Response of ventilator-dependent patients to delayed opening of exhalation valve
Response of ventilator-dependent patients to delayed opening of exhalation valve
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DOI：
10.1164/rccm.2107143
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发表时间：
2002-07-01
影响因子：
24.7
通讯作者：
Roberts, D
中科院分区：
文献类型：
--
作者：
Younes, M;Kun, J;Roberts, D
在传统的机械通气中，充气周期通常延长到神经性呼气(TEN)，潜在地加剧动态过度充气(DH)。我们希望确定当这种情况发生时，患者对卫生署的防御程度。这种防御可能包括延长TEN(定时反应)和/或呼气肌招募(神经肌肉反应)。50名患者在比例辅助模式下进行呼吸，使我们能够无创地推断这些反应。以随机的间隔，通过短暂延迟呼气瓣的打开(闭塞)来延迟单次呼吸的呼气(T-OCC=0.78+/-0.34秒)。时间反应是从10分的变化中评估出来的。神经肌肉反应是通过在相似的呼气流量持续时间(DeltaV(等时间))内解除阻塞后呼气容量与非阻塞呼吸中呼气容量之间的差值来评估的。没有证据表明有急性神经肌肉反应；DeltaV(等时)平均为0.005+/-0.023 L(NS)。50名患者中有45名患者显著延长了10岁。然而，定时响应仅抵消了到期延迟的36%+/-20%。由于缺乏神经肌肉反应和较弱的时间反应，大多数患者在闭塞后呼吸中的差值增加(差值差值=0.10+/-0.08 L，p=2e-10)。我们得出结论，呼吸机依赖患者对呼气值延迟开放的急性代偿性反应较弱。因此，这种不同步性往往会加剧脱氢症。
In conventional mechanical ventilation, the inflation cycle often extends into neural expiration (TEN), potentially exacerbating dynamic hyperinflation (DH). We wished to determine the extent to which patients defend against DH when this happens. Such defense may include prolongation of TEN (timing response) and/or expiratory muscle recruitment (neuromuscular response). Fifty patients were ventilated in the Proportional Assist mode, allowing us to infer these responses noninvasively. At random intervals, exhalation of single breaths was delayed by briefly delaying the opening of exhalation valve (occlusion) (T-occ = 0.78 +/- 0.34 seconds). Timing response was assessed from the change in TEN. Neuromuscular response was assessed from the difference between volume exhaled after release of occlusion and volume exhaled in unoccluded breaths over a similar expiratory flow duration (DeltaV(iso-time)). There was no evidence of an acute neuromuscular response; DeltaV(iso-time) averaged 0.005 +/- 0.023 L (NS). Forty-five of 50 patients significantly lengthened TEN. However, the timing response offset only 36 +/- 20% of the delay in expiration. Because of absent neuromuscular responses and weak timing responses, DH increased in most patients in postocclusion breaths (DeltaDH = 0.10 +/- 0.08 L, p = 2E - 10). We conclude that acute compensatory responses to delays in opening of exhalation value are weak in ventilator-dependent patients. As a result, such nonsynchrony tends to exacerbate DH.