正常人呼气相高分辨CT研究

目的探讨正常人呼气相HRCT扫描所见,分析其相关影像学表现。方法对28例正常人行吸气相加呼气相HRCT扫描,定量分析扫描结果。结果吸气相与呼气相HRCT比较,肺野CT值平均上升(224.84±97.98)Hu(70.14~544.05Hu);呼气相全肺野CT值上升幅度与其面积减少正相关,相关系数r=0.693,P<0.001。仰卧位时双肺承重区域CT值上升幅度大于非承重区域,P<0.001;俯卧位测试结果与之相同,P<0.001。呼气相CT值增加幅度随年龄的增加而降低。结论正常受试者呼气相肺野CT值较吸气相平均上升224.84Hu;正常人呼气相HRCT肺野CT值上升程度与肺野面积减少正相关;正常人呼气相HRCT承重区CT值上升幅度大于非承重区,与体位无关;正常人呼气相CT值增加幅度随年龄增加而减低。     

双相高分辨率CT对慢阻肺的定量诊断价值分析

目的：评价双相高分辨率CT（HRCT）对慢性阻塞性肺疾病（COPD）的定量诊断价值。方法：对87例COPD患者分别进行吸气相、呼气相HRCT扫描，分析其HRCT表现，统计双肺吸-呼气相的平均密度差值（VD）和面积缩小率（AD）以及呼气相空气潴留评分值与患者同期肺功能检测指标进行相关性分析。结果：81例患者呼气相HRCT上出现空气潴留征；超出了吸气相异常征象的范围，双肺VD和AD、空气潴留评分值与肺功能检测指标显著相关（P〈O．05）。结论：呼气相HRCT可以辅助吸气相HRCT评价COPD病变程度，空气潴留征能够定量分析并反映患者的肺功能状况。     

成人正常肺吸气相-呼气相HRCT表现

目的评价肺吸气相-呼气相HRCT的正常表现.方法健康成人46例,分别行吸气末及呼气末HRCT检查,分析气管形态、径线及面积的变化,肺衰减及肺面积的变化.结果吸气相时气管为圆形或椭圆形,呼气相时气管大多数(63%)为马蹄形;呼气相气管横断面积较吸气相平均减小(23±9)%,前后径及横径平均分别减小(22±8)%、(15±7)%,气管面积缩小的百分比与前后径及横径缩小的百分比成正相关(r=0.633,0.393,P<0.01).呼气相较吸气相肺衰减增加,以肺野后部及肺底水平增加为著(P<0.01);呼气相肺衰减梯度较吸气相明显,且以肺底为著(P<0.01);呼气相肺横断面积减小,平均减小(21±9)%;隆突水平肺衰减增加与肺面积减小呈正比(r=0.702, P<0.01).呼气相时28.3%(13/46)可见马赛克征.结论肺吸气相-呼气相HRCT的正常表现不同.呼气相HRCT的气管形态大多为马蹄形,气管面积减小,前后径减小为主;呼气相时肺横断面积减小与肺衰减值增加呈正相关性,肺前后部衰减梯度明显,且以肺底为著.     

肺部深吸气及深呼气相HRCT在小支气管扩张诊断中的价值

目的：评价HRCT在肺小支管扩张诊断中的价值。材料与方法：对48例临床怀疑为支气管扩张的患者分别进行常规螺旋CT扫描和深吸气及深呼气相HRCT扫描。将螺旋CT与HRCT扫描结果进行对照分析，找出HRCT在小支气管扩张诊断中的优势及深吸气与深呼气相HRCT的特点。结果：48例患者中，螺旋CT发现支气管扩张38例，深吸气HRCT发现支气管扩张43例。同时，深呼气相HRCT能清晰的显示病变肺叶的空气潴留征。结论：深吸气相HRCT扫描对诊断支气管扩张比常规CT有更大的优越性，对临床怀疑支气管扩张的患者，应首选HRCT检查。     

