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Sleep in the Intensive Care Unit: A Review Lisa M. Pulak and Louise Jensen J Intensive Care Med published online 10 June 2014 DOI: 10.1177/0885066614538749 The online version of this article can be found at: http://jic.sagepub.com/content/early/2014/06/03/0885066614538749

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Article

Sleep in the Intensive Care Unit: A Review

Journal of Intensive Care Medicine 1-10 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0885066614538749 jic.sagepub.com

Lisa M. Pulak, RN, NP, MN1, and Louise Jensen, RN, PhD2

Abstract Patients in the intensive care unit (ICU) are susceptible to sleep deprivation. Disrupted sleep is associated with increased morbidity and mortality in the critically ill patients. The etiology of sleep disruption is multifactorial. The article reviews the literature on sleep in the ICU, the effects of sleep deprivation, and strategies to promote sleep in the ICU. Until the impact of disrupted sleep is better explained, it is appropriate to provide critically ill patients with consolidated, restorative sleep. Keywords sleep, intensive care, sleep deprivation, sleep quality, sleep in critical care

Promoting rest and sleep is integral to the critically ill patients. Sleep is essential for energy conservation and restoring the mind. Sleep provides the necessary energy for patients to participate in therapy. With intense nursing care, patients in the intensive care unit (ICU) are susceptible to sleep deprivation.1 Although patients may achieve an acceptable amount of sleep during a 24-hour period while receiving care in the ICU, this sleep is fragmented and has a significantly abnormal architecture.2 Sleep deprivation impairs cognition, ranging from apathy and confusion to delirium, all of which may lead to increased morbidity and mortality.3,4 Disrupted sleep is associated with immune dysfunction, impaired resistance to infection, as well as alterations in nitrogen balance and wound healing.5 Factors contributing to sleep deprivation are multifactorial and include the type and severity of illness, pathophysiology of acute illness or injury, pain, medications used in treatment, and the ICU environment.6

Sleep Stages Sleep is a temporal phenomenon that is regulated by homeostatic and circadian processes. This system has connections to organs and tissues, relaying information from a centrally created circadian rhythm.7 The circadian rhythm, a period of approximately 24 hours, is regulated by the suprachiasmatic nucleus located in the hypothalamus. The circadian pacemaker stimulates changes in the daily patterns of sleep–wake and activity–rest. Sleep also has infradian (longer than a day) and ultradian (shorter than a day) rhythms. Homeostasis is the result of the coordinated physiologic processes that maintain most steady states in an organism. In humans, the need for sleep is proportional to the preceding time of wake. ‘‘Normal’’ sleep is categorized by nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

Classically, NREM sleep was divided into 4 stages, representing a continuum of sleep. Stage 1 is the transition from wakefulness to sleep. Individuals have a sleep latency period of 10 to 20 minutes before beginning NREM stage 1 sleep. Initiation of sleep is short lived accounting for only 2% to 5% of total sleep time (TST). It is the lightest stage of sleep. An increased amount or percentage of stage 1 sleep typically suggests sleep fragmentation due to a sleep disorder. Nonrapid eye movement stage 2 sleep typically accounts for 40% to 55% of TST. It is characterized by slowing of electroencephalogram (EEG) frequency and lasts 10 to 25 minutes, progressing into NREM stages 3 and 4 sleep. Stages 3 and 4 are referred to as deep sleep or slow wave sleep (SWS). It is a deeper, more restful sleep with a high arousal threshold. Most SWS occurs in the first third of the night. Slow wave sleep comprises 13% to 23% of sleep and decreases markedly with age.8 The American Academy of Sleep Medicine no longer divides NREM sleep into 4 stages, with stage 4 deleted. Sleep stages 1 to 3 are referred to as N1, N2, and N3, with N3 reflecting SWS; REM is referred to as stage R. In REM sleep, the EEG resembles wakefulness but muscle activity is greatly reduced. Rapid eye movement sleep is

1 NP Medical Assessment Unit, Royal Alexandra Hospital, Edmonton, Alberta, Canada 2 Faculty of Nursing, University of Alberta, 4-256 Edmonton Clinic Health Academy, Edmonton, Alberta, Canada

Received September 9, 2013, and in revised form March 11, 2014. Accepted for publication March 13, 2014. Corresponding Author: Louise Jensen, Faculty of Nursing, University of Alberta, 4-256 Edmonton Clinic Health Academy, Edmonton, Alberta, Canada T6G 1C9. Email: [email protected]

