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Background In this prospective observational study, we evaluated the effects of fluid bolus (FB) on venous-to-arterial carbon dioxide tension (PvaCO2) in 42 adult critically ill patients with pre-infusion PvaCO2 > 6 mmHg. Results FB caused a decrease in PvaCO2, from 8.7 [7.6−10.9] mmHg to 6.9 [5.8−8.6] mmHg (p < 0.01). PvaCO2 decreased independently of pre-infusion cardiac index and PvaCO2 changes during FB were not correlated with changes in central venous oxygen saturation (ScvO2) whatever pre-infusion CI. Pre-infusion levels of PvaCO2 were inversely correlated with decreases in PvaCO2 during FB and a pre-infusion PvaCO2 value < 7.7 mmHg could exclude a decrease in PvaCO2 during FB (AUC: 0.79, 95%CI 0.64–0.93; Sensitivity, 91%; Specificity, 55%; p < 0.01). Conclusions Fluid bolus decreased abnormal PvaCO2 levels independently of pre-infusion CI. Low baseline PvaCO2 values suggest that a positive response to FB is unlikely., SCOPUS: ar.j, info:eu-repo/semantics/published

So far, only a few studies have examined and confirmed the correlation between end-expiratory carbon dioxide partial pressure (PETCO2) and arterial carbon dioxide tension (PaCO2) during invasive mechanical ventilation in critically ill patients. This study aimed to observe the correlation between PaCO2 and PETCO2 in patients on invasive mechanical ventilation. This was a cross-sectional study of adult patients on invasive mechanical ventilation enrolled between June 2018 and March 2019. Patients requiring invasive mechanical ventilation underwent one of the following mechanical ventilation modes: assisted/controlled ventilation, synchronized intermittent mandatory ventilation, and spontaneous breathing. Subsequently, the difference and correlation between PETCO2 and PaCO2 were analyzed. A total of 184 patients with 298 pairs of PETCO2-PaCO2 data were included in the analysis. Without distinguishing the ventilator mode, there was significant positive correlation between PETCO2 and PaCO2. In different ventilator modes, the correlation coefficient was 0.81 for synchronized intermittent mandatory ventilation, 0.47 for assisted/controlled ventilation, and 0.55 for spontaneous breathing, respectively. In patients with chronic obstructive pulmonary disease (r = 0.80), multiple trauma (r = 0.64), severe pneumonia (r = 0.60), gastrointestinal surgery (r = 0.57), and cerebrovascular diseases (r = 0.53), PETCO2 and PaCO2 were positively correlated. For oxygenation index

Objective: This study aimed to determine the association between venous–arterial CO2 difference (Pv-aCO2) and clinical outcomes of interest in children with severe sepsis and septic shock. Design: An analytical observational study of a prospective cohort was conducted. Setting: The study was carried out from January 2015 to January 2018 in the pediatric intensive care unit of a referral hospital. Materials and methods: Of a total of 1159 patients who were admitted to pediatric critical care, 375 had severe sepsis and septic shock, of which 67 fulfilled the inclusion criteria. Arterial and venous gases were drawn simultaneously with a transthoracic echocardiogram, Pv-aCO2, and other measures of tissue perfusion such as arterial lactate, venous, and evolution to multiple organ failure. Measurements and main results: Half (53.7%) of the patients were under 24 months old, with a slight predominance of male patients. The main site of infection was the lungs in 56% of the cases, with a 91.2% survival rate. Patients who died had a higher venous lactate level (interquartile range 16.2–33.6, p = 0.02). However, there was no correlation between myocardial dysfunction seen on echocardiogram and a Pv-aCO2 greater than 6 mm Hg in children with severe sepsis and septic shock (r = 0.13). Pv-aCO2 and central venous saturation had low sensitivity to detect multiple organ failure and poor correlation with the number of compromised systems (r = 0.8). Conclusion: Pv-aCO2 was not associated with myocardial dysfunction, measured by echocardiogram, in children with severe sepsis and septic shock. It also did not correlate with the number of organs involved or mortality.

BACKGROUND In a previous study, we found a rebound of arterial carbon dioxide tension (PaCO2 ) after stopping THAM buffer administration. We hypothesized that this was due to reduced pulmonary CO2 elimination during THAM administration. The aim of this study was to investigate this hypothesis in an experimental porcine hypercapnic model. METHODS In seven, initially normoventilated, anesthetized pigs (22-27 kg) minute ventilation was reduced by 66% for 7 h. Two hours after commencing hypoventilation, THAM was infused IV for 3 h in a dose targeting a pH of 7.35 followed by a 2 h observation period. Acid-base status, blood-gas content and exhaled CO2 were measured. RESULTS THAM raised pH (7.07 ± 0.04 to 7.41 ± 0.04, P < 0.05) and lowered PaCO2 (15.2 ± 1.4 to 12.2 ± 1.1 kPa, P < 0.05). After the infusion, pH decreased and PaCO2 increased again. At the end of the observation period, pH and PaCO2 were 7.24 ± 0.03 and 16.6 ± 1.2 kPa, respectively (P < 0.05). Pulmonary CO2 excretion decreased from 109 ± 12 to 74 ± 12 ml/min (P < 0.05) during the THAM infusion but returned at the end of the observation period to 111 ± 15 ml/min (P < 0.05). The estimated reduction of pulmonary CO2 elimination during the infusion was 5800 ml. CONCLUSIONS In this respiratory acidosis model, THAM reduced PaCO2 , but seemed not to increase the total CO2 elimination due to decreased pulmonary CO2 excretion, suggesting only cautious use of THAM in hypercapnic acidosis.

