Search

Background: Despite the fervent scientific effort, a state-of-the art assessment of the different causes of hypoxemia (shunt, ventilation-perfusion mismatch, and diffusion limitation) in COVID-19 acute respiratory distress syndrome (ARDS) is currently lacking. In this study, the authors hypothesized a multifactorial genesis of hypoxemia and aimed to measure the relative contribution of each of the different mechanism and their relationship with the distribution of tissue and blood within the lung., Methods: In this cross-sectional study, the authors prospectively enrolled 10 patients with COVID-19 ARDS who had been intubated for less than 7 days. The multiple inert gas elimination technique (MIGET) and a dual-energy computed tomography (DECT) were performed and quantitatively analyzed for both tissue and blood volume. Variables related to the respiratory mechanics and invasive hemodynamics (PiCCO [Getinge, Sweden]) were also recorded., Results: The sample (51 ± 15 yr; Pao2/Fio2, 172 ± 86 mmHg) had a mortality of 50%. The MIGET showed a shunt of 25 ± 16% and a dead space of 53 ± 11%. Ventilation and perfusion were mismatched (LogSD, Q, 0.86 ± 0.33). Unexpectedly, evidence of diffusion limitation or postpulmonary shunting was also found. In the well aerated regions, the blood volume was in excess compared to the tissue, while the opposite happened in the atelectasis. Shunt was proportional to the blood volume of the atelectasis (R2 = 0.70, P = 0.003). V˙A/Q˙T mismatch was correlated with the blood volume of the poorly aerated tissue (R2 = 0.54, P = 0.016). The overperfusion coefficient was related to Pao2/Fio2 (R2 = 0.66, P = 0.002), excess tissue mass (R2 = 0.84, P < 0.001), and Etco2/Paco2 (R2 = 0.63, P = 0.004)., Conclusions: These data support the hypothesis of a highly multifactorial genesis of hypoxemia. Moreover, recent evidence from post-mortem studies (i.e., opening of intrapulmonary bronchopulmonary anastomosis) may explain the findings regarding the postpulmonary shunting. The hyperperfusion might be related to the disease severity., (Copyright © 2023 American Society of Anesthesiologists. All Rights Reserved.)

