Factors that impact on sleep in intensive care patients

Factors that impact on sleep in intensive care patients

Intensive and Critical Care Nursing (2009) 25, 314—322 available at www.sciencedirect.com journal homepage: www.elsevier.com/iccn REVIEW Factors t...

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Intensive and Critical Care Nursing (2009) 25, 314—322

available at www.sciencedirect.com

journal homepage: www.elsevier.com/iccn

REVIEW

Factors that impact on sleep in intensive care patients Agness. C. Tembo a,∗, Vicki Parker b,1 a

Registered Nurse Intensive Care Unit, John Hunter Hospital, The University of Newcastle, Callaghan Campus, Callaghan, NSW 2308, Australia b John Hunter Hospital, HRMC, Lookout Road, New Lambton, NSW 2305, Australia Accepted 24 July 2009

KEYWORDS Sleep; Mechanical ventilation; Critical illness; Intensive care units

Summary This literature review shows that sleep is important for healing and survival of critical illness (Richardson et al., 2007; Straham and Brown, 2004). Sleep deprivation impinges on recovery, ability to resist infection, brings about neurological problems such as delirium, respiratory problems because it weakens upper air way muscles thus prolonging the duration of ventilation, ICU stay and complicating periods just after extubation (Friese, 2008; Parthasarathy and Tobin, 2004). Noise, pain and discomfort (Jacobi et al., 2002; Honkus, 2003) modes of ventilation and drugs have been cited as causes of sleep deprivation in critically ill patients (Friese, 2008; Parthasarathy and Tobin, 2004). The inability of nurses to accurately assess patients’ sleep has also been cited as a concern while polysonography has been cited as the most effective way of assessing patients’ sleep despite the difficulties associated with it. While some of these causes of sleep disruption can not be easily alleviated, every effort must be made to promote REM and SWS sleep. More research is needed to find solutions to sleep disruption in ICU. More research is needed to ascertain the impact of mechanical ventilation on sleep disruption and more focused ways of sleep assessment are needed. Nurses need to minimise disruptions by clustering their care at night in order to allow patients to have the much needed REM sleep. Furthermore, more specific way of sleep assessment in the critically ill. © 2009 Elsevier Ltd. All rights reserved.

Introduction Over time, studies have shown that sleep is important in the critically ill for healing and survival (Richardson et al., 2007; Honkus, 2003; Pandharipande and Ely, 2006) and yet there is



Corresponding author. Tel.: +61 2 4951 1592. E-mail addresses: [email protected] (Agness.C. Tembo), [email protected] (V. Parker). 1 Tel.: +61 2 4921 4506.

consistent evidence reporting that patients in ICU still do not have enough sleep (Feeley and Gardner, 2006). This paper presents the literature available on factors that impact on sleep in ICU, the consequences of sleep disruption and the possible recommendations for practice, nursing education and future research to enhance sleep in the critically ill.

Methods This review explored research reports and other relevant literature that examined sleep disruption in ICU

0964-3397/$ — see front matter © 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.iccn.2009.07.002

Factors that impact on sleep in intensive care patients patients over the last decade. The aim of the review was to identify factors consistently reported as contributing to sleep disturbance, strategies employed to assess and promote sleep, changes in sedation practice and their implications on sleep related outcomes for patients. The literature search was conducted in order to answer the following questions: What factors impact on patients’ ability to sleep in ICU? How do these factors operate to interfere with sleep? What are the consequences of sleep disturbance for patients’ recovery? A literature search from Medline, CINAHL, Proquest and psychinfo databases was conducted. The search was conducted using the following inclusion criteria: all full text articles written in English, using the search terms, sleep in ICU, sleep deprivation, critical illness, intensive care units and nursing. Three hundred hits were achieved overall. The search was narrowed through combining terms and limiting to those published since 2000, identifying twenty two articles, of which eight were literature reviews, five were qualitative studies and nine were quantitative studies. Fourteen articles were American, five were European and three were Australasian. A summary of studies reviewed is presented in Table 1 .

