Factors associated with carbon dioxide transfer in an experimental model of severe acute kidney injury and hypoventilation during high bicarbonate continuous renal replacement therapy and oxygenation membrane support.

OBJECTIVE: To investigate the factors influencing carbon dioxide transfer in a system that integrates an oxygenation membrane in series with high-bicarbonate continuous veno-venous hemodialysis in hypercapnic animals. METHODS: In an experimental setting, we induced severe acute kidney injury and hypercapnia in five female Landrace pigs. Subsequently, we initiated high (40mEq/L) bicarbonate continuous veno-venous hemodialysis with an oxygenation membrane in series to maintain a pH above 7.25. At intervals of 1 hour, 6 hours, and 12 hours following the initiation of continuous veno-venous hemodialysis, we performed standardized sweep gas flow titration to quantify carbon dioxide transfer. We evaluated factors associated with carbon dioxide transfer through the membrane lung with a mixed linear model. RESULTS: A total of 20 sweep gas flow titration procedures were conducted, yielding 84 measurements of carbon dioxide transfer. Multivariate analysis revealed associations among the following (coefficients ± standard errors): core temperature (+7.8 ± 1.6 °C, p < 0.001), premembrane partial pressure of carbon dioxide (+0.2 ± 0.1/mmHg, p < 0.001), hemoglobin level (+3.5 ± 0.6/g/dL, p < 0.001), sweep gas flow (+6.2 ± 0.2/L/minute, p < 0.001), and arterial oxygen saturation (-0.5 ± 0.2%, p = 0.019). Among these variables, and within the physiological ranges evaluated, sweep gas flow was the primary modifiable factor influencing the efficacy of low-blood-flow carbon dioxide removal. CONCLUSION: Sweep gas flow is the main carbon dioxide removal-related variable during continuous veno-venous hemodialysis with a high bicarbonate level coupled with an oxygenator. Other carbon dioxide transfer modulating variables included the hemoglobin level, arterial oxygen saturation, partial pressure of carbon dioxide and core temperature. These results should be interpreted as exploratory to inform other well-designed experimental or clinical studies.

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients.

OBJECTIVES: Under a constant inspired concentration, the uptake of a volatile anesthetic into the arterial blood should mainly be governed by alveolar ventilation, according to the assumption that the patient's cardiac output remains stable during anesthesia. We investigated whether ventilation volume affects the rate of desflurane uptake by examining arterial blood concentrations. METHOD: Thirty female patients were randomly allocated into the following three groups: hyperventilation, normal ventilation and hypoventilation. Hemodynamic variables were measured using a Finometer, inspiratory and end-tidal concentrations of desflurane were measured by infrared analysis, and the desflurane concentration in the arterial blood (Ades) was analyzed by gas chromatography. RESULTS: During the first 10 minutes after the administration of desflurane, the Ades was highest in the hyperventilation group, and this value was significantly different from those obtained for the normal and hypoventilation groups. In addition, hyperventilation significantly increased the slope of Ades-over-time during the first 5 minutes compared with patients experiencing normal ventilation and hypoventilation, but there were no differences in these slopes during the periods from 5-10, 10-20 and 20-40 minutes after the administration of desflurane. This finding indicates that there were no differences in desflurane uptake between the three groups after the first 5 minutes within desflurane administration. CONCLUSIONS: Hyperventilation accelerated the rate of the rise in Ades following desflurane administration, which was time-dependent with respect to different alveolar ventilations levels.

Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

OBJECTIVES: Under a constant inspired concentration, the uptake of a volatile anesthetic into the arterial blood should mainly be governed by alveolar ventilation, according to the assumption that the patient's cardiac output remains stable during anesthesia. We investigated whether ventilation volume affects the rate of desflurane uptake by examining arterial blood concentrations. METHOD: Thirty female patients were randomly allocated into the following three groups: hyperventilation, normal ventilation and hypoventilation. Hemodynamic variables were measured using a Finometer, inspiratory and end-tidal concentrations of desflurane were measured by infrared analysis, and the desflurane concentration in the arterial blood (Ades) was analyzed by gas chromatography. RESULTS: During the first 10 minutes after the administration of desflurane, the Ades was highest in the hyperventilation group, and this value was significantly different from those obtained for the normal and hypoventilation groups. In addition, hyperventilation significantly increased the slope of Ades-over-time during the first 5 minutes compared with patients experiencing normal ventilation and hypoventilation, but there were no differences in these slopes during the periods from 5-10, 10-20 and 20-40 minutes after the administration of desflurane. This finding indicates that there were no differences in desflurane uptake between the three groups after the first 5 minutes within desflurane administration. CONCLUSIONS: Hyperventilation accelerated the rate of the rise in Ades following desflurane administration, which was time-dependent with respect to different alveolar ventilations levels.

Carbon dioxide monitoring during long-term noninvasive respiratory support in children.