Study objectives To determine the relationships between partial pressure of arterial carbon dioxide (PaCO 2 ), prescribed minute ventilation (MV), and neurologic outcome in patients resuscitated from cardiac arrest. Methods This was a retrospective cohort study utilizing a multicenter database of adult patients with return of spontaneous circulation (ROSC) after cardiac arrest. The primary outcome was neurologic status at hospital discharge, defined by Cerebral Performance Category (CPC) score: CPC 1–2 was favorable, CPC 3–5 was poor. We compared rates of initial normocarbia (PaCO 2 31–49mmHg) and mean sequential PaCO 2 measurements obtained over the first 24h. We also assessed the influence of MV on the PaCO 2 at initial, 6, 12, 18, and 24h after cardiac arrest using univariate linear regression. Results One hundred and fourteen patients from 3 institutions met inclusion criteria. Overall, 46/114 (40.4%, 95% CI: 31.4–49.4%) patients survived to hospital discharge, and 33/114 (28.9%, 20.6–37.2%) had CPC 1–2 at the time of discharge. A total of 38.9% (95% CI: 29.9–47.9%) of patients had initial normocarbia; 43.2% (28.6–57.8%) of these patients were discharged with CPC 1–2, compared with 20.3% (10.8–29.8%) of dyscarbic patients. By 6h, neurologic outcomes were not significantly associated with PaCO 2 . Prescribed MV was not associated with PaCO 2 at any time point with the exception of a weak correlation at hour 18. Conclusion Initial normocarbia was associated with favorable neurological outcome in patients resuscitated from cardiac arrest. This relationship was not seen at subsequent time points. There was no significant association between prescribed MV and PaCO 2 or neurologic outcome.

Introduction Arterial carbon dioxide tension (PaCO 2 ) abnormalities are common after cardiac arrest (CA). Maintaining a normal PaCO 2 makes physiological sense and is recommended as a therapeutic target after CA, but few studies have examined the association between PaCO 2 and patient outcomes. This systematic review and meta-analysis aimed to assess the effect of a low or high PaCO 2 on patient outcomes after CA. Methods We searched MEDLINE, EMBASE, CINAHL and Cochrane CENTRAL, for studies that evaluated the association between PaCO 2 and outcomes after CA. The primary outcome was hospital survival. Secondary outcomes included neurological status at the end of each study's follow up period, hospital discharge destination and 30-day survival. Meta-analysis was conducted if statistical heterogeneity was low. Results The systematic review included nine studies; eight provided sufficient quantitative data for meta-analysis. Using PaCO 2 cut-points of 45mmHg to define hypo- and hypercarbia, normocarbia was associated with increased hospital survival (odds ratio [OR] 1.30, 95% confidence interval [CI] 1.23, 1.38). Normocarbia was also associated with a good neurological outcome (cerebral performance category score 1 or 2) compared to hypercarbia (OR 1.69, 95% CI 1.13, 2.51) when the analysis also included an additional study with a slightly different definition for normocarbia (PaCO 2 30–50mmHg). Conclusions From the limited data it appears PaCO 2 has an important U-shape association with survival and outcomes after CA, consistent with international resuscitation guidelines' recommendation that normocarbia be targeted during post-resuscitation care.

Introduction The magnitude of the secondary response to chronic respiratory acidosis, that is, change in plasma bicarbonate concentration ([HCO3−]) per mm Hg change in arterial carbon dioxide tension (PaCO2), remains uncertain. Retrospective observations yielded Δ[HCO3−]/ΔPaCO2 slopes of 0.35 to 0.51 mEq/l per mm Hg, but all studies have methodologic flaws. Methods We studied prospectively 28 stable outpatients with steady-state chronic hypercapnia. Patients did not have other disorders and were not taking medications that could affect acid−base status. We obtained 2 measurements of arterial blood gases and plasma chemistries within a 10-day period. Results Steady-state PaCO2 ranged from 44.2 to 68.8 mm Hg. For the entire cohort, mean (± SD) steady-state plasma acid−base values were as follows: PaCO2, 52.8 ± 6.0 mm Hg; [HCO3−], 29.9 ± 3.0 mEq/l, and pH, 7.37 ± 0.02. Least-squares regression for steady-state [HCO3−] versus PaCO2 had a slope of 0.476 mEq/l per mm Hg (95% CI = 0.414–0.538, P < 0.01; r = 0.95) and that for steady-state pH versus PaCO2 had a slope of −0.0012 units per mm Hg (95% CI = −0.0021 to −0.0003, P = 0.01; r = −0.47). These data allowed estimation of the 95% prediction intervals for plasma [HCO3−] and pH at different levels of PaCO2 applicable to patients with steady-state chronic hypercapnia. Conclusion In steady-state chronic hypercapnia up to 70 mm Hg, the Δ[HCO3−]/ΔPaCO2 slope equaled 0.48 mEq/l per mm Hg, sufficient to maintain systemic acidity between the mid-normal range and mild acidemia. The estimated 95% prediction intervals enable differentiation between simple chronic respiratory acidosis and hypercapnia coexisting with additional acid−base disorders.

Hypocarbia during the first 12 h of life is associated with mortality and disability in neonatal hypoxic ischemic encephalopathy (HIE). Notable variation in arterial carbon dioxide tension (PaCO2) during the first 4 d of life is related to severe intraventricular hemorrhages in preterm infants. We examined the association between PaCO2 during 72 h of whole-body therapeutic hypothermia for neonatal HIE and 2-year neurodevelopmental outcomes.A retrospective review of 23 term neonates treated with whole-body hypothermia documented clinical, demographic and arterial blood gas data. Comparisons were made across good and severe neurodevelopmental outcome groups at 2 years of age.Severe neurodevelopmental outcomes were documented in 8 of 23 toddlers. There were no significant differences between outcome groups with regard to the number of patients with hypocarbic means or measurements. There were also no significant differences with mean PaCO2, PaO2, pH, time-weighted cumulative hypocarbia, and PaCO2 range. The severe neurodevelopmental outcomes group had a significantly higher mean PaCO2 standard deviation (p = 0.04; 95% CI, -5.46 to -0.39).Severe neurodevelopmental outcomes were significantly associated with high PaCO2 variability over 72 h in whole-body-cooled HIE neonates. Mitigating these fluctuations may be a potential management strategy.