Factors that contribute to sleep disturbance in ICU patients Numerous factors were reported to contribute to sleep disturbance in ICU. Specific types of environment together with the invasive and persistent nature of management strategies employed in ICU make it difficult to identify and alleviate causes of sleep deprivation. Evidence suggested that sleep disruption is most likely due to a combination of intrinsic and external factors which impact differently across patients according to each particular circumstance. Individual patient illness and prior experiences, together with fluctuating severity of illness impact on the potential to achieve effective sleep. Particular causes identified included pain and discomfort, nursing and medical procedures, mechanical ventilation, ICU environment (including noise), pharmacological agents and severity of underlying disease (Drouot et al., 2008; Reishtein, 2005; De Jong et al., 2005; Honkus, 2003). Table 1 identifies the studies examined, the methods used by each and their limitations.

Environmental factors Noise was widely cited as the most common cause of sleep disruption in the critically ill (Honkus, 2003; Drouot et al., 2008). Noise from equipment such as alarms from the monitors, ventilators and other equipment, together with staff related noise and ringing telephones were commonly reported causes of sleep disruption in ICU (Kass, 2008; Coyer et al., 2007). Noise initiated a sequence of physiological changes including vasoconstriction, raised diastolic blood pressure, pupil dilatation and muscle tension (Honkus, 2003). Furthermore, noise was implicated to cause sympathetic system stimulus, resulting in release of adrenaline which prevented relaxation and consequently prevented

315 the patient from falling asleep. Although noise was one of the most often cited factors responsible for sleep deprivation, Stanchina et al. (2005) argued that the degree of noise did not affect the frequency of sleep disruption. In a study conducted by Freedman et al. (2001) where the aim was to establish the effect of environmental noise on sleep disruption in ICU, it was revealed that indeed noise was responsible for disruption of quality of sleep but not necessarily quantity of sleep. Freedman et al. (2001) used continuous polysomnography (PSG) and environmental noise measurements for 24—48 hours in 22 patients, two of whom were not mechanically ventilated. Their study showed that environmental noise was responsible for 11—17% of arousals and awakenings from sleep. However, Freedman et al.’s (2001) study was small (n = 22) and included only two ICUs. In Olson et al.’s (2001) observational study, which aimed to determine whether reduction of external environmental stimuli was associated with increased frequency of sleep interruption, the control group had more interruptions than the intervention group. This study was also limited by the inclusion of neurological patients only and also by relatively small numbers (intervention group = 118, control group 122). Furthermore, this study employed observation as the only method of data collection which meant that the quality of sleep was not addressed. Stanchina et al. (2005) also did an observational study which included PSG on four healthy subjects with a view to establishing whether or not sleep disruption would be low with white noise in ICU. Their findings were that sleep disruption did not increase with peak noise. However, the limitations of that study were that it was not done in an ICU environment, rather noise was generated artificially which may not reflect the true variation of the amplitude in a unit over time. Also their sample size was small (n = 4).

Nursing interactions/procedures Nursing interactions and procedures with patients were also noted among the factors that were responsible for sleep disruptions in the critically ill. Tamburri et al. (2004) conducted an observational study in which they reviewed fifty records of patients from four ICUs in order to establish the number of times nurses performed procedures with patients during the night, over 147 nights. Tamburri et al. (2004) found that there were more interactions with patients at midnight and less at around 03:00 hrs in the morning and only 9 out of 147 nights had a 2—3 hour period of uninterrupted sleep. However, this was a retrospective (review) study in which the patients were neither observed nor interviewed. While this study established that disruptions do occur that prevent protracted periods of sleep, it unfortunately relied solely on written nurse records without observation of actual practice. Furthermore, the study did not provide room for assessment of quality of sleep — polysomnography (PSG) or any tool for measuring quality of sleep was not used. The lack of knowledge among nurses about the nature of sleep, sleep physiology, the psychological and physical benefits of sleep was a factor that was attributed to nurses disrupting patients’ sleep by doing procedures at frequent and awkward hours of the night (Honkus, 2003). However, Olson et al.’s (2001) study showed that while nurses were knowledge-

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Table 1

Summary of studies reviewed. Type and aim of study

Number of participants

Method

Results

Limitations

Olson et al. (2001)

Observational study. To determine if reduction of external environmental stimuli is associated with increased frequency of sleep in neurocritical care units.

