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 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

Mathematically arterialised venous blood is a stable representation of patient acid-base status at steady state following acute transient changes in ventilation

Hyper- or hypoventilation are commonly occurring stress responses to arterial puncture around the time of blood sampling and have been shown to rapidly alter arterial blood acid–base parameters. This study aimed to evaluate a physiology-based mathematical method to transform peripheral venous blood acid–base values into mathematically arterialised equivalents following acute, transient changes in ventilation. Data from thirty patients scheduled for elective surgery were analysed using the physiology-based method. These data described ventilator changes simulating ‘hyper-’ or ‘hypoventilation’ at arterial puncture and included acid–base status from simultaneously drawn blood samples from arterial and peripheral venous catheters at baseline and following ventilatory change. Venous blood was used to calculate mathematically arterialised equivalents using the physiology-based method; baseline values were analysed using Bland–Altman plots. When compared to baseline, measured arterial and calculated arterialised values at each time point within limits of pH: ± 0.03 and PCO(2): ± 0.5 kPa, were considered ‘not different from baseline’. Percentage of values considered not different from baseline were calculated at each sampling timepoint following hyper- and hypoventilation. For the physiological method, bias and limits of agreement for pH and PCO(2) were -0.001 (-0.022 to 0.020) and -0.02 (-0.37 to 0.33) kPa at baseline, respectively. 60 s following a change in ventilation, 100% of the mathematically arterialised values of pH and PCO(2) were not different from baseline, compared to less than 40% of the measured arterial values at the same timepoint. In clinical situations where transient breath-holding or hyperventilation may compromise the accuracy of arterial blood samples, arterialised venous blood is a stable representative of steady state arterial blood

Skeletal muscle oxygenation during cycling at different power output and cadence

The selection of cadence during cycling may be determined by a number of factors, including the degree of oxygenation in the exercising skeletal muscle. The purpose of this study was to determine the degree of muscle oxygenation associated with different cycling cadences and exercise intensities, and its putative role in the choice of self‐selected cadence during cycling. We recorded cardiopulmonary and metabolic responses to cycling at exercise intensities of 70% and 90% of the ventilatory threshold (Tvent), and used near‐infrared spectroscopy to determine tissue saturation index as a measure of skeletal muscle (vastus lateralis) oxygenation. Twelve participants cycled at cadences of 30, 50, 70, 90, and 110 revolutions per minute (rpm), each for 4 min, in a randomized sequence, interspersed with active recovery periods. Despite cardiopulmonary and metabolic responses being greater at 90% than at 70% Tvent, and at 110 rpm compared with lower cadences, vastus lateralis oxygenation was not different between the two exercise intensities and five cadences tested. Our results indicate that skeletal muscle tissue saturation index is not substantially affected during cycling for short periods of time at constant, moderate exercise intensity at cadences between 30 and 110 rpm, suggesting that skeletal muscle oxygenation may not be an important negative feedback signal in the choice of self‐selected cadence during cycling at moderate exercise intensity