Department of Emergency and Critical Care Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
BMC Anesthesiol. 2013 Dec 5;13(1):47. doi: 10.1186/1471-2253-13-47.
Although endotracheal suctioning induces alveolar derecruitment during mechanical ventilation, it is not clear whether repeated endotracheal suctioning exacerbates lung injuries. The present study aimed to determine whether repeated open endotracheal suctioning (OS) exacerbates lung injury compared to closed endotracheal suctioning (CS) during mechanical ventilation in an animal model of acute respiratory distress syndrome (ARDS).
Briefly, thirty six Japanese white rabbits were initially ventilated in pressure-controlled mode with a constant tidal volume (6 mL/kg). Then, lung injury was induced by repeated saline lavage. The rabbits were divided into four groups, namely: a) OS; b) CS; c) control with ARDS only; d) and healthy control (HC) without ARDS. Animals in all the groups were then ventilated with positive end expiratory pressure (PEEP) at 10 cm H2O. CS was performed using 6 French-closed suctioning catheters connected to endotracheal tube under the following conditions: a) a suctioning time and pressure of 10 sec and 140 mm Hg, respectively; and b) a suction depth of 2 cm (length of adapter) plus tracheal tube. OS was performed using the same conditions described for CS, except the ventilator was disconnected from the animals. Each endotracheal suctioning was performed at an interval of 30 min.
PaO2/FIO2 (P/F) ratio for CS, control and HC groups remained at >400 for 6 hours, whereas that of the OS group progressively declined to 300 (p < 0.05), with each suctioning. However, no difference was observed either in lung injury score (histology) or in the expression pattern of inflammatory cytokines (tumor necrosis factor-α and interleukin-6) after 6 hours between the OS and CS groups in the circulatory as well as the pulmonary tissues.
Progressive arterial desaturation under conditions of repeated endotracheal suctioning is greater in OS than in CS time-dependently. However, OS does not exacerbate lung injury during mechanical ventilation when observed over a longer time span (6 hours) of repeated endotracheal suctioning, based on morphological and molecular analysis.
虽然气管内吸引在机械通气过程中会引起肺泡萎陷,但尚不清楚反复气管内吸引是否会加重肺损伤。本研究旨在确定在急性呼吸窘迫综合征(ARDS)动物模型中,与密闭式气管内吸引(CS)相比,反复开放式气管内吸引(OS)是否会加重机械通气期间的肺损伤。
简要地说,36 只日本白兔最初在压力控制模式下通气,潮气量恒定(6mL/kg)。然后,通过反复生理盐水灌洗诱导肺损伤。将兔子分为四组:a)OS;b)CS;c)仅 ARDS 的对照组;d)无 ARDS 的健康对照组(HC)。所有组的动物随后在呼气末正压(PEEP)为 10cmH2O 下通气。CS 使用 6 法国密闭式吸引导管在以下条件下连接到气管导管:a)吸引时间和压力分别为 10 秒和 140mmHg;b)吸引深度为 2cm(适配器长度)加气管导管。OS 采用与 CS 相同的条件进行,只是呼吸机与动物断开连接。每次气管内吸引间隔 30 分钟。
CS、对照组和 HC 组的 PaO2/FIO2(P/F)比值在 6 小时内保持在>400,而 OS 组的比值则逐渐下降到 300(p<0.05),每次吸引时均如此。然而,在 6 小时后,无论是在循环系统还是在肺组织中,OS 组和 CS 组的肺损伤评分(组织学)或炎症细胞因子(肿瘤坏死因子-α和白细胞介素-6)的表达模式均无差异。
在重复气管内吸引的情况下,OS 引起的进行性动脉血氧饱和度下降比 CS 更为明显,呈时间依赖性。然而,基于形态学和分子分析,在重复气管内吸引的较长时间(6 小时)内,OS 并没有加重机械通气期间的肺损伤。