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

TLDR
In this paper, the authors investigated the isolated effects of changes in ventilation on ∆PCO2, eight pigs were studied in a prospective observational cohort, and the changes from baseline were analysed using repeated measures ANOVA with post-hoc analysis using Bonferroni's correction.
Abstract
Background Early diagnosis of shock is a predetermining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO2 difference (∆PCO2) 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 ∆PCO2, thereby misrepresenting the patient status. This study aimed to determine the influences of acute changes in ventilation on ∆PCO2 and understand its clinical implications. Methods To investigate the isolated effects of changes in ventilation on ∆PCO2, 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 EtCO2 of 5±0.5 kPa (VT = 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. ∆PCO2 changes from baseline were analysed using repeated measures ANOVA with post-hoc analysis using Bonferroni’s correction. Results ∆PCO2 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 ∆PCO2, increasing maximally to 1.35±0.29 kPa (10.1±2.2 mm Hg). A corresponding decrease in the ∆PCO2 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 PCO2, leading to inaccurate calculations of the ∆PCO2, 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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Citations
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Veno‐arterial CO2 difference and lactate for prediction of early mortality after cardiac arrest

TL;DR: In this paper , the authors evaluated the ability of veno-arterial pCO2 difference (∆pCO2; central venous CO2 − arterial CO2) and lactate to predict early mortality in postcardiac arrest patients.
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Agreement between CO2 gap determined from peripheral blood and mixed venous blood in septic shock patients

TL;DR: In this article , a single-centre, observational clinical study on septic shocked and invasively ventilated patients during the first 24 hours from admission in ICU was conducted.
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Venous Minus Arterial Carbon Dioxide Gradients in the Monitoring of Tissue Perfusion and Oxygenation: A Narrative Review

TL;DR: In this paper , the authors analyzed the physiologic determinants of Pcv-aCO2 and Pmv-a CO2/Ca-cvO2 and their potential usefulness and limitations for the monitoring of critically ill patients.
References
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TL;DR: In this paper, the authors systematically searched 15 citation databases for population-level estimates of sepsis incidence rates and fatality in adult populations using consensus criteria and published in the last 36 years.
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Metabolic acidosis: pathophysiology, diagnosis and management

TL;DR: Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response.
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