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characterized by inhibition of spinal motor neurons leading to muscle atonia (tonic REM) with intermittent bursts of REM and distal muscle twitches (phasic REM). Rapid eye movement sleep is considered to be restful sleep and has a variable arousal threshold. Dreaming is associated with REM sleep, which originates in the pons. Rapid eye movement sleep occurs approximately 70 to 90 minutes after sleep onset, with the first REM period lasting a few minutes. Rapid eye movement periods cycle every 90 minutes, alternating with NREM stages, which accounts for 45% to 55% of TST. Rapid eye movement periods increase in length and intensity as the night progresses.8,9 Rapid eye movement sleep is associated with the greatest instability of respiratory and cardiac function. Rapid eye movement sleep is predominantly a parasympathetic (vagal) state, but during aphasic REM sleep, there are sudden bursts of sympathetic nervous system activity. These bursts can be associated with sudden increases in arterial blood pressure, cardiac or cerebral ischemia, cardiac arrhythmias, and sudden changes in heart rate (HR) and respiratory rate (RR). Short central apneas and hypopneas are also common during REM sleep.8

Measurement of Sleep Polysomnography (PSG), often considered the criterion standard of sleep measurement,10 uses EEG, chin electromyography, and electrooculography collected continuously over the duration of the time period of interest.2 These data are used to score sleep stages, including NREM and REM sleep, and wake. Sleep stages and related physiologic phenomena are usually scored in 30-second epochs, although other time periods may be used. Other patterns in EEG, such as brief electrophysiologic arousals and seizure activity, can be evaluated. Polysomnography also often includes evaluation of cardiorespiratory variables, such as respiratory effort, nasal/oral airflow, and oxygen saturation, to determine the presence of sleep-disordered breathing. Other physiologic data can also be evaluated (eg, gastric pH and end-tidal CO2) if appropriate sensors are added. However, PSG requires skilled technicians and interpretation. Consequently, PSG is costly and logistically challenging in the ICU.2 Alternative surrogate techniques to assess sleep in the ICU have been utilized such as actigraphy and bispectral index analysis (BIS). Actigraphy measures the level of activity at the wrist to discern wakefulness judged by movement, with rest or sleep estimated from stillness.11 Actigraphy tends to overestimate TST compared to PSG, as it has a higher sensitivity for detecting sleep, but is less reliable in detecting wakefulness (ie, reduced sleep specificity). The BIS integrates EEG data to provide a scaled numerical value from 0 to 100, with a larger value representing a higher degree of consciousness. The BIS has the potential to estimate sleep depth, although it has not yet shown clinical benefit in ICU care.12 Compared to PSG, subjective survey instruments, such as the Richards-Campbell Sleep Questionnaire, have been investigated for ICU sleep measurement. However, there remains concerns with patient’s self-reports while sedated

or delirious. Kamdar et al12 further found that nurses’ ratings overestimated patients’ ratings of sleep quality.

Sleep in the ICU Critical illness is associated with profound and rapidly changing alterations in physiologic, emotional, and functional status and symptoms. These changes are likely to be associated with similarly rapid changes in sleep patterns.13 Sleep deprivation and disruption are very apparent in the ICU where critical care protocols routinely and severely deprive patients of sleep at a time when the need for adequate rest is perhaps most essential. Friese5 found sleep architecture was markedly abnormal in critically ill patients, with the vast majority of sleep being superficial (NREM stages 1 and 2), with very little deep or restorative NREM stages 3 and 4 and REM sleep. Hilton14 found a significant decrease in TST compared with controls, with only 50% of sleep occurring during the night. Night sleep was characterized by extreme fragmentation, an overrepresentation of stage 1 and NREM sleep (49% of TST), reduced or absent SWS and REM sleep (3.6% of TST), almost nonexistent NREM stage 4 sleep (0.1% of TST), and circadian rhythm abnormalities. In the ICU, approximately 50% of sleep hours occur during the day in short bouts, which makes it difficult for patients to achieve REM sleep.15 In fact, although TST may be normal, an increased percentage of wakefulness, NREM stage 1 sleep, and decreased amounts of NREM stages 2 and 3 and REM sleep were consistently noted.15 Average sleep time was 8.28 hours over 24 hours in severely fragmented superficial stages (NREM stages 1 and 2), whereas only 0.29% was spent in NREM stages 3 and 4 sleep. Rapid eye movement sleep accounted for only 3.3% of the TST.8 A telephone interview with a random sample of 60 ICU patients was conducted after discharge using the Basic Nordic Sleep Questionnaire and 2 other questions estimating the quality of sleep before and after their stay in ICU. Sleep disturbances were described in one-half of the patients during the ICU stay and in one-third 6 to 12 months after discharge.16

