Investigation of Sleep in the Intensive Care Unit (ICU-SLEEP)

项目总结/摘要：重症监护病房（ICU-SLEEP）的睡眠调查 睡眠剥夺是ICU经历中最常见的抱怨之一。ICU睡眠往往是 轻度和非恢复性睡眠（与深度/恢复性睡眠相反），严重碎片化，分布 白天和晚上，而不是集中在夜间。睡眠不足的病人会患上 睡眠债，一种注意力和记忆力受损的状况，以及认知能力下降。ICU中的睡眠障碍 不仅来自光和噪音污染，还来自干扰大脑活动的药物， 恢复性睡眠睡眠不足也被认为是急性脑梗死的一个主要可改变的风险因素 脑病，也称为谵妄。谵妄是一种急性意识模糊状态，影响高达80%的ICU 是住院老年患者可预防的发病率和死亡率的六大主要原因之一。 许多从谵妄中幸存下来的患者会经历长期的认知障碍和独立性丧失。 目前在ICU中用于治疗睡眠问题的药物（例如苯二氮卓类、抗精神病药）不 诱导自然睡眠且不能防止谵妄。相反，我们发现α2-肾上腺素受体激动剂 右美托咪定可诱导仿生睡眠，这是一种脑状态，其脑电图（EEG）模式 活动、脑血流量和功能连接接近恢复性睡眠。此外，最近 在手术后患者中进行的大型临床试验表明， 大大降低了精神错乱的风险。目前尚不清楚这种益处是否与改善睡眠有关， 在ICU中睡眠更好的患者是否具有更好的长期认知结果。我们的中央 一种假设是睡眠剥夺在很大程度上介导了短期和长期的认知障碍 与危重病患者的谵妄有关。为了验证这一假设，我们的具体目标是 系统地确定1）预防性右美托咪定对睡眠质量的影响，2） 给予右美托咪定（整夜vs仅在夜晚开始时），2）睡眠剥夺对 短期认知功能和谵妄，和3）睡眠剥夺的贡献，长期 危重病后的神经精神病学结局。在这些研究结束时，我们将扩大 我们对危重病患者睡眠生理学的了解以及睡眠与谵妄的关系;评估了一种新的 先发制人的治疗策略，以促进睡眠和防止谵妄，并制定了一个理解， 睡眠如何影响危重病后的神经心理学结果。因此，我们的研究将提供至关重要的 指导个体化的方法，以保持这种脆弱患者的长期大脑健康 人口

PROJECT SUMMARY / ABSTRACT: Investigation of Sleep in the Intensive Care Unit (ICU-SLEEP) Sleep deprivation is among the most common complaints about the ICU experience. ICU sleep tends to be light and non-restorative (as opposed to deep / restorative sleep), severely fragmented, and distributed throughout the day and night rather than consolidated into nighttime hours. Sleep deprived patients suffer from sleep debt, a condition of impaired attention and memory, and cognitive slowing. Sleep disturbances in the ICU arise not only from light and noise pollution, but also from drugs that interfere with brain activity involved in restorative sleep. Sleep deprivation has also been suggested as a major modifiable risk factors for acute encephalopathy, also known as delirium. Delirium is an acute state of confusion that affects up to 80% of ICU patients, and is one of six leading causes of preventable morbidity and mortality in hospitalized elderly patients. Many patients who survive delirium experience long-term cognitive impairment and loss of independence. Current medications used in the ICU to treat sleep problems (e.g. benzodiazepines, antipsychotics) do not induce natural sleep and do not prevent delirium. In contrast, we have found that the α2-adrenoceptor agonist dexmedetomidine can induce biomimetic sleep, a brain state whose pattern of electroencephalogram (EEG) activity, cerebral blood flow, and functional connectivity approximates restorative sleep. Moreover, a recent large clinical trial in post-surgical patients suggests that low-dose dexmedetomidine given overnight substantially reduces the risk of delirium. It is unknown whether this benefit is linked to improved sleep, or whether patients with better sleep while in the ICU have better long-term cognitive outcomes. Our central hypothesis is that sleep deprivation substantially mediates both the short- and long-term cognitive impairments associated with delirium in critical illness. To test this hypothesis, our specific aims are designed to systematically determine 1) the impact of prophylactic dexmedetomidine on sleep quality, 2) the optimal way to give dexmedetomidine (all night vs at the beginning of the night only), 2) the impact of sleep deprivation on short-term cognitive function and delirium, and 3) the contribution of sleep deprivation to long-term neuropsychiatric outcome following critical illness. At the conclusion of these studies, we will have expanded our knowledge of sleep physiology in critical illness and relationship of sleep with delirium; evaluated a new preemptive therapeutic strategy to promote sleep and prevent delirium, and developed an understanding of how sleep impacts neuropsychological outcomes after critical illness. Our studies will thus will provide crucial guidance for individualized approaches to preserving long-term brain health in this vulnerable patient population.