Sleep Alterations and Management
Nurses who have an appreciation of the importance of sleep place a higher priority on protection of patients’ sleep.1 Health care providers interrupt patients’ sleep for assessment, treatments, or interventions, and environmental noise, pain, or anxiety can also disturb it.2 Although prioritizing care is essential, the consequence of sleep interruptions is not merely sleep-deprived patients; alterations in sleep patterns can result in chronic sleep problems, poor recovery, and decreased quality of life.1 To facilitate sleep and healing, critical care nurses need to understand the essentials of sleep and chronobiology, the effect of pharmacologic therapy on sleep, and the consequences of disrupted sleep. The purpose of this chapter is to acquaint nurses with the characteristics of normal human sleep and chronobiology, changes in sleep associated with aging and pharmacologic treatment, and abnormal sleep patterns that may affect critically ill patients. Evidence-based nursing care for critically ill patients with sleep disturbances is discussed.
Normal Human Sleep
Sleep Physiology
Humans spend about one third of their lives engaged in a process known as sleep. Although little is now known about the physiologic process or the depths to which it affects us, researchers are learning more about sleep every day. The behavioral definition of sleep is a reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment.3 Sleep is a basic human need, just as food and water are. For patients to regain and maintain their optimal physical and emotional health, they must be able to get adequate amounts of quality sleep. To help patients obtain their optimal amount of sleep, a nurse must first understand what constitutes normal sleep and how the nursing plan of care can contribute to accomplishing this goal.
Polysomnography (PSG) is the collection of multiple channels of physiologic data to assess sleep and its disorders using various electrodes.4 Electroencephalographic (EEG) electrodes are attached to the patient’s scalp to measure brain waves. Changes in the EEG frequency (number of waveforms) and amplitude (height of waveform) over the course of the study allow the sleep to be scored into stages. Sleep stages are distinguished primarily by the EEG waveforms they produce. Sleep is scored by each 30-second epoch or segment of the tracing. The criteria for scoring sleep in infants differ from those used for adults.4
Electrooculography (EOG) measures eye movement activity. The study can help to determine when the patient is in rapid eye movement (REM) sleep; it also can establish when sleep onset occurs as reflected by slow, rolling eye movements.4 Electromyography (EMG) involves leads placed over various muscle groups. When placed over the chin, the leads can help detect muscle atonia associated with REM sleep. Intercostal leads detect respiratory effort, whereas leads over the anterior tibialis detect leg movements that may be causing the patient to arouse. The electrocardiogram (ECG) shows any cardiac abnormalities, oximetry monitors the oxygen saturation levels, and piezoelastic bands around the chest and abdomen detect respiratory disorders such as apnea. Thermocouples are used to monitor airflow through the nose and mouth.4
Sleep Stages
Humans experience three states of being. They are awake, in REM sleep, or in non–rapid eye movement (NREM) sleep. NREM sleep usually occupies 70% to 75% of the sleep cycle, with REM sleep comprising 20% to 25%.5 Some theorize that NREM sleep is a restorative period that relieves the stresses of waking activities, whereas REM sleep serves to refuel creative brain stores.
Non-Rapid Eye Movement Sleep
Stage N1 comprises 2% to 5% of a night’s sleep and is demonstrated by an EEG pattern of low-voltage, mixed-frequency waveforms with vertex sharp waves.5 The EOG during stage N1 may demonstrate slow, side-to-side eye movements. A patient with severely disrupted sleep may experience an increase in the amount of stage N1 sleep throughout the sleep cycle. As a patient makes the transition from awake to asleep, a brief memory impairment may occur.4 As a result, the patient may not remember educational or care instructions given by the nurse during the transition between sleep and wake states. Stage N2 sleep occupies about 45% to 55% of the night, with sleep deepening and a higher arousal threshold being required to awaken the patient. Changes seen in the EEG pattern include sleep spindles and K complexes.5 As stage N2 continues, high-voltage, slow-wave activity begins to appear.4 When these slow waves represent 20% of the EEG activity per page, the criteria are met for stage N3 sleep, which constitutes 15% to 20% of the cycle.5 In stage N3 sleep, slow waves continue to develop until 50% of the EEG waveforms are slow wave. This stage of sleep is often referred to as slow-wave sleep.5
NREM sleep is dominated by the parasympathetic nervous system. The body tries to maintain a homeostatic regulation, and this causes a decreased level of energy expenditure. Blood pressure, heart and respiratory rates, and the metabolic rate return to basal levels. EMG levels are lower in NREM as opposed to wake states but not as low as in REM sleep. Sweating or shivering that a patient may experience with temperature extremes occurs during NREM sleep but ceases during REM sleep.3 During slow-wave sleep, 80% of the total daily growth-stimulating hormone is released, which works to stimulate protein synthesis while sparing catabolic breakdown. The release of other hormones, such as prolactin and testosterone, suggests that anabolism is occurring during slow-wave sleep. Cortisol release peaks during early morning hours, whereas melatonin is released only during darkness, and thyroid-stimulating hormone is inhibited during sleep. The activities associated with stage N3 sleep include protein synthesis and tissue repair, such as the repair of epithelial cells and specialized cells of the brain, skin, bone marrow, and gastric mucosa.6
Rapid Eye Movement Sleep
REM sleep occupies about 20% to 25% of the night in healthy young adults and is sometimes known as the dream stage. However, dreaming is not the exclusive property of any one stage. REM can be viewed as a highly active brain in a paralyzed body and is frequently referred to as a paradoxic sleep. The paradox is that some areas of the brain remain very active, whereas others are suppressed. EEG waveforms are relatively slow voltage and sawtooth waves are present. Increased cortical activity occurs, with the EEG pattern resembling those of the wake state. Synchronized bursts of rapid, side-to-side eye movements with suppressed EMG activity (muscle atonia) are seen, indicating functional paralysis of the skeletal muscles.7
The sympathetic nervous system predominates during REM sleep. Oxygen consumption increases, and blood pressure, cardiac output, and respiratory and heart rates become variable. The body’s response to decreased oxygen levels and increased carbon dioxide levels is lowest during REM sleep. Cardiac efferent vagus nerve tone is generally suppressed during REM sleep, and irregular breathing patterns can lead to oxygen reduction, particularly in patients with pulmonary or cardiac disease. An increase in premature ventricular contractions and tachydysrhythmias may be associated with respiratory pauses during REM sleep. Arterial pressure surges and increases in heart rate, coronary arterial tone, and blood viscosity may cause the combination of plaque rupture and hypercoagulability in persons with cardiac disease.7
Sleep Cycles
NREM and REM sleep cycles alternate (Fig. 7-1) throughout the night. Sleep onset usually occurs in stage 1 sleep, progressing through stages 2 and 3, then going back to stage 2, at which time the person usually enters REM. This first cycle typically takes about 70 to 100 minutes, with later cycles lasting 90 to 120 minutes. Four to five cycles are completed during normal adult sleep. NREM sleep predominates during the first third of the night, whereas REM is more prominent during the last third. Brief episodes of wakefulness (usually less than 5%) tend to intrude later into the night and are usually not remembered the next morning.5
Chronobiology
Circadian System
Many body systems cycle with approximately a 24-hour period, hence the name circadian rhythm (from circa [“about”] and dies [“day”]).8 Among these systems is the sleep-wake rhythm. A bundle of cells in the anterior hypothalamus, known as the suprachiasmatic nucleus, functions as the pacemaker for these rhythms. The circadian system facilitates cycling of the prescribed functions within a predictable period, but the functions are also influenced by other conditions, such as social activity, posture, and physical environment.8
Under normal conditions, a person’s rhythms interact and influence one another. For example, when body temperature is becoming lower, a person is more likely to sleep, and as the body temperature rises in early morning hours, people awaken. Another example is the melatonin cycle, which tends to run in synchrony with the sleep-wake cycle.8
External influences such as posture, exercise, and light also influence the sleep circadian rhythm. These external influences, known as zeitgebers, can shift the rhythm, causing it to peak at different times, or fragment it. Light is the most influential zeitgeber for sleep8; critical care nurses therefore need to limit the light in the environment during nocturnal hours to facilitate sleep and circadian continuity in their patients.9
Homeostatic Mechanism
The recent history of the sleep obtained by an individual also influences timing and depth of sleep. Known as the homeostatic process of sleep regulation, this determinant of sleep is linked to how much sleep the individual has had previously. Essentially, someone who is sleep-deprived will sleep more readily, regardless of circadian phase, whereas someone who is well rested will not fall asleep readily.10,11 The amount of slow-wave sleep (stage N3) reflects sleep intensity, and individuals recovering from sleep deprivation have increased amounts of slow-wave sleep.11
Circadian and Homeostatic Interaction
Circadian and homeostatic processes function together to ensure optimal sleep for an individual. In essence, these studies have shown that homeostatic processes primarily regulate slow-wave activity and that the ratio of REM to NREM sleep is primarily regulated by the interaction of circadian and homeostatic processes.11
Pharmacology
Hypnotic benzodiazepines remain the medications of choice to treat insomnia. Insomnia is a patient complaint of inability to initiate or maintain sleep, and prescriptions for treatment of insomnia cost more than $1 billion annually.12 Acute stress, such as admission to a critical care unit, may cause some patients to experience acute sleep-onset insomnia. Hypnotics tend to promote lighter sleep stages and have a higher lipophilicity, which can cause the elderly to experience an increased drug half-life.12 Care should be used in the administration and dosage of hypnotics in the elderly. This age group may experience night terrors, nightmares, and increased agitation. The metabolism of hypnotics in elderly patients can be inhibited by the use of steroids, or it can be accelerated in those who smoke. Hypnotics may also produce anterograde amnesia, which is a memory failure of information processed after the medication is consumed. Patients with normal ventilation should not be affected by the mild respiratory depression caused by hypnotics, although patients with chronic obstructive pulmonary disease (COPD) or sleep-disordered breathing may be affected.13
Wake-promoting medications produce increased arousal, behavioral activation, and alertness. They can be divided into three classes: direct-acting sympathomimetics (e.g. phenylephrine), indirect-acting sympathomimetics (e.g., methylphenidate, amphetamine, mazindol), and stimulants that are not sympathomimetics (e.g., caffeine). Common side effects can include irritability and sweating, with talkativeness, anorexia, gastrointestinal complaints, dyskinesias, insomnia, and palpitations occurring less frequently.14 Wake-promoting medications can be used for patients who experience disabling symptoms of sleepiness resulting from narcolepsy, idiopathic central nervous system hypersomnia, or sleep deprivation. Wake-promoting medications should be used only when sustained alertness is required for the individual or for reasons of public safety.
