Nieman Gary F, Kaczka David W, Andrews Penny L, Ghosh Auyon, Al-Khalisy Hassan, Camporota Luigi, Satalin Joshua, Herrmann Jacob, Habashi Nader M
Department of Surgery, Upstate Medical University, Syracuse, NY 13210, USA.
Departments of Anesthesia, Radiology and Biomedical Engineering, University of Iowa, Iowa City, IA 52242, USA.
J Clin Med. 2023 Jul 12;12(14):4633. doi: 10.3390/jcm12144633.
Acute respiratory distress syndrome (ARDS) is associated with a heterogeneous pattern of injury throughout the lung parenchyma that alters regional alveolar opening and collapse time constants. Such heterogeneity leads to atelectasis and repetitive alveolar collapse and expansion (RACE). The net effect is a progressive loss of lung volume with secondary ventilator-induced lung injury (VILI). Previous concepts of ARDS pathophysiology envisioned a two-compartment system: a small amount of normally aerated lung tissue in the non-dependent regions (termed "baby lung"); and a collapsed and edematous tissue in dependent regions. Based on such compartmentalization, two protective ventilation strategies have been developed: (1) a "protective lung approach" (PLA), designed to reduce overdistension in the remaining aerated compartment using a low tidal volume; and (2) an "open lung approach" (OLA), which first attempts to open the collapsed lung tissue over a short time frame (seconds or minutes) with an initial recruitment maneuver, and then stabilize newly recruited tissue using titrated positive end-expiratory pressure (PEEP). A more recent understanding of ARDS pathophysiology identifies regional alveolar instability and collapse (i.e., hidden micro-atelectasis) in both lung compartments as a primary VILI mechanism. Based on this understanding, we propose an alternative strategy to ventilating the injured lung, which we term a "stabilize lung approach" (SLA). The SLA is designed to immediately stabilize the lung and reduce RACE while gradually reopening collapsed tissue over hours or days. At the core of SLA is time-controlled adaptive ventilation (TCAV), a method to adjust the parameters of the airway pressure release ventilation (APRV) modality. Since the acutely injured lung at any given airway pressure requires more time for alveolar recruitment and less time for alveolar collapse, SLA adjusts inspiratory and expiratory durations and inflation pressure levels. The TCAV method SLA reverses the open first and stabilize second OLA method by: (i) immediately stabilizing lung tissue using a very brief exhalation time (≤0.5 s), so that alveoli simply do not have sufficient time to collapse. The exhalation duration is personalized and adaptive to individual respiratory mechanical properties (i.e., elastic recoil); and (ii) gradually recruiting collapsed lung tissue using an inflate and brake ratchet combined with an extended inspiratory duration (4-6 s) method. Translational animal studies, clinical statistical analysis, and case reports support the use of TCAV as an efficacious lung protective strategy.
急性呼吸窘迫综合征（ARDS）与整个肺实质的异质性损伤模式相关，这种损伤模式会改变局部肺泡的开放和塌陷时间常数。这种异质性会导致肺不张以及反复的肺泡塌陷和扩张（RACE）。其最终结果是肺容积逐渐减少，并继发呼吸机诱导的肺损伤（VILI）。以往关于ARDS病理生理学的概念设想为一个双室系统：非下垂部位有少量正常通气的肺组织（称为“婴儿肺”）；下垂部位则是塌陷和水肿的组织。基于这种分区，已开发出两种保护性通气策略：（1）“保护性肺方法”（PLA），旨在使用低潮气量减少剩余通气腔室的过度扩张；（2）“开放肺方法”（OLA），该方法首先尝试在短时间内（数秒或数分钟）通过初始复张操作使塌陷的肺组织复张，然后使用滴定式呼气末正压（PEEP）稳定新复张的组织。对ARDS病理生理学的最新认识将两个肺腔室中的局部肺泡不稳定和塌陷（即隐匿性微肺不张）确定为主要的VILI机制。基于这一认识，我们提出了一种用于通气损伤肺的替代策略，我们称之为“稳定肺方法”（SLA）。SLA旨在立即稳定肺并减少RACE，同时在数小时或数天内逐渐使塌陷的组织重新开放。SLA的核心是时间控制的适应性通气（TCAV），这是一种调整气道压力释放通气（APRV）模式参数的方法。由于在任何给定气道压力下，急性损伤的肺需要更多时间进行肺泡复张，而肺泡塌陷所需时间较少，SLA会调整吸气和呼气持续时间以及充气压力水平。SLA的TCAV方法通过以下方式颠倒了先开放后稳定的OLA方法：（i）使用非常短暂的呼气时间（≤0.5秒）立即稳定肺组织，以使肺泡根本没有足够的时间塌陷。呼气持续时间是个性化的，并适应个体呼吸力学特性（即弹性回缩）；（ii）使用充气和制动棘轮结合延长吸气持续时间（4 - 6秒）的方法逐渐使塌陷的肺组织复张。转化动物研究、临床统计分析和病例报告支持将TCAV用作一种有效的肺保护策略。
