Sleep in Critically Ill Patients Requiring Mechanical Ventilation* Andrew B. Cooper, MD; Kristine S. Thornley, BSc, RPSGT; G. Bryan Young, MD; Arthur S. Slutsky, MD, FCCP; Thomas E. Stewart, MD; and Patrick J. Hanly, MD Study objectives: To objectively measure sleep in critically ill patients requiring mechanical ventilation and to define selection criteria for future studies of sleep continuity in this population. Design: Prospective cohort analysis. Setting: University teaching hospital medical-surgical ICU. Patients: Twenty critically ill (APACHE II [acute physiology and chronic health evaluation II] acute physiology score [APS], 10  5), mechanically ventilated adults (male 12, female 8, age 62  15 years) with mild to moderate acute lung injury (lung injury score, 1.8  0.9) 10  7 days after admission to the ICU. Measurements and results: Patients were divided into three groups based on 24-h polysomnog- raphy (PSG) findings. No patient demonstrated normal sleep. In the “disrupted sleep” group (n  8), electrophysiologic sleep was identified and was distributed throughout the day (6:00 AM to 10:00 PM; 4.0  2.9 h) and night (10:00 PM to 6:00 AM; 3.0  1.9 h) with equivalent proportions of non–rapid eye movement (NREM) and rapid eye movement (REM) sleep. Nocturnal sleep efficiency was severely reduced (38  24%) with an increased proportion of stage 1 NREM sleep (40  28% total sleep time [TST]) and a reduced proportion of REM sleep (10  14% TST). Severe sleep fragmentation was reflected by a high frequency of arousals (20  17/h) and awakenings (22  25/h). Electrophysiologic sleep was not identifiable in the PSG recordings of the remaining patients. These were classified either as “atypical sleep” (n  5), characterized by transitions from stage 1 NREM to slow wave sleep with a virtual absence of stage 2 NREM and reduced stage REM sleep, or “coma” (n  7), characterized by > 50% delta or theta EEG activity with (n  5) and without (n  2) evidence of EEG activation either spontaneously or in response to deep painful stimuli. The combined atypical sleep and coma groups had a higher APS (13  4 vs 6  4) and higher doses of sedative medications than the disrupted sleep group. Conclusion: Sleep, as it is conventionally measured, was identified only in a subgroup of critically ill patients requiring mechanical ventilation and was severely disrupted. We have proposed specific criteria to select patients for future studies to evaluate potential causes of sleep disruption in this population. (CHEST 2000; 117:809 – 818) Key words: critical care; mechanical ventilation; polysomnography; sleep deprivation; sleep stages Abbreviations: APACHE II = acute physiology and chronic health evaluation II; APS = acute physiology score; EMG = electromyogram; EOG = electro-oculogram; GCS = Glasgow coma scale; LIS = lung injury score; NREM = nonrapid eye movement; REM = rapid eye movement; SE = sleep efficiency; SWS = slow wave sleep; TSP = total study period; TST = total sleep time S leep disruption has been recognized as a compli- cation of acute illness for at least 20 years. It is characterized by reduced nocturnal sleep efficiency and altered sleep architecture with increased wake- fulness and stage 1 non–rapid eye movement (NREM) sleep, together with reduced slow wave (SWS) and rapid eye movement (REM) sleep. 1–10 Sleep disruption in critically ill, mechanically ven- tilated patients may have a multifactorial cause. Acute illnesses are associated with abnormal sleep architecture. 4,5,7,9,11,12 The ICU environment, in which loud noises 13,14 and frequent care-related interruptions 14,15 are prevalent, may interfere with continuity of sleep. Medications commonly pre- scribed for patient comfort also have marked effects on sleep. 16 It is possible that dyssynchronous pa- *From the Division of Respirology and the Critical Care Medi- cine Program, University of Toronto (Drs. Cooper, Slutsky, Stewart, and Hanley), St. Michael’s Hospital, Wellesley Site, Sleep Laboratory, Toronto (Ms. Thornley and Dr. Hanly), and the Division of Neurology, University of Western Ontario, Lon- don (Dr. Young), Ontario, Canada. Funded, in part, by grants from the Ontario Thoracic Society. Manuscript received April 13, 1999; revision accepted September 7, 1999. Correspondence to: Patrick J. Hanly, MD, Division of Respirol- ogy, St. Michael’s Hospital, 30 Bond St, Suite 6049, Toronto, ON, Canada M5B 1W8 CHEST / 117 / 3 / MARCH, 2000 809 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21941/ on 06/21/2017