Background: Positron emission tomography (PET) imaging of anaesthetized pig brains is a useful tool in neuroscience. Stable cerebral blood flow (CBF) is essential for PET, since variations can affect the distribution of several radiotracers. However, the effect of physiological factors regulating CBF is unresolved and therefore knowledge of optimal anaesthesia and monitoring of pigs in PET studies is sparse. The aim of this study was therefore to determine if and how physiological variables and the duration of anaesthesia affected CBF as measured by PET using (15O)-water in isoflurane-N2O anaesthetized domestic female pigs. First, we examined how physiological monitoring parameters were associated with CBF, and which parameters should be monitored and if possible kept constant, during studies where a stable CBF is important. Secondly, we examined how the duration of anaesthesia affected CBF and the monitoring parameters. Results: No significant statistical correlations were found between CBF and the nine monitoring variables. However, we found that arterial carbon dioxide tension (PaCO2) and body temperature were important predictors of CBF that should be observed and kept constant. In addition, we found that long-duration anaesthesia was significantly correlated with high heart rate, low arterial oxygen tension, and high body temperature, but not with CBF. Conclusions: The findings indicate that PaCO2 and body temperature are crucial for maintaining stable levels of CBF and thus optimizing PET imaging of molecular mechanisms in the brain of anaesthetized pigs. Therefore, as a minimum these two variables should be monitored and kept constant. Furthermore, the duration of anaesthesia should be kept constant to avoid variations in monitoring variables.

Aim The harmful effect of hypocapnia on the neonatal brain emphasizes the importance of monitoring arterial carbon dioxide tension (PaCO2). Transcutaneous monitoring of carbon dioxide (tcPCO2) reduces the need for arterial blood sampling. Drawbacks are high electrode temperature causing risks of skin burning. The aim was to determine the accuracy and precision of tcPCO2 at reduced electrode temperature. Methods Forty newborns (GA 24.9-41.7) were included. Two tc-monitors were applied (TCM4, Radiometer, Copenhagen). Arterial blood gas sampling and monitoring of tcPCO2-level at different electrode temperatures was done simultaneously (39°C, 40°C, 41 °C, 42°C, 44°C). Difference of PaCO2-tcPCO2 was expressed as a percentage of the mean. Results Mean PaCO2 was 5.8kPa [3,2; 7.9]. Bias (PaCO2 -tcPCO2) increased from 5% at 44°C to 17% at 39°C, but did not differ significantly between 41°C and 40°C. The precision of the tcPCO2 at each temperature ranged from +7-10%. After correction for the temperature-dependent over-reading, we found increasing PaCO2 — tcPCO2 difference with increasing PaCO2, approx. 2% pr. kPa increase of CO2. Only mild transient erythema was observed. Conclusion A lower electrode temperature in tcPCO2-monitoring increases systematic overreading of the tc-electrode. However, in very preterm babies, monitoring at 40°C or 41°C is possible provided a bias correction of 12-15% is applied.

The influence of induced changes in arterial blood pressure and pCO2 on the pressure-volume characteristics of the cerebrospinal fluid space, was evaluated experimentally using dogs. The pressure-volume curve was not appreciably affected by variations in pCO2. The arterial pressure, on the contrary, was found to be a major determinant of the gradient dP/dV of the steep part of the curve, i.e. the high pressure elastance of the system. Variations in mean arterial pressure in the interval 25-230 mmHg produced approximately a 5-fold change in the elastance. The relationship was nonlinear, with relatively less effect from changes in the arterial blood pressure in the higher pressure range. An interpretation on the mechanics involved is presented.

Traumatic brain injury has a devastating impact on society, utilizing many resources and disproportionately affecting the young. Recent evidence demonstrates the early care of the brain injured patient impacts patient outcomes. While prevention of systolic hypotension and hypoxia are mainstays of prehospital management of the injured patient ventilatory management performed in the prehospital environment has recently been shown to impact outcomes. Hypocapnea from hyperventilation has been shown in several trials to cause deleterious effects from cerebral vasoconstriction and ischemia. The importance of balancing the prevention of both hypocapnea and hypercapnea has led to the idea of a target ventilation range for arterial carbon dioxide tension, the ideal way to achieve this balance in the prehospital setting remains elusive. This article reviews the background, physiologic effects, impact on outcomes, and implications for prehospital care of prehospital ventilation.

Supplemental Digital Content is available in the text, The objective of this study was to examine the repeatability of blood gas (BG) parameters and their derived variables such as the central venous-to-arterial carbon dioxide tension difference (▵Pco2) and the ratio of ▵Pco2 over the central arteriovenous oxygen content difference (▵Pco2/C(a-cv)O2) and to determine the smallest detectable changes in individual patients. A total of 192 patients with arterial and central venous catheters were included prospectively. Two subsequent arterial and central venous blood samples were collected immediately one after the other and analyzed using the same point-of-care BG analyzer. The samples were analyzed for arterial and venous BG parameters, ▵Pco2, and ▵Pco2/C(a-cv)O2 ratio. Repeatability was expressed as the smallest detectable difference (SDD) and the least significant change (LSC). A change in value of these parameters exceeding the SDD or the LSC should be regarded as real. The SDDs for arterial carbon dioxide tension, arterial oxygen saturation, central venous oxygen saturation (ScvO2), and ▵Pco2 were small: ±2.06 mm Hg, ±1.23%, 2.92%, and ±1.98 mm Hg, respectively, whereas the SDDs for arterial oxygen tension (Pao2) and ▵Pco2/C(a-cv)O2 were high: ±9.09 mm Hg and ±0.57 mm Hg/mL, respectively. The LSCs (%) for these variables were 5.06, 1.27, 4.44, 32.4, 9.51, and 38.5, respectively. The repeatability of all these variables was good except for Pao2 and ▵Pco2/C(a-cv)O2 ratio for which we observed an important inherent variability. Expressed as SDD, a ScvO2 change value of at least ±3% should be considered as true. The clinician must be aware that an apparent change in these variables in an individual patient might represent only an inherent variation.

