Engineering Approach to the Ventilatory Pump

呼吸泵的工程方法

基本信息

批准号：
7256228
负责人：
Aladin M Boriek
金额：
$ 32.11万
依托单位：
BAYLOR COLLEGE OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-08-01 至 2009-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7256228
关键词：
Breathing Canis familiaris Cause of Death Chest wall structure Chronic Chronic Obstructive Airway Disease Clinical Complement Condition Data Disease Electron Beam Tomography Engineering Evaluation Failure Fluoroscopy Frequencies Goals Health Human Individual Knowledge Lung Lung diseases Lung volume reduction surgery Measures Mechanics Mediating Membrane Modeling Morbidity - disease rate Motion Muscle Muscle Contraction Muscle Fibers Muscle function Operative Surgical Procedures Patients Property Publishing Pulmonary Emphysema Pump Rate Relative (related person)Respiratory Diaphragm Respiratory Failure Scanning Shapes Slice Speed Staging Stress Structural Models Structure Techniques Testing Total Lung Capacity base cost expiration functional restoration human subject improved in vivo interest kinematics lung volume mathematical model membrane model mortality pressure productivity loss programs respiratory rib bone structure theories

项目摘要

DESCRIPTION (provided by applicant): Respiratory failure is a major cause of morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). However, the mechanical determinants of ventilatory pump function are still not well understood. Our goal is to use an engineering approach to investigate the mechanical factors that mediate pump failure in COPD. Hyperinflation of the lungs and extreme diaphragm shortening can distort the sheet of the diaphragm, cause loss of its membrane curvature, and reduce its muscle force. This will severely limit the function of the ventilatory pump. Our objective is to build a general model of diaphragm mechanics that can be utilized to evaluate the effect of lung volume reduction surgery on respiratory pump function in patients with severe emphysema. We will extend our knowledge of diaphragm and chest wall mechanics in dogs, and will begin to apply the same principles and approaches to the study of ventilatory mechanics in normal human subjects and patients with severe emphysema before and after lung volume reduction surgery (LVRS). Finally, we will develop a comprehensive theory of diaphragm mechanics that can eventually be used to predict diaphragm muscle function in both healthy and diseased states. We will achieve this objective with in vivo studies of diaphragm mechanics in dogs and humans complemented with mathematical modeling techniques. Our specific aims are: Specific Aim #1: To determine how hyperinflation of the lungs alters the pressure generating ability of the diaphragm during simultaneous sub-maximal and maximal activation of both hemi-diaphragms. Hypothesis 1: Extreme muscle contraction of both hemi-diaphragms at high frequencies of stimulation and at lower lung volumes causes flattening and distortion of the membrane of the diaphragm, and therefore its generating ability of pressure is severely compromised. Specific Aim #2: To develop a comprehensive mechanical model of the diaphragm. Hypothesis 3: A comprehensive mechanical model of the diaphragm that utilizes both structure and constitutive relationships of the diaphragm should provide sufficient quantitative information on the evaluation of the pressure generating ability of the ventilatory pump. Specific Aim #3: To evaluate diaphragm function in patients with end-stage emphysema before and after LVRS, and in normal humans. Hypothesis 2a: In normal individuals, muscle fibers are oriented along the direction of maximum principal curvature, Hypothesis 2b: In severe emphysema patients, the diaphragm is comparatively flattened, and after LVRS, there is a gain in diaphragm muscle fiber curvature. Therefore, membrane tension is transmitted into trans-diaphragmatic pressure more effectively than before the surgery. Once we obtained the distribution of principal curvatures we will use our model of diaphragm mechanics developed in Aim 2 to predict diaphragm function in normal individuals and patients with severe emphysema before and after LVRS. The completion of these aims will significantly enhance our fundamental understanding of the ventilatory pump function in health and disease.

描述（由申请人提供）：呼吸衰竭是慢性阻塞性肺疾病（COPD）患者发病率和死亡率的主要原因。但是，通气泵功能的机械决定因素仍未得到充分了解。我们的目标是使用工程方法研究介导COPD中泵衰竭的机械因素。肺的过度充气和极端的隔膜缩短会使隔膜的薄片扭曲，导致其膜曲率损失，并减少其肌肉力。这将严重限制通风泵的功能。我们的目标是建立一个通用的隔膜力学模型，该模型可用于评估严重肺气肿患者肺部体积减少手术对呼吸泵功能的影响。我们将扩展对狗的隔膜和胸壁力学的了解，并将开始在正常人类受试者和患有严重肺气肿的患者中对通气力学的研究应用相同的原理和方法，并在肺部体积减少手术（LVRS）之前和之后。最后，我们将开发一种隔膜力学的综合理论，该理论最终可用于预测健康和患病状态的隔膜肌肉功能。我们将通过对狗和人类的隔膜力学的体内研究来实现这一目标，并辅以数学建模技术。我们的具体目的是：特定目标＃1：确定肺部过度充气如何改变同时下半二脑片的同时亚最大激活和最大激活期间膜片产生的压力产生能力。假设1：在刺激的高频和下肺体积下，两种小尖端的极端肌肉收缩会导致膜片的膜的变平和变形，因此其压力的产生能力严重损害。特定目的＃2：开发隔膜的综合机械模型。假设3：使用隔膜的结构和组成关系的膜片的综合机械模型应提供有关评估通气泵的压力产生能力的足够的定量信息。特定目的＃3：评估LVR前后末期肺气肿的患者以及正常人类的隔膜功能。假设2a：在正常个体中，肌肉纤维沿最大主曲率的方向定向，假设2b：在严重的肺气肿患者中，隔膜相对扁平，在LVR之后，diaphragm肌肉纤维纤维曲率会增加。因此，与手术前相比，膜张力更有效地传播到跨diaphragmatragic压力中。一旦获得了主曲线的分布，我们将使用在AIM 2中开发的隔膜力学模型来预测正常个体和LVR之前和之后患有严重肺气肿的患者的隔膜功能。这些目标的完成将显着增强我们对健康和疾病中通气泵功能的基本理解。