Background: International guidelines suggest using a higher (> 10 cm H 2 O) positive end-expiratory pressure (PEEP) in patients with moderate-to-severe ARDS due to COVID-19. However, even if oxygenation generally improves with a higher PEEP, compliance, and Paco 2 frequently do not, as if recruitment was small., Research Question: Is the potential for lung recruitment small in patients with early ARDS due to COVID-19?, Study Design and Methods: Forty patients with ARDS due to COVID-19 were studied in the supine position within 3 days of endotracheal intubation. They all underwent a PEEP trial, in which oxygenation, compliance, and Paco 2 were measured with 5, 10, and 15 cm H 2 O of PEEP, and all other ventilatory settings unchanged. Twenty underwent a whole-lung static CT scan at 5 and 45 cm H 2 O, and the other 20 at 5 and 15 cm H 2 O of airway pressure. Recruitment and hyperinflation were defined as a decrease in the volume of the non-aerated (density above -100 HU) and an increase in the volume of the over-aerated (density below -900 HU) lung compartments, respectively., Results: From 5 to 15 cm H 2 O, oxygenation improved in 36 (90%) patients but compliance only in 11 (28%) and Paco 2 only in 14 (35%). From 5 to 45 cm H 2 O, recruitment was 351 (161-462) mL and hyperinflation 465 (220-681) mL. From 5 to 15 cm H 2 O, recruitment was 168 (110-202) mL and hyperinflation 121 (63-270) mL. Hyperinflation variably developed in all patients and exceeded recruitment in more than half of them., Interpretation: Patients with early ARDS due to COVID-19, ventilated in the supine position, present with a large potential for lung recruitment. Even so, their compliance and Paco 2 do not generally improve with a higher PEEP, possibly because of hyperinflation., (Copyright © 2021 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Purpose: This study aimed at investigating the mechanisms underlying the oxygenation response to proning and recruitment maneuvers in coronavirus disease 2019 (COVID-19) pneumonia., Methods: Twenty-five patients with COVID-19 pneumonia, at variable times since admission (from 1 to 3 weeks), underwent computed tomography (CT) lung scans, gas-exchange and lung-mechanics measurement in supine and prone positions at 5 cmH 2 O and during recruiting maneuver (supine, 35 cmH 2 O). Within the non-aerated tissue, we differentiated the atelectatic and consolidated tissue (recruitable and non-recruitable at 35 cmH 2 O of airway pressure). Positive/negative response to proning/recruitment was defined as increase/decrease of PaO 2 /FiO 2 . Apparent perfusion ratio was computed as venous admixture/non aerated tissue fraction., Results: The average values of venous admixture and PaO 2 /FiO 2 ratio were similar in supine-5 and prone-5. However, the PaO 2 /FiO 2 changes (increasing in 65% of the patients and decreasing in 35%, from supine to prone) correlated with the balance between resolution of dorsal atelectasis and formation of ventral atelectasis (p = 0.002). Dorsal consolidated tissue determined this balance, being inversely related with dorsal recruitment (p = 0.012). From supine-5 to supine-35, the apparent perfusion ratio increased from 1.38 ± 0.71 to 2.15 ± 1.15 (p = 0.004) while PaO 2 /FiO 2 ratio increased in 52% and decreased in 48% of patients. Non-responders had consolidated tissue fraction of 0.27 ± 0.1 vs. 0.18 ± 0.1 in the responding cohort (p = 0.04). Consolidated tissue, PaCO 2 and respiratory system elastance were higher in patients assessed late (all p < 0.05), suggesting, all together, "fibrotic-like" changes of the lung over time., Conclusion: The amount of consolidated tissue was higher in patients assessed during the third week and determined the oxygenation responses following pronation and recruitment maneuvers., (© 2021. The Author(s).)

COVID-19 infection may lead to acute respiratory distress syndrome (CARDS) where severe gas exchange derangements may be associated, at least in the early stages, only with minor pulmonary infiltrates. This may suggest that the shunt associated to the gasless lung parenchyma is not sufficient to explain CARDS hypoxemia. We designed an algorithm (Vent ri Q lar ), based on the same conceptual grounds described by J.B. West in 1969. We set 498 ventilation-perfusion (V A /Q) compartments and, after calculating their blood composition (PO 2 , PCO 2 , and pH), we randomly chose 10 6 combinations of five parameters controlling a bimodal distribution of blood flow. The solutions were accepted if the predicted PaO 2 and PaCO 2 were within 10% of the patient's values. We assumed that the shunt fraction equaled the fraction of non-aerated lung tissue at the CT quantitative analysis. Five critically-ill patients later deceased were studied. The PaO 2 /FiO 2 was 91.1 ± 18.6 mmHg and PaCO 2 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 V A /Q (Q mean  = 0.06 ± 0.02) and a smaller fraction in regions with moderately high V A /Q. Overall LogSD, Q was 1.66 ± 0.14, suggestive of high V A /Q inequality. Our data suggest that shunt alone cannot completely account for the observed hypoxemia and a significant V A /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. NEW & NOTEWORTHY Hypothesizing that the non-aerated lung fraction as evaluated by the quantitative analysis of the lung computed tomography (CT) equals shunt (V A /Q = 0), we used a computational approach to estimate the magnitude of the ventilation-perfusion inequality in severe COVID-19. The results show that a severe hyperperfusion of poorly ventilated lung region is likely the cause of the observed hypoxemia. The extensive microthrombosis or abnormal vasodilation of the pulmonary circulation may represent the pathophysiological mechanism of such V A /Q distribution.

