© 2003 American Thoracic Society
Contribution of the Intensive Care Unit Environment to Sleep Disruption in Mechanically Ventilated Patients and Healthy SubjectsDepartment of Medicine, St. Michael's Hospital; Department of Critical Care Medicine, Sunnybrook and Women's College Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada Correspondence and requests for reprints should be addressed to Patrick J. Hanly, M.D., Room 6-049, St. Michael's Hospital, 30 Bond Street, Toronto, ON, M5B 1W8 Canada. E-mail: hanlyp{at}smh.toronto.on.ca
Recent studies have challenged the traditional hypothesis that excessive environmental noise is central to the etiology of sleep disruption in the intensive care unit (ICU). We characterized potentially disruptive ICU noise stimuli and patient-care activities and determined their relative contributions to sleep disruption. Furthermore, we studied the effect of noise in isolation by placing healthy subjects in the ICU in both normal and noise-reduced locations. Seven mechanically ventilated patients and six healthy subjects were studied by continuous 24-hour polysomnography with time-synchronized environmental monitoring. Sound elevations occurred 36.5 ± 20.1 times per hour of sleep and were responsible for 20.9 ± 11.3% of total arousals and awakenings. Patient-care activities occurred 7.8 ± 4.2 times per hour of sleep and were responsible for 7.1 ± 4.4% of total arousals and awakenings. Healthy subjects slept relatively well in the typically loud ICU environment and experienced a quantitative, but not qualitative, improvement in sleep in a noise-reduced, single-patient ICU room. Our data indicate that noise and patient-care activities account for less than 30% of arousals and awakenings and suggest that other elements of the critically ill patient's environment or treatment should be investigated in the pathogenesis of ICU sleep disruption.
Key Words: sleep disruption • intensive care unit noise • polysomnography Previous studies have determined that acutely ill patients in the intensive care unit (ICU) suffer unique sleep disturbances (1–8). Sleep is fragmented by frequent arousals and awakenings, resulting in decreased or absent slow-wave and REM sleep. The circadian rhythm of sleep is distorted, with nearly half of the total sleep time occurring during the daytime. Although sleep disruption in ICU patients has been unequivocally confirmed, little is known about its etiology. However, potential sleep-disrupting factors such as noise, frequent patient-care activities, medication effects, acute and chronic illness, and dyssynchrony between the patient and the ventilator are hypothesized as being the causes of this syndrome. Environmental stimuli, particularly noise, have been presumed to be the most disruptive factors in the ICU. Although numerous studies have documented excessive noise levels in the ICU (9–14), the link to sleep disruption has, until recently, been only indirectly established through simulated laboratory studies on healthy subjects (15–17) and correlations between noise levels and arousal frequencies in ICU patients (18). Studies on healthy subjects in sleep laboratories indicated that audiotape recordings of ICU noise disrupted sleep and that reducing noise, either through earplugs or on "quiet" control nights, improved sleep. However, a sleep laboratory cannot simulate the full auditory and visual experience of the ICU. In addition, the studies were only performed for an 8-hour nocturnal period rather than over 24 hours. Therefore, a more realistic evaluation of the effects of the ICU environment would be obtained by studying patients and healthy subjects in the ICU for at least a 24-hour period, with polysomnography (PSG) and time-synchronized recording of environmental variables to quantify their contribution to sleep disruption. Two studies by Freedman and colleagues (8, 19) re-evaluated the contribution of noise to sleep disruption in ICU patients. A detailed questionnaire administered to patients after discharge from the ICU indicated that assessment of vital signs and phlebotomy were considered more disruptive than noise (19). This study had a large sample size and was thorough in its design and analysis but was limited by potential recall bias and the lack of objective measurement of sleep quality. The subsequent study (8), using PSG and time-synchronized recording of environmental noise, directly linked noise to arousals from sleep and determined that noise was responsible for only 15% of all arousals and awakenings. Although it was the first study to demonstrate that common noise elevations directly cause arousals in ICU patients, other environmental factors such as patient-care activities were not assessed. Furthermore, the extent to which different noise sources, such as alarms or conversation, contributed to sleep disruption was not documented. Therefore, the relative contribution of noise and other components of the ICU environment to the pathogenesis of ICU sleep disruption are unknown. Because previous studies have not used PSG for objective sleep quality assessment, or have used simulated ICU environments or have not evaluated factors other than noise, the impact of these potential sleep disruptors on sleep continuity has been incompletely assessed. The objectives of our study were to (1) determine the prevalence of excessive noise and patient-care activities over a 24-hour period, (2) determine the relative impact of these factors on sleep continuity, (3) monitor healthy, unattended individuals in the actual ICU environment to examine, in isolation, the effect of noise on sleep quality as compared with that in critically ill patients, and (4) evaluate the effectiveness of a noise-reduction strategy by monitoring these healthy subjects in a single room in the ICU.
