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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.

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.

Background and aims: 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 need of arterial blood sampling. Drawbacks are high electrode temperature causing short application time and risks of skin burning. The aim of this study 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). The metabolic constant was 0.53 kPa. Arterial blood gas sampling and recording of the tcPCO2-level at different electrode temperatures was done simultaneously (39°C, 40°C, 41°C, 42°C, 44°C). The Bland and Altman method was used for analysis. PaCO2-tcPCO2 difference was expressed in fraction of the mean. Results: Mean PaCO2 was 5.8 kPa {3,2; 7.9}. The mean PaCO2 - tcPCO2 difference (bias) increased from 5% at 44°C to 17% at 39°C, but did not differ significantly between 41°C and 40°C (14.8% vs. 11.8%). The precision of the tcPCO2 at each temperature ranged from +7% to +10%. After correction for the temperature-dependent overreading, the Bland-Altman plot showed increasing PaCO2 - tcPCO2 difference with increasing PaCO2, approx. 2% pr. kPa increase of CO2. Sequence of electrode temperatures did not matter. Only mild transient erythema was observed. Conclusions: 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 bias correction of 12-15%.

Effect of Weaning Inhaled Nitric Oxide (INO) on Arterial Carbon Dioxide Tension (pCO2) and pH

Cerebral Vasoreactivity to Arterial Carbon Dioxide Tension in Premature Infants: Effect of Ibuprofen

The purpose of this study was to measure cerebral blood flow (CBF), cerebral blood volume (CBV) and its response to changes in arterial carbon dioxide tension (CBVR) by NIRS in 21 term newborn infants who had suffered birth asphyxia. All had clinical and biochemical (base deficit ≥ 15 mmol/l) evidence of asphyxia and were studied during ihc first 24 hours. Eight of the 21 infants died and neurodevelopmental examination in survivors at one year of age showed that 7 had major neurological impairments; the remaining 6 infants were normal or had minor impairments. Results (mean ± SEM) were as follows: Values for CBF and CBV were significantly higher than previously defined normal values and for CBVR lower. The extern of the abnormalities was related to the severity of adverse outcome (ANOVA p

81 Response of cerebral blood volume to changes in arterial carbon dioxide tension in newborn infants

The aim of this study was to find out whether the intracerebral concentration of cytochrome aa3 ([CytO2]) (the terminal enzyme of the respiratory electron transport chain) altered in response to changes in arterial carbon dioxide tension (PaCO2).

The effect on the arterial carbon dioxide tension of assisting spontaneously breathing patients under halothane anaesthesia has been studied. A reduction in PaCO2 is usually seen, but it was reduced below 40 torr in only 30 per cent of cases, while a rise was recorded in 20 per cent.

Summary Nineteen newborn lambs, spontaneously breathing room air, were hemorrhaged of 50% of their measured blood volume over a 30-min period. They were then observed for the following 90 min. No fluid or blood was reinfused during the study. Eight of the 19 lambs survived beyond the study period, the other 11 died at the end of the hemorrhage or during the recovery period. All lambs became hypotensive and bradycardic during the hemorrhage. All became tachycardic after the hemorrhage. Blood pressure of the survivors returned towards baseline levels whereas it continued to fall in the non-survivors. All animals became anemic, acidotic, and hypocarbic but remained normoxemic. Myocardial blood flow fell to approximately 50% of baseline levels in both survivors and non-survivors during, and at the end of the hemorrhage. It returned to near baseline levels in the survivors by 90 min posthemorrhage. Cerebral blood flow remained at baseline levels during the hemorrhage in the survivors but cerebral oxygen delivery decreased. Flow rose 10% above baseline levels 90 min after hemorrhage but oxygen delivery remained low. In the non-survivors, cerebral blood flow fell to 60% of baseline and cerebral oxygen delivery was 50% of baseline by the end of the hemorrhage. A group of five lambs was hemorrhaged and studied in the same fashion as the 19, except that they breathed 4.5% CO2 beginning 15 min before the hemorrhage, during the hemorrhage and 90 min recovery period. Four of these five survived the study period. They remained normocarbic and became more acidotic than the animals that breathed room air. Blood pressure and heart rate fell during hemorrhage but these decreases were less than in either group of room air breathing animals. During recovery they became tachy­ cardic and blood pressure returned to baseline levels. Myocardial blood flow increased 20% above baseline by the end of hemorrhage and 40% above baseline by 90 min posthemorrhage. Cerebral blood flow increased 40% above baseline during the hemorrhage and remained at that level at the end of hemorrhage and 90 min afterwards. The increase in brain blood flow was sufficient to maintain oxygen delivery to the brain at baseline levels throughout the experiment.

Based on measurements of arterial CO2 tension in 132 adult patients, a curve was constructed relating fresh gas inflow and arterial CO2 tension for a modified Mapleson D system. In patients on controlled ventilation using a ventilating volume greater than the predicted respiratory minute volume, it was found that the arterial Pco2 can be predicted from the fresh gas inflow with an accuracy sufficient to be clinically useful.