Effects of Sleep Deprivation Achieving restorative sleep in the ICU remains a challenge for most patients. There are strong correlations of sleep disruption with systemic illness and mortality.8,17 The ICU is geared toward specifically treating organ failures and providing a high level of nursing care. However, these benefits come at a substantial physiological and psychological discomfort to the patients.18

Immune Function Despite controversy, the notion that sleep loss leads to impaired defense mechanisms and renders the individual more susceptible to infection has gained increased acceptance.19 Sleep is particularly important for initiating effective adaptive immune responses that eventually produce long-lasting immunological memory.20 The basis for this influence is a bidirectional communication

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between the central nervous system (CNS) and the immune system and direct innervation of the immune system by the autonomic nervous system.20 Interleukin 1 (IL-1) and tumor necrosis factor have been shown to regulate NREM sleep; therefore, loss of sleep may result in impairment of host defenses against infection. Significant reduction in the number and phagocytic activity of lymphocytes was found to be decreased by 13% as compared with nonsleep-deprived individuals. Interleukin 2 was also found to be suppressed.21 Benedict et al22 found that IL-7 levels were increased during normal sleep. Interleukin 7 facilitates the transition of CD8þ effector to memory T-cells and lengthens survival of the T-cell memory cells.23 Natural killer T-cell activity was found to be negatively correlated with severity of insomnia.21 Sleep restriction can also result in reduced antioxidant activity (catalase and glutathione), decreased spleen weight, alterations in leukocyte and lymphocyte counts, and the production of serum antibodies without the presence of an antigen.24 Thus, sleep deprivation can potentially affect healing, both in terms of tissue repair and cellular immune function. Prolonged sleep deprivation and the accompanying stress response invoke a persistent production of proinflammatory cytokines, producing a chronic low-grade inflammation and also immunodeficiency.20

Hormonal Systems and Metabolism Sleep deprivation results in extensive changes to homeostatic mechanisms and markedly affects neuroendocrine stress systems. Sareli and Schwab19 found that sleep deprivation reduced body temperature and weight, despite increased energy expenditure. Schmid et al25 found significant decreases in basal glucagon after 1 night of sleep deprivation along with other changes in glucose hormonal regulation. Other investigators have found increased insulin resistance with sleep loss. Spiegel et al26 found that sleep-deprived patients showed decreased glucose tolerance, insulin resistance, lower thyrotropin, and elevated evening cortisol levels. Sleep deprivation has been shown to induce the onset of a catabolic state.27 Wakefulness enhances catabolism, while sleep shifts metabolism in favor of anabolism. Urinary nitrogen secretion increases markedly with sleep reversal (change in diurnal activity) and sleep deprivation.27 During sleep, especially SWS, growth hormone is secreted that rapidly stimulates protein and RNA synthesis and amino acid uptake by cells. Important circadian variations occur in protein synthesis and cellular division, with peak activity occurring during sleep.27 Sleep-deprived patients are found to have higher oxygen consumption, carbon dioxide production, HR, and catecholamine levels, likely as a stress response.28 Fanfulla et al29 demonstrated a relationship between sleep quality and acid–base balance, which had not been previously described. A higher pH was associated with a reduced quantity and quality of sleep in terms of less SWS and more arousals. The presence of alkalosis, including respiratory alkalosis with hypocapnia, increases neuronal excitability, seizure activity, and spontaneous and/or asynchronous firing of cortical neurons.

Thermoregulation Body temperature and thermoregulation are regulated, in part, by sleep and circadian rhythms. In normal individuals, core body temperature peaks late in the day and declines before sleep onset. Temperature sensitivity decreases during NREM sleep, and REM sleep is characterized by variations in body temperature based on the surroundings and loss of compensatory responses, such as shivering and sweating. Body temperature reaches a nadir during the latter part of sleep, following a temperature rise preceding awakening.12

Pulmonary Mechanics White et al30 found that ventilatory response to hypercapnia and hypoxemia was reduced after sleep deprivation. Chen and Tang31 showed that after 30 hours of sleep deprivation, inspiratory muscle endurance was reduced as evidenced by a reduced product of inspiratory muscle load and sustained time, whereas forced expiratory volume in 1 second and forced vital capacity were unaltered. Acute sleep deprivation has been shown to decrease central motor output to upper airway muscles in response to hypercapnia. In patients with severe sleep disordered breathing, this could potentially lead to respiratory failure. It is possible that by reducing respiratory muscle endurance or compromising pulmonary function, sleep disruption may hamper the ability of mechanically ventilated patients to be weaned. These studies were performed in healthy volunteers however, and may not apply to the critically ill patients, who are characterized by a unique pattern of sleep disturbance rather than continuous sleep deprivation.

