Intra-arterial and extra-arterial pH, PCO2 and PO2 monitors

In vitro blood gas analysers inherently limit the frequency of serial blood gas measurements because of blood loss and cost. In vivo blood gas monitors eliminate an inherent cost and blood loss associated with measurement. Optode microsensing is a technology that can be readily adapted to in vivo measurement of pH, PCO₂ and PO₂. Optode-based intra-arterial devices that display continuