible and neck region, visualization of tremors, and measurements with electrical signals of muscle activity, such as electromyography (EMG). Objective Assessment of Shivering via Direct Observation Keen observation skills will allow detection of changes in the condition of the skin. Piloerection, or goose bumps, occurs first as the body attempts to shunt blood from the peripheral compartment to stop heat loss. 31 While trying to diminish Table Bedside Shivering Assessment Scale a Score Type of shivering None Mild Moderate Severe a Data from Badjatia et al. 16 the loss of heat, the body begins shivering in an attempt to produce heat and raise its temperature. Because the increasing intensity of shivering correlates with increasing metabolic consumption of nutrients and oxygen, identifying and quantifying shivering as early as possible are desirable. 16 The Bedside Shivering Assessment Scale (BSAS) 16 was developed to quantify the shivering in adults that occurs during TTM. This 4- point scale (see Table) was validated against resting energy expenditure, oxygen consumption, and carbon dioxide production as measured by indirect calorimetry. In 50 neurocritical care patients who had shivering assessed by using the BSAS, 80% underwent induced normothermia for fever control, and shivering occurred in 64%. The BSAS score provided an accurate representation of the initial and ongoing metabolic stress that occurred during shivering. A BSAS score of 2 to 3 was associated with a resting energy expenditure of 2303 to 3686 kcal/d compared with patients with a BSAS score of 0 to 1, who expended approximately 1390 to 1730 kcal/d. 16 These results indicate that the BSAS is a reliable tool Location No shivering is detected on palpation of the masseter, neck, or chest muscles Shivering localized to the neck and thorax only Shivering involves gross movement of the upper extremities (in addition to neck and thorax) Shivering involves gross movements of the trunk and upper and lower extremities for determining the metabolic consequences of shivering. One benefit of mild hypothermia is the decrease in cerebral metabolic rate. Therefore, untreated shivering may negate the benefits of TTM. 16 The increase in metabolic consumption associated with shivering provides evidence of the need to assess patients for shivering and to treat patients with a BSAS score of 1 or greater. Ongoing assessment is vital to monitor the effectiveness of interventions to reduce shivering. Objective Assessment of Shivering via Technology Additional objective means to assess shivering include measuring muscle activity with electrodes. In the past, shivering was studied by using EMG recordings. 32 Shivering produces a tremor frequency of 200 Hz or 4 to 8 cycles per minute of waves identified as a waxing and waning pattern on EMGs. 27 EMG electrodes are usually placed on the pectoralis major muscle groups bilaterally because shivering usually starts in muscle groups in this region. 33 The EMG system is a challenge; it requires specialized equipment, complex testing, and interpretation of the data. Unlike the laboratory or clinic, 36 CriticalCareNurse Vol 32, No. 1, FEBRUARY

5 the ICU it is not a feasible location for using continuous EMG to measure shivering. Therefore, in clinical practice, use of the BSAS seems to be prudent for assessing patients for shivering. Nursing Care and Implementation of the BSAS Nurses who provide care during the cooling and rewarming phases of TTM are instrumental in ensuring patients overall safety. The primary nursing responsibilities are maintaining stable hemodynamic and ventilatory status, promoting oxygenation, monitoring electrolyte changes, ensuring that target temperatures are achieved, and administering appropriate medications to provide analgesia and sedation. The goals are to diminish secondary injury and improve neurological outcome. Because untreated shivering may negate the beneficial effects of TTM, the BSAS should be used throughout the phases of TTM. Clinicians should determine the BSAS score at least hourly; the score should be determined more frequently during the induction of cooling and the rewarming phase after mild hypothermia when shivering is more likely to occur. Using the BSAS to detect shivering requires less than 1 minute. Because shivering is deleterious, it warrants recognition and prompt intervention. To use the BSAS, begin by palpating the patient s neck, masseter, and chest muscles to determine if the patient is shivering. The absence of any shivering in this part of the body is scored as 0. Shivering visible on the neck and thorax is scored as 1. Moderate shivering includes shivering of the neck and chest muscles and involvement of the upper extremities and is scored as 2. Movement of the neck, chest, and all extremities indicates severe shivering, a BSAS score of 3. Therefore, a higher BSAS score indicates a more severe state of shivering. Determining the BSAS score frequently provides information to guide clinicians in using appropriate therapeutic interventions to manage shivering. Documenting the BSAS score along with hourly vital signs ensures continual reassessment and guides interventions. The assessments determine the evolving needs of the patient and establish the efficacy of both nonpharmacological and pharmacological agents. Therapeutic Strategies for the Treatment of Shivering Strategies to counter shivering include both nonpharmacological and pharmacological interventions. The methods chosen to counter shivering should begin with the least invasive and proceed to more aggressive means. Nonpharmacological Methods A nonpharmacological, noninvasive treatment for shivering is the application of surface counterwarming. Previous clinical studies 34 focused on local warming of the hands, feet, and face of patients to reduce shivering. Skin temperature is thought to influence at least 20% of the shivering threshold. Skin warming increases the mean temperature by 4ºC, an increase that may blunt the shivering response. 35 In a recent study, 36 the effects of surface counterwarming of the entire body were investigated in 50 neurocritical care patients who required fever control and hypothermia. The study had 3 phases: counterwarming, removal of the counterwarming device, and reapplication of counterwarming. BSAS scores increased during the initial phase and improved in the third phase, reapplication of counterwarming. Surface warming is an effective adjunct in suppressing the shiver reflex. 36 Counterwarming devices that blow warm air on the skin can be set to 40ºC to 43ºC. Pharmacological Methods Several pharmacological agents are used to treat and blunt the thermoregulatory response of shivering. The agents are often used synergistically to effectively reduce the shiver reflex. In one study, 37 meperidine (Demerol) decreased both shivering and the vasoconstriction threshold in 9 healthy volunteers. In another study, 38 a combination of low-dose buspirone (Buspar, 20 mg) and lowdose meperidine (25 mg) decreased the shivering threshold without causing respiratory compromise. In another study, 39 dexmedetomidine (Precedex) plus meperidine reduced the shivering threshold in 10 healthy male volunteers. The use of dexmed - etomidine to counter shivering is considered off label. Doses range from 0.2 to 1.5 µg/kg per hour, greater than the approved dosing. Patients who have seizures or renal failure or who take monamine oxidase inhibitors should not be given meperidine because it can decrease the seizure threshold in some patients. In patients with bradycardia, dexmedetomidine may not be the drug of choice because it can slow the heart rate further, leading to an unstable hemodynamic status. CriticalCareNurse Vol 32, No. 1, FEBRUARY

6 Alternatively, infusion of magnesium sulfate at 500 mg/h is beneficial in facilitating the cooling process because of the agent s vasodilating properties. 40 When administering magnesium, clinicians should routinely monitor a patient s magnesium levels at least every 8 hours to maintain and achieve a minimum serum level of 2.5 to 3.5 mg/dl. Because magnesium can cause hypotension, blood pressure should be measured hourly. Another pharmacological option is propofol (Diprivan) 10 to 50 µg/kg per minute. Propofol is a powerful anesthetic agent that decreases vasoconstriction and shivering thresholds. 22 Like magnesium, propofol can cause hypotension. Hourly monitoring of hemodynamic status and reassessment of sedation levels are imperative. If shivering cannot be abolished with the previously mentioned agents, neuromuscular blockade with medications such as vecuronium (Norcuron) may be used. Patients given a neuromuscular blocker must be receiving mechanical ventilation and concurrent sedatives or analgesics. The neuronal activity responsible for eliciting the shiver reflex remains intact despite cessation of vasomotor response caused by paralytic agents. 