Delirium Delirium continues as a significant complication of an acute illness. Available data show that delirium develops in 20% to 50% of patients with low severity of illness and in up to 80% of patients requiring mechanical ventilation.32 Association between delirium and sleep disturbance in the ICU is suggested, although medications used to control delirium may in fact be contributing to deleterious effects on sleep and overall psychiatric outcomes. Drouot et al10 combined EEG spectral analysis and visual quantitative EEG analysis during sleep and wakefulness and identified subclinical alterations in sleep/ wake states, which may affect one-third of conscious nonsedated ICU patients with respiratory failure. These abnormalities may reflect a subclinical form of brain dysfunction that may be associated with an increased risk of delirium.

Causes of Sleep Deprivation in the ICU Mechanical Ventilation Effects Critically ill, mechanically ventilated patients have long been known to have poor sleep quality.33 Major causes of sleep disturbance associated with mechanical ventilation include patient–ventilator asynchronies, central apneas due to

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overventilation, and inadequate ventilatory support due to improper settings or air leaks leading to increased respiratory effort.34 Mechanical ventilation is used primarily to improve gas exchange and achieve respiratory muscle rest. To achieve this goal, it is important that a patient does not make respiratory efforts out of synchrony with the cycling of the ventilator. The operation of a ventilator, however, including its alarms, may disrupt sleep. Selecting a ventilator mode has a marked influence on the quality of sleep in a critically ill patient, and a patient’s response to ventilator settings can differ significantly between sleep and wakefulness.35 Parthasarathy and Tobin35 showed an increase in central apneas when the ventilatory mode was switched from assistcontrol ventilation (ACV) to pressure support ventilation (PSV). Central apneas can cause hypoxia and hypercapnia with consequent increase in respiratory effort, and all 3 factors can cause arousal from sleep. The patients who developed central apneas did so more frequently during PSV than during pressure support with added dead space, and, in turn, more frequently than during ACV. Assist-control ventilation has been associated with increased NREM stages 1 and 2 sleep and reduced wakefulness during the first part of the night when compared to low levels of PSV. Assist-control ventilation was also associated with significant increases in NREM stages 3 and 4 sleep during the second part of the night.35 Sleep fragmentation followed a similar trend. Compared with ACV, the increase in apneas during PSV, with and without dead space, was associated with a proportional increase in the number of awakenings. Central apneas during PSV may worsen sleep quality. Sleep fragmentation during PSV resulted from an increased frequency of awakenings rather than arousals. These data suggest that not only the frequency but also the degree of sleep fragmentation was greater during PSV.

Noninvasive Ventilation Effects Patients with hypercapnic respiratory failure requiring >24 hours of noninvasive ventilation (NIV) exhibit marked sleep disturbances as assessed by PSG. Sleep alterations including circadian sleep cycle disruption and shorter REM sleep time were associated with subsequent delirium and late NIV failure.11,36 Cooper et al37 studied sleep quality in mechanically ventilated patients. In 8 patients with electrophysiological features of sleep, 42 arousals and awakenings occurred per hour of sleep. This level of sleep fragmentation is similar to that seen in patients with obstructive sleep apnea who have excessive daytime sleepiness and impaired cognition.38

Medication Effects The mainstay of treatment for sleep disturbances has been sedative–hypnotics, although these compounds may have adverse effects including rebound insomnia, falls, tolerance, withdrawal, and delirium.39 Medications can affect sleep in various ways. They may contribute to disturbed sleep and adversely affect normal sleep physiology and architecture.