健康成人肺脏在动脉螺旋CT扫描中正常表现的定量研究

目的:研究正常人肺脏深呼、吸气末动态螺旋CT扫描的表现,初步确定其正常值范围。材料与方法:对55例健康成人进行呼、吸气末HRCT扫描及肺功能检查PFTs。以呼、吸气末肺野密度变化、象素指数PI值及面积变化率为CT评价指标。比较上述指标在左、右肺,上、中、下肺区及前、后肺区的变化规律,并比较全肺法和局部感兴趣区ROI法对肺野密度测量结果的相关性。结果:健康成人深呼、吸气末全肺平均CT值分别为-6815±386Hu和-8391±211HuP<001,其差值为1576±361Hu。呼、吸气末CT值左、右肺间无统计学差异P>01;上、中、下肺区吸气末平均CT值无差异P>005,呼气末CT值上肺区低于下肺区,呼、吸气末CT值差值下肺区最大,上肺区最小P<005。肺脏CT值分布呈前-后节段性差异,肺前部的呼、吸气末平均CT值及其差值变化均比肺后部低P<005,以呼气末更显著。深吸气末平均PI值为2962%12%～528%,深呼气末为065%0%～17%,两者有显著性差异P<0001。肺野面积变化率为384%,上肺区面积减少显著P<001。局部ROI法与全肺法测量的全肺平均CT值结果有显著相关性。结论:肺野密度、PI及面积变化率的测算是定量评估正常人肺脏动态CT表现及其功能很有价值的影像方法。ROI法较全肺法测量简便易行     

阻塞性肺气肿定量CT与肺功能检查相关性的实验研究

目的 通过实验研究探讨阻塞性肺气肿HRCT密度定量与肺功能检查间的相关性。方法 随机将45只大白鼠中的30只制成COPD模型，15只作为对照组。对实验动物做CT全肺扫描，测量两肺上、中和下三区的平均密度值。统计分析这些测量值与肺功能检查结果。结果 实验组动物的CT肺密度改变与PET、IP Slope的变化有着较密切的相关性，r值分别为0.82和0.87，P值均＜0.01。结论 阻塞性肺气肿HRCT密度定量能间接的反映阻塞性肺气肿的呼气阻力和呼吸肌力的变化。     

正常成人肺高分辨率CT的吸气相和呼气相的定量研究

目的　研究正常成人肺HRCT呼气相表现和对其进行定量分析。方法　分析 10 7例 2 0～ 70岁健康志愿者的肺呼气相HRCT表现 ,计算双肺吸呼气相密度差值 (VD)和面积缩小率 (AR)并对其影响因素进行统计学分析。结果　各年龄组内男女之间的VD和AR无显著性差异 ;年龄与左、右肺VD和AR之间存在显著相关 ;左、右肺VD和AR之间有显著性差异。结论　年龄为健康成人肺HRCT的吸呼气相密度差值和面积缩小率的主要影响因素。     

肺高分辨率CT的呼气相定量研究及其与肺功能的关系

目的：对患者呼气相HRCT上空气潴留征的范围进行定量分析，并分析其与肺功能试验（PFT）指标的关系。方法：55例肺弥漫性病变的患者进行吸气相、呼气相HRCT和肺功能试验检查，统计双肺吸－呼气相密度差值（VD）和面积缩小率（AD）、空气潴留评分值并与肺功能试验指标进行相关性分析。结果：空气潴留征象普遍存在；双肺VD和AD、空气潴留评分值与肺功能试验指标显著相关（P＜0．05）。结论：呼气相HRCT上的空气潴留征可以定量分析，能够反映患者的肺功能状况。     

呼气相肺CT扫描空气潴留的价值与临床意义

呼气相CT扫描作为肺功能成像的一种手段和吸气相CT扫描的补充,不仅提供了肺组织的病理解剖学信息,也提供了肺组织局部病理生理学信息.国内外许多学者利用呼气相扫描进行了一系列的研究,探讨呼气相扫描时肺部的形态、密度的变化与肺通气功能间的关系[1-4].空气潴留作为小气道病变的CT征象,与肺功能的改变有一定的相关性[2].本文就空气潴留程度与肺功能指标的相关性进行研究,并评价其临床意义.     

螺旋CT双相扫描在肺气肿诊断与功能评价中的价值探讨

目的：探讨螺旋CT双呼吸相扫描对肺气肿诊断与功能评价的价值。方法：50例健康志愿者和30例肺气肿患者行全肺双相扫描及局部感兴趣区HRCT薄层扫描,计算全肺、肺内各区双相肺容积减少百分比及CT临界值。结果：（1）50岁以上正常人双相肺容积减少百分比为45％－65％,重度肺气肿患者为20％－30％,中度患者为32％－48％;（2）肺气肿CT临界值为：深吸气相－953．30,深呼气相－914．62HU。结论：螺旋CT双相肺容积测定结合HRCT薄层扫描,对评估肺功能尤其是局部肺功能及诊断早期肺气肿有重大价值。     