41 Because the incidence of seizures after cardiac arrest can be as high as 34%, continuous electro - encephalographic monitoring is necessary to monitor for seizure activity. 5 Case Study MM, a 50-year-old man, sustained a cardiac arrest in the grocery store. Cardiopulmonary resuscitation was initiated by a bystander and was continued by paramedics for 20 minutes. Return of spontaneous Patient s temperature, C To computed tomography: machine unplugged 33 0 Patient s temperature Patient s temperature set point Water temperature (right axis) Figure 1 Patient s temperature and machine water temperature changes. A. Patient s body temperature increasing greater than the projected temperature increase plotted in green due to shivering. B. Water response in machine shows a decrease in water temperature. Cessation of shivering occurs, leading to stabilization of rewarming. Note: Patient was taken to computed tomography during rewarming (blue lines show decrease in water temperature when water machine was unplugged and the patient was transported). circulation occurred upon arrival at the emergency department. After his airway was secured and his blood pressure was optimized, MM was unresponsive. TTM with mild hypothermia was started in the emergency department with iced saline and a cooling system. The patient was sedated and analgesia was provided. After 24 hours at 33ºC, rewarming of MM was initiated at a rate of 0.25ºC/h. When the ICU nurse noted his temperature had increased to 34.5ºC and that the water temperature in the machine had decreased markedly (Figure 1), MM had a BSAS score of 2. Application of a counterwarming device reduced the BSAS score to 1 for 30 minutes, but the shivering returned B A to a BSAS score of 2 (Figure 2). Because sedation had been maximized, the intensivist ordered a bolus of meperidine. Reassessment 15 minutes later revealed a BSAS score of 0. Rewarming continued until MM s body temperature returned to 37ºC. Twenty-four hours later, the patient s temperature increased to 38.3ºC. After he did not respond to acetaminophen, the ICU nurse restarted the cooling device to lower MM s temperature to 37ºC. Anticipating the possibility that shivering might begin, the nurse began assessing for the presence of shivering by using the BSAS every 15 minutes. MM had been weaned from sedation 6 hours before initiation of cooling 5 Water temperature, C 38 CriticalCareNurse Vol 32, No. 1, FEBRUARY

7 Patient s temperature, C B A Figure 2 Patient s body temperature began to increase (A) when shivering commenced. Notice decrease in water temperature (B) with shivering. Interventions instituted to decrease shivering result in return to baseline. for fever control. Twenty minutes after starting the cooling device, the ICU nurse noted piloerection on the patient s arms. Assessment of shivering revealed a humming or vibration in the chest and mandible regions for a BSAS score of 1. A counterwarming device was applied, and the BSAS score decreased to 0. The nurse s ability to use a standardized tool to assess for the presence of shivering assisted in patient management. Minimizing the adverse impact of shivering enabled the ICU Water temperature, C Patient s temperature Patient s temperature set point Water temperature (right axis) To learn more about shivering management in the critical care setting, read Optimal Management of Shivering During Therapeutic Hypothermia After Cardiac Arrest by Logan et al in Critical Care Nurse, 2011; 31:e18-e30. Available at team to reach therapeutic temperature goals. MM was extubated on day 3 and was transferred to acute rehabilitation on day 7. Later he was discharged home, and he returned to his normal activities of daily living. Conclusion Acute cerebral resuscitation via therapeutic hypothermia may ameliorate the destructive processes of ischemiareperfusion injury, favorably improving survival and neurological outcome. Untreated shivering as a sequela of TTM may negate the benefits of the intervention. Failure to detect and recognize shivering creates unintended adverse metabolic and hemodynamic effects. Currently, the BSAS is the only validated bedside tool that ICU clinicians can use to monitor shivering. The usefulness of the tool includes the ability to measure the degree of shivering during TTM. This information can indicate the efficacy of the interventions intended to blunt thermoregulatory defenses. Furthermore, use of the BSAS allows the ICU team to continually evaluate patients responses to interventions. Nurses are at the forefront in caring for patients undergoing cooling therapy. Knowledge and understanding of the harmful effects of shivering are important to effect care and prevent secondary injury. CCN Now that you ve read the article, create or contribute to an online discussion about this topic using eletters. Just visit and click Submit a response in either the full-text or PDF view of the article. Financial Disclosures None reported. References 1. American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiac care, part 7.5: postresuscitation support. Circulation. 