Patients receiving paralytics along with sedation showed REM sleep was completely absent. Medications may affect the CNS directly by penetrating the blood–brain barrier or indirectly by affecting a medical or psychiatric illness that results in altered sleep. Some may disrupt sleep by their effect on preexisting sleep disorders and others have an equally disruptive effect when withdrawn abruptly.40 Drug withdrawal can also alter sleep architecture and precipitate delirium and requires consideration in any patient using long-term medications that influence sleep.12 Sedatives. Sedation is a nonphysiological, nonessential state and is not circadian or fully reversible with external stimuli. The most common ICU sedatives are those that interact with g-aminobutyric acid (GABA) receptors in the CNS. g-Aminobutyric acid activation is part of the endogenous sleep pathway; however, it is a late event in naturally occurring sleep.41 At low doses, benzodiazepines and propofol suppress SWS and may decrease REM sleep. They shorten sleep latency, decrease arousals, and increase NREM stage 2 sleep. Higher doses are associated with a characteristic slowing of the EEG and both can lead to a burst suppression pattern, thus the EEG shows more of a comatose pattern. With repeated use, benzodiazepines can completely abolish NREM stage 4 sleep.40,42 Propofol administration to achieve the recommended level of sedation in critically ill patients further worsens the already impaired sleep quality of these patients.43 Dexmedetomidine has a different relationship with sleep than GABA agonist sedatives. Its effects are closer to the onset of the naturally occurring sleep pathway in the CNS.41 Dexmedetomidine, an a-agonist, is believed to inhibit norepinephrine release by the locus coeruleus, thus leading to a sequence of events that more closely resembles natural sleep physiologically and clinically.40 Dexmedetomidine preserves a natural sleep pattern and induces cooperative sedation in which patients are easily arousable, leads to less impairment in cognitive function, and has an opioid sparing effect as well.44 Analgesics. Opioids are the mainstay of treatment for pain and discomfort in critically ill patients. They interact with the natural sleep pathway by way of the pontothalamic arousal pathway.45 Even single doses of opioids potently suppress SWS.46 Rapid eye movement sleep suppression by opioids is a dose-dependent phenomenon.47 Opioids increase NREM stage 2 sleep and also increase wakefulness. However, if pain is a predominant cause of disturbed sleep, the overall effects of opioids would likely be to improve sleep.48 Even nonsteroidal anti-inflammatory medications can adversely affect sleep by decreasing sleep efficiency and increasing awakenings. These effects may be because of inhibition of prostaglandin synthesis, decreased melatonin secretion, attenuation in nocturnal body temperature, or gastric irritation.49 Although it should be emphasized that these medications have an important role in patient comfort, the right balance of sedative and analgesic administration is required.50 Benzodiazepines and opioids can

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lower upper airway tone during sleep, contributing to obstruction and apnea, as well as sleep fragmentation. Cardiovascular medications. The use of b-blockers has become commonplace for the critically ill patients.51 Their effects on sleep are variable and depend on their lipid solubility; it is their ability to cross the blood–brain barrier that is believed to be related to their CNS side effects. The most lipid soluble (ie, propranolol) drugs have the greatest tendency to disrupt sleep.52 They have been found to be associated with nightmares, insomnia, and REM sleep suppression. Amiodarone, a highly effective antiarrhythmic, has neurological side effects in up to 40% of patients on a therapeutic dose. These include insomnia and nightmares.53 Adrenergic receptor agonists may cross the blood–brain barrier under certain conditions leading to CNS side effects.54 Patients with sepsis and those simultaneously anesthetized with propofol are more vulnerable to CNS side effects on sleep. Norepinephrine, epinephrine, and dopamine are associated with insomnia and suppression of REM sleep and SWS.55 Respiratory medications. Patients on mechanical ventilation and those who have acute or chronic respiratory conditions with symptoms are likely to receive inhaled b-adrenergic receptor agonists while in the ICU. Central nervous system stimulation with associated restlessness and insomnia is a well-known adverse effect. The overall effect on sleep may be positive, however, if they alleviate dyspnea and desaturations, which have been demonstrated to be associated with arousals from sleep.56 Corticosteroids. The effects of corticosteroids on sleep depend on the type and dose of the medication. They have been associated with REM sleep suppression and an increase in nocturnal awakenings. Their CNS stimulatory adverse effects, the hypermania or steroid ‘‘psychosis,’’ can cause insomnia.57 Antipsychotics. Antipsychotics have become a mainstay of the care for the agitated critically ill patients. Haloperidol in single doses has been shown to increase sleep efficiency and NREM stage 2 sleep, with little effect on slow wave activity and REM sleep.58 Atypical antipsychotics such as olanzapine and risperidone increase TST efficiency and SWS.58 Off-label medications. Medications such as diphenhydramine are deliriogenic. Additionally, sedating antidepressants such as trazodone, amitriptyline, and mirtazapine have not been studied for use in insomnia and have important potential side effects including hypotension, arrhythmias, and anticholinergic syndrome.12

Environmental Effects Patients in the ICU are invariably anxious. They rarely have preparation for their admission and are puzzled and worried by the strange surroundings. This is even more so when the

patient is unable to communicate, sedated, or unable to move from chemical or physical restraints. Fear, apprehension, and constant worry cause low morale and sleep disturbances. In addition, the patient’s sleep is often interrupted by the health care team for procedures and assessments, despite the increased sophistication of monitoring systems that should decrease the hands-on manipulation of the sleeping patients.59 Nursing activities require a well-lighted environment, increasing the disturbance for patients. It is inevitable that noise will be created while preparing and conducting patient care activities. Thus, noise and light levels, drugs, pain, and critical illnesses affect the quality of sleep and may lead to sleep deprivation.60