Subject Recruitment The study was approved by the research ethics boards of both participating institutions. Patients or their substitute decision-makers provided written consent to participate in the protocol. Patients admitted to the Critical Care Unit of Sunnybrook and Women's College Health Sciences Centre were screened for eligibility according to previously published exclusion criteria for reliable PSG (7). Selection criteria were endotracheal intubation and anticipated mechanical ventilation for a further 24 hours. Healthy volunteers were recruited by advertising on the St. Michael's Hospital e-mail network and were excluded on the basis of previous medical history, sleep disorders, or exposure to the ICU environment.
Study Protocol
PSG
Environmental Monitoring Each subject's immediate environment was continuously monitored using a sound meter and infrared camera synchronized to the PSG. In addition to background sound intensity, the magnitude, source, and disruptive effect of each abrupt sound elevation above 10 dB(A) (A-weighted decibel scale) was recorded. Each interaction between the patient and a member of the critical care team, sleep technician, or visitor that occurred during sleep was classified by type, and its effect on sleep continuity was documented.
Statistical Analysis
Prevalence of Eligible Patients In all, 3,443 patient-days (daily screening result for an individual patient) were screened, 1,048 (30.4%) of which were new, representing the first patient-day, and 2,395 (69.6%) of which were repeats, representing subsequent patient-days. A total of 1,296 (37.6%) patient-days passed screening criteria for reliable PSG. Of the excluded patient-days, 42.7% of exclusions were due to central nervous system injury, 21.7% to Glasgow Coma Scale ranking below 10, and 8.8% to morphine equivalent sedation above 10 µg/kg/hour. Other factors, such as general anesthesia in the preceding 24 hours (4.2%), drug overdose (0.9%), and anticipated death in the following 24 hours (0.5%), were less common reasons for exclusion.
Subject Demographics
Sleep diaries of the healthy subjects indicated that they maintained a regular nocturnal sleep schedule, with an estimated total sleep time of 7.3 ± 0.8 hours. Epworth Sleepiness Scale scores were normal (< 6) for all subjects (mean 2.6 ± 2.0) (23). All subjects were naive to PSG and the ICU environment and had no history of sleep disorders.
Sound Intensities in the ICU Locations
Sleep Quality in the ICU In comparison with healthy subjects in the open-plan ICU, there was a tendency toward poorer sleep quality in the patient group (Table 3) . Patients tended to have a higher awakening index and shorter sleep time compared with healthy subjects. The percentages of Stage 1 and Stage 2 non-REM and REM sleep were similar between patients and healthy subjects; however, slow-wave sleep was significantly lower compared with healthy subjects. Approximately half of patients' sleep occurred during the daytime (6:00 A.M. to 10:00 P.M.), whereas the sleep of healthy subjects tended to be more nocturnal (Figures 2 and 3) .
Healthy subjects in the single room experienced significant improvements in total sleep time and night sleep compared with the open ICU (Table 3, Figure 4) . However, sleep architecture and arousal and awakening indices were not significantly different between the open ICU and the single room. No differences existed in any variable between those healthy subjects randomized to the single room first and those placed in the open ICU first. No healthy subject or patient demonstrated evidence of sleep apnea syndrome.
Impact of Noise on Sleep Quality The majority of healthy subjects' total arousals and awakenings in the open ICU were caused by sound peaks (Table 4) , whereas a minority of patients' arousals and awakenings were caused by sound. Of the sound "peaks," abrupt elevations of over 10 dB(A) as defined in METHODS, 11.7 ± 8.3% resulted in an arousal or awakening in the patients' ICU. If peaks reaching 75 dB or greater are considered separately, 30.8 ± 17.9% resulted in an arousal or awakening in the patients' open ICU. Peak decibel thresholds that resulted in arousals or awakenings did not differ by sleep stage in any subject group. Although the magnitude of the sound level increase that resulted in an awakening was similar in all three locations, all other sound peak measures were significantly lower in the single room than in the other two locations.
In critically ill patients in the open ICU, no single noise source was predominantly responsible for sound-induced sleep disruption. In the healthy subjects in the open ICU, alarm noises were less disruptive than were conversation or staff activities. The proportions of different noise types responsible for sleep disruption were not significantly different between patients and healthy subjects in the open ICU. However, noise resulting from staff activities was the predominant source of sound-induced sleep disruption in the single room. The great majority of these arousals and awakenings (75.4 ± 14.4% and 81.9 ± 27.7%) was associated specifically with the opening of the main door of the ICU, which was in close proximity to the single room. Without the main-door effect on the single room, the arousal and awakening indices would have been 9.5 ± 2.9 events/hour, which would have been significantly different from the arousal and awakening indices in the open ICU (p < 0.05).
