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利用肺气体交换评估肺部疾病中的分流和无效腔:理论方法与实践基础

Using pulmonary gas exchange to estimate shunt and deadspace in lung disease: theoretical approach and practical basis.

作者信息

Wagner Peter D, Malhotra Atul, Prisk G Kim

机构信息

Division of Pulmonary, Critical Care, Sleep Medicine and Physiology, University of California, San Diego, California.

出版信息

J Appl Physiol (1985). 2022 Apr 1;132(4):1104-1113. doi: 10.1152/japplphysiol.00621.2021. Epub 2022 Mar 24.

Abstract

The common pulmonary consequence of SARS-CoV-2 infection is pneumonia, but vascular clot may also contribute to COVID pathogenesis. Imaging and hemodynamic approaches to identifying diffuse pulmonary vascular obstruction (PVO) in COVID (or acute lung injury generally) are problematic particularly when pneumonia is widespread throughout the lung and hemodynamic consequences are buffered by pulmonary vascular recruitment and distention. Although stimulated by COVID-19, we propose a generally applicable bedside gas exchange approach to identifying PVO occurring alone or in combination with pneumonia, addressing both its theoretical and practical aspects. It is based on knowing that poorly (or non) ventilated regions, as occur in pneumonia, affect O more than CO, whereas poorly (or non) perfused regions, as seen in PVO, affect CO more than O. Exhaled O and CO concentrations at the mouth are measured over several ambient-air breaths, to determine mean alveolar Po and Pco. A single arterial blood sample is taken over several of these breaths for arterial Po and Pco. The resulting alveolar-arterial Po and Pco differences (AaPo, aAPco) are converted to corresponding physiological shunt and deadspace values using the Riley and Cournand 3-compartment model. For example, a 30% shunt (from pneumonia) with no alveolar deadspace produces an AaPO of almost 50 torr, but an aAPco of only 3 torr. In contrast, a 30% alveolar deadspace (from PVO) without shunt leads to an AaPO of only 12 torr, but an aAPco of 9 torr. This approach can identify and quantify physiological shunt and deadspace when present singly or in combination. Identifying pulmonary vascular obstruction in the presence of pneumonia (e.g., in COVID-19) is difficult. We present here conversion of bedside measurements of arterial and alveolar Po and Pco into values for shunt and deadspace-when both coexist-using Riley and Cournand's 3-compartment gas exchange model. Deadspace values higher than expected from shunt alone indicate high ventilation/perfusion ratio areas likely reflecting (micro)vascular obstruction.

摘要

新型冠状病毒2(SARS-CoV-2)感染常见的肺部后果是肺炎,但血管内血栓形成也可能在新冠病毒病发病机制中起作用。对于识别新冠病毒病(或一般的急性肺损伤)中弥漫性肺血管阻塞(PVO)的影像学和血流动力学方法存在问题,特别是当肺炎广泛累及全肺且血流动力学后果因肺血管募集和扩张而得到缓冲时。尽管受到新冠病毒病19(COVID-19)的启发,但我们提出了一种普遍适用的床边气体交换方法,用于识别单独发生或与肺炎合并发生的PVO,并阐述其理论和实践方面。其依据是了解到,如肺炎中出现的通气不良(或无通气)区域对氧(O)的影响大于对二氧化碳(CO)的影响,而如PVO中所见的灌注不良(或无灌注)区域对CO的影响大于对O的影响。在几次呼吸环境空气的过程中测量口腔呼出的O和CO浓度,以确定平均肺泡氧分压(Po)和二氧化碳分压(Pco)。在这些呼吸过程中的几次呼吸期间采集一份动脉血样本,用于检测动脉血氧分压(Po)和二氧化碳分压(Pco)。使用赖利(Riley)和库南德(Cournand)的三室模型,将由此产生的肺泡-动脉氧分压差(AaPo)和肺泡-动脉二氧化碳分压差(aAPco)转换为相应的生理分流和死腔值。例如,由肺炎导致的30%分流(无肺泡死腔)会产生近50托(torr)的AaPO,但aAPco仅为3托。相比之下,由PVO导致的30%肺泡死腔(无分流)会导致AaPO仅为12托,但aAPco为9托。这种方法可以单独或联合存在时识别和量化生理分流和死腔。在存在肺炎(如在COVID-19中)的情况下识别肺血管阻塞很困难。我们在此介绍如何使用赖利和库南德的三室气体交换模型,将动脉和肺泡Po和Pco的床边测量值转换为分流和死腔值(当两者共存时)。高于仅由分流预期值的死腔值表明可能反映(微)血管阻塞的高通气/灌注比区域。

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