Background: Several reports have demonstrated substantial mean differences between arterial carbon dioxide tension (PaCO2) and end-tidal carbon dioxide tension (ETCO2) in children under anesthesia. Aim: We explored the importance of the (a-ET) PCO2 gradient in a pediatric population receiving general anesthesia, with special attention to the relative effects of age and weight. Methods: After induction of general anesthesia, 129 children, ASA I or II, and between 1 day and 15 years old, had an endotracheal tube placed and mechanical ventilation initiated. After reaching a steady-state ETCO2, an arterial blood sample was obtained and the PaCO2 measured. Results: The mean (a-ET) PCO2 was 1.6 ± 4.3 mmHg for the entire pediatric population. There was a significant negative correlation between (a-ET) PCO2 and age and weight (r =-0.42, P

Objectives: To assess the appropriateness of arterial carbon dioxide tension control in a group of 92 patients with traumatic brain injury who, despite receiving advanced prehospital care, showed no improved outcome in comparison with a group homogeneous but for a lower level of prehospital care. Methods: A retrospective registration of the early in-hospital arterial carbon dioxide tension of the patients intubated and ventilated on scene. Patients were excluded if the arterial carbon dioxide tension did not reflect prehospital ventilation or its alteration might have been intentional or unavoidable. Results: Arterial carbon dioxide tension was normal (35-45 mmHg) in only six of the 16 suitable cases (37.5%), was elevated (>45 mmHg) in three cases (18.75%), low (25-35 mmHg) in five cases (31.25%), and extremely low (

We compared the performance of mainstream capnometry as a measure of arterial carbon dioxide tension (Paco2) with sidestream recordings in adult neurosurgical patients undergoing supine craniotomy. Two hundred and forty patients were randomly assigned so that the end-tidal carbon dioxide tension (PEco2) was measured using either a mainstream or sidestream infrared capnometer. All patients received propofol anaesthesia and ventilation was adjusted according to clinical requirement. Arterial blood gas analyses were performed after induction, prior to dural incision, during surgery and before wound closure. Simultaneous haemodynamic and ventilatory parameters were also recorded. For 1007 paired measurements of PEco2 and Paco2 (mainstream, n = 503; sidestream, n = 504), the mean (SD) mainstream arterial to end-tidal carbon dioxide tension difference, 0.64 (0.16) kPa, was smaller than the corresponding sidestream values, 0.99 (0.40) kPa (p < 0.001). The limits of agreement for the mainstream analyser, 0.32-0.96 kPa, were also narrower than the sidestream recordings, 0.19-1.79 kPa (p < 0.001). In both capnometers, the arterial to end-tidal difference in carbon dioxide tension did not change with time. However, there was greater within-patient variation in the sidestream group. Our study showed that mainstream PEco2 provided a more accurate estimation of Paco2 than sidestream measurement.

An open system of delivery of supplemental oxygen was compared with a closed system during endotracheal suction (ETS) at zero end-expiratory pressure (ZEEP) and 10 cm H2O positive end-expiratory pressure (PEEP). Four protocols in a 2 x 2 design were administered in random order to 12 anesthetized and oleic acid-injured animals. Statistically significant differences were found between protocols for arterial carbon dioxide tension (PaCO2), arterial oxygen saturation (SaO2), airway pressure (Paw), right atrial pressure (Pra), intrathoracic pressure (Pit), arterial pressure, and right ventricular afterload. Intrathoracic pressure and systolic aortic pressure differed between open and closed systems. Statistically significant differences between ZEEP and PEEP were found for PaCO2, SaO2, Paw, Pra, Pit, aortic pressure, and right ventricular afterload. Suctioning through a closed system made little difference in subject responses, but clinically significant differences existed when suctioning subjects on and off PEEP.

Transcutaneous carbon dioxide (PtCO2) monitoring offers a potential non-invasive and continuous means to determine the arterial carbon dioxide tension (PaCO2). Studies investigating the use of PtCO2 monitoring in the adult emergency department (ED) are limited. To date, the lack of ED studies, especially those looking at clinical outcome and treatment alteration, some technical and cost limitations make it difficult to recommend widespread use of PtCO2 monitoring in the ED. However, there is a potential future use of PtCO2 monitoring in combination with peripheral venous blood gas (pVBG) values in ED patients with acute exacerbations of chronic obstructive pulmonary disease.

There are little data on the effects of propofol on cerebral blood volume (CBV). We studied the effects of changes in PaCO(2) on CBV and cerebral blood flow (CBF) during propofol anesthesia in eight New Zealand white rabbits. We also investigated the effects of propofol over time on CBV and CBF during normocapnia (control group). At normocapnia, the mean (+/- SD) CBV and CBF values were 2.41 +/- 0.68 mL/100 g and 56 +/- 28 mL/100 g/min, respectively,. When PaCO(2) was reduced from 41 to 27 mm Hg, no significant change in either CBV or CBF was observed (P0.10). However, increasing PaCO(2) from 41 to 58 mm Hg resulted in a 30% increase in CBV (3.08 +/- 0.86 mL/100 g, P0.05) and a 91% increase in CBF (97 +/- 39 mL/100 g/min, P0.01). In the control group, there were no significant changes in CBV and CBF (P0.10) during 2 h of propofol anesthesia. These results indicate that, during propofol anesthesia, cerebrovascular reactivity of blood flow and blood volume is maintained during hypercapnia but is markedly diminished during hypocapnia.During propofol anesthesia in rabbits with normal brains, a reduction in the arterial carbon dioxide level may not always be accompanied by a reduction in brain blood flow and blood volume.

