Abstract:
Acute respiratory distress syndrome (ARDS) alters the dynamics of lung inflation during mechanical ventilation. Repetitive alveolar collapse and expansion (RACE) predisposes the lung to ventilator-induced lung injury (VILI). Two broad approaches are currently used to minimize VILI: (1) low tidal volume (LVT) with low-moderate positive end-expiratory pressure (PEEP); and (2) open lung approach (OLA). The LVT approach attempts to protect already open lung tissue from overdistension, while simultaneously resting collapsed tissue by excluding it from the cycle of mechanical ventilation. By contrast, the OLA attempts to reinflate potentially recruitable lung, usually over a period of seconds to minutes using higher PEEP used to prevent progressive loss of end-expiratory lung volume (EELV) and RACE. However, even with these protective strategies, clinical studies have shown that ARDS-related mortality remains unacceptably high with a scarcity of effective interventions over the last two decades. One of the main limitations these varied interventions demonstrate to benefit is the observed clinical and pathologic heterogeneity in ARDS. We have developed an alternative ventilation strategy known as the Time Controlled Adaptive Ventilation (TCAV) method of applying the Airway Pressure Release Ventilation (APRV) mode, which takes advantage of the heterogeneous time- and pressure-dependent collapse and reopening of lung units. The TCAV method is a closed-loop system where the expiratory duration personalizes VT and EELV. Personalization of TCAV is informed and tuned with changes in respiratory system compliance (CRS) measured by the slope of the expiratory flow curve during passive exhalation. Two potentially beneficial features of TCAV are: (i) the expiratory duration is personalized to a given patient\'s lung physiology, which promotes alveolar stabilization by halting the progressive collapse of alveoli, thereby minimizing the time for the reopened lung to collapse again in the next expiration, and (ii) an extended inspiratory phase at a fixed inflation pressure after alveolar stabilization gradually reopens a small amount of tissue with each breath. Subsequently, densely collapsed regions are slowly ratcheted open over a period of hours, or even days. Thus, TCAV has the potential to minimize VILI, reducing ARDS-related morbidity and mortality.
摘要:
急性呼吸窘迫综合征(ARDS)改变了机械通气期间肺部充气的动力学。反复肺泡塌陷和扩张(RACE)使肺容易发生呼吸机诱导的肺损伤(VILI)。目前使用两种广泛的方法来最小化VILI:(1)低潮气量(LVT)和低中度呼气末正压(PEEP);(2)开放肺方法(OLA)。LVT方法试图保护已经开放的肺组织免受过度扩张,同时通过将塌陷的组织排除在机械通气周期之外,使其静止。相比之下,OLA试图重新膨胀潜在的可招募的肺,通常在数秒至数分钟的时间内,使用较高的PEEP来防止呼气末肺容积(EELV)和RACE的进行性损失。然而,即使有了这些保护策略,临床研究表明,在过去20年中,ARDS相关死亡率仍然高得令人无法接受,缺乏有效的干预措施.这些不同的干预措施证明受益的主要限制之一是观察到的ARDS的临床和病理异质性。我们开发了一种替代通气策略,称为时间控制自适应通气(TCAV)方法,用于应用气道压力释放通气(APRV)模式,它利用了不同的时间和压力依赖性塌陷和肺单位重新开放。TCAV方法是闭环系统,其中呼气持续时间个性化VT和EELV。通过被动呼气期间呼气流量曲线的斜率测量的呼吸系统顺应性(CRS)的变化来告知和调整TCAV的个性化。TCAV的两个潜在的有益特征是:(i)呼气持续时间针对给定患者的肺生理而个性化,通过阻止肺泡的进行性塌陷来促进肺泡的稳定,从而最大限度地减少重新开放的肺在下一次呼气中再次塌陷的时间,和(ii)在肺泡稳定后,在固定的充气压力下延长的吸气阶段随着每次呼吸逐渐重新打开少量组织。随后,密集塌陷的区域在几个小时内缓慢地逐渐张开,甚至几天。因此,TCAV有可能最小化VILI,降低ARDS相关发病率和死亡率。