2005;112:IV84-IV Nolan JP, Morley PT, Vanden Hoek TL, et al; International Liaison Committee on Resuscitation. Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Circulation. 2003;108(1): Bernard SA, Gray T, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346: 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(22):1756]. N Engl J Med. 2002;346(8); Seder D, Van der Kloot TE. Methods of cooling: practical aspects of therapeutic temperature management. Crit Care Med. 2009;37(7 suppl):s211-s Jordan J, Carhuapoma J. Hypothermia: comparing technology. J Neurol Sci. 2007;261(1): Badjatia N. Celsius control system. Neurocrit Care. 2004;1: Mayer S, Kowalski RG, Presciutti M, et al. Clinical trial of a novel surface cooling system for fever control in neurocritical care patients. Crit Care Med. 2004;2(12): Schreckinger M, Marion D. Contemporary management of therapeutic intracranial hypertension: is there a role for therapeutic hypothermia? Neurocrit Care. 2009;11: Stravitz RT, Larsen FS. Therapeutic hypothermia for acute liver failure. Crit Care Med. 2009;37(7 suppl):s258-s Jamarillo A, Illanes S, Diaz V. Is hypothermia useful in malignant ischemic stroke? Current status and future perspectives. J Neurol Sci. 2008;266: Hemmen T, Lyden P. Induced hypothermia for acute stroke. Stroke. 2007;38: Konstas A, Choi J, Spellman J. Neuroprotection for ischemic stroke using hypothermia. Neurocrit Care. 2006;4: Nagoa S, Irie K, Kawai N, Nakamura T, Kunishio K, Matsumoto Y. The use of mild hypothermia for patients with severe vaso - spasm: a preliminary report. J Clin Neurosci. 2003;10(2): CriticalCareNurse Vol 32, No. 1, FEBRUARY

8 15. Badjatia N. Hyperthermia and fever control in brain injury. Crit Care Med. 2009;37(7 suppl):s250-s Badjatia N, Strongilis E, Gordon E, et al. Metabolic impact of shivering during therapeutic temperature modulation: the Bedside Shivering Assessment Scale. Stroke. 2008; 39(12): Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009;37(7 suppl):s186-s Sanders AB. Therapeutic hypothermia after cardiac arrest. Curr Opin Crit Care. 2006;12: Boulant J. Neuronal basis of Hammel s model for set-point thermoregulation. J Appl Physiol. 2006;100(4): Boulant JA. Role of the preoptic-anterior hypothalamus in thermoregulation and fever. Clin Infect Dis. 2000;31(suppl 5):S157-S Hammel HT, Hardy JD, Fusco MM. Thermoregulatory responses to hypothalamic cooling in unanesthesized dogs. Am J Physiol. 1960;198: Sessler DI. Thermoregulatory defense mechanisms. Crit Care Med. 2009;37(7 suppl): S203-S Mahmood MA, Zwiefler RM. Progress in shivering control. J Neurol Sci. 2007;261: Hemingway A. Shivering. Physiol Rev. 1963; 43: Gilbert GJ. Thermoregulation: recent concepts and remaining questions. Neurology. 2008;70(21): Eyolfson DA, Tikuisis P, Xu X, Weseen G, Giesbrecht GG. Measurement and prediction of peak shivering intensity in humans. Eur J Appl Physiol. 2001;84: Dewitte J, Sessler DI. Perioperative shivering. Anesthesiology. 2002;96: Ralley F, Wyands JE, Ramsay JG, Carli F, MacSullivan R. The effects of shivering on oxygen consumption and carbon dioxide production in patients rewarming from hypothermic cardiopulmonary bypass. Can J Anaesth. 1988;35(4): Vassilieff N, Rosencher N, Sessler D, Conseiller C. Shivering threshold during spinal anesthesia is reduced in elderly patients. Anesthesiology. 1995;83(6): Badjatia N, Kowalski RG, Schmidt JM, et al. Predictors and clinical implications of shivering during therapeutic normothermia. Neurocrit Care. 2007;6(3): Landsberg L, Saville ME, Young JB. Sympathoadrenal system and regulation of thermogenesis. Am J Physiol. 1984;247:E181-E Tikusis P, Bell DG, Jacobs I. Shivering onset, metabolic response and convective heat transfer during cold air exposure. J Appl Physiol. 