Noise Levels The World Health Organization’s (WHO) external review policy on community noise has produced guidelines that identify specific noise levels within hospital environments. The recommendations include noise levels not exceeding 35 dB(A) during the night and 40 dB(A) during the day, contrasting with a quiet bedroom at night being 20 to 30 dB(A). When compared with ward-based environments, the noise intensity within the ICU far exceeds the ward environment.61 In early studies, researchers found that noise levels in an ICU ranged from 59 to 83 dB(A), enough to stimulate cardiovascular and endocrine systems as well as disrupt sleep as a result of noiseinduced stress modulation.62 Later work continued to show the average noise level in ICU to be 55 to 66 dB(A), far exceeding the WHO recommendation, with peaks reaching as high as 85 dB(A).63-65 The exact source of excessive noise pollution within an ICU is multifactorial for the very reason of close proximity care and the array of medical instrumentation attached to patients.64 Balogh et al63 suggested that the majority of the noise in an ICU was created by mechanical alarms. Apart from medical equipment, Cmiel et al66 concluded that nursing and other allied health care staff are responsible for approximately 80% of the noise produced within an ICU. Intensive care unit nursing staff seem to have limited appreciation/knowledge of the psychophysiological effects of exposure to noise; nursing care remains consistent throughout a 24-hour period and ritualistic practices of subduing lighting during the night make little difference in noise levels.63 Moreover, nursing staff thought that because the majority of patients were critically ill, sedated, and mechanically ventilated, the need for noise reduction was not applicable.63 However, research of Johansson et al67 showed that we can no longer claim that patients are too critically ill to reflect on surrounding sounds and noises. Her findings indicated that there is a need to reduce disturbing and unexpected sounds and noises around critically ill patients in order to facilitate well-being, sleep, and recovery. The shifts between silence and disturbing sounds create stress and are later connected to delusional memories of the ICU. Although numerous studies have documented excessive noise levels in the ICU, the link to sleep disruption has, until recently, been indirectly established only through simulated

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laboratory studies with healthy individuals.68,69 Freedman et al15 used PSG and time-synchronized recording of environmental noise, directly linked to noise arousals from sleep and determined that noise was responsible for only 15% of all arousals and awakenings. In 2003, using PSG and an actual ICU, Gabor et al70 found that although loud noise and frequent patient care activities were prevalent, they were responsible for only a small proportion of the observed sleep disruption. Healthy individuals slept relatively well in this potentially disruptive environment and although noise accounted for a significant proportion of sleep disruption, its extent was not pathologic. High-peak noise may be more disruptive than general background noise; however, as noted even peaks were not found that problematic. Therefore, the relative contribution of noise and other components of the ICU environment to the pathogenesis of ICU sleep disruption are largely unknown and remain a complex issue.70-72

alternative to the pharmacological approach. In fact, recent clinical practice guidelines from the American College of Critical Care Medicine on the use of sedatives and analgesics in the critically ill adult advocate the use of nonpharmacological methods to promote sleep.74,75 Optimizing patient comfort and ensuring that patients receive adequate restorative sleep while in the ICU are daunting tasks. It is unlikely that addressing 1 or 2 ICU environmental factors contributing to sleep disruption would have a profound effect on correcting ICU sleep deprivation. Several issues can be addressed including controlling noise levels, using diurnal lighting practices, employing appropriate pharmacological interventions, providing uninterrupted sleep times, psychological support, ventilator synchrony, effective pain therapy, relaxation techniques, and music therapy.

