ALTERNATIVE MODES OF MECHANICAL VENTILATION

我们研究机械通气替代模式的目标 是评估机械通气策略，其结果是 在向全身组织提供最佳氧气的同时 产生最小的不利影响。 在 (a) 正常肺部，(b) 肺水肿，以及 (c) 肺部急性气流阻塞 由支气管痉挛引起的，我们将采用和评估非常规 机械通气的模式。 提议的替代模式 通气包括高频振荡通气 (HFOV)、连续流通气 CFV) 和体外 膜氧合（ECMO），单独或与 某种形式的传统机械通气 (CMV)。 三 提出了几组实验 (i) 机制评估 CFV 和 HFOV 期间的气相传质。 这些 在麻醉的狗和猪身上进行的实验， 肺部水肿、支气管收缩或硬气道 模型，将确定气道内气体混合的机制 在不同的气道代和不同的平行路径之间，以及 将这些流动模式与气体传输效率联系起来。 这些 实验应确定总体调整策略 肺泡通气量及其区域间的均匀性。 (二) 在第二组实验中，我们将应用这些替代方案 急性低氧血症模型中的通气方式 呼吸衰竭或支气管收缩以维持气体 交流，尽量减少不良影响。 对此我们提出四点要求 问题： 1）在相同的平均肺泡压下，如何 通过水肿液的最佳重新分布最大化氧合 （肺部水肿）或通过调整通气模式 （支气管痉挛）？ 2) 平均胸内压和峰值胸内压可以是 单独或组合使用任何给定的通气模式减少， 这种减少是否会改善心输出量和全身氧气 送货？ 3）周期性肺泡压力波动如何 影响水肿的积累和清除？ 4）是否循环 高肺泡压力的应用进一步导致肺损伤，并且可以 机械通气的替代模式减少了这种额外的 短期或长期的损害？ （三）在解决这两个问题时 上面详述的广泛问题我们应该已经学会如何最好地 在低压肺水肿或肺水肿时应用机械通气 哮喘持续状态患者。 在第三组实验中， 我们的长期目标是在临床中评估这些方法 在急性病患者中进行的试验。 在此过程中，我们将评估 基本的气体交换和血流动力学异常表现在 急性低氧性呼吸衰竭，然后测试各种方法 以早期动物研究结果为指导的方法。

Our goal in studying Alternative Modes of Mechanical Ventilation is to evaluate strategies of mechanical ventilation which result in the optimal delivery of oxygen to systemic tissues while incurring the minimum adverse effects. In (a) normal lungs, (b) in pulmonary edema, and (c) in lungs with acute airflow obstruction caused by bronchospasm, we will employ and evaluate nonconventional modes of mechanical ventilation. The proposed alternative modes of ventilation include high frequency oscillatory ventilation (HFOV), continuous flow ventilation CFV), and extra-corporeal membrane oxygenation (ECMO), either alone or in combination with some form of conventional mechanical ventilation (CMV). Three groups of experiments are proposed (i) Evaluation of the mechanisms of gas phase mass transport during CFV and HFOV. These experiments, performed in anesthetized dogs and pigs with normal, edematous, or bronchoconstricted lungs, or in hardware airway models, will identify mechanisms of gas mixing within the airways at various airway generations and among various parallel paths, and will relate these flow patterns to gas transport efficiency. These experiments should identify strategies for adjusting overall alveolar ventilation as well as its uniformity among regions. (ii) In the second group of experiments, we will apply these alternative ventilation modalities in models of either acute hypoxemic respiratory failure or bronchoconstriction in order to maintain gas exchange and minimize adverse effect. In this regard we ask four questions: 1) At the same mean alveolar pressure, how can oxygenation be maximized by optimal redistribution of edema fluid (edematous lungs) or by adjustment of ventilatory mode (bronchospasm)? 2) Can mean and peak intrathoracic pressures be reduced with any given ventilatory mode alone or in combination, and does this reduction improve cardiac output and systemic oxygen delivery? 3) How does cyclic alveolar pressure fluctuation influence edema accumulation and clearance? 4) Does cyclic application of high alveolar pressures further lung injury, and can alternative modes of mechanical ventilation abate such additional damage in the short or long term? (iii) In addressing the two broad issues detailed above we should have learned how best to apply mechanical ventilation in low pressure pulmonary edema or in patients in status asthmaticus. In the third group of experiments, our long range goal is to evaluate these approaches in clinical trials in acutely ill patients. In doing so we will evaluate the fundamental gas exchange and hemodynamic abnormalities manifest in acute hypoxemic respiratory failure, then test various modalities in an approach directed by results of earlier animal studies.