Purpose: To investigate whether COVID-19-ARDS differs from all-cause ARDS., Methods: Thirty-two consecutive, mechanically ventilated COVID-19-ARDS patients were compared to two historical ARDS sub-populations 1:1 matched for PaO 2 /FiO 2 or for compliance of the respiratory system. Gas exchange, hemodynamics and respiratory mechanics were recorded at 5 and 15 cmH 2 O PEEP. CT scan variables were measured at 5 cmH 2 O PEEP., Results: Anthropometric characteristics were similar in COVID-19-ARDS, PaO 2 /FiO 2 -matched-ARDS and Compliance-matched-ARDS. The PaO 2 /FiO 2 -matched-ARDS and COVID-19-ARDS populations (both with PaO 2 /FiO 2 106 ± 59 mmHg) had different respiratory system compliances (Crs) (39 ± 11 vs 49.9 ± 15.4 ml/cmH 2 O, p = 0.03). The Compliance-matched-ARDS and COVID-19-ARDS had similar Crs (50.1 ± 15.7 and 49.9 ± 15.4 ml/cmH 2 O, respectively) but significantly lower PaO 2 /FiO 2 for the same Crs (160 ± 62 vs 106.5 ± 59.6 mmHg, p < 0.001). The three populations had similar lung weights but COVID-19-ARDS had significantly higher lung gas volume (PaO 2 /FiO 2 -matched-ARDS 930 ± 644 ml, COVID-19-ARDS 1670 ± 791 ml and Compliance-matched-ARDS 1301 ± 627 ml, p < 0.05). The venous admixture was significantly related to the non-aerated tissue in PaO 2 /FiO 2 -matched-ARDS and Compliance-matched-ARDS (p < 0.001) but unrelated in COVID-19-ARDS (p = 0.75), suggesting that hypoxemia was not only due to the extent of non-aerated tissue. Increasing PEEP from 5 to 15 cmH 2 O improved oxygenation in all groups. However, while lung mechanics and dead space improved in PaO 2 /FiO 2 -matched-ARDS, suggesting recruitment as primary mechanism, they remained unmodified or worsened in COVID-19-ARDS and Compliance-matched-ARDS, suggesting lower recruitment potential and/or blood flow redistribution., Conclusions: COVID-19-ARDS is a subset of ARDS characterized overall by higher compliance and lung gas volume for a given PaO 2 /FiO 2 , at least when considered within the timeframe of our study.

The article offers information on the coronavirus disease (COVID-19) pneumonia that are defined as acute respiratory distress syndrome (ARDS) learn about its respiratory treatment. Topics include examines that the gas and ventilation side are relatively preserved and the hypoxemia must primarily derive from the perfusion side.

Pulmonary parenchymal and vascular damage are frequently reported in COVID-19 patients and can be assessed with unenhanced chest computed tomography (CT), widely used as a triaging exam. Integrating clinical data, chest CT features, and CT-derived vascular metrics, we aimed to build a predictive model of in-hospital mortality using univariate analysis (Mann–Whitney U test) and machine learning models (support vectors machines (SVM) and multilayer perceptrons (MLP)). Patients with RT-PCR-confirmed SARS-CoV-2 infection and unenhanced chest CT performed on emergency department admission were included after retrieving their outcome (discharge or death), with an 85/15% training/test dataset split. Out of 897 patients, the 229 (26%) patients who died during hospitalization had higher median pulmonary artery diameter (29.0 mm) than patients who survived (27.0 mm, p < 0.001) and higher median ascending aortic diameter (36.6 mm versus 34.0 mm, p < 0.001). SVM and MLP best models considered the same ten input features, yielding a 0.747 (precision 0.522, recall 0.800) and 0.844 (precision 0.680, recall 0.567) area under the curve, respectively. In this model integrating clinical and radiological data, pulmonary artery diameter was the third most important predictor after age and parenchymal involvement extent, contributing to reliable in-hospital mortality prediction, highlighting the value of vascular metrics in improving patient stratification. [ABSTRACT FROM AUTHOR]

The article focuses on a study regarding coronavirus disease (COVID-19) which does not lead to a typical acute respiratory distress syndrome.