Light Levels

Noise represents an easily modifiable factor that may impact patients sleep patterns in the ICU. Patient satisfaction is said to go up when the unit is less noisy and sleep is improved.76 The introduction of guidelines by Walder et al77 to decrease noise levels included relocating all acoustic alarms to outside the patient’s rooms; adapting all mechanical alarms (pumps and ventilators) to nighttime environment; closing the door or curtain if this can be safely done; and discouraging noisy tasks at night such as garbage emptying and linen collection. Richardson et al78 recorded patient perceptions of sleep, while wearing soft foam earplugs to reduce ambient noise. Even when wearing earplugs, patients reported that noise was the highest factor in preventing sleep. It may be that earplugs do not adequately block high noise levels common in critical care settings or perhaps because of raised consciousness of the earplugs themselves, which resulted in a heightened patient awareness of environmental noise. This study indicated that earplugs may help some patients sleep in a noisy environment but not all find them easy to use or comfortable to wear. Hu et al79 found that use of earplugs and eye masks in patients not only improved subjective sleep quality but also increased the amount of REM sleep and nocturnal melatonin levels in a simulated ICU environment. The masking of noise has been demonstrated to improve sleep quantity and to reduce the number of nighttime awakenings.13 There is a likelihood that patients continually exposed to low-level white noise or repetitive sounds do not exhibit the telltale signs of ICU delirium—instead patients get ‘‘used to’’ the noise.62 Williamson80 tested the effect of ocean sounds on the sleep of postoperative cardiac surgery patients and showed that the subjective sleep scores of the patients in the intervention group were significantly higher than those in the control group who had no masking sound in the room. The intervention group reported a better quality of sleep, fewer awakenings, quicker return to sleep following awakenings, and deeper sleep.

The light–dark cycle is probably the most powerful entraining factor in the human sleep–wake cycle and ultimately development of restful surroundings. If normal entraining factors are removed or disrupted, the human sleep–wake cycle may deviate from its normal 24-hour period. Even with the traditional dimming of the lights in the ICU, nocturnal light levels in an ICU vary from 5 to 1400 lux.8 Light levels between 100 and 500 lux are known to affect melatonin secretion and have an effect on the circadian pacemaker.9 Dunn et al73 recorded activity that was occurring or not occurring, while various light sources were illuminated. The activity associated with the greatest amount of light exposure was obtaining samples for laboratory tests, while the second activity most often recorded while the light was on was ‘‘none.’’ This suggested a lack of simple vigilance on the part of health care providers.

Patient Care Activities Gabor et al70 found that patient care activities that include nursing visits, assessment of vital signs, and administering medications occurred 8 times/h of sleep. Approximately 20% of patient care activities resulted in an arousal or awakening, accounting for only 7% of observed sleep disruption. Therefore, patient care activities, although frequent, were not a predominant source of sleep disruption in ICU patients.

Strategies for Promoting Sleep in the ICU The cause of sleep disruptions and abnormal sleep architecture during recovery from acute illness or injury in the ICU remains poorly defined. However, it is likely that the both acute physiologic changes from illness or injury and extrinsic factors contribute to abnormal sleep in this patient population. By modifying these extrinsic factors, patients may achieve better more physiologic sleep during recovery.5 Although largely unexamined in the ICU, the use of complementary and alternative therapies to promote sleep may offer a promising

Noise Reduction

Light Levels Guidelines of Walder et al77 to control nighttime light resulted in a significantly lower mean disturbance and fewer periods

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with high light levels. It was found that it was more comfortable for patients to have a continuous indirect low-grade light than an oscillation between low and high levels at each intervention. It was concluded that light variation should be avoided, that the light level be sufficiently high to allow for patient care but low enough to let patients sleep. The use of eye masks to decrease nighttime waking from light was studied by Richardson et al.78 They found that patients reported the most common factor that helped them sleep was eye masks, although many patients reported them to be uncomfortable, hot and tight, and contributed to a sense of claustrophobia. In general, the normal 24-hour light–dark cycle should be stimulated and maintained by dimming or turning off lights during the night and encouraging a bright environment during the day.

Patient Care Activities Celik et al81 found that nursing activities in the ICU were focused on activities seen to maximize physiological stability. It also showed that nurses more frequently applied care activities between 0200 and 0500 hours. Consequently, a protocol was developed that limited nursing activities such as cardiac monitoring, high–low alarm checks, turning and position changes, vital signs, and phlebotomy between 0000 and 0600. In another sleep protocol developed by Edwards and Schuring,59 nursing care activities were limited to decreasing patient disturbances between 0100 and 0500 during the night shift. This protocol included decreasing sound and light, administering sleep medications, and changing the timing of nursing activities. It was suggested that the critical care team should limit disturbance in the ICU between the hours of 2400 to 0500. Dennis et al82 implemented a quiet time protocol with reduced light and noise to promote rest for neuro-ICU patients and found patients were 1.6 times more likely to be found asleep during this time. Furthermore, the evolution of newer technologies, faster real-time computing abilities, and miniaturization of ventilator technology can bring the control of breathing to the bedside and benefit the critically ill patients.83,84

