A description of nurses' decision-making in managing electrocardiographic monitor alarms.

AIMS AND OBJECTIVES: To describe the cues and factors that nurses use in their decision-making when responding to clinical alarms. BACKGROUND: Alarms are designed to be very sensitive, and as a result, they are not very specific. Lack of adherence to the practice standards for electrocardiographic monitoring in hospital settings has been observed, resulting in overuse of the electrocardiographic monitoring. Monitoring without consideration of clinical indicators uses scarce healthcare resources and may even produce untoward circumstances because of alarm fatigue. With so many false alarms, alarm fatigue represents a symptom of a larger problem. It cannot be fixed until all of the factors that contribute to its existence have been examined. DESIGN: This was a qualitative descriptive study. METHOD: This study was conducted at an academic medical centre located in the Northeast United States. Eight participants were enrolled using purposive sampling. Nurses were observed for two three-hour periods. Following each observation, the nurse was interviewed using the critical decision method to describe the cognitive processes related to the alarm activities. Qualitative data from the conducted interviews were analysed via an a priori framework founded in the critical decision method. RESULTS: This study reveals information, experience, guidance and decision-making as the four prominent categories contributing to nurses' decision-making in relation to alarm management. Managing technology was a category not identified a priori that emerged in the data analysis. CONCLUSION: Nurses revealed a breadth of information needed to adequately identify and interpret monitor alarms, and how they used that information to put the alarms into the particular context of an individual patient's situations. RELEVANCE TO CLINICAL PRACTICE: Understanding the cues and factors nurses use when responding to cardiac alarms will guide the development of learning experiences and inform policies to guide practice.

The diurnal rhythm of hypocretin in young and old F344 rats.

STUDY OBJECTIVES: Hypocretins (HCRT-1 and HCRT-2), also known as orexins, are neuropeptides localized in neurons surrounding the perifornical region of the posterior hypothalamus. These neurons project to major arousal centers in the brain and are implicated in regulating wakefulness. In young rats and monkeys, levels of HCRT-1 are highest at the end of the wake-active period and lowest toward the end of the sleep period. However, the effects of age on the diurnal rhythm of HCRT-1 are not known. DESIGN: To provide such data, cerebrospinal fluid (CSF) was collected from the cisterna magna of young (2-month-old, n = 9), middle-aged (12 months, n = 10), and old (24 months, n = 10) F344 rats at 4-hour intervals, (beginning at zeitgeber [ZT]0, lights on). CSF was collected once from each rat every 4 days at 1 ZT point. After collecting the CSF at all of the time points, the rats were kept awake by gentle handling for 8 hours (ZT 0-ZT8), and the CSF was collected again at the end of the sleep-deprivation procedure. HCRT-1 levels in the CSF were determined by radioimmunoassay SETTINGS: Basic neuroscience research lab. MEASUREMENTS AND RESULTS: Old rats had significantly less HCRT-1 in the CSF versus young and middle-aged rats (P < .002) during the lights-on and lights-off periods and over the 24-hour period. In old rats, significantly low levels of HCRT-1 were evident at the end of the lights-off period (predominantly wake-active period). The old rats continued to have less HCRT-1 even after 8 hours of prolonged waking. Northern blot analysis did not show a difference in pre-proHCRT mRNA between age groups. CONCLUSIONS: In old rats there is a 10% decline in CSF HCRT-1 over the 24-hour period. Functionally, if there is less HCRT-1, which our findings indicated, and there is also a decline in HCRT receptor mRNA, as has been previously found, then the overall consequence would be diminished action of HCRT at target sites. This would diminish the waking drive, which in the elderly could contribute to the increased tendency to fall asleep during the normal wake period.

Sleep rhythmicity and homeostasis in mice with targeted disruption of mPeriod genes.

In mammals, sleep is regulated by circadian and homeostatic mechanisms. The circadian component, residing in the suprachiasmatic nucleus (SCN), regulates the timing of sleep, whereas homeostatic factors determine the amount of sleep. It is believed that these two processes regulating sleep are independent because sleep amount is unchanged after SCN lesions. However, because such lesions necessarily damage neuronal connectivity, it is preferable to investigate this question in a genetic model that overcomes the confounding influence of circadian rhythmicity. Mice with disruption of both mouse Period genes (mPer)1 and mPer2 have a robust diurnal sleep-wake rhythm in an entrained light-dark cycle but lose rhythmicity in a free-run condition. Here, we examine the role of the mPer genes on the rhythmic and homeostatic regulation of sleep. In entrained conditions, when averaged over the 24-h period, there were no significant differences in waking, slow-wave sleep (SWS), or rapid eye movement (REM) sleep between mPer1, mPer2, mPer3, mPer1-mPer2 double-mutant, and wild-type mice. The mice were then kept awake for 6 h (light period 6-12), and the mPer mutants exhibited increased sleep drive, indicating an intact sleep homeostatic response in the absence of the mPer genes. In free-run conditions (constant darkness), the mPer1-mPer2 double mutants became arrhythmic, but they continued to maintain their sleep levels even after 36 days in free-running conditions. Although mPer1 and mPer2 represent key elements of the molecular clock in the SCN, they are not required for homeostatic regulation of the daily amounts of waking, SWS, or REM sleep.