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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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Detalles Bibliográficos
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
Descripción
Sumario: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.