239. 118 control group. 121 intervention group.

Noise and light reduction from 02:00 h to 04:00 h and from 14:00 h to 16:00 h. Data collected at 02:45 h, 03:30 h, 14:45 h PM and 15:30 h from patients with GCS of 10 or greater. 1446 observations in the control group. 1529 observations in the intervention group.

Intervention group had more sleep than the control group — reduction of environmental stimuli was associated with increased sleep time.

Single centre study. One type of patients (neuropatients). Observational study hence likely more focused on quantity than quality of sleep. Done over specific short periods of time.

Tamburri et al. (2004)

Randomised retrospective review of medical records. Establish common causes of sleep deprivation in critically ill patients. Discuss nocturnal care that impact on sleep in ICU. Describe interventions to increase opportunities for sleep in critically ill patients.

50 records from 4 ICUs.

50 medical records were reviewed for care activities from 7 PM to 7 AM retrospectively in 4 critical care units. Established frequency, types and pattern of nocturnal care interactions with patients in the 4 ICUs. Analysed relationships among the interactions and patient variables, i.e. age, sex, acuity. Analysed the differences in style of nocturnal care among the 4 ICUs.

Data was based on 147 nights. Mean interaction of care was 42.7. Most frequent at midnight and least frequent at 03:00 h. Only 9 had 2—3 h uninterrupted hours for sleep out of 147 nights of study. Increased frequency of care at night gave patients with less periods for uninterrupted sleep.

There was room for assumption because the study was a retrospective review of medical records. Patients were neither assessed nor interviewed. Difficult to account for quality of sleep.

Agness.C. Tembo, V. Parker

Author

Animal randomised study. Establish whether sleep interruption after septic insult was associated with increased mortality regardless of age.

33 control. 29 young and 35 old C57BL/6L male mice aged 2 months (young) and 9 months (old).

Animals underwent caecal ligation and puncture and then randomised to have sleep interruption for 48 h at 30 s on/90 s off intervals. Outcome was survival at 5 days post-CLP Kaplan—Meier survival analysis with long-rank test used to determine differences in mortality.

Freedman et al. (2001)

Effect of environmental noise on sleep disruption in ICU.

20MV patients. 2 non-MV.

Continuous PSG and environmental noise measurements for 24—48 h.

Franzen et al. (2008)

Pilot study. Examined relationships between effects of sleep deprivation on subjective and objective measures of sleepiness and effect, and psychomotor vigilance performance.

15 sleep deprived group. 14 non-sleep deprived healthy subjects.

Controlled lab. Conditions data collected following day. Subjective reports mood and sleepiness (multiple sleep latency test and spontaneous oscillations in pupil diameter effective reactivity/regulation and psychomotor vigilance performance.

Increased wakefulness time for both light and dark cycles. Young mice mortality increased from 31% (post-CLP) to 67% with sleep interruption. Old mice mortality increased from 18% post-CLP to 50% with sleep interruption. Abnormal sleep cycle in patients. TST 8.8 ± 5.0 h raises fragmented sleep and non-consolidated environmental noise responsible for 11.5—17% of arousal and xxx from sleep respecting qualitative sleep is disrupted even though quantity of sleep is not. All 9 domains were subjectively and objectively affected.

Small sample. Sleep was only quantified and no quality was accounted for Study was not done in an ICU environment.

2 centre study. Small sample.

Factors that impact on sleep in intensive care patients

Friese et al. (2009)

Small sample size. Not ICU based study. Quality and quantity of sleep. Self-reporting could have been influenced by individual traits.