Wake-promoting medications possess a high abuse potential. A sequence of euphoria, dysphoria, paranoia, and psychosis can occur after a single exposure, and sustained use can lead to cognitive and behavioral disorders. Proper dosing and a structured management plan are recommended for wake-promoting medication use. This includes providing patient education with treatment goals, beginning with low doses, emphasizing good sleep hygiene such as naps, and adjusting the dosage according to clinical information. Wake-promoting medications should be included as part of a treatment plan only to decrease excessive somnolence. Sustained use of high-dose wake-promoting medications can lead to cognitive and behavioral disorders.15 Effective sleep hygiene and attention to other substances or medications that can affect sleep may be beneficial for patients who want to avoid the abuse potential.
Many people use alcohol to assist them in falling asleep. Alcohol is a central nervous system sedative and will cause suppression of REM sleep. More than two alcoholic drinks may cause an increase in NREM stages 1 and 2 and decrease the onset of slow-wave sleep. Alcohol also may cause shallow, fragmented sleep and may precipitate or aggravate an existing obstructive sleep apnea (OSA) condition. In the 2008 National Sleep Foundation survey, 8% reported self-medicating for insomnia with alcohol. Of those polled, 20% reported using alcohol, over-the-counter medications (7%), prescription sleep medications (3%), or alternative therapy or herbal supplements (2%).16
Patients with illness may respond differently to medications than do healthy patients. Patients may come to the critical care unit with impaired sleep or poor cognitive function. Beta-blockers, a commonly used class of medications in critical care, are known to produce nightmares and have disruptive effects on sleep quality in some individuals.17 The effect of various drug combinations are not well known.
The critical care nurse should assess the patient’s need for sedative and analgesic medications. The nurse has a responsibility to administer these medications in the most efficient manner to promote sleep and to monitor effectiveness. This can be achieved through assessment, including a medication history, diagnostic test results, and review of the patient’s medical history. Information from that assessment assists the nurse in formulating a nursing diagnosis with outcome criteria and interventions. Evaluation of the patient ensures attainment of the desired outcomes.18
Sleep Pattern Disturbance
Description
Sleep disturbance in critically ill patients is defined as insufficient duration or stages of sleep that results in discomfort and interferes with quality of life. When ill, most people need more sleep than usual, and sleep seems to promote recovery. Studies have demonstrated that the nocturnal sleep of patients in critical care units is severely disturbed, even though many receive medications to promote sleep.1,19,20
Etiology and Pathophysiology
Normal sleep is a period of decreased physiologic workload for the cardiovascular system. Insufficient sleep in acutely and critically ill patients has been associated with physiologic and psychologic exhaustion and may delay recovery from illness. These effects include mental status changes resulting in delirium.21 A general consensus among sleep experts and researchers is that sleep deprivation results in psychologic alterations such as changes in mood and performance, fatigue, increased irritability, and feelings of persecution.1,22
The intensification of pain related to sleep disturbance is a significant problem in acutely and critically ill patients. Sunshine and colleagues related a potential theory for pain alleviation from massage therapy that is linked to quiet or restorative sleep. During deep sleep, somatostatin is normally released. Without this substance, pain is experienced. Substance P is released when an individual is deprived of deep sleep, and substance P is noted for causing pain. When people are deprived of deep sleep, they may have less somatostatin and increased substance P, which results in greater pain and more sleep disruption.23
Sleep disturbance in critically ill patients may stem from psychologic stress associated with critical illness and the critical care environment, surgical stress, noise, interruptions for care, painful procedures or physiologic processes, excessive bright light, and muscular and joint discomfort resulting from bed rest.22 Of 84 patients’ recollections about sleep-disturbing factors in the critical care unit, the most frequently mentioned factors included an inability to get comfortable or lie comfortably (recalled by 70% of patients), inability to perform one’s usual routine before going to sleep (57%), anxiety (55%), and pain (54%).24 The stressful nature of the critical care environment and uncertainty and worry regarding the outcomes of a critical illness may explain why some patients have such difficulty sleeping while hospitalized. These concerns are not culturally isolated. A Swedish study identified pain, anxiety, and environmental noise among factors that interfered with sleep.25 However, perhaps because of staffing issues and general work flow, nurses tend to provide labor-intensive tasks during early morning hours.2
