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正常受试者睡眠期间辅助通气时周期性呼吸的易感性。

Susceptibility to periodic breathing with assisted ventilation during sleep in normal subjects.

作者信息

Meza S, Mendez M, Ostrowski M, Younes M

机构信息

Respiratory Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3A 1R8.

出版信息

J Appl Physiol (1985). 1998 Nov;85(5):1929-40. doi: 10.1152/jappl.1998.85.5.1929.

Abstract

Assisted ventilation with pressure support (PSV) or proportional assist (PAV) ventilation has the potential to produce periodic breathing (PB) during sleep. We hypothesized that PB will develop when PSV level exceeds the product of spontaneous tidal volume (VT) and elastance (VTsp . E) but that the actual level at which PB will develop [PSV(PB)] will be influenced by the DeltaPCO2 (difference between eupneic PCO2 and CO2 apneic threshold) and by DeltaRR [response of respiratory rate (RR) to PSV]. We also wished to determine the PAV level at which PB develops to assess inherent ventilatory stability in normal subjects. Twelve normal subjects underwent polysomnography while connected to a PSV/PAV ventilator prototype. Level of assist with either mode was increased in small steps (2-5 min each) until PB developed or the subject awakened. End-tidal PCO2, VT, RR, and airway pressure (Paw) were continuously monitored, and the pressure generated by respiratory muscle (Pmus) was calculated. The pressure amplification factor (PAF) at the highest PAV level was calculated from [(DeltaPaw + Pmus)/Pmus], where DeltaPaw is peak Paw - continuous positive airway pressure. PB with central apneas developed in 11 of 12 subjects on PSV. DeltaPCO2 ranged from 1.5 to 5.8 Torr. Changes in RR with PSV were small and bidirectional (+1.1 to -3.5 min-1). With use of stepwise regression, PSV(PB) was significantly correlated with VTsp (P = 0.001), E (P = 0.00009), DeltaPCO2 (P = 0.007), and DeltaRR (P = 0.006). The final regression model was as follows: PSV(PB) = 11.1 VTsp + 0.3E - 0.4 DeltaPCO2 - 0.34 DeltaRR - 3.4 (r = 0.98). PB developed in five subjects on PAV at amplification factors of 1.5-3.4. It failed to occur in seven subjects, despite PAF of up to 7.6. We conclude that 1) a PCO2 apneic threshold exists during sleep at 1.5-5.8 Torr below eupneic PCO2, 2) the development of PB during PSV is entirely predictable during sleep, and 3) the inherent susceptibility to PB varies considerably among normal subjects.

摘要

压力支持通气(PSV)或比例辅助通气(PAV)在睡眠期间有可能导致周期性呼吸(PB)。我们假设,当PSV水平超过自主潮气量(VT)与弹性的乘积(VTsp·E)时,会出现PB,但PB出现时的实际水平[PSV(PB)]将受ΔPCO2(平静呼吸PCO2与CO2呼吸暂停阈值之间的差值)和ΔRR[呼吸频率(RR)对PSV的反应]的影响。我们还希望确定PB出现时的PAV水平,以评估正常受试者固有的通气稳定性。12名正常受试者连接到PSV/PAV呼吸机原型时接受了多导睡眠图检查。两种模式下的辅助水平以小步长(每次2 - 5分钟)增加,直到出现PB或受试者醒来。持续监测呼气末PCO2、VT、RR和气道压力(Paw),并计算呼吸肌产生的压力(Pmus)。最高PAV水平时的压力放大因子(PAF)由[(ΔPaw + Pmus)/Pmus]计算得出,其中ΔPaw是Paw峰值 - 持续气道正压。12名接受PSV的受试者中有11名出现了伴有中枢性呼吸暂停的PB。ΔPCO2范围为1.5至5.8托。RR随PSV的变化较小且呈双向(+1.1至 - 3.5次/分钟)。使用逐步回归分析,PSV(PB)与VTsp显著相关(P = 0.001)、E(P = 0.00009)、ΔPCO2(P = 0.007)和ΔRR(P = 0.006)。最终回归模型如下:PSV(PB)= 11.1VTsp + 0.3E - 0.4ΔPCO2 - 0.34ΔRR - 3.4(r = 0.98)。5名接受PAV的受试者在放大因子为1.5 - 3.4时出现了PB。7名受试者尽管PAF高达7.6但未出现PB。我们得出结论:1)睡眠期间存在一个PCO2呼吸暂停阈值,比平静呼吸PCO2低1.5 - 5.8托;2)睡眠期间PSV期间PB的发生完全可预测;3)正常受试者中PB的固有易感性差异很大。

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