Physiology and Pathophysiology of Sleep Apnea Transition from acute to chronic hypercapnia in patients with periodic breathing : predictions from a computer model
Physiology and Pathophysiology of Sleep Apnea Transition from acute to chronic hypercapnia in patients with periodic breathing : predictions from a computer model
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2006
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通讯作者：
R. Norman;R. Goldring;Jeremy M. Clain;Beno W. Oppenheimer;A. Charney;D. Rapoport;K. Berger
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作者：
R. Norman;R. Goldring;Jeremy M. Clain;Beno W. Oppenheimer;A. Charney;D. Rapoport;K. Berger
诺曼、罗伯特·G、罗伯塔·m·戈德林、杰里米·m·克莱恩、贝诺·w·奥本海默、艾伦·n·查尼、大卫·m·拉波波特和肯尼斯·i·伯杰。周期性呼吸患者从急性到慢性高碳酸血症的转变：来自计算机模型的预测。中国生物医学工程学报（英文版），2006,31(2):393 - 398。2005年12月29日首次出版；doi: 10.1152 / japplphysiol.00502.2005。急性高碳酸血症可在周期性呼吸期间由呼吸暂停和/或低通气期间异常通气模式与事件间期代偿性通气反应之间的不平衡引起。然而，这种急性高碳酸血症在清醒状态下转变为慢性持续性高碳酸血症的原因尚不清楚。我们假设呼吸-肾脏相互作用将在这一转变中发挥关键作用。由于这种转变在临床上不易解决，我们修改了先前发表的全身二氧化碳动力学模型，加入了呼吸控制和肾脏碳酸氢盐动力学。我们强制执行8小时周期性呼吸（睡眠）和16小时常规通气（清醒）的模式，重复20天。干预措施包括改变初始清醒呼吸CO2反应和在生理范围内改变肾脏碳酸氢盐排泄率。结果表明，周期性呼吸时的急性高碳酸血症可转变为清醒时的慢性持续性高碳酸血症。虽然急性高碳酸血症可能仅归因于周期性呼吸，但从急性到慢性高碳酸血症的转变需要肾脏碳酸氢盐动力学减慢，通气CO2反应性降低，或两者兼而有之。因此，该模型表明，碳酸氢盐排泄时间常数与呼吸控制之间的相互作用导致碳酸氢盐浓度在下一段睡眠前无法完全正常化，并通过通气驱动的钝化而持续高碳酸血症。这些呼吸-肾脏相互作用在随后的睡眠期间产生累积效应，最终导致慢性高碳酸血症的自我延续状态。
Norman, Robert G., Roberta M. Goldring, Jeremy M. Clain, Beno W. Oppenheimer, Alan N. Charney, David M. Rapoport, and Kenneth I. Berger. Transition from acute to chronic hypercapnia in patients with periodic breathing: predictions from a computer model. J Appl Physiol 100: 1733–1741, 2006. First published December 29, 2005; doi:10.1152/japplphysiol.00502.2005.—Acute hypercapnia may develop during periodic breathing from an imbalance between abnormal ventilatory patterns during apnea and/or hypopnea and compensatory ventilatory response in the interevent periods. However, transition of this acute hypercapnia into chronic sustained hypercapnia during wakefulness remains unexplained. We hypothesized that respiratory-renal interactions would play a critical role in this transition. Because this transition cannot be readily addressed clinically, we modified a previously published model of whole-body CO2 kinetics by adding respiratory control and renal bicarbonate kinetics. We enforced a pattern of 8 h of periodic breathing (sleep) and 16 h of regular ventilation (wakefulness) repeated for 20 days. Interventions included varying the initial awake respiratory CO2 response and varying the rate of renal bicarbonate excretion within the physiological range. The results showed that acute hypercapnia during periodic breathing could transition into chronic sustained hypercapnia during wakefulness. Although acute hypercapnia could be attributed to periodic breathing alone, transition from acute to chronic hypercapnia required either slowing of renal bicarbonate kinetics, reduction of ventilatory CO2 responsiveness, or both. Thus the model showed that the interaction between the time constant for bicarbonate excretion and respiratory control results in both failure of bicarbonate concentration to fully normalize before the next period of sleep and persistence of hypercapnia through blunting of ventilatory drive. These respiratory-renal interactions create a cumulative effect over subsequent periods of sleep that eventually results in a self-perpetuating state of chronic hypercapnia.