Impact of Patient-Care Activities on Sleep Quality
Subjective Perception of Sleep-Disrupting Factors Sleep quality in the open ICU was rated as significantly worse than in the single room (p < 0.05) and worse than at home (p < 0.05, Table 6) . In the open ICU, subjects identified alarms and staff conversation as the most disruptive environmental noises, a result identical to that observed by Freedman in a survey of ICU patients at discharge (19). Subjects rated noise from televisions and pagers as least disruptive, again similar to ICU patients (19). In the single room, noise and its component sources were not considered significantly disruptive to sleep.
This is the first study to systemically determine the contribution of the ICU environment to sleep disruption in both patients and healthy subjects and to estimate the effectiveness of a noise reduction strategy. Our findings demonstrate that although loud noise and frequent patient-care activities were prevalent in the ICU environment, 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 in this group, its extent was not pathologic. A quantitative improvement in sleep quality was observed as a result of noise reduction; however, there was no change in sleep architecture. Numerous studies have examined noise levels in the ICU, and all have concluded that they exceed Environmental Protection Agency recommendations for hospitals, which are less than 45 dB(A) during the daytime and greater than 35 dB(A) at night (24). Rather, mean sound levels are usually in the 55–65 dB(A) range, with sound peaks greater than 80 dB(A) (8–14). In contrast to previous studies, we quantified all sound peaks that increased by more than 10 dB(A) (which represents a doubling of sound intensity) because the change in noise may be as important to the pathogenesis of sleep disruption as the actual decibel level achieved (8). We observed 37 and 72 sound peaks/hour of sleep in the open ICUs of patients and healthy subjects, respectively, which indicated frequent noise spiking. Consequently, we conclude that our open ICUs are sources of excessive noise that may cause sleep disruption, which is consistent with the previous literature. Many studies have demonstrated unequivocal sleep disruption in critically ill patients, characterized by extreme sleep fragmentation, an overrepresentation of Stage 1 and Stage 2 non-REM sleep, reduced or absent slow-wave sleep and REM sleep, and circadian rhythm abnormalities (1–8). We observed similar findings in our patient cohort. Healthy subjects in the open ICU experienced a modest decrease in the proportion of slow-wave sleep and REM sleep and a concomitant increase in the proportion of Stage 1 and Stage 2 non-REM sleep, perhaps partly due to unrestricted daytime napping, as approximately 30% of sleep occurred during the day. The frequency of arousals and awakenings was within normal limits (25), supporting the more recent finding (8) that noise, which was the only known environmental factor intruding on the sleep of the healthy subjects, is not a significant source of sleep disruption. Only 20% of arousals and awakenings in our ICU patient cohort were identifiably due to noise peaks, demonstrating that, in contradiction of traditional hypotheses, environmental noise is not responsible for the majority of ICU sleep disruption instances. Although noise peaks occurred frequently, only 12% of these peaks, and 35% of peaks greater than 75 dB(A), resulted in an arousal or awakening. Noise was responsible for the majority of sleep disruption in healthy subjects, likely because other potential sources of sleep disruption such as patient-care activities and mechanical ventilation did not exist. Previous work on arousal responses to acoustic stimulation in healthy individuals observed that 35% of sound spikes of 85 dB intensity resulted in an arousal (26), which is similar to our results with a threshold of 75 dB. These investigators observed sleep stage–dependent changes in arousal frequency for a fixed sound intensity, whereas we observed no significant differences in the peak sound intensity that caused sleep disruption across sleep stages and between patients and healthy subjects. This is also the first study to directly quantify the effect of patient-care activities on sleep continuity. In the first study to characterize sleep disruption in the ICU by PSG, Hilton (1) monitored patient-care activities. However, she did not directly determine their contribution to sleep disruption with PSG synchronization. In our study, patient-care activities (which included nursing visits, assessment of vital signs, and administering medications) occurred approximately 8 times per hour of sleep, which is in contrast with the occurrence of noise spikes 37 times per hour of sleep. Approximately 20% of patient-care activities resulted in an arousal or an awakening, which accounted for only 7% of observed sleep disruption. Therefore, patient-care activities, although frequent, were not a predominant source of sleep disruption in ICU patients. We used a questionnaire to subjectively assess the relative contribution of different sleep-disrupting factors (19). In contrast to the findings of Freedman and coworkers, our healthy subjects perceived noise as highly disruptive to sleep in the open ICU, presumably because the more disruptive factors from their study (phlebotomy, assessment of vital signs) are not relevant to healthy subjects. As with Freedman and colleagues, however, our healthy subjects perceived that sleep in the ICU was worse than at home. We observed that conversation and alarms were perceived to be the most disruptive noises, whereas noise from televisions, telephones, and pagers were rated as the least disruptive. Subject perceptions did not match the objective PSG–environmental data. For example, alarms were rated second to conversation in terms of sleep disruption, yet they were responsible for only 20–25% of arousals and awakenings. We suspect that subjects may subconsciously bias their observations on the basis of the perceived degree of irritation from these noises while awake; clearly, the transient nature of arousals and awakenings makes it difficult for the subject to recall the event and its cause. Two previous studies have attempted to reduce noise in the ICU (27, 28). Walder and coworkers (27) were partially successful in reducing noise and light levels, and Kahn and colleagues (28), through a detailed and comprehensive behavior modification program, significantly reduced mean peak noise levels and the number of sound peaks less than 80 dB(A). However, neither of these studies assessed the impact of these changes on sleep quality. Two overnight studies on healthy subjects by Topf and coworkers (15, 16) and one by Wallace and colleagues (17) simulated an ICU environment in the sleep laboratory by using audiotape-recorded ICU noise. Reduction of noise, either by stopping the audiotape or the use of earplugs, was associated with improved sleep quality. However, these studies were not performed for 24 hours, and the sleep laboratory cannot simulate the full auditory and visual experience of the ICU. In addition to being performed completely in the ICU, our study objectively assessed sleep quality in both the loud and noise-reduced environments. Although there was a quantitative improvement in sleep in the single room, sleep architecture was nearly identical and arousal frequencies were normal in both locations. Mean and mean maximum sound intensities were significantly reduced in the single room, as were the number of extremely loud (>75 dB[A]) sound peaks and the mean peak decibel level; however, the frequency of sound spikes remained elevated, essentially the same as that experienced by our patient cohort. This may be one explanation for a lack of improvement in sleep continuity despite a reduction in overall sound intensity and may suggest that the frequency and nature of sound peaks are important contributors to noise-induced sleep disruption. The single room was chosen as a realistic location for noise reduction because it is physically isolated from the main open ICU. Any ICU noise registered in the single room originated from "leakage" from the main ICU. In our case, this was particularly evident with respect to the main door of the ICU, which was responsible for a disproportionate amount of sleep disruption. However, when sleep disruption caused by the main door was excluded, the arousal and awakening indices of subjects in the single room were significantly lower than the arousal and awakening indices of subjects in the open ICU. Despite the effect of the main door, total sleep time and nocturnal sleep time improved significantly in the single room, perhaps because the noise-reduced location is more conducive to a return to sleep after an arousal or awakening. Alternatively, the comparative lack of visual and other distractions in the single room may have also played a role. Reductions in the frequency of irritating noises, noise intensity, and visual distractions, in addition to a longer total sleep time, may have contributed to the subjective rating of improved sleep quality in the single room despite no improvement in arousal and awakening indices. Our study has a number of limitations, which should be noted. First, our sample sizes were small, which limited the power of our statistical analyses. Nevertheless, our adherence to strict inclusion and exclusion criteria enabled us to avoid a wide heterogeneity in our data, which resulted in relatively consistent PSG findings despite the fact that we recruited patients and healthy subjects over a wide age range. Second, the design of the study did not allow healthy subjects to adapt to the ICU environment and habituate to noise intensity, which may have occurred in our patients admitted to the ICU for prolonged periods. However, habituation to noise among our healthy individuals would be expected to reduce the prevalence of noise-related sleep disruption even further. Therefore, our finding that excessive noise did not pathologically disrupt the sleep of healthy subjects, without the opportunity to habituate to noise, coupled with our observations in ICU patients, strengthens our suggestion that noise is not a major sleep disrupter in the ICU. Given that the elements of the ICU environment assessed in this study, namely sound and patient-care activities, together accounted for less than 30% of observed sleep disruption, a significant proportion of sleep disruption in mechanically ventilated ICU patients remains unexplained. One possibility is dyssynchrony between the patient and the ventilator. Preliminary data (29) suggest that this may be dependent on the mode of ventilation, but this requires further study. If patient–ventilator dyssynchrony is determined to be a major source of sleep disruption, this may be corrected by altering the mode of mechanical ventilation with the hope and expectation that improvement of sleep quality will ultimately benefit the clinical outcome of critically ill patients.
The authors are indebted to Dr. Hans Kunov and Dr. Taha Jaffer at the Institute for Biomaterial and Biomedical Engineering and the Edwards S. Rogers Department of Electrical and Computer Engineering, University of Toronto, who designed and built the apparatus for time-synchronization of PSG and environmental variables, and the Canadian Intensive Care Foundation and the St. Michael's Hospital Foundation for financial support of this work.
Supported by St. Michael's Hospital Foundation; Canadian Intensive Care Foundation; Department of Anesthesia, University of Toronto; and Department of Anaesthesia, Sunnybrook and Women's College Health Sciences Centre. This article has an online supplement, which is accessible from this issue's table of contents online at www.atsjournals.org Received in original form January 31, 2002; accepted in final form November 22, 2002
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