Pain Control and Comfort Analgesics should be given at least 30 minutes before ‘‘bedtime’’ and advocate for protocols that provide a steady state of pain control such as round-the-clock dosing, continuous infusions, patient-controlled analgesia, or epidural pumps.85 Consistent sleep patterns and uninterrupted blocks of time that allow for sleep are important. Ancillary departments such as radiology and other support services can be asked to plan diagnostic testing and procedures around rest times. Caregivers should schedule bedside activities so that several interventions can be completed in 1 visit.85 Taking the time to explain procedures scheduled and answering questions may give the patient peace of mind they need to sleep, as well as telling them what to expect the next

day, such as scheduled tests or procedures.85 Something as simple as a clean gown, removing tubes or lines from under the patient, and providing properly fitted continuous positive airway pressure (PAP)/bilevel PAP masks or devices may relax them enough to fall asleep. Routine bedtime care, such as teeth brushing, hair brushing, or face washing, are simple but effective interventions.85

Massage Massage therapy promotes a significant decrease in cortisol levels and increase in active neurotransmitters, such as serotonin and dopamine.86 Massage may also promote parasympathetic activation, which results in reductions in HR, blood pressure, and breathing and increases in release of endorphins and decreases in stress levels.87 Effleurage, a type of massage, is a technique that has been used over the centuries in numerous cultures and adopted in nursing as a traditional nonpharmacological means of promoting rest and relaxation. Effleurage strokes are performed in a slow, rhythmic fashion using firm steady pressure. The palms of the hands are used to perform gliding strokes over large body areas such as the back. Contact is maintained with the skin whenever possible.88 Richards et al39 found that physiological indicators of the relaxation response were reported by patients after administration of a massage intervention; these included reductions in HR, RR, muscle tension, and oxygen consumption. These data suggest that a simple 3-minute backrub can actually enhance patient comfort and relaxation and have a positive effect on cardiovascular parameters.

Music Therapy Although a significant body of research exists examining the effect of music therapy on anxiety, few studies have explored sleep as an outcome measure. The effect of music on the sleep of postoperative cardiac surgery patients by Zimmerman et al89 revealed that recipients of music therapy had significantly higher sleep scores indicating better sleep than the control group who had no intervention. Intensive care unit nurses can easily integrate music therapy into a patient’s plan of care with a library of recorded musical selections. The characteristics of music best suited for sleep and relaxation promotion are a tempo of approximately 60 beats/min, are composed primarily of low tones, and are played predominantly by strings.90

Melatonin Therapy Melatonin secretion normally increases at night and increases in the early morning hours. In contrast, cortisol secretion falls. Both are biological markers of the circadian rhythm.79 Nocturnal secretion of melatonin synchronizes the sleep–wake and dark– light cycles, and disruption to the normal timing and amplitude of the circadian rhythm of melatonin secretion is associated with reduced sleep. Reduction in plasma melatonin levels, low melatonin secretion, and lack of circadian increase in melatonin has been found in critical care patients undergoing mechanical

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ventilation.91 In contrast to other sedatives and hypnotics, melatonin causes minimal side effects even in extremely high doses (700 mg/d). Tolerance to melatonin does not seem to develop during treatment as it does with other sedatives, so there is no need for increasing doses for sleep induction.91 Melatonin therapy has been shown to be effective in the resetting of sleep–wake cycles and the entrainment of circadian rhythms.79 Bourne et al92 found that melatonin therapy was associated with a 1-hour increase in nocturnal sleep compared with placebo, corresponding to an increase of 47% sleep improvement. However, effective treatment is dependent on the correct timing of light and melatonin in relation to the circadian clock to avoid precipitating phase shifts in the wrong direction.

Conclusion Patients admitted to the ICU are susceptible to severe sleep deprivation. The cause appears to be multifactorial, including the patient’s underlying illness, medications used in treatment, and the ICU environment. Despite gaps in current knowledge, mounting evidence suggests an interaction between sleep, delirium, and morbidity and mortality in the critically ill patients. The nature of the interaction is complex and difficult to clearly define. Attempting to ascertain the relative importance of restorative sleep, within the framework of critically ill patients, multiple comorbidities, and polypharmacy, remains a difficult challenge. A vast body of data suggests an impact of sleep patterns on immune mechanisms, respiratory function, hormonal homeostasis, metabolism, and neurocognition. Furthermore, disrupted sleep in the critical care setting is perceived by patients to be extremely distressing. Until such time that the impact of disrupted sleep in the critical care setting is better explained, it is appropriate to provide patients with consolidated, restorative sleep, if this can be safely achieved. Therapy should be directed at all potential causes of sleep deprivation, with particular attention given to creating an environment that is both diurnal and conducive to sleep. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

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