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318

Table 1 (Continued ) Type and aim of study

Number of participants

Method

Results

Limitations

Parthasarathy and Tobin (2002)

Effect of ventilator mode on quality of sleep on critically ill patients to determine whether presence of a back rate on assist-control ventilation would reduce apnoea-related arousals and improved quality of sleep.

11 critically ill patients.

More arousals and awakenings in patients on PSV than on patients on ACV (79 ± 7 as compared to 54 ± 7 events per hour). More central apnoeas and heart failure in the 6 patients on PSV as compared to patients on ACV (83% as opposed to 20%) Central apneas reduced to 44% from 83% with addition of dead space

Sample size was s mall (n = 11). Single centre study. One type of ventilator.

Stanchina et al. (2005)

Observational study. White noise added to the ICU environment would lower arousals by reducing the magnitude of changing noise levels.

4 patients.

Puritan Bennett 7200 ventilator was initially set in the assist-control mode with a backup rate of 4 breaths per minute and tidal volume (VT) of 8 ml/kg. Over 5—10 min of quiet wakefulness, the patient’s respiratory rate on the ventilator was measured. The backup rate on assist-control ventilation was then set at 4 breaths below the patient’s respiratory rate and kept at that setting for the rest of the study. Pressure support adjusted to achieve a VT equivalent to that during assist-control ventilation — 8 ml/kg. Randomised patients to receive at least 2 h each of the following three modes: assist-control ventilation, pressure support alone, and pressure support with dead space. PSG, CO2 monitors, EEG, pulse oxymetry. End-tidal studies done performed between 22:00 h and 06:00 h apneas, electroencephalogram (EEG) arousals and awakenings manually scored. Elastance and resistance of the respiratory system were measured. Mechanical inspiratory time (TI), expiratory time (TE), total respiratory cycle time (Ttot), end-tidal CO2 , and VT measured breath-by-breath. Apnea threshold was determined from the end-tidal CO2 of the breath immediately before the onset of an apnea. PSG under 2 baseline exposure to ICU noise. 3 exposure to ICU noise and inject frequency white noise. Peak noise levels recorded for each arousal from sleep.

Results. 1178 arousals index. Increased during noise but did not lower with white noise ICU noise might ICU noise and white noise versus ICU noise condition 17.7 ± 0.4 h 17.5 ± 0.3 h. Peak noise was not the main determinant of sleep disruption from ICU noise.

Small number of patients. Noise levels could have been amplified because they were recorded. Study did not take place in real ICU environment. Healthy subjects.

Agness.C. Tembo, V. Parker

Author

Factors that impact on sleep in intensive care patients able about the importance of sleep, they found it hard to organise their procedures to give their patients even a two hour break because such was the nature of their responsibility as critical care nurses.

Mechanical ventilation modes Depending on the mode of ventilation, mechanical ventilation was one of the factors that negatively impacted on sleep in critically ill patients. Parthasarathy and Tobin (2002) conducted a study in which they looked at the impact of pressure support ventilation (PSV) versus assist-controlled ventilation (ACV). Their findings revealed that there were more arousals in 1 hour (79 ± 7 versus 54 ± 7) in patients on PSV than in the patients on ACV. However, Parthasarathy and Tobin’s (2002) study was conducted in 2002, involving now outdated Puritan—Bennett 7200 ventilators. No more recent studies were located to verify these findings (Reishtein, 2005). Parthasarathy and Tobin (2002) sample size (n = 11) could be considered a limitation together with the fact that it was a single centre study. Equipment and procedures to do with mechanical ventilation such as masks, endotracheal tubes, suctioning, physical restraints, bite blocks and nasogastric tubes also contributed to sleep disturbance (Parthasarathy and Tobin, 2004). However, more research is needed to understand how this impact on sleep and how this phenomenon can be minimised.

