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      Effect of Reducing Interns' Weekly Work Hours on Sleep and Attentional Failures

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          Abstract

          Knowledge of the physiological effects of extended (24 hours or more) work shifts in postgraduate medical training is limited. We aimed to quantify work hours, sleep, and attentional failures among first-year residents (postgraduate year 1) during a traditional rotation schedule that included extended work shifts and during an intervention schedule that limited scheduled work hours to 16 or fewer consecutive hours. Twenty interns were studied during two three-week rotations in intensive care units, each during both the traditional and the intervention schedule. Subjects completed daily sleep logs that were validated with regular weekly episodes (72 to 96 hours) of continuous polysomnography (r=0.94) and work logs that were validated by means of direct observation by study staff (r=0.98). Seventeen of 20 interns worked more than 80 hours per week during the traditional schedule (mean, 84.9; range, 74.2 to 92.1). All interns worked less than 80 hours per week during the intervention schedule (mean, 65.4; range, 57.6 to 76.3). On average, interns worked 19.5 hours per week less (P<0.001), slept 5.8 hours per week more (P<0.001), slept more in the 24 hours preceding each working hour (P<0.001), and had less than half the rate of attentional failures while working during on-call nights (P=0.02) on the intervention schedule as compared with the traditional schedule. Eliminating interns' extended work shifts in an intensive care unit significantly increased sleep and decreased attentional failures during night work hours. Copyright 2004 Massachusetts Medical Society.

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          Most cited references26

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          Dose-response relationship for light intensity and ocular and electroencephalographic correlates of human alertness.

          Light can elicit both circadian and acute physiological responses in humans. In a dose response protocol men and women were exposed to illuminances ranging from 3 to 9100 lux for 6.5 h during the early biological night after they had been exposed to <3 lux for several hours. Light exerted an acute alerting response as assessed by a reduction in the incidence of slow-eye movements, a reduction of EEG activity in the theta-alpha frequencies (power density in the 5-9 Hz range) as well as a reduction in self-reported sleepiness. This alerting response was positively correlated with the degree of melatonin suppression by light. In accordance with the dose response function for circadian resetting and melatonin suppression, the responses of all three indices of alertness to variations in illuminance were consistent with a logistic dose response curve. Half of the maximum alerting response to bright light of 9100 lux was obtained with room light of approximately 100 lux. This sensitivity to light indicates that variations in illuminance within the range of typical, ambient, room light (90-180 lux) can have a significant impact on subjective alertness and its electrophysiologic concomitants in humans during the early biological night.
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            Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response study

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              Paradoxical timing of the circadian rhythm of sleep propensity serves to consolidate sleep and wakefulness in humans.

              The contribution of the circadian pacemaker and the sleep homeostat to sleep tendency and consolidation was quantified by forced desynchrony of the sleep-wake cycle from the circadian pacemaker in eight men who lived in time-isolation for 33-36 days. Analysis of 175 polygraphically recorded sleep episodes revealed that the circadian pacemaker and the sleep homeostat contribute about equally to sleep consolidation, and that the phase relationship between these oscillatory processes during entrainment to the 24-h day is uniquely timed to facilitate the ability to maintain a consolidated bout of sleep at night and a consolidated bout of wakefulness throughout the day.
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                Author and article information

                Journal
                New England Journal of Medicine
                N Engl J Med
                Massachusetts Medical Society
                0028-4793
                1533-4406
                October 28 2004
                October 28 2004
                : 351
                : 18
                : 1829-1837
                Article
                10.1056/NEJMoa041404
                15509816
                b022cd22-007d-4bd2-b49b-6595856b9816
                © 2004
                History

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