1996;72(6): Van Ooijen AM, van Marken Lichtenbelt WD, van Steenhoven A, Westerterp KR. Cold-induced heat production preceding shivering. Br J Nutr. 2005;93(3): Doufas AG, Wahhwa A, Lin C, Shah Y, Hanni K, Sessler D. Neither arm nor face warming reduces the shivering threshold in unanesthetized humans. Stroke. 2003;34: Cheng C, Matsukawa T, Sessler DI, et al. Increasing mean skin temperature linearly reduces the core-temperature thresholds for vasoconstriction and shivering in humans. Anesthesiology. 1995;82(5): Badjatia N, Strongilis E, Presciutti M, et al. Metabolic benefits of skin counter warming during therapeutic temperature modulation. Crit Care Med. 2009;37(6): Kurz A, Takehiko I, Sessler D, et al. Meperidine decreases the shivering threshold twice as much as the vasoconstriction threshold. Anesthesiology. 1997;86(5): Mokhtarani M, Mahgoub AN, Marioka N, et al. Buspirone and meperidine synergistically reduce the shivering threshold. Anesth Analg. 2001;93: Doufas AG, Lin C, Suleman MI, et al. Dexmedetomidine and meperidine additively reduce the shivering threshold in humans. Stroke. 2003;34(5): Zweifler RM,Voorhees ME, Mahmood MA, Parnell M. Magnesium increases the rate of hypothermia via surface cooling and improves comfort. Stroke. 2004;35: Van Zanten AR, Polderman KH. Blowing hot and cold? Skin counter warming to prevent shivering during therapeutic cooling. Crit Care Med. 2009;37(6): CriticalCareNurse Vol 32, No. 1, FEBRUARY

9 CCN Fast Facts CriticalCareNurse The journal for high acuity, progressive, and critical care Shivering Management During Therapeutic Temperature Modulation: Nurses Perspective Facts Therapeutic temperature modulation (TTM), which incorporates mild hypothermia and maintenance of normothermia, is being used to manage patients resuscitated after cardiac arrest. Methods of modulating temperature include intravenous infusion of cold fluids and surface or endovascular cooling. During this therapy, the shiver response is activated as a defense mechanism in response to an altered set-point temperature and causes metabolic and hemodynamic stress for patients. Because the deleterious effects of shivering further compromise already vulnerable patients, detection of shivering is an important bedside activity during TTM. Assessments of shivering include both subjective and objective methods. Subjective reports of shivering by patients can be documented, but the intensity of the shivering should be quantified. Methods to objectively measure the onset and severity of shivering include observation of piloerection (erection of hair on the skin of Table Bedside Shivering Assessment Scale a Score Type of shivering None Mild Moderate Severe a Data from Badjatia et al. 1 Location No shivering is detected on palpation of the masseter, neck, or chest muscles Shivering localized to the neck and thorax only Shivering involves gross movement of the upper extremities (in addition to neck and thorax) Shivering involves gross movements of the trunk and upper and lower extremities the arms and legs), tactile confirmation of a vibration in the mandible and neck region, visualization of tremors, and measurements with electrical signals of muscle activity, such as electromyography. The Bedside Shivering Assessment Scale (BSAS) 1 was developed to quantify the shivering in adults that occurs during TTM. This 4-point scale (see Table) was validated against resting energy expenditure, oxygen consumption, and carbon dioxide production as measured by indirect calorimetry. The BSAS can be used to determine the efficacy of interventions intended to blunt thermoregulatory defenses and can provide continual evalu ation of patients responses to the interventions. Currently, the BSAS is the only validated bedside tool that intensive care unit clinicians can use to monitor shivering. The usefulness of the tool includes the ability to measure the degree of shivering during TTM. This information can indicate the efficacy of the interventions intended to blunt thermoregulatory defenses. Furthermore, use of the BSAS allows the intensive care unit team to continually evaluate patients responses to interventions. Nurses are at the forefront in caring for patients undergoing cooling therapy. Knowledge and understanding of the harmful effects of shivering are important to effect care and prevent secondary injury. CCN Reference 1. Badjatia N, Strongilis E, Gordon E, et al. Metabolic impact of shivering during therapeutic temperature modulation: the Bedside Shivering Assessment Scale. Stroke. 2008;39(12): Presciutti M, Bader MK, Hepburn M. Shivering management during therapeutic temperature modulation: nurses perspective. Crit Care Nurse. 2012;32(1): CriticalCareNurse Vol 32, No. 1, FEBRUARY

