Browsing by Subject "PCO2"
Now showing items 1-4 of 4
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(2021)Background Normoventilation is crucial for many critically ill patients. Ventilation is routinely guided by end-tidal capnography during prehospital anaesthesia, based on the assumption of the gap between arterial partial pressure of carbon dioxide (PaCO2) and end-tidal carbon dioxide partial pressure (PetCO(2)) of approximately 0.5 kPa (3.8 mmHg). Methods We retrospectively analysed the airway registry and patient chart data of patients who had been anaesthetised and intubated endotracheally by the prehospital critical care team and had their prehospital arterial blood gases analysed. Bland-Altman analysis was used to estimate the bias and limits of agreement. Results Altogether 502 patients were included in the study, with a median age of 58 years. The most common patient groups were post-resuscitation (155, 31%), neurological emergencies (96, 19%), intoxication (75, 15%) and trauma (68, 14%). The median of the gap between PaCO2 and PetCO(2) was 1.3 kPa (interquartile range 0.7 to 2.2) (9.8 (5.3-16.5) mmHg). Mean bias of PetCO(2) was -1.6 kPa/12.0 mmHg (standard deviation 1.7 kPa/12.8 mmHg) with 95% confidence limits of agreement -4.9 to 1.9 kPa (-36.8 to 14.3 mmHg). The gap was >= 1.0 kPa (>7.5 mmHg) in 297 (66%, 95% confidence interval 55 to 63) patients. Conclusion Our results suggest that end-tidal capnography alone might not be an adequate method to achieve normoventilation for critically ill patients intubated and mechanically ventilated in prehospital setting. Thus, an arterial blood gas analysis might be useful to recognize patients with an increased gap between PaCO2 and PetCO(2).
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(2020)Brain interstitial pH (pHbrain) alterations play an important role in the mechanisms of neuronal injury in neonatal hypoxic-ischemic encephalopathy (HIE) induced by perinatal asphyxia. The newborn pig is an established large animal model to study HIE, however, only limited information on pHbrain alterations is available in this species and it is restricted to experimental perinatal asphyxia (PA) and the immediate reventilation. Therefore, we sought to determine pHbrain over the first 24h of HIE development in piglets. Anaesthetized, ventilated newborn pigs (n = 16) were instrumented to control major physiological parameters. pHbrain was determined in the parietal cortex using a pH-selective microelectrode. PA was induced by ventilation with a gas mixture containing 6%O2-20%CO2 for 20 min, followed by reventilation with air for 24h, then the brains were processed for histopathology assessment. The core temperature was maintained unchanged during PA (38.4±0.1 vs 38.3±0.1°C, at baseline versus the end of PA, respectively; mean±SEM). In the arterial blood, PA resulted in severe hypoxia (PaO2: 65±4 vs 23±1*mmHg, *p
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(2018)Arterial blood gas (ABG) analysis is the traditional method for measuring the partial pressure of carbon dioxide. In mechanically ventilated patients a continuous noninvasive monitoring of carbon dioxide would obviously be attractive. In the current study, we present a novel formula for noninvasive estimation of arterial carbon dioxide. Eighty-one datasets were collected from 19 anesthetized and mechanically ventilated pigs. Eleven animals were mechanically ventilated without interventions. In the remaining eight pigs the partial pressure of carbon dioxide was manipulated. The new formula (Formula 1) is PaCO2 = PETCO2 + k(PETO2 - PaO2) where PaO2 was calculated from the oxygen saturation. We tested the agreements of this novel formula and compared it to a traditional method using the baseline PaCO2 - ETCO2 gap added to subsequently measured, end-tidal carbon dioxide levels (Formula 2). The mean difference between PaCO2 and calculated carbon dioxide (Formula 1) was 0.16 kPa (+/- SE 1.17). The mean difference between PaCO2 and carbon dioxide with Formula 2 was 0.66 kPa (+/- SE 0.18). With a mixed linear model excluding cases with cardiorespiratory collapse, there was a significant difference between formulae (p <0.001), as well as significant interaction between formulae and time (p <0.001). In this preliminary animal study, this novel formula appears to have a reasonable agreement with PaCO2 values measured with ABG analysis, but needs further validation in human patients.
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(2020)Background Controlling arterial carbon dioxide is paramount in mechanically ventilated patients, and an accurate and continuous noninvasive monitoring method would optimize management in dynamic situations. In this study, we validated and further refined formulas for estimating partial pressure of carbon dioxide with respiratory gas and pulse oximetry data in mechanically ventilated cardiac arrest patients. Methods A total of 4741 data sets were collected retrospectively from 233 resuscitated patients undergoing therapeutic hypothermia. The original formula used to analyze the data is PaCO2-est1 = PETCO2 + k[(PIO2 - PETCO2) - PaO2]. To achieve better accuracy, we further modified the formula to PaCO2-est2 = k(1)*PETCO2 + k(2)*(PIO2 - PETCO2) + k(3)*(100-SpO(2)). The coefficients were determined by identifying the minimal difference between the measured and calculated arterial carbon dioxide values in a development set. The accuracy of these two methods was compared with the estimation of the partial pressure of carbon dioxide using end-tidal carbon dioxide. Results With PaCO2-est1, the mean difference between the partial pressure of carbon dioxide, and the estimated carbon dioxide was 0.08 kPa (SE +/- 0.003); with PaCO2-est2 the difference was 0.036 kPa (SE +/- 0.009). The mean difference between the partial pressure of carbon dioxide and end-tidal carbon dioxide was 0.72 kPa (SE +/- 0.01). In a mixed linear model, there was a significant difference between the estimation using end-tidal carbon dioxide and PaCO2-est1 (P <.001) and PaCO2-est2 (P <.001) respectively. Conclusions This novel formula appears to provide an accurate, continuous, and noninvasive estimation of arterial carbon dioxide.
