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• W4301431657 abstract "ViewpointLast Word on Viewpoint: Revisiting the effects of the reciprocal function between alveolar ventilation and CO2 partial pressure (PACO2) on PACO2 homeostasis at rest and in exercisePhilippe HaouziPhilippe HaouziDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, Hershey, PennsylvaniaPublished Online:04 Oct 2022https://doi.org/10.1152/japplphysiol.00501.2022MoreSectionsPDF (147 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat to the editor: The kinetics of changes in alveolar PCO2 (PACO2) is affected by body CO2 stores and the circulatory status through the kinetics of the rate at which CO2 is exchanged in the lungs (volume of CO2 exchanged in the lungs per unit of time). This is what the alveolar equation is telling us.Indeed, PACO2 is not dictated by the ratio between the rate of CO2 production and alveolar ventilation (1) but is determined by the ratio between the rate at which CO2 is exchanged in the lungs and alveolar ventilation (2), buffered only by the volume of CO2 stored in the lungs, i.e., in the functional residual capacity (FRC). The confusion stems from the use of one and only one symbol to describe different physiological notions: it is indeed unclear why the symbol V̇co2 has been adopted by respiratory physiologists to describe: 1) the rate at which CO2 is produced in (by) the different tissues (the metabolic rate), 2) the rate at which CO2 is exchanged in the tissues and between the tissues and the blood, 3) the rate at which CO2 is exchanged in the lungs (between the blood and the alveolar regions), and 4) the rate of CO2 exchanged by the lungs (between the alveolar regions and the atmosphere: FECO2.V̇E). This distinction has important practical implications since these rates are only equal in steady-state conditions (3) but differ, for instance, during acute change in cardiac output, blood flow redistribution, or modifications in body CO2 stores (like at the onset of exercise or when transitioning to hyperventilation or hypoventilation or when a rapid change in venous return occurs to name a few). Such a dissociation can also result from multifarious acute medical conditions (from pulmonary embolism to hemorrhagic shock) and a complex transfer function (including time delay and time constant) between the metabolic rate and the rate of CO2 exchanged in the lungs (change in flow and CO2 buffer systems) must be considered when trying to understand the pathophysiology of periodic breathing for instance.Yet, regardless of the changes in body CO2 store and/or circulation, changes in PACO2 and their kinetics are strictly proportional to the rate at which CO2 is exchanged in the lungs, and inversely proportional to alveolar ventilation (modulated only by the volume of CO2 in FRC). Cardiac output and body CO2 store are not forgotten by the alveolar gas equation, they are already “encapsulated” or included in the rate at which CO2 is exchanged in the lungs—the product of cardiac output and the difference in mixed venous and arterial CO2 content. Any factor affecting the rate at which CO2 is exchanged in the lungs or its kinetics in any acute medical condition (sedation, reduction in pulmonary blood flow, and acute changes in mechanical ventilatory support) must certainly be characterized and understood when dealing with ICU patients, but their impact on alveolar and thus on arterial PCO2 only depends on the very simple and often counterintuitive alveolar gas equation. The use of the same symbol (V̇co2) to describe quite different rates of CO2 exchange in the body does not make easier the task of understanding some intriguing implications of the reciprocal relationship between alveolar PCO2 and alveolar ventilation (2).DISCLOSURESNo conflicts of interest, financial or otherwise, are declared by the author.AUTHOR CONTRIBUTIONSP.H. conceived and designed research; analyzed data; and drafted manuscript.REFERENCES1. Giosa L, Roveri G, Busana M. Commentary on Viewpoint: Revisiting the effects of the reciprocal function between alveolar ventilation and CO2 partial pressure (PaCO2) on PaCO2 homeostasis at rest and in exercise. J Appl Physiol (1985). doi:10.1152/japplphysiol.00468.2022. Link | Google Scholar2. Haouzi P. Revisiting the effects of the reciprocal function between alveolar ventilation and CO2 partial pressure (PaCO2) on PaCO2 homeostasis at rest and in exercise. J Appl Physiol (1985). doi:10.1152/japplphysiol.00058.2022. Link | Google Scholar3. Otis AB. Quantitative relationships in steady-state gas exchange. In: Handbook of Physiology. Respiration, edited by Fenn WO, Rahn H. Washington DC: American Physiological Society, 1964, vol. 1, sect. 3, p. 681–698.Google ScholarAUTHOR NOTESCorrespondence: P. Haouzi ([email protected].psu.edu). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Related ArticlesCommentary on Viewpoint: Revisiting the effects of the reciprocal function between alveolar ventilation and CO2 partial pressure (PACO2) on PACO2 homeostasis at rest and in exercise 04 Oct 2022Journal of Applied PhysiologyRevisiting the effects of the reciprocal function between alveolar ventilation and CO2 partial pressure (PACO2) on PACO2 homeostasis at rest and in exercise 04 Oct 2022Journal of Applied Physiology More from this issue > Volume 133Issue 4October 2022Pages 918-918 Crossmark Copyright & PermissionsCopyright © 2022 the American Physiological Society.https://doi.org/10.1152/japplphysiol.00501.2022PubMed36194685History Received 26 August 2022 Accepted 6 September 2022 Published online 4 October 2022 Published in print 1 October 2022 Metrics" @default.
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