INTRODUCTION: Routine monitoring of noninvasive respiratory support relies on nocturnal pulse oximetry and daytime arterial blood gases, without systematic nocturnal carbon dioxide recording. The aim of the study was to assess if overnight pulse oximetry and daytime blood gases are sufficiently accurate to detect nocturnal hypoventilation in children receiving long-term noninvasive respiratory support. MATERIALS AND METHODS: Pulse oximetry and carbon dioxide pressure measured by capillary arterialized blood gases and a combined transcutaneous carbon dioxide and pulse oximetry (PtcCO(2)/SpO(2)) monitor were compared in 65 patients (asthma, n = 16, recurrent bronchitis, n = 8, lung infection, n = 8, cystic fibrosis, n = 15, interstitial lung disease, n = 6, neuromuscular disease, n = 12). Daytime capillary arterialized blood gases and nocturnal recording of pulse oximetry and carbon dioxide by means of a combined PtcCO(2)/SpO(2) monitor were performed in 50 other patients receiving nocturnal noninvasive respiratory support at home. RESULTS: A correlation was observed between pulse oximetry (r = 0.832, P < 0.0001) and carbon dioxide pressure (r = 0.644, P < 0.0001) measured by capillary arterialized blood gases and the combined PtcCO(2)/SpO(2) monitor. Twenty-one of the 50 patients (42%) on long-term noninvasive respiratory support presented nocturnal hypercapnia, defined by a PtcCO(2) value >50 mmHg, without nocturnal hypoxemia. Daytime capillary arterialized carbon dioxide levels were normal in 18 of these 21 patients. CONCLUSIONS: Nocturnal hypercapnia may occur in children receiving nocturnal noninvasive respiratory support at home. Nocturnal pulse oximetry and daytime arterial blood gases are not sufficiently accurate to diagnose nocturnal hypercapnia, underlying the importance of a systematic carbon dioxide monitoring in children receiving noninvasive respiratory support.

Comparison of a sidestream capnograph and a mainstream capnograph in mechanically ventilated dogs.

OBJECTIVE: To compare the ability of a sidestream capnograph and a mainstream capnograph to measure end-tidal CO2 (ETCO2) and provide accurate estimates of PaCO2 in mechanically ventilated dogs. DESIGN: Randomized, double Latin square. ANIMALS: 6 healthy adult dogs. PROCEDURE: Anesthesia was induced and neuromuscular blockade achieved by IV administration of pancuronium bromide. Mechanical ventilation was used to induce conditions of standard ventilation, hyperventilation, and hypoventilation. While tidal volume was held constant, changes in minute volume ventilation and PaCO2 were made by changing the respiratory rate. Arterial blood gas analysis was performed and ETCO2 measurements were obtained by use of either a mainstream or a sidestream capnographic analyzer. RESULTS: A linear regression model and bias analysis were used to compare PaCO2 and ETCO2 measurements; ETCO2 measurements obtained by both capnographs correlated well with PaCO2. Compared with PaCO2, mainstream ETCO2 values differed by 3.15 +/- 4.89 mm Hg (mean bias +/- SD), whereas the bias observed with the sidestream ETCO2 system was significantly higher (5.65 +/- 5.57 mm Hg). Regardless of the device used to measure ETCO2, bias increased as PaCO2 exceeded 60 mm Hg. CONCLUSIONS AND CLINICAL RELEVANCE: RelevancehAlthough the mainstream cas slightly more accurate, both methods of ETCO2 measurement correlated well with PaCO2 and reflected changes in the ventilatory status. However, ETCO2 values > 45 mm Hg may inaccurately reflect the severity of hypoventilation as PaCO2 may be underestimated during conditions of hypercapnia (PaCO2 > 60 mm Hg).

Mechanisms for episodes of hypoxemia in preterm infants undergoing mechanical ventilation.

OBJECTIVE: To ascertain possible mechanisms implicated in the development of transient episodes of hypoxemia (oxygen saturation < 85%) frequently observed in preterm infants undergoing mechanical ventilation, even after the acute phase of respiratory failure has passed. STUDY DESIGN: Tidal flow, airway and esophageal pressure, and oxygen saturation were continuously recorded in 10 infants (mean +/- SD, birth weight 733 +/- 149 gm, gestational age 25.5 +/- 2.2 weeks, age 26.3 +/- 11.9 days) who had repeated episodes of hypoxemia without any evident cause. Measurements of minute ventilation (VE) inspiratory compliance (Ci), and inspiratory resistance (Ri) were compared before and during episodes of hypoxemia. RESULTS: All episodes of hypoxemia were preceded by an active exhalation that produced a mean decrease in end-expiratory lung volume of 6.4 +/- 2.8 ml/kg. The reduction in lung volume was immediately followed by a sudden decrease in tidal flow and volume, despite continuation of mechanical ventilation at the same rate and peak pressure. The resulting hypoventilation was associated with a drop in Ci to approximately one half and an increase in Ri to more than double the baseline values. Approximately 30 seconds after the beginning of hypoventilation, the arterial oxygen saturation reached a hypoxemic level (oxygen saturation < 85%)> CONCLUSION: Most hypoxemic episodes were triggered by an expiratory effort that produced a large decrease in lung volume. This reduction in lung volume probably leads to closure of small airways and the development of intrapulmonary shunts, which would explain the rapid development of hypoxemia.

Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation.

The effect of rapid or slow infusion of hypertonic sodium bicarbonate on acid-base balance and serum osmolality was studied in 36 acidotic newborn dogs. Respiratory acidosis and hypoxia were produced by mechanically fixed hypoventilation. One group of animals breathed 100% O2 to prevent hypoxemia. Rapid infusion of HCO3- in acidotic and hypoxic animals resulted in only a transient (1 minute) and small (0.05 pH units) elevation of arterial pH followed by a continuous fall, resulting in a lower pH and a worsened metabolic condition than in the nontreated controls. In nonhypoxic acidotic animals, rapid infusion of HCO3- had little effect on arterial pH. PaCO2 increased suddenly by 17 Torr in hypoxic and, by 13 Torr, in nonhypoxic animals. There was a concomitant fall in PaO2 (15 Torr). Serum osmolality rose rapidly after rapid infusion of HCO3-. Rapid infusion of hypertonic bicarbonate into an animal or infant whose ventilation is fixed thus results in a less than predicted elevation of arterial pH. PaCO2 rises, PaO2 falls, and serum osmolality rises. The net result may be a worsening rather than an improvement in the animals' metabolic state.