SLEEP-INDUCED PERIODIC BREATHING AND APNEA - A THEORETICAL-STUDY
SLEEP-INDUCED PERIODIC BREATHING AND APNEA - A THEORETICAL-STUDY
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DOI：
10.1152/jappl.1991.70.5.2014
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发表时间：
1991-05-01
影响因子：
3.3
通讯作者：
PACK, AI
中科院分区：
文献类型：
--
作者：
KHOO, MCK;GOTTSCHALK, A;PACK, AI
为了阐明导致睡眠呼吸障碍的机制，我们开发了一种数学模型，该模型允许呼吸的化学控制、睡眠-觉醒状态的变化和上呼吸道通畅性的变化之间的动态相互作用。 睡眠期间稳态动脉 PCO2 的增加与 CO2 的通气反应呈负相关。 尽管化学反应性降低，但在浅睡眠阶段，呼吸的化学控制变得不太稳定，因为“植物增益”（即血气对通气变化的反应性）随之增加。 睡眠开始期间“觉醒驱力”的撤退代表着对呼吸控制的强烈扰动：这种驱力撤退的幅度和速率越高，有利于不稳定。 这些结果可能解释了浅睡眠和入睡期间观察到的周期性呼吸发生率较高的原因。 睡眠开始和觉醒之间的重复交替也可能导致周期性通气。 如果还包括上呼吸道阻塞的可能性，则不稳定的可能性会进一步加剧。 在具有高控制器增益的系统中，不稳定性主要通过化学反射过度补偿来调节。 然而，在化疗反应性低下的系统中，快速入睡和大的血气波动会引发反复发作的觉醒和呼吸过度，与可能或可能不阻塞的呼吸暂停交替出现。 在这些极端之间，较短周期持续时间（几乎等于 36 秒）的化学反射介导的振荡和较长波长（几乎等于 60-80 秒）状态驱动振荡之间的相互作用可能会产生更复杂的模式。
To elucidate the mechanisms that lead to sleep-disordered breathing, we have developed a mathematical model that allows for dynamic interactions among the chemical control of respiration, changes in sleep-waking state, and changes in upper airway patency. The increase in steady-state arterial PCO2 accompanying sleep is shown to be inversely related to the ventilatory response to CO2. Chemical control of respiration becomes less stable during the light stage of sleep, despite a reduction in chemoresponsiveness, due to a concomitant increase in "plant gain" (i.e., responsiveness of blood gases to ventilatory changes). The withdrawal of the "wakefulness drive" during sleep onset represents a strong perturbation to respiratory control: higher magnitudes and rates of withdrawal of this drive favor instability. These results may account for the higher incidence of periodic breathing observed during light sleep and sleep onset. Periodic ventilation can also result from repetitive alternations between sleep onset and arousal. The potential for instability is further compounded if the possibility of upper airway occlusion is also included. In systems with high controller gains, instability is mediated primarily through chemoreflex overcompensation. However, in systems with depressed chemoresponsiveness, rapid sleep onset and large blood gas fluctuations trigger repetitive episodes of arousal and hyperpnea alternating with apneas that may or may not be obstructive. Between these extremes, more complex patterns can arise from the interaction between chemoreflex-mediated oscillations of shorter-cycle-duration (almost equal to 36 s) and longer-wavelength (almost equal to 60-80 s) state-driven oscillations.