电焊烟尘与矽尘所致肺部异常的早期HRCT表现的对比研究

目的比较电焊烟尘与矽尘所致肺部的早期HRCT表现,探讨其病理学意义。方法对456例焊尘及矽尘作业者进行肺部HRCT检查,男性443人,女性13人,年龄22-75岁,平均年龄44．0岁,工龄0．5-29年,平均工龄13．1年。采用GENX／i螺旋CT扫描仪,深吸气末HRCT采用层厚1-2mm,间隔10mm,轴面扫描,扫描速度1s／r,高分辨率重建,扫描范围自肺尖至横膈。分析HRCT的异常表现,观察肺窗窗宽为1200HU,窗位为－700HU,纵隔窗窗宽为400HU,窗位-30HU。结果456例粉尘作业者中346例可见不同程度异常。早期肺部异常主要表现为小叶内分支状线影增多（187,41．01％）,电焊工肺部表现较矽尘作业者更加显著：51例（11．18％）可见小叶间隔增厚,矽尘较焊尘更易出现小叶间隔增厚（χ^2=10．109,P=-0．003）;82例（17．98％）可见边缘清晰结节,焊尘结节分布相对较均匀,大小一致,小叶中心分布,密度相对较低,而矽尘结节密度较高,大小不均匀,可合并肺结构及血管束的扭曲和变形：47例（10．31％）表现为磨玻璃密度结节,位于小叶中心,其中42例见于焊尘作业者。29（6.36％）例肺内可见磨玻璃影,其中18例见于焊尘。72例（15．79％）可见不同程度肺气肿改变,矽尘作业者肺气肿明显多于电焊工（χ^2=24．206,P=-0．000）。结论不同粉尘的致纤维化作用的不同,HRCT有助于对粉尘的致纤维化进行早期评估。     

慢性阻塞性肺疾病呼吸双相高分辨CT肺定量指标与肺功能相关性

目的探讨64排螺旋CT高分辨CT肺定量指标与肺功能检查各项指标的相关性及呼吸双相肺CT扫描对肺气肿的诊断价值。方法78例慢性阻塞性肺疾病患者分为轻度组8例,中度组28例,重度组26例与极重度组16例,4组均行呼吸双相全肺高分辨率CT检查,检测深吸气末、深呼气末肺密度、呼吸双相肺密度差及肺容积,分析肺密度与肺容积和肺功能各指标的相关性。结果4组深吸气末与深呼气末肺密度比较差异均有统计学意义（P〈0．05）;4组第1秒用力呼气量（forced expiratory volume in one second, FEV1 ）、用力肺活量（forced vital capacity, FVC）及FEV1／FVC比值比较差异均有统计学意义（P〈0．05）;随疾病严重程度增加,深吸气末与深呼气末肺容积均相应增加,但4组间比较差异均无统计学意义（P〉O．05）;胸部重建后深吸气末及深呼气末肺容积与FVC、FEV2、FEV1／FVC有明显相关性（P〈0．01）;深呼气末肺容积与残气量占最大肺总量百分比预计值间有明显相关性（P〈0．05）;深吸气相肺密度与FEV。／FVC、残气量值有明显相关性（P〈O．05）。结论64排螺旋CT呼吸双相高分辨率肺定量指标与肺功能测定具有良好相关性,可用于评价肺气肿严重程度。     

Role of autoPEEP in the optimization of the respiratory pattern in patients with acute parenchymatous lung diseases

The paper presents the results of a study of the impact of autoPEEP (positive end-expiratory pressure) on gas exchange in the lungs, their biomechanical characteristics, the transport and consumption of oxygen by inverting the inspiration/expiration ratio under the volume-controlled mechanical ventilation of the lung (VCMVL) in patients with acute parenchymatous lung lesion, as well as how to choose the optimum inspiration/expiration ratio in VCMVL by analyzing the pattern of total PEEP (the sum of positioning and autoPEEP) in this group of patients.     

多平面重建对肺内孤立结节的评价

目的:探讨多层螺旋CT多平面重建技术(MPR)对肺内孤立性结节(SPN)的诊断价值。资料与方法:39例SPN行多层螺旋CT扫描、轴位HRCT扫描及薄层冠状位、矢状位MPR重建。图像分析分为2种方法,方法A为螺旋CT轴位图像结合轴位HRCT图像,方法B为螺旋CT轴位图像结合薄层冠状和矢状位多平面重建图像。判断方法A和方法B对SPN基本形态和基本征象的评价有无不同。结果:方法A和方法B对39例SPN基本形态和征象评价的差别无统计学意义。螺旋CT结合轴位HRCT的方法将2例炎症误诊为肺癌,螺旋CT结合MPR图像则作出正确诊断。与MPR图像比较分析后发现,轴位图像未能真实显示病灶的基本形态。结论:薄层MPR在显示SPN的基本征象方面同HRCT的作用相同、在评价SPN的基本形态方面优于单纯轴位CT。     

超声观察呼吸运动对脑静脉颅外回流的影响

目的 探讨不同体位条件下呼吸运动对脑静脉颅外回流的影响.方法 嘱40名健康志愿者分别取坐位和仰卧位,以超声观测颈内静脉和椎静脉在平静呼吸、深吸气末和深呼气末时的血流量变化.结果 卧位平静呼吸时,颈内静脉和椎静脉血流量分别占脑血流总量的66.94％和4.17％;深吸气末颈内静脉所占比例增至86.61％,椎静脉所占比例减至1.69％.坐位平静呼吸时,颈内静脉和椎静脉血流量分别占脑血流总量的18.08％和14.73％;深吸气末颈内静脉所占比例增至89.68％,椎静脉所占比例减至1.86％.在深呼气末,卧位和坐位时颈内静脉、椎静脉血流量与平静呼吸时的差异均无统计学意义.结论 卧位和坐位时,深吸气均使得脑静脉通过颈内静脉向颅外回流的比例显著增加.     

Altered alveolar mechanics in the acutely injured lung

OBJECTIVES: Alterations in alveolar mechanics (i.e., the dynamic change in alveolar size during tidal ventilation) are thought to play a critical role in acute lung injuries such as acute respiratory distress syndrome (ARDS). In this study, we describe and quantify the dynamic changes in alveolar mechanics of individual alveoli in a porcine ARDS model by direct visualization using in vivo microscopy. DESIGN: Prospective, observational, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Pigs were anesthetized and placed on mechanical ventilation, underwent a left thoracotomy, and were separated into the following two groups post hoc: a control group of instrumented animals with no lung injury (n = 5), and a lung injury group in which lung injury was induced by tracheal Tween instillation, causing surfactant deactivation (n = 5). Pulmonary and systemic hemodynamics, blood gases, lung pressures, subpleural blood flow (laser Doppler), and alveolar mechanics (in vivo microscopy) were measured in both groups. Alveolar size was measured at peak inspiration (I) and end expiration (E) on individual subpleural alveoli by image analysis. Histologic sections of lung tissue were taken at necropsy from the injury group. MEASUREMENTS AND MAIN RESULTS: In the acutely injured lung, three distinct alveolar inflation-deflation patterns were observed and classified: type I alveoli (n = 37) changed size minimally (I - EDelta = 367 +/- 88 microm2) during tidal ventilation; type II alveoli (n = 37) changed size dramatically (I - EDelta = 9326 +/- 1010 microm2) with tidal ventilation but did not totally collapse at end expiration; and type III alveoli (n = 12) demonstrated an even greater size change than did type II alveoli (I - EDelta = 15,418 +/- 1995 microm2), and were distinguished from type II in that they totally collapsed at end expiration (atelectasis) and reinflated during inspiration. We have termed the abnormal alveolar inflation pattern of type II and III alveoli "repetitive alveolar collapse and expansion" (RACE). RACE describes all alveoli that visibly change volume with ventilation, regardless of whether these alveoli collapse totally (type III) at end expiration. Thus, the term "collapse" in RACE refers to a visibly obvious collapse of the alveolus during expiration, whether this collapse is total or partial. In the normal lung, all alveoli measured exhibited type I mechanics. Alveoli were significantly larger at peak inspiration in type II (18,266 +/- 1317 microm2, n = 37) and III (15,418 +/- 1995 microm2, n = 12) alveoli as compared with type I (8214 +/- 655 microm2, n = 37). Tween caused a heterogenous lung injury with areas of normal alveolar mechanics adjacent to areas of abnormal alveolar mechanics. Subsequent histologic sections from normal areas exhibited no pathology, whereas lung tissue from areas with RACE mechanics demonstrated alveolar collapse, atelectasis, and leukocyte infiltration. CONCLUSION: Alveolar mechanics are altered in the acutely injured lung as demonstrated by the development of alveolar instability (RACE) and the increase in alveolar size at peak inspiration. Alveolar instability varied from alveolus to alveolus in the same microscopic field and included alveoli that changed area greatly with tidal ventilation but remained patent at end expiration and those that totally collapsed and reexpanded with each breath. Thus, alterations in alveolar mechanics in the acutely injured lung are complex, and attempts to assess what may be occurring at the alveolar level from analysis of inflection points on the whole-lung pressure/volume curve are likely to be erroneous. We speculate that the mechanism of ventilator-induced lung injury may involve altered alveolar mechanics, specifically RACE and alveolar overdistension.