We compared the accuracy and reliability of a validated, physiological simulator and six intensive care specialists in predicting changes in arterial oxygen tension (PaO(2)), arterial carbon dioxide tension (PaCO(2)) and pH following adjustment of mechanical ventilation. Twenty-five data sets were collected before and after routine alterations in ventilator settings. Fractional inspired oxygen was adjusted in all patients and minute volume was adjusted in 13 patients. The simulator was more accurate and consistent than all the physicians in predicting the magnitude of PaO(2) and pH change. The simulator had a larger bias in estimating the magnitude of change of PaCO(2) than four of the physicians, but was more consistent than all but one of the physicians. The simulator may prove to be a useful tool in the management of mechanical ventilation. Incorporation into mechanical ventilators in a passive predictive role or an active 'closed-loop' ventilation management system are potential roles for physiological simulation.

Within the setting of trauma, there are many indications for intubation and ventilation, but the ultimate aims are always the same. These are to ensure airway patency and security, provide an acceptable level of arterial oxygenation at the lowest possible inspired oxygen concentration, control arterial carbon dioxide tension and optimize pulmonary and systemic blood flow. The clinical situation, developing trends, and the experience of the individual concerned will all influence the decision to intubate and ventilate the patient who has suffered trauma. This paper considers the ‘rule-of-thumb’ indications for intubation in the emergency room and discusses the factors which may influence their interpretation.

Although there are data demonstrating reversal of cerebral vasospasm with magnesium sulfate, there is little information on the effects of magnesium on the normal intact cerebral vasculature. This study investigated the actions of magnesium on cerebral blood flow (CBF) velocity, cardiovascular variables, and arterial gas tensions. Magnesium sulfate was infused into awake, adult sheep at rates of 3 and 6 mmol/min to a total of 15 and 30 mmol, respectively. Direct arterial pressure, cardiac output, and CBF velocity were measured using chronically implanted catheters and a sagittal sinus Doppler flow probe. Arterial blood was sampled for magnesium concentrations and blood gas analysis. Infusion of both 15 and 30 mmol of magnesium increased CBF velocity by 14% (P = .056) and 24% (P = .023), respectively. These increases were accompanied by increases in arterial carbon dioxide tension (PaCO2) of 12% (P = .033) and 17% (P = .048). Multiple linear regression analysis revealed that both PaCO2 (P = .00037) and magnesium (P = .0012) were important predictors of CBF velocity.

The effect of modified ultrafiltration (MUF) after cardiopulmonary bypass for paediatric cardiac surgery was evaluated in 138 children with moderate to severe congenital heart disease. The median age was 0.4 years (0 days to 6.5 years), and the weight 5.3 kg (2.2-20 kg). The operation was discontinued in six cases, three because of technical problems and three because of unstable circulation. One-hundred-and-thirty-four patients were ultrafiltrated for a median of 12 min (2-27 min) with an ultrafiltrate of median 44 ml/kg (6-118 ml/kg). Haematocrit was significantly increased from 28% (20-39%) to 36% (26-51%) and systolic arterial pressure from 56 mmHg (30-85 mmHg) to 74.0 mmHg (32-118 mmHg). Furthermore arterial oxygenation was significantly increased from 30.8 kPa (4.8-70.4 kPa) to 34.1 kPa (4.9-80.6 kPa), and arterial carbon dioxide tension from 4.8 kPa (3.1-7.3 kPa) to 5.1 kPa (3.1-7.6 kPa). Heart rate was significantly reduced from 145 beats/min (92-201 beats/min) to 136 beats/min (88-200 beats/min). There were no significant differences in central venous pressure, left atrial pressure and base excess before and after MUF. MUF increases systolic blood pressure, haematocrit, arterial oxygen and carbon dioxide tension coming off bypass in paediatric cardiac surgery and reduces heart rate and postoperative fluid overload.

To study the relationship between arterial PCO2 (PaCO2) and transcutaneous PCO2 (tcPCO2) intermittent 2-min total umbilical cord occlusions were performed with a 3-min interval (n = 12) in 5 fetal sheep, tcPCO2 was measured continuously. Arterial acid-base balance was analyzed at the end of occlusion periods and at the end of occlusion intervals. During each occlusion, PaCO2 increased 1.9 kPa (p0.001) and pH decreased 0.07 units (p0.001). Partial recovery occurred between occlusion intervals resulting in development of mild fetal acidemia. The quick fluctuations in PaCO2 during occlusions were not followed by tcPCO2, but tcPCO2 was capable following the trend in PaCO2. Measurement of tcPCO2 may therefore be an additional tool in the detection of the development of fetal acidemia.

Introduction: The purpose of this study was to determine the strength of the relationship between arterial oxygen tension (Pao 2 ) and transcutaneous oxygen (Ptco 2 ), and arterial carbon dioxide tension (Paco 2 ) and transcutaneous carbon dioxide (Ptcco 2 ) of premature neonates during fixed-wing air transport. Method: The study admitted 37 randomly selected intubated or nonintubated neonates who received oxygen by mechanical ventilation or face mask and required at least a 1-hour fixed-wing flight. Arterial blood gas samples were taken from the umbilical artery catheter at the end of three 15-minute intervals and stored in an ice slurry for analysis (Radiometer ABL300) on arrival at the receiving hospital. Transcutaneous monitor readings (Radiometer Tina 3) were recorded with each arterial sample. Results: A correlation of 0.88 ( p 2 and Ptco 2 and 0.86 ( p 2 and Ptcco 2 existed. Conclusion: Despite strong correlation, the range of difference between the individual transcutaneous values and actual blood oxygen values were from 0 to 31. This difference was not due to change in cabin pressure. Considering the flight environment (cabin temperature, pressure changes, and weather), these values are remarkably stable.

