关键词: Adaptive-Servo Ventilation (ASV) apneic threshold bi-level positive pressure therapy (BPAP) central apnea continuous positive pressure therapy (CPAP) controller gain hypocapnia loop gain plant gain

Mesh : Humans Sleep Apnea, Central Hypocapnia / complications Respiration Sleep Heart Failure

来  源:   DOI:10.1093/sleep/zsac113   PDF(Pubmed)

Abstract:
Central sleep apnea is not a single disorder; it can present as an isolated disorder or as a part of other clinical syndromes. In some conditions, such as heart failure, central apneic events are due to transient inhibition of ventilatory motor output during sleep, owing to the overlapping influences of sleep and hypocapnia. Specifically, the sleep state is associated with removal of wakefulness drive to breathe; thus, rendering ventilatory motor output dependent on the metabolic ventilatory control system, principally PaCO2. Accordingly, central apnea occurs when PaCO2 is reduced below the \"apneic threshold\". Our understanding of the pathophysiology of central sleep apnea has evolved appreciably over the past decade; accordingly, in disorders such as heart failure, central apnea is viewed as a form of breathing instability, manifesting as recurrent cycles of apnea/hypopnea, alternating with hyperpnea. In other words, ventilatory control operates as a negative-feedback closed-loop system to maintain homeostasis of blood gas tensions within a relatively narrow physiologic range, principally PaCO2. Therefore, many authors have adopted the engineering concept of \"loop gain\" (LG) as a measure of ventilatory instability and susceptibility to central apnea. Increased LG promotes breathing instabilities in a number of medical disorders. In some other conditions, such as with use of opioids, central apnea occurs due to inhibition of rhythm generation within the brainstem. This review will address the pathogenesis, pathophysiologic classification, and the multitude of clinical conditions that are associated with central apnea, and highlight areas of uncertainty.
摘要:
中枢性睡眠呼吸暂停不是一种单一的疾病;它可以表现为孤立的疾病或其他临床综合征的一部分。在某些情况下,比如心力衰竭,中枢呼吸暂停事件是由于睡眠期间通气运动输出的短暂抑制,由于睡眠和低碳酸血症的重叠影响。具体来说,睡眠状态与消除清醒驱动呼吸有关;因此,根据代谢通气控制系统渲染通气运动输出,主要是PaCO2。因此,当PaCO2降低到“呼吸暂停阈值”以下时,就会发生中枢呼吸暂停。在过去的十年中,我们对中枢性睡眠呼吸暂停的病理生理学的理解有了明显的发展。在心力衰竭等疾病中,中枢呼吸暂停被视为呼吸不稳定的一种形式,表现为呼吸暂停/呼吸不足的反复循环,交替呼吸过度。换句话说,通气控制作为负反馈闭环系统,将血气张力的稳态维持在相对狭窄的生理范围内。主要是PaCO2。因此,许多作者采用了"环路增益"(LG)的工程概念作为衡量呼吸不稳定和对中枢呼吸暂停的敏感性的指标.LG的增加促进了许多医学疾病中的呼吸不稳定性。在其他条件下,比如使用阿片类药物,中枢神经性呼吸暂停是由于脑干内节律生成的抑制而发生的。这篇综述将针对发病机制,病理生理分类,以及与中枢呼吸暂停相关的多种临床状况,并强调不确定的领域。
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