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Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation

BACKGROUND: Early diagnosis of shock is a predetermining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO(2) difference (∆PCO(2)) over 0.8 kPa (6 mm Hg) is indicative of low blood flow states. Disturbances around the time of blood sampling could result in ina...

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Autores principales: Shastri, Lisha, Kjærgaard, Benedict, Rees, Stephen Edward, Thomsen, Lars Pilegaard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7978276/
https://www.ncbi.nlm.nih.gov/pubmed/33737311
http://dx.doi.org/10.1136/bmjresp-2021-000886
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author Shastri, Lisha
Kjærgaard, Benedict
Rees, Stephen Edward
Thomsen, Lars Pilegaard
author_facet Shastri, Lisha
Kjærgaard, Benedict
Rees, Stephen Edward
Thomsen, Lars Pilegaard
author_sort Shastri, Lisha
collection PubMed
description BACKGROUND: Early diagnosis of shock is a predetermining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO(2) difference (∆PCO(2)) over 0.8 kPa (6 mm Hg) is indicative of low blood flow states. Disturbances around the time of blood sampling could result in inaccurate calculations of ∆PCO(2), thereby misrepresenting the patient status. This study aimed to determine the influences of acute changes in ventilation on ∆PCO(2) and understand its clinical implications. METHODS: To investigate the isolated effects of changes in ventilation on ∆PCO(2), eight pigs were studied in a prospective observational cohort. Arterial and central venous catheters were inserted following anaesthetisation. Baseline ventilator settings were titrated to achieve an EtCO(2) of 5±0.5 kPa (V(T) = 8 mL/kg, Freq = 14 ± 2/min). Blood was sampled simultaneously from both catheters at baseline and 30, 60, 90, 120, 180 and 240 s after a change in ventilation. Pigs were subjected to both hyperventilation and hypoventilation, wherein the respiratory frequency was doubled or halved from baseline. ∆PCO(2) changes from baseline were analysed using repeated measures ANOVA with post-hoc analysis using Bonferroni’s correction. RESULTS: ∆PCO(2) at baseline for all pigs was 0.76±0.29 kPa (5.7±2.2 mm Hg). Following hyperventilation, there was a rapid increase in the ∆PCO(2), increasing maximally to 1.35±0.29 kPa (10.1±2.2 mm Hg). A corresponding decrease in the ∆PCO(2) was seen following hypoventilation, decreasing maximally to 0.23±0.31 kPa (1.7±2.3 mm Hg). These changes were statistically significant from baseline 30 s after the change in ventilation. CONCLUSION: Disturbances around the time of blood sampling can rapidly affect the PCO(2), leading to inaccurate calculations of the ∆PCO(2), resulting in misinterpretation of patient status. Care should be taken when interpreting blood gases, if there is doubt as to the presence of acute and transient changes in ventilation.
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spelling pubmed-79782762021-03-30 Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation Shastri, Lisha Kjærgaard, Benedict Rees, Stephen Edward Thomsen, Lars Pilegaard BMJ Open Respir Res Critical Care BACKGROUND: Early diagnosis of shock is a predetermining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO(2) difference (∆PCO(2)) over 0.8 kPa (6 mm Hg) is indicative of low blood flow states. Disturbances around the time of blood sampling could result in inaccurate calculations of ∆PCO(2), thereby misrepresenting the patient status. This study aimed to determine the influences of acute changes in ventilation on ∆PCO(2) and understand its clinical implications. METHODS: To investigate the isolated effects of changes in ventilation on ∆PCO(2), eight pigs were studied in a prospective observational cohort. Arterial and central venous catheters were inserted following anaesthetisation. Baseline ventilator settings were titrated to achieve an EtCO(2) of 5±0.5 kPa (V(T) = 8 mL/kg, Freq = 14 ± 2/min). Blood was sampled simultaneously from both catheters at baseline and 30, 60, 90, 120, 180 and 240 s after a change in ventilation. Pigs were subjected to both hyperventilation and hypoventilation, wherein the respiratory frequency was doubled or halved from baseline. ∆PCO(2) changes from baseline were analysed using repeated measures ANOVA with post-hoc analysis using Bonferroni’s correction. RESULTS: ∆PCO(2) at baseline for all pigs was 0.76±0.29 kPa (5.7±2.2 mm Hg). Following hyperventilation, there was a rapid increase in the ∆PCO(2), increasing maximally to 1.35±0.29 kPa (10.1±2.2 mm Hg). A corresponding decrease in the ∆PCO(2) was seen following hypoventilation, decreasing maximally to 0.23±0.31 kPa (1.7±2.3 mm Hg). These changes were statistically significant from baseline 30 s after the change in ventilation. CONCLUSION: Disturbances around the time of blood sampling can rapidly affect the PCO(2), leading to inaccurate calculations of the ∆PCO(2), resulting in misinterpretation of patient status. Care should be taken when interpreting blood gases, if there is doubt as to the presence of acute and transient changes in ventilation. BMJ Publishing Group 2021-03-18 /pmc/articles/PMC7978276/ /pubmed/33737311 http://dx.doi.org/10.1136/bmjresp-2021-000886 Text en © Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ http://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Critical Care
Shastri, Lisha
Kjærgaard, Benedict
Rees, Stephen Edward
Thomsen, Lars Pilegaard
Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title_full Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title_fullStr Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title_full_unstemmed Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title_short Changes in central venous to arterial carbon dioxide gap (PCO(2) gap) in response to acute changes in ventilation
title_sort changes in central venous to arterial carbon dioxide gap (pco(2) gap) in response to acute changes in ventilation
topic Critical Care
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7978276/
https://www.ncbi.nlm.nih.gov/pubmed/33737311
http://dx.doi.org/10.1136/bmjresp-2021-000886
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