Blood gases, tidal volumes, and respiratory rates were measured preoperatively and during surgery with intermittent positive pressure breathing of 50 per cent oxygen. The ventilator was set to provide a tidal volume and rate closely approximating that in the awake state.

The Suwa nomogram was devised to predict the amount of mechanical dead space which must be added to a ventilated patient’s breathing circuit to achieve a normal arterial carbon dioxide tension of 40 mm Hg from a hypocapnoeiac level. The reliability of the mathematical analysis from which the nomogram was derived, together with the Suwa nomogram itself, were assessed in nine patients in respiratory failure. The results from 26 samples verified the mathematical analysis with a difference of ± 1 mm Hg from the predicted value of 40 mm Hg for arterial carbon dioxide tension when mechanical dead space was added. The mechanical dead space predicted by the Suwa nomogram to achieve an arterial carbon dioxide tension of 40 mm Hg was shown to have a potential error of ± 3.23 mm Hg. It was shown that the mathematical analysis warranted more use than the Suwa nomogram because of superior accuracy.

Responses of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2) were studied by near infrared spectroscopy during the first week of life in 12 newborn infants, 11 of whom were receiving mechanical ventilation. 5 of the infants were thought to have normal brains, and 7 had various forms of cerebral injury. In the normal infants, increases in PaCO2 of about 1-2kPa caused cerebral blood volume to increase by 0.5 to 1.8ml.100g−1.kPa−1: the size of the increase appeared to be gestation-dependent. Estimated cerebral blood flow increased correspondingly. In the 7 infants with cerebral injuries the responses to changes in PaCO2 were usually less. In 3 term infants who had been severely birth-asphyxiated they were absent or grossly reduced and all 3 had elevated cerebral blood volumes. 3 of the 7 infants died and all 4 survivors had loss of brain tissue. We conclude that: 1) the sensitivity of the cerebral vasculature to PaCO2 probably increases with gestation, 2) cerebral injury is associated with diminished or absent responses to PaCO2.

Measurement of arterial carbon dioxide tension (paCO2) is an invasive technique for determining the adequacy of ventilation and, therefore, is associated with possible morbidity. Consequently, a non-invasive means for estimating paCO2 is desirable. A Chemetron mass spectrometer (MS) with a response time of 0.68 sec to 63% of a step change in CO2 and analytic accuracy for CO2 of ± 2% was used to measure PECO2 of neonates on IPPV/CPAP. Gas was continually sampled from 1.0 cm beyond the plastic adapter of an oral ET tube via a catheter with inner diameter 0.38 mm. 9 neonates (mean BW 2182g, range 870-3440; mean GA 33.8 wk, range 26-40) with cardiopulmonary diseases (5 HMD, 2 aspiration, 1 each PDA, CHD, BPD, pneumothorax) were studied at an initial mean age of 82 hrs (6/9 < 72 hrs), 75 paired comparisons of PECO2 and paCO2 had a correlation of 0.69 (p < 0.001) and a mean gradient (paCO2-PECO2) of 8.3 torr (range +23 to -3). 61.3% of the gradients were ≤ 10 torr. We conclude that the MS is a useful monitoring device but that the correlation between paCO2 and PECO2 was adversely affected by the relatively long response time of the total system. We speculate that reduction of this parameter would enhance the usefulness of the MS by increasing the correlation and decreasing the gradient.

Previous studies in adults have shown that CO2 is a major factor in cerebral blood flow regulation. The present study investigates the effect of hyperventilation on cerebral and other organs blood flow in 8 newborn lambs 15 days old. Following chronic catheterization,blood gases, Hct, Hb, pH, lactates, pyruvates, and regional blood flows using the microsphere technique were obtained prior to and following hyperventilation. Mean values for blood flow ± SD in ml/min/100g tissue at a baseline PaCO2 of 36 mmHg and after hyperventilation to 20 and 12 mmHg respectively were: brain - from 118 ± 14 to 83 ± 10 to 59 ± 17 (p < 0.05); adrenal - from 418 ± 60 to 365 ± 45 to 303 ± 40 (p < 0.05); kidney - from 458 ± 49 to 408 ± 31 (p < 0.05) to 201 ± 42 (p < 0.01); heart - from 111 ± 32 to 88 ± 21 to 59 ± 15 (NS). Cardiac output did not significantly change from a mean value ± SD in ml/min/kg of 197 ± 39 to 161 ± 33 to 108 ± 24 at 20 and 12 mmHg respectively. There was no change in whole blood buffer base with acute changes in PaCO2. This data demonstrates that hyperventilation reduced organ blood flow independent of cardiac output. Cerebral blood flow in the newborn lambs as in the adults seems sensitive to changes in PaCO2 with the reduction being most marked (50% from baseline value) at a PaCO2 of 12 mmHg. These data also suggest that a similar mechanism may be responsible for the reduction in renal and adrenal blood flows.