Intrinsic factors Intrinsic factors such as the severity of the underlying critical illness were noted to play a part in sleep disruption (Drouot et al., 2008; Parthasarathy and Tobin, 2004). In particular, the severity of critical illness was associated with increased production of catecholamines which caused sleep disturbance (Parthasarathy and Tobin, 2004; Pandharipande and Ely, 2006). Furthermore, inflammatory mediators produced in sepsis were also believed to play a role in disrupting normal sleep patterns (Friese, 2008; Reishtein, 2005). However, very little literature was found supporting this phenomenon. Freedman et al. (2001) conducted a study using continuous monitoring with PSG for 24—48 hours in which 17 mechanically ventilated patients were not sedated and not deeply unconscious and found that the patients had disrupted sleep. The participants were observed to have 11.6 arousals in 1 hour. Although the patients slept around the clock, most of the sleep occurred between 6:00 and 22:00 hr which are normal wakefulness hours and the sleep architecture was disturbed. However, Freedman et al.’s (2001) study had a small sample size. Apart from the fact that critical illness was examined as one of many factors that impact simultaneously, other intrinsic factors were also highlighted such as drugs. Drugs used in critical care such as benzodiazepines, opioids, continuous infusions of inotropes (catecholamines), antihypertensives, antipsychotics, antidepressants including anticonvulsants were among the drugs that caused sleep disruption in ICU patients (Drouot et al., 2008; Parthasarathy and Tobin, 2004). Having noted intrinsic factors that contributed to sleep disruption in ICU patients, there was not much research that had dealt with the intrinsic factors such

319 as catecholamines. Some literature recommended the use of propofol and precidex instead of benzodiapines like midazolum and opioids like morphine as the former promotes better quantity and quality of sleep (Drouot et al., 2008; Parthasarathy and Tobin, 2004). However, these are all literature reviews; there was no original study found supporting these assumptions. Polysomnography (PSG) was the most reliable tool for assessing sleep in critically ill patients (Parthasarathy and Tobin, 2004; Pandharipande and Ely, 2006; Drouot et al., 2008). However the difficulties associated with its use in intensive care could not be overlooked. Using nurses’ observation and inspection, in spite of being readily available to assess sleep in critically ill patients, was deemed unreliable because they were believed to result in over estimation of quantity of sleep and possibly, did not account for quality of sleep (Parthasarathy and Tobin, 2004). Pain and discomfort were found to contribute to sleep disturbance. Pain was attributed to surgical and medical procedures and the lines that were used as part of the therapies (Jacobi et al., 2002; Honkus, 2003). However, optimal pain relief in critically ill patients is difficult because patients are unable to communicate due to mechanical ventilation devices and sedation (Coyer et al., 2007). Discomfort was attributed to the uncomfortable hospital beds, inability to assume usual comfortable positions for sleeping and also not being able to do usual bed time rituals such as having a glass of milk or reading a good book (Honkus, 2003). Monitoring equipment along with uncomfortable room temperatures that were not regulated to patients’ comfort contributed to discomfort and thus, caused sleep disturbance (Honkus, 2003). Without communication, however, it is difficult or rather impossible to determine patient’s feelings unless a patient was shivering, had a high temperature or felt hot to touch. Sedatives and analgesics used to promote sleep and comfort during mechanical ventilation were among the contributing factors to sleep deprivation (Drouot et al., 2008; Parthasarathy and Tobin, 2004; Pandharipande and Ely, 2006). Midazolum produced increased levels of catecholamines which led to sleep disruption (Parthasarathy and Tobin, 2004). However, there was no data available to support this. While benzodiapines shortened the time to fall asleep and sleep disruptions, increased length and efficiency of sleep (Drouot et al., 2008; Honkus, 2003; Jacobi et al., 2002; Pandharipande and Ely, 2006), they suppressed rapid eye movement sleep (REM) and slow sleep because at low doses, they increased the number of spindles and at high doses, they reduced the EEG amplitude and frequency. REM sleep and slow wave sleep (most restorative sleep stage) were also suppressed by narcotics because they caused dose dependent slowing of EEG. Hence drug induced sleep could mimic natural sleep without producing the physiological benefits which true sleep produced. Non-benzodiazepine sedatives such as zolpiclone and zolpidem were recommended. However, zolpidem could produce very harmful side effects in hospitalised patients as there were a few reports to the effect that zolpidem caused sleep driving and sleep walking (Friese, 2008; quality and safety branch, NSW Department of Health, 2008). Precidex a sedative — analgesic was found to promote slow wave sleep because it did not suppress SWS and it inhibited the secre-

