PURPOSE: To access the effect of propofol administration on sleep quality in critically ill patients ventilated on assisted modes. METHODS: This was a randomized crossover physiological study conducted in an adult ICU at a tertiary hospital. Two nights' polysomnography was performed in mechanically ventilated critically ill patients with and withoutpropofol infusion, while respiratory variables were continuously recorded. Arterial blood gasses were measured in the beginning and at the end of the study. The rate of propofol infusion was adjusted to maintain a sedation level of 3 on the Ramsay scale. Sleep architecture was analyzed manually using predetermined criteria. Patient-ventilator asynchrony was evaluated breath by breath using the flow-time and airway pressure-time waveforms. RESULTS:Twelve patients were studied. Respiratory variables, patient-ventilator asynchrony, and arterial blood gasses did not differ between experimental conditions. With or without propofol all patients demonstrated abnormal sleep architecture, expressed by lack of sequential progression through sleep stages and their abnormal distribution. Sleep efficiency, sleep fragmentation, and sleep stage distribution (1, 2, and slow wave) did not differ with or without propofol. Compared to without propofol, both the number of patients exhibiting REM sleep (p = 0.02) and the percentage of REM sleep (p = 0.04) decreased significantly with propofol. CONCLUSIONS: In critically ill patients ventilated on assisted modes, propofol administration to achieve the recommended level of sedation suppresses the REM sleep stage and further worsens the poor sleep quality of these patients.
RCT Entities:
PURPOSE: To access the effect of propofol administration on sleep quality in critically illpatients ventilated on assisted modes. METHODS: This was a randomized crossover physiological study conducted in an adult ICU at a tertiary hospital. Two nights' polysomnography was performed in mechanically ventilated critically illpatients with and without propofol infusion, while respiratory variables were continuously recorded. Arterial blood gasses were measured in the beginning and at the end of the study. The rate of propofol infusion was adjusted to maintain a sedation level of 3 on the Ramsay scale. Sleep architecture was analyzed manually using predetermined criteria. Patient-ventilator asynchrony was evaluated breath by breath using the flow-time and airway pressure-time waveforms. RESULTS: Twelve patients were studied. Respiratory variables, patient-ventilator asynchrony, and arterial blood gasses did not differ between experimental conditions. With or without propofol all patients demonstrated abnormal sleep architecture, expressed by lack of sequential progression through sleep stages and their abnormal distribution. Sleep efficiency, sleep fragmentation, and sleep stage distribution (1, 2, and slow wave) did not differ with or without propofol. Compared to without propofol, both the number of patients exhibiting REM sleep (p = 0.02) and the percentage of REM sleep (p = 0.04) decreased significantly with propofol. CONCLUSIONS: In critically illpatients ventilated on assisted modes, propofol administration to achieve the recommended level of sedation suppresses the REM sleep stage and further worsens the poor sleep quality of these patients.
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