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Hypoxaemia in COVID-19: many pieces to a complex puzzle

Mattia Busana, Luigi Camporota, Luciano Gattinoni
European Respiratory Review 2022 31: 220090; DOI: 10.1183/16000617.0090-2022
Mattia Busana
1Dept of Anesthesiology, University Medical Center Göttingen, Göttingen, Germany
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Luigi Camporota
2Dept of Adult Critical Care, Guy's and St Thomas’ NHS Foundation Trust, Health Centre for Human and Applied Physiological Sciences, London, UK
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Luciano Gattinoni
1Dept of Anesthesiology, University Medical Center Göttingen, Göttingen, Germany
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Abstract

Hypoxaemia from COVID-19 is likely a consequence of multiple causes https://bit.ly/3yXCJGZ

Reply to G. Harutyunyan and co-workers:

We read with interest the comments from G. Harutyunyan and co-workers on our coronavirus disease 2019 (COVID-19) pathophysiology review [1]. Without doubt we recognise that new data emerge every day and present knowledge must be reassessed in the face of new evidence. In this regard, the authors dive deep into the putative effects of pathological changes in the oxygen–haemoglobin dissociation curve (OHDC) as an additional cause of hypoxaemia in COVID-19. While interesting, this aspect is not completely new. Indeed, since the early days of COVID-19 some authors have speculated over the very same issue and conducted clinical and preclinical studies. Renoux et al. [2], for example, described no changes in the OHDC between seven COVID-19 patients and 14 comparable matched non-COVID-19 (control and septic) subjects. The findings of Daniel et al. [3] are along the same line: no change in the OHDC. Gille et al. [4] published a larger study on 100 COVID-19 patients and also found no deviation of the P50 (the partial pressure of oxygen at which haemoglobin is 50% saturated) in COVID-19. The largest study (3518 patients) by Vogel et al. [5] even found a left shift (increased affinity) of the OHDC with a P50 of 23.4 mmHg. Therefore, we are quite confident to say that the theory of haemoglobin with altered oxygen affinity is not significant enough to be responsible for the severity of hypoxaemia seen in patients with COVID-19.

Nevertheless, the pathophysiology of hypoxaemia in COVID-19 still has some secrets that are waiting to be revealed. We published a computational study showing that even an extreme degree of ventilation–perfusion mismatch is per se not sufficient to completely explain the hypoxaemia [6]. It is therefore likely that other mechanisms, or a combination of mechanisms, play a role. Interestingly, some recent evidence coming from autoptic studies show, among the other mechanisms, openings of intrapulmonary bronchopulmonary anastomosis [7, 8] that may well be the source of intrapulmonary shunt not associated with lung parenchymal consolidation. Moreover, the pathological enlargement of COVID-19 pulmonary vessels would cause an increase in oxygen equilibration time within the capillary, a phenomenon commonly called “diffusion limitation”. We believe that only through a rigorous measurement of ventilation–perfusion distribution, we may deepen our understanding of the problem and close the circle, explaining why in COVID-19 the degree of lung consolidation is often not proportional to hypoxaemia severity.

Footnotes

  • Provenance: Invited article, peer reviewed.

  • Conflict of interest: M. Busana has nothing to disclose.

  • Conflict of interest: L. Camporota has nothing to disclose.

  • Conflict of interest: L. Gattinoni reports receiving grants or contracts from DIMAR srl, outside the submitted work. Consulting fees received from SIDAM srl and General Electrics, outside the submitted work. Payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from General Electrics, outside the submitted work.

  • Received May 10, 2022.
  • Accepted May 17, 2022.
  • Copyright ©The authors 2022
http://creativecommons.org/licenses/by-nc/4.0/

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References

  1. ↵
    1. Gattinoni L,
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    COVID-19 pneumonia: pathophysiology and management. Eur Respir Rev 2021; 30: 210138. doi:10.1183/16000617.0138-2021
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Renoux C,
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    Impact of COVID-19 on red blood cell rheology. Br J Haematol 2021; 192: e108–e111. doi:10.1111/bjh.17306
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    1. Busana M,
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    The impact of ventilation - perfusion inequality in COVID-19: a computational model. J Appl Physiol (1985) 2021; 130: 865–876. doi:10.1152/japplphysiol.00871.2020
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    1. Galambos C,
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    . Intrapulmonary bronchopulmonary anastomoses in COVID-19 respiratory failure. Eur Respir J 2021; 58: 2004397. doi:10.1183/13993003.04397-2020
    OpenUrlAbstract/FREE Full Text
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    1. Ackermann M,
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    The bronchial circulation in COVID-19 pneumonia. Am J Respir Crit Care Med 2022; 205: 121–125. doi:10.1164/rccm.202103-0594IM
    OpenUrl
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Hypoxaemia in COVID-19: many pieces to a complex puzzle
Mattia Busana, Luigi Camporota, Luciano Gattinoni
European Respiratory Review Jun 2022, 31 (164) 220090; DOI: 10.1183/16000617.0090-2022

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Hypoxaemia in COVID-19: many pieces to a complex puzzle
Mattia Busana, Luigi Camporota, Luciano Gattinoni
European Respiratory Review Jun 2022, 31 (164) 220090; DOI: 10.1183/16000617.0090-2022
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