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Agness.C. Tembo, V. Parker

Figure 1

The multisystem impact of sleep deprivation on critically ill patients.

tion of noradrenaline which inhibited slow wave sleep (SWS) (Friese, 2008). Contrary to Friese’s finding, Jacobi et al.’s (2002) extensive literature review found that precidex suppressed SWS. Jacobi et al. (2002) was based on older findings where as Friese’s work was more recent. Other medications such as beta blockers like metoprolol and propranolol caused sleep disturbance because of their ability to easily cross the blood brain barrier and cause night mares (Friese, 2008). Despite the fact that metholdopa increased REM sleep and reduced SWS, it caused sleep disruption because it caused nightmares (Honkus, 2003). Continuous infusions of inotropes (catecholamines) for blood pressure support and to increase cardiac output also caused sleep deprivation in ICU patients because they stimulated the reticular activating system (Friese, 2008). The negative impact of these drugs on the patients’ experience of ICU is considered justified given their life saving impact. Diuretics were reported to disturb sleep because they cause urinary frequency. Angiotensin-converting enzyme inhibitors, calcium channel blockers, anticonvulsants, corticosteroids, theophylline, neuroleptics, antihistamines, anticonvulsants and antidepressants negatively impacted on patients’ sleep Pandharipande and Ely (2006) and Honkus (2003). But once again, REM inhibiting drugs were not the only reason why patients had disrupted sleep (Reishtein, 2005). Similarly, Freedman et al.’s (2001) study found that most of their patients who were not on REM inhibiting drugs also experienced sleep disruption. Most of the data above is based on literature reviews so more research is needed to substantiate these claims. Continuous lighting in ICU also contributed to sleep disruption Reishtein (2005) as it interfered with the biological clock which is responsible for regulation of the wake—sleep cycle (circadian rhythm) (Pandharipande and Ely, 2006; Jacobi et al., 2002). However, De Jong et al. (2005) states that some studies have not found sudden changes in lighting to affect patients’ sleep. The accuracy of sleep assessment by nurses was questioned by Honkus (2003) and supported by Drouot et al.

(2008) who suggested that in many instances nurses are reported to assess sleep merely through observation which resulted in overestimation of sleep duration and failure to account for sleep fragmentation. PSG was found to be a more reliable method in assessing sleep in critically ill ventilated patients (Drouot et al., 2008; Reishtein, 2005). However, this method is impractical in ICU as it requires attachment of electrodes to the patients’ heads. It is more added work for the already overburdened nurses and it is an inconvenience to the patients themselves. Furthermore, it needs specialised staff to use it. Other writers suggested the use of the bisectral index (Reishtein, 2005), but that was an inconvenience to the patients and specialised staff were needed to use it.

Consequences of sleep disturbance The complex nature of sleep disturbance makes it hard to assess and alleviate. The very fact that the causes are multi factorial and that it affects all the body systems makes it a challenging syndrome which needs a multi disciplinary approach. Prolonged failure to experience effective sleep has detrimental effects on almost all body systems. It hinders the body’s normal defence mechanisms designed to deal with insult from injury or illness as well as diminishing cognitive capacity and emotional resilience (Friese, 2008). In Fig. 1 we summarise complications of sleep deprivation. Sleep disruption can lead to agitation, a situation which results in increased levels of catecholamines in the plasma. Sleep deprivation also causes delirium (Kass, 2008) and post-traumatic stress disorder, withdrawal symptoms, neurocognitive dysfunction (Franzen et al., 2007), depression and continued sleep disruption (Friese, 2008). However, McQuire et al. (2000) contend that sleep deprivation is actually not the cause of delirium but that it is delirium which causes sleep deprivation. More often than not, agitated and delirious patients are managed by administration of large doses of sedatives whose metabolites can linger