10 CE Test Test ID C121: Shivering Management During Therapeutic Temperature Modulation: Nurses Perspective Learning objectives: 1. Describe the physiological processes of temperature control 2. Identify subjective and objective measurements for assessment of shivering in patients undergoing therapeutic temperature modulation (TTM) 3. Discuss nursing implications associated with shivering and appropriate interventions to manage shivering during TTM 1. Which of the following are thought to be responsible for the ability of the body to regulate its temperature and adapt to changes in maintaining homeostasis? a. Sensory neurons in the hypothalamus b. Effector neurons in the hypothalamus c. Afferent receptors in the skin and periphery d. Efferent receptors in the central and peripheral nervous systems 2. Mild therapeutic hypothermia is defined as a body temperature within what range? a. 33ºC and 35ºC b. 32ºC and 34ºC c. 31ºC and 33ºC d. 30ºC and 32ºC 3. What is the main goal of therapeutic temperature modulation (TTM)? a. Improved cerebral perfusion pressure b. Prevention of ischemia-reperfusion injury to body cells c. Reduction of destructive molecular changes in the brain d. Decreased cellular metabolism and oxygen consumption 4. What specific parameter should be monitored in a patient receiving an infusion of propofol during TTM? A. Electroencephalogram b. Blood glucose c. Patellar reflexes d. Heart rate and rhythm 5. Which of the following groups of patients are most susceptible to shivering at a core body temperature of 35 C? a. Young women b. Elderly men c. Patients with high serum calcium levels d. Patients with low serum magnesium levels 6. Patients with what Bedside Shivering Assessment Scale (BSAS) should be treated for shivering? a. BSAS of 3 or greater b. BSAS of 1 or greater c. BSAS of 3 or less d. BSAS of 1 or less 7. A patient who is shivering after cardiac surgery would be expected to have which of the following? a. Low mixed venous oxygen level b. Decreased mean arterial pressure c. Increased mixed venous oxygen consumption d. Decreased arteriovenous shunting 8. The shivering mechanism is activated with what change in body temperature? a. Decrease of 1ºC less than the set point b. Decrease of 2ºC less than the set point c. Decrease of 1ºC less than the vasoconstriction threshold d. Decrease of 2ºC less than the vasoconstriction threshold 9. Shivering occurs most frequently during which of the following phases of TTM? a. Induction of cooling and maintenance phase b. Induction of cooling and rewarming phase c. Induction of cooling d. Rewarming phase 10. Which medication used to treat shivering during TTM should be avoided in patients who have seizures? a. Meperidine b. Buspirone c. Dexmedetomide d. Propofol 11. Shivering usually starts in which of the following muscle groups? a. The sternocleidomastoid region b. The trapezius region c. The pectoralis major region d. The latissimus dorsi region 12. The presence of which of the following would warrant a score of 1 on the BSAS? a. Absence of shivering b. Shivering present in the neck, thorax, and upper and lower extremities c. Shivering in the neck and chest muscles only d. Shivering in the muscles of the neck, masseter, chest, and upper extremities 1. qa Test answers: Mark only one box for your answer to each question. You may photocopy this form. 2. qa 3. qa Test ID: C121 Form expires: February 1, 2014 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP: Category A Test writer: Ann Lystrup, RN, BSN, CEN, CFRN, CSPI, CCRN For faster processing, take this CE test online at ( CE Articles in this issue ) or mail this entire page to: AACN, 101 Columbia Aliso Viejo, CA qa 5. qa Program evaluation 6. qa Yes No Objective 1 was met q q Objective 2 was met q q Objective 3 was met q q Content was relevant to my nursing practice q q My expectations were met q q This method of CE is effective for this content q q The level of difficulty of this test was: q easy q medium q difficult To complete this program, it took me hours/minutes. Name Member # Address City State ZIP Country Phone RN Lic. 1/St RN Lic. 2/St Payment by: q Visa q M/C q AMEX q Discover q Check Card # Expiration Date Signature The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure. 7. qa 8. qa 9. qa 10. qa 11. qa 12. qa

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