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The impact of ventilation - perfusion inequality in COVID-19: a computational model
Journal of Applied Physiology ( IF 3.3 ) Pub Date : 2021-01-13 , DOI: 10.1152/japplphysiol.00871.2020
Mattia Busana 1 , Lorenzo Giosa 2 , Massimo Cressoni 3 , Alessio Gasperetti 4 , Luca Di Girolamo 5 , Alessandra Martinelli 6 , Aurelio Sonzogni 7 , Luca Lorini 6 , Maria Michela Palumbo 1 , Federica Romitti 1 , Simone Gattarello 1 , Irene Steinberg 1 , Peter Herrmann 1 , Konrad Meissner 1 , Michael Quintel 1 , Luciano Gattinoni 1
Affiliation  

COVID-19 infection may lead to an Acute Respiratory Distress Syndrome where severe gas exchange derangements may be associated, at least in the early stages, only with minor pulmonary infiltrates. This suggests that the shunt associated to the gasless lung parenchyma is not sufficient to explain CARDS hypoxemia. We designed an algorithm (VentriQlar), based on the same conceptual grounds described by J.B West in 1969. We set 499 ventilation-perfusion (VA/Q) compartments and, after calculating their blood composition (PO2, PCO2 and pH), we randomly chose 106 combinations of five parameters controlling a bimodal distribution of blood flow. The solutions were accepted if the predicted PaO2 and PaCO2 were within 10% of the patient's values. We assumed that shunt fraction equaled the fraction of non-aerated lung tissue at the CT quantitative analysis. Five critically-ill patients later deceased were studied. The PaO2/FiO2 was 91.1±18.6 mmHg and PaCO2 69.0±16.1 mmHg. Cardiac output was 9.58±0.99 l/min. The fraction of non-aerated tissue was 0.33±0.06. The model showed that a large fraction of the blood flow was likely distributed in regions with very low VA/Q (Qmean=0.06±0.02) and a smaller fraction in regions with moderately high VA/Q. Overall LogSD, Q was 1.66 ± 0.14, suggestive of high VA/Q inequality. Data suggest that shunt alone cannot completely account for the observed hypoxemia and a significant VA/Q inequality must be present in COVID-19. The high cardiac output and the extensive microthrombosis later found in the autopsy further support the hypothesis of a pathological perfusion of non/poorly ventilated lung tissue.

中文翻译:

COVID-19 中通气-灌注不平等的影响:计算模型

COVID-19 感染可能导致急性呼吸窘迫综合征,其中可能与严重的气体交换紊乱有关,至少在早期阶段,只有轻微的肺部浸润。这表明与无气肺实质相关的分流不足以解释 CARDS 低氧血症。我们设计了一种算法 (Vent ri Q lar ),基于 JB West 在 1969 年描述的相同概念基础。我们设置了 499 个通气-灌注 (V A / Q) 隔室,并在计算它们的血液成分 (PO 2,PCO 2和 pH 值),我们随机选择了 10 6控制血流双峰分布的五个参数的组合。如果预测的 PaO 2和 PaCO 2在患者值的 10% 以内,则接受这些解决方案。我们假设分流分数等于 CT 定量分析中未充气肺组织的分数。研究了后来死亡的五名危重患者。PaO 2 /FiO 2为91.1±18.6 mmHg,PaCO 2 为69.0±16.1 mmHg。心输出量为 9.58±0.99 l/min。未充气组织的分数为0.33±0.06。该模型表明,大部分血流可能分布在 V A /Q(Q均值)非常低的区域=0.06±0.02) 并且在具有中等高 V A /Q 的区域中的比例较小。总体 LogSD,Q 为 1.66 ± 0.14,表明高 VA/Q 不平等。数据表明,单独的分流不能完全解释观察到的低氧血症,并且COVID-19 中必须存在显着的 V A / Q 不平等。后来在尸检中发现的高心输出量和广泛的微血栓进一步支持了非/通气不良肺组织病理性灌注的假设。
更新日期:2021-01-14
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