Factors that impact on sleep in intensive care patients around in adipose tissue and cause prolonged effects that can lead to prolonged ventilation and ICU stay (Honkus, 2003; Parthasarathy and Tobin, 2004). Sleep deprivation can also reduce pain tolerance and increased fatigue on sympathetic nerve centres (Kass, 2008). This scenario, inadvertently, leads to increased need for pain control thus using more drugs that again contribute to sleep deprivation and so, the cycle goes on. Lee et al. (2007), based on her study of six older people, found that sleep deprivation also led to short term memory loss. Furthermore, sleep deprivation causes cognitive impairment (Franzen et al., 2008) which can lead to post-traumatic stress disorder. Sleep deprivation increases sympathetic activity which in turn leads to nocturnal high blood pressure (Parthasarathy and Tobin, 2004). Elevated serum catecholamines can result in arrhythmias and worsening of cardiac failure and consequently, death (Parthasarathy and Tobin, 2004). However, inotropes and other cardiovascular drugs also cause dysrythmias as side effects. Hence more research is needed to find out whether or not dysrythmias are more pronounced in patients on with sleep disturbance. Sleep deprivation blunts chemoreceptor response which reduces the respiratory system’s ability to compensate for the respiratory loads during mechanical ventilation and after extubation (Pandharipande and Ely, 2006; Parthasarathy and Tobin, 2004) which further leads to decreased hypercapneic and hypoxic ventilatory responsiveness resulting in ineffective gas exchange (Honkus, 2003). Apneas and hypopneas have also been reported among the complications of sleep deprivation (Friese, 2008). Dysfunction of upper airway musculature leads to more respiratory problems especially during weaning from ventilation and immediately after extubation (Honkus, 2003). Sleep deprivation in critically ill patients decreases killer cell and lymphokyne killer cell activity (Friese, 2008; Parthasarathy and Tobin, 2004; Honkus, 2003) by fifty percent (Parthasarathy and Tobin, 2004) which can result in reduction of immunity to fight and resist infection, delayed healing, altered tissue repair and consequently, prolonged ICU and hospital stay (Friese, 2008; Honkus, 2003). Furthermore, Honkus (2003) and Friese (2008), maintain that the prolonged secretion of cortisol in sleep deprived critically ill patients also contributes to reduced healing and makes patients susceptible to infection and delayed recovery. Literature also shows that sleep deprivation sends the body into a catabolic state which affects the immune system and healing (Friese, 2008; Kass, 2008; Honkus, 2003).

Implications/recommendations Clinical implications Modification of environmental factors such as noise, mechanical ventilation modes, and minimising arousals due to procedures could help promote sleep in the critically ill. Sleep deprivation can be reduced by employing the following measures: • Noise reduction. • Avoid/minimise use of sleep inhibiting pharmacological agents.

321 • • • •

Facilitate uninterrupted adequate sleep time. Ensure ventilator synchrony. Encourage use of non-sleep inhibiting drugs. Promote comfort and relaxation.

Implications for nurse practice/education • The importance of sleep especially in critically ill patients needs to be incorporated into nurse education and proper assessment for quality of sleep needs to be emphasised. Specific focused sleep assessment using the right tools such as PSG need to be done to accurately determine patients’ sleep patterns. • Nurses must cluster their work so that unnecessary disruptions are avoided. • Proper temperature regulation and noise reduction could help promote sleep.

Implications for research • More research is needed into proper and effective ways of monitoring and assessing quality of sleep in critically ill patients. • More research to establish whether or not modes of mechanical ventilation still cause sleep deprivation with the introduction of new ventilators. • More research to establish whether or not inotropes and cardiovascular agents commonly used in ICU that cause sleep deprivation is needed and alternative drugs to be recommended.

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