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气流阻力在成人呼吸窘迫综合征患者中的作用。

The role of airflow resistance in patients with the adult respiratory distress syndrome.

作者信息

Wright P E, Bernard G R

机构信息

Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232.

出版信息

Am Rev Respir Dis. 1989 May;139(5):1169-74. doi: 10.1164/ajrccm/139.5.1169.

Abstract

Although reduced lung compliance is a hallmark of the adult respiratory distress syndrome (ARDS), the role of increased airflow resistance in this disorder has not been well studied. Because animal models of ARDS show marked increases in airflow resistance and because mediators known to participate in lung parenchymal injury have also been implicated in models of increased airway reactivity, we hypothesized that increased airflow resistance is a major contributor to altered lung mechanics in human ARDS. We studied 10 mechanically ventilated patients with ARDS (criteria: PaO2 less than or equal to 70 mm Hg breathing FIO2 greater than or equal to 0.4; bilateral pulmonary roentgenographic infiltrates; Ppaw less than or equal to 18 mm Hg) measuring dynamic (Cdyn) and static (Cstat) compliance, airflow resistance across the lungs (RL), shunt fraction (QS/QT breathing FIO2 = 1.0), minute ventilation (VE), (a/A)PO2, dead space to tidal volume ratio (VD/VT), airflow (pneumotachograph), transpulmonary pressure (intratracheal pressure minus esophageal pressure) and volume (integrated from flow) at 50 L/min peak flow rate. Airflow resistance was uniformly elevated and averaged six times normal (5.32 +/- 0.92 cm H2O/L/s versus 0.88 +/- 0.08) (p less than 0.05). Cdyn correlated directly with (a/A)PO2. RL correlated with peak pressure, but did not correlate with VE, shunt, (a/A)PO2, or VD/VT. We conclude that increased pulmonary airflow resistance contributes significantly to the altered lung mechanics in ARDS. These data are consistent with studies of animal models of ARDS and long-term survivors of ARDS and may be secondary to tissue factors, airway hyperreactivity, or airway inflammation.

摘要

尽管肺顺应性降低是成人呼吸窘迫综合征(ARDS)的一个标志,但气流阻力增加在该病症中的作用尚未得到充分研究。由于ARDS动物模型显示气流阻力显著增加,并且已知参与肺实质损伤的介质也与气道反应性增加的模型有关,我们推测气流阻力增加是人类ARDS肺力学改变的主要原因。我们研究了10例机械通气的ARDS患者(标准:吸入氧分数(FIO2)≥0.4时动脉血氧分压(PaO2)≤70 mmHg;双侧肺部X线浸润;气道平台压(Ppaw)≤18 mmHg),测量了动态(Cdyn)和静态(Cstat)顺应性、肺的气流阻力(RL)、分流分数(呼吸FIO2 = 1.0时的QS/QT)、分钟通气量(VE)、(a/A)PO2、死腔与潮气量之比(VD/VT)、气流(呼吸流速仪)、跨肺压(气管内压减去食管压)以及在50 L/min峰值流速时的容积(由流量积分得出)。气流阻力均显著升高,平均为正常的6倍(5.32±0.92 cm H2O/L/s对比0.88±0.08)(p<0.05)。Cdyn与(a/A)PO2直接相关。RL与峰值压力相关,但与VE、分流、(a/A)PO2或VD/VT无关。我们得出结论,肺气流阻力增加对ARDS中肺力学的改变有显著影响。这些数据与ARDS动物模型及ARDS长期存活者的研究一致,可能继发于组织因素、气道高反应性或气道炎症。

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