Literature DB >> 30571287

Revisiting atelectasis in lung units with low ventilation/perfusion ratios.

James P Butler1,2,3, Atul Malhotra4, Stephen H Loring5.   

Abstract

Patients on high inspired O2 concentrations are at risk of atelectasis, a problem that has been quantitatively assessed using analysis of ratio of ventilation to perfusion (V̇a/Q̇) equations. This approach ignores the potential of the elastic properties of the lung to support gas exchange through "apneic" oxygenation in units with no tidal ventilation, and is based on an error in the conservation of mass equations. To fill this gap, we correct the error and compare the pressure drops associated with apneic gas exchange with the pressure differences that can be supported by lung recoil. We analyze a worst case scenario: a small test unit in the Weibel model A tree structure with zero tidal ventilation, 100% inspired O2, the rest of the lung being normally ventilated tidally. We first computed the gas flux to the (unventilated) test unit and estimated the associated pressure drops. We then computed the difference in local gas pressure relative to the surrounding lung that would cause the unit to collapse. We compared these two, and finally computed the degree of airway narrowing that would effect change from the stable (apneic gas exchange) regime to the unstable regime leading to collapse. We find that except under extreme conditions of loss of airway caliber exceeding roughly 90%, lung recoil is sufficient to maintain oxygenation through convective transport alone. We further argue that the fundamental V̇a/Q̇ equations are invalid in these circumstances, and that the issue of atelectasis in low V̇a/Q̇ will require modifications to account for this additional mode of gas exchange. NEW & NOTEWORTHY Breathing high concentrations of oxygen increases the likelihood of atelectasis because of oxygen absorption, which is thought to be inevitable in regions with relatively low ventilation/perfusion ratios. However, airspaces of the lung resist collapse because of the forces of interdependence, and can, with low or even zero active tidal ventilation, draw in an inspiratory flow of oxygen sufficient to replace the oxygen consumed, thus preventing collapse of airspaces served by all but the most narrowed airways.

Entities:  

Keywords:  absorption atelectasis; alveolar collapse; apneic gas exchange; lung

Mesh:

Substances:

Year:  2018        PMID: 30571287      PMCID: PMC6734073          DOI: 10.1152/japplphysiol.00354.2018

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


  9 in total

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Journal:  J Appl Physiol (1985)       Date:  2007-01-04

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Authors:  Lennart K A Lundblad; John Thompson-Figueroa; Gilman B Allen; Lisa Rinaldi; Ryan J Norton; Charles G Irvin; Jason H T Bates
Journal:  Am J Respir Crit Care Med       Date:  2007-01-25       Impact factor: 21.405

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Journal:  J Physiol       Date:  1974-10       Impact factor: 5.182

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Authors:  P D Wagner; H A Saltzman; J B West
Journal:  J Appl Physiol       Date:  1974-05       Impact factor: 3.531

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Journal:  J Appl Physiol (1985)       Date:  2003-12-05

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Journal:  Lancet       Date:  1995-06-03       Impact factor: 79.321

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Authors:  Niels D Nielsen; Benedict Kjaergaard; Jacob Koefoed-Nielsen; Christian O Steensen; Anders Larsson
Journal:  ASAIO J       Date:  2008 Jul-Aug       Impact factor: 2.872

  9 in total
  1 in total

Review 1.  The POOR Get POORer: A Hypothesis for the Pathogenesis of Ventilator-induced Lung Injury.

Authors:  Donald P Gaver; Gary F Nieman; Louis A Gatto; Maurizio Cereda; Nader M Habashi; Jason H T Bates
Journal:  Am J Respir Crit Care Med       Date:  2020-10-15       Impact factor: 21.405

  1 in total

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