To investigate changes of cerebral arteriovenous oxygen content difference (AVDO2) induced by surgical incision and to determine carbon dioxide (CO2) reactivity of the cerebral circulation during sevoflurane and isoflurane anaesthesia. Twenty-one ASA 1–2 patients undergoing elective surgery for supratentorial tumours were randomly allocated to receive either 1.3 MAC sevoflurane/N2O anaesthesia (n =10) or equi-MAC isoflurane/N2O anaesthesia (n = 11). Before and after incision, haemodynamic measurements and AVDO2 determinations were performed. After opening the dura, AVDO2 was determined before and after the respiration rate was increased by 50%. Incision produced an increase in mean arterial pressure from 69 ±11 to 97 ±22 mmHg (mean ±SD) (P < 0.0005) and from 71 ±6 to 89 ±12 mmHg (P < 0.0001) in the sevoflurane and isoflurane groups, respectively, whereas the heart rate increased from 60 ±9 to 72 ±8 bpm (P < 0.001) and from 65 ±6 to 70 ±7 bpm (P < 0.001), respectively. Arterial carbon dioxide tension (PaCO2) was increased from 33.6 ±2.3 to 34.6 ±1.8 mmHg (P < 0.05) with incision in the sevoflurane group. The AVDO2 was decreased from 6.5 ±1.6 to 5.3 ±1.6 vol% (P < 0.0005) in the sevoflurane group and from 6.7 ±1.1 to 6.0 ±1.1 vol% (P < 0.01) in the isoflurane group. The % change of AVDO2 was larger in the sevoflurane group than in the isoflurane group (−18.3 ±8.4% vs −9.1 ±9.0%; P < 0.05) but no difference remained after the postincisional AVDO2 value of the sevoflurane group was corrected for pre-incisional PaCO2. Carbon dioxide reactivity, calculated as the percent change in AVDO2 per mmHg change in PaCO2, was 6.1 ±3.0% mmHg−1 in the sevoflurane group and 5.9 ±2.4% · mmHg−1 in the isoflurane group (P = NS). Sevoflurane and isoflurane are associated with similar impairment of cerebral flow-metabolism coupling at incision, while CO2 reactivity is maintained during both anaesthetics. Etudier les changements de la difference arterioveineuse du contenu en oxygene cerebral (AVDO2) produits par l’incision et determiner la reactivite au gaz carbonique (CO2) de la circulation cerebrale sous anesthesie au sevoflurane et a l’isoflurane. Vingt et un patients ASA 1 et 2 subissant une chirurgie non urgente pour tumeur supratentorielle ont ete aleatoirement assignes a recevoir soit une anesthesie au sevoflurane/N2O 1,3 MAC (n = 10) soit une anesthesie a l’isoflurane/N2O equi-MAC (n = 11). Avant et apres l’incision, les mesures hemodynamiques ont ete effectuees et AVDO2 determinee. Apres l’ouverture de la dure-mere, AVDO2 a ete calculee avant et apres une augmentation de la frequence respiratoire de 50%. L’incision a provoque une augmentation de la pression arterielle moyenne respective de 69 ±11 a 97 ±22 mmHg (moyenne ±ET) (P < 0,0005) et 71 ±6 a 89 ±12 (P < 0,0001) dans les groupes sevoflurane et isoflurane; la frequence cardiaque augmentait respectivement de 60 ±9 a 72 ±8 bpm (P < 0,001) et de 65 ±6 a 70 ±7 bpm (P < 0,001). Dans le groupe sevoflurane, la PaCO2 augmentait de 33,6 ±2,3 a 34,6 ±1,8 (P < 0,05) avec l’incision. Dans le groupe sevoflurane, AVDO2 diminuait de 6,5 ±1,6 a 5,3 ±1,6 vol% (P < 0,0005) et dans le groupe isoflurane, de 6,7 ±1,1 a 6,0 ±1,1 vol% (P < 0,01). Le pourcentage de changement de AVDO2 etait plus important dans le groupe sevoflurane que dans le groupe isoflurane (−18,3 ±8,4% vs −9,1 ±9,0%; P < 0,05); cette difference est disparue une fois la valeur post-incision du groupe sevoflurane corrigee pour la valeur de PaCO2 pre-incision. La reactivite du gaz carbonique, calculee en pourcentage de changement en AVDO2 par mmHg de changement de PaCO2 etait 6,1 ±3,0% · mmHg−1 dans le groupe sevoflurane et 5,9 ±2,4% · mmHg−1 dans le groupe isoflurane (P = NS). Le sevoflurane et l’isoflurane sont associes a une perturbation identique du couplage debit-metabolisme a l’incision, alors que la reactivite au CO2 est maintenue avec les deux anesthesiques.

Jugular bulb oximetry provides the first bedside available information on cerebral oxygen utilization. An extensive analysis was made of all initial jugular bulb oximetry data obtained in 150 patients within the first 12 h after severe traumatic brain' injury. These data revealed initial abnormal jugular bulb saturation values in 57 patients (= 38% of study population), with a predominance of jugular bulb desaturation (observed in 45 patients). This confirms earlier reports that revealed a high incidence of disturbed and inadequate cerebral perfusion in the first hours after brain injury. Jugular bulb desaturation was especially related to systemic causes (such as a lowered cerebral perfusion pressure observed in 29 patients, and a lowered arterial carbon dioxide tension in 24 patients). These findings could have important implications for the emergency management of severely head-injured patients, as outcome might possibly be improved by better attention to all systemic factors that might reduce cerebral perfusion in the early hours after traumatic insult.

There is much controversy about the optimal bloodgas management of hypothermic patients, whether the hypothermia is caused by accidents or induced before operations. The surgeons and anestesiologists have acquired more clinical experience the last years when operating patients in hypothermia. The comparative physiology has given increased information about the blood gas strategy of heterothermic endotherms and poikilothermic ectotherms during lowering of their core temperature. There are two types of strategies which have been used in clinical medicine the last years in the blood gas management of patients in hypothermia: pH-stat method and alpha-stat method. In the pH-stat method, the arterial carbon dioxide tension (pCO2(a)) is maintained at 5.3 kPa (40 mmHg) and the pH is maintained at 7.40 when measured at the actual temperature. It is then necessary to add CO2 to the inspired gas. In the alpha-method, the arterial carbon dioxide tension and the pH are maintained at 5.3 kPa and 7.40 when measured at +37 degrees C. When a patient is cooled down, the pH-value will increase and the pCO2-value and the pO2-value will decrease with lowering of the temperature if measured at the patients temperature. Both the pH-stat and alpha-stat strategies have theoretical disadvantages. For the optimal myocardial function the alpha-stat method is the method of choice. The pH-stat method may result in loss of autoregulation in the brain (coupling of the cerebral blood flow with the metabolic rate in the brain). By increasing the cerebral blood flow beyond the metabolic requirements, the pH-stat method may lead to cerebral microembolisation and intracranial hypertension. In Norway the alpha-stat strategy is the preferred method.

The difference between mixed venous blood carbon dioxide tension (PvCO(2)) and arterial carbon dioxide tension (PaCO(2)), called ∆PCO(2) has been proposed to better characterize the hemodynamic status. It depends on the global carbon dioxide (CO(2)) production, on cardiac output and on the complex relation between CO(2) tension and CO(2) content. The aim of this review is to detail the physiological background allowing adequate interpretation of ∆PCO(2) at the bedside. Clinical and experimental data support the use of ∆PCO(2) as a valuable help in the decision-making process in patients with hemodynamic instability. The difference between central venous CO(2) tension and arterial CO(2) tension, which is easy to obtain can substitute for ∆PCO(2) to assess the adequacy of cardiac output. Differences between local tissue CO(2) tension and arterial CO(2) tension can also be obtained and provide data on the adequacy of local blood flow to the local metabolic conditions.

Study A lipid emulsion containing 10 percent medium-chain triglycerides (MCT) and 10 percent long-chain triglycerides (LCT) was infused at a rate of 1 ml/kg/h (3.3 mg/kg/min) for 2 h, in 12 patients (2 males, 10 females; mean age, 54 ± 3 (SEM) years; range, 34 to 67 years) 24 h after open-heart surgery (mitral valve replacement). Methods Hemodynamic factors (pulmonary and radial artery indwelling catheters), oxygen and carbon dioxide partial pressures, oxygen saturation, oxygen delivery and consumption, and intrapulmonary shunt fraction were obtained before, during, and after lipid infusion (for 2 h), at 30-s intervals, along with some metabolic indexes (triglycerides, free fatty acids, glucose, insulin, lactate, acetoacetate). Results No statistically significant changes in heart rate, cardiac index, systemic and pulmonary pressures and resistances, central venous and pulmonary capillary pressures, or arterial oxygen partial pressure were observed during infusion. Arterial carbon dioxide partial pressure values were constantly reduced throughout and after the end of lipid infusion, as compared with baseline values, while oxygen consumption was increased significantly without any change in oxygen delivery. No adverse effects on intrapulmonary shunt fraction were observed. Statistically significant increases of triglycerides, free fatty acids, acetoacetate and insulin (peak values at end of the lipid infusion) were found in comparison with baseline values. Plasma glucose increased significantly during lipid infusion and remained higher than baseline values until the end of the study. Lactate levels were unchanged, except for a slight decrease at the end of the study, without any derangement of acid-base equilibrium. Neither arrhythmias nor adverse clinical reactions were observed as a consequence of lipid infusion. Conclusion Fat emulsions containing both MCT and LCT, when given at 3.3 mg/kg/min for 120 min following valvular heart surgery, do not exert negative cardiopulmonary effects, and could represent a source of rapidly metabolized substrates.

Summary We have used nitric oxide in the treatment of four children admitted to the paediatric intensive care unit with acute, severe respiratory failure. Administration resulted in an improvement in arterial oxygenation range 1.3–18.4 kPa (9.9–140 mmHg): mean 6.7 kPa (51 mmHg) and a reduction in arterial carbon dioxide tension range 0.6–1.2 kPa (4.5–9 mmHg): mean 0.9 kPa (6.8 mmHg). No adverse effects were encountered following administration for a duration of 3–12 days at a dose of 40–64 parts per million.

Background: Transcutaneous measurement of carbon dioxide is routinely done at the earlobe site. In patients receiving non invasive ventilation or in the intensive care setting with necklines, an alternate measurement site would be useful. The infraclavicular site has major blood vessels in its viscinity. We started to use the infraclavicular site for transcutaneous measurements of carbon dioxide using a new digital sensor. Aim: Comparison of transcutaneous carbon dioxide with arterial carbon dioxide at the infraclavicular site. Methods: We retrospectively compared transcutaneous carbon dioxide at the infraclavicular site with arterial carbon dioxide in 50 samples. The Sentec Digital Monitoring System (SentecAG, Therwil, Switzerland) was used. The V-Sign digital sensor was placed on the infraclavicular site at the medial two third and one third point from the sternoclavicular joint and acromioclavicular jont. Results: When comparing PtcCO2 with PaCO2 values, the Bland-Altman analysis revealed a bias of 0.15 mmHg (95% CI: [-0.76; 1.05]) with a precision of 3.18 mmHg. Linear regression analysis describes the relationship between the two methods. The slope of the linear model was 0.85. ± 0.04 and the intercept was 5.78±1.58 (RSE = 2.8, R2 = 0.91). Conclusion: The measurement of transcutaneous carbon dioxide at the infraclavicular site is feasible with a digital sensor and has a good correlation with the carbon dioxide values obtained from the arterial blood gas.

End-tidal carbon dioxide tension (PetCO2) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on PetCO2 being an accurate surrogate for arterial carbon dioxide tension (PaCO2), the latter being the physiologically relevant variable. This study tested the hypothesis that PetCO2 provides an accurate assessment of PaCO2 during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress ( N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in PetCO2 ( N = 7). PetCO2 and PaCO2 decreased during heat stress ( P < 0.001); however, there was no group difference between PaCO2 and PetCO2 ( P = 0.36) nor was there a significant interaction between thermal condition and measurement technique ( P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, PetCO2 and PaCO2 at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between PaCO2 and PetCO2 while normothermic ( P = 0.14) and following a 1.0 ± 0.2°C ( P = 0.21) and 1.4 ± 0.2°C ( P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of PetCO2 and PaCO2 were similar ( P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in PetCO2 (7.5 ± 2.8 mmHg) and PaCO2 (6.6 ± 3.4 mmHg) were similar ( P = 0.31). These data indicate that mean PetCO2 reflects mean PaCO2 during the evaluated conditions.

Blood gases were analyzed in dogs with pulmonary heartworm (HW) disease. The arterial oxygen tension (PaO2) in dogs with mild signs of dirofilariasis (mildly affected group, n = 48, 85.7 +/- 8.2 mmHg) and in dogs with signs of right heart failure (severely affected group, n = 13, 76.4 +/- 11.6 mmHg) was lower (p0.01) than in dogs without HW infection (HW-free group, n = 19, 91.5 +/- 7.3 mmHg). Only 2 dogs in the severely affected group had a PaO2 less than 60 mmHg. The arterial carbon dioxide tension (PaCO2, p0.01) and mixed venous O2 (p0.01) and CO2 (p0.01) tensions were lower, and alveolar-arterial oxygen difference (AaDO2, p0.01) was greater in the severely affected group than in the HW-free and mildly affected groups. Arterial pH and bicarbonate (HCO3-) concentrations were lower (p0.01) in both affected groups than in the HW-free groups. The anion gap level was not different among the 3 groups. Serum lactic acid level in the severely affected group was higher (p0.01) than in the HW-free and mildly affected groups. However, a slightly higher serum lactic acid concentration was found only in 2 dogs of the severely affected group (3.84 mmol/l and 3.82 mmol/l). The PaO2 (r = -0.62) and AaDO2 (r = 0.66) correlated significantly (p0.01) with mean pulmonary arterial pressure. One week after HW removal, blood gases, pH and HCO3- concentration remained unchanged in the mildly affected group. In the severely affected group, blood gas values were the same, but pH and HCO3- concentration improved slightly.

1. Respiratory alkalosis is defined as a pH above 7.45 due to an arterial carbon dioxide tension less than 35 mmHg.

Objective: Cheyne Stokes respiration (CSR) is frequently seen in the patients with heart failure (HF) and it increases mortality. In the present study, we aimed to evaluate acute effects of adaptive servo ventilation (ASV) on CSR and neurohormones in the patients with HF. Methods: Nineteen males and 1 female patients with HF in the functional capacity of NYHA II-III were included into the study prospectively. One night polysomnography (PSG) was performed to all patients. In addition to medical treatment, 10 patients having CSR were applied ASV in another night together with PSG.. Arterial blood gases, plasma epinephrine and norepinephrine, serum N-terminal -pro-B type brain natriuretic peptide (NT-pro-BNP) were studied in the first night and after ASV treatment. A Wilcoxon test was used for comparison of parameters before and after treatment; and Mann-Whitney-U test was used for comparison of parameters between the patients with CSR and without CSR. Results: Mean age of 10 patients with CSR was 62.2±11.1 years. Their etiologies were ischemic in 9 patients and idiopathic dilated cardiomyopathy in 1 patient. While there were no significant differences in the levels of PaCO2, HCO3, PH, before and after treatment; PaO2 (75.3 mmHg) and SatO2 (94.7%) significantly increased after the therapy (84.7 mmHg, 96.5% and p=0.007 and p=0.008 respectively). While NT-proBNP (3029.6±1450.5 pg/ml), norepinephrine (625.4±304.7 pg/ml) and epinephrine (65.4±24.1 pg/ml) were higher than normal before ASV treatment, all of them showed significant reductions after treatment (1694.0±925.9 pg/mvl, 333.9±165.4 pg/ml and 45.0±20.5 pg/ml; p=0.005, p=0.005 and p=0.02, respectively). Conclusions: One night ASV treatment improves CSR, partial pressure of oxygen in arterial blood, and oxygen saturation and provides significant reductions in plasma catecholamines and NT-proBNP levels in the patients with HF and CSR. Prospective studies are needed to evaluate long-term effects of ASV treatment on morbidity and mortality in the patients with HF. © Copyright 2009 by AVES Yayincilik Ltd.

To the Editors: Obesity hypoventilation syndrome (OHS) is commonly defined as a combination of obesity (body mass index (BMI) >30 kg·m−2), waking arterial hypercapnia (arterial carbon dioxide tension ( P a,CO2) >6.0 kPa (45 mmHg)) and sleep-disordered breathing. Essential to the diagnosis is exclusion of other causes of alveolar hypoventilation 1. The lack of a standardised definition of OHS in general, and of OHS–obstructive sleep apnoea relationships in particular, leads to confusion. One of the main aspects that has not been clarified is the assessment of OHS severity. This appears to be directly related to the degree of hypercapnia, the degree of hypoxaemia and the presence of complications 2, 3. Nevertheless, …

Summary Doxapram, 0.05 mg/kg bodyweight/min, was infused during the second hour of 2 h halothane anaesthesia in six ponies. Two of the ponies were anaesthetised on a second occasion as controls and given 5 per cent dextrose in place of the doxapram. Respiratory depression typical of halothane anaesthesia in ponies developed in the first hour of anaesthesia and continued during the second hour in the control animals. During doxapram infusion arterial carbon dioxide tension decreased and pH increased. Arterial blood pressure increased but there was no change in pulse rate, the electrocardiogram or arterial oxygen tension. Anaesthesia lightened during doxapram infusion necessitating an increase in the vapouriser setting in order to prevent arousal. Recovery from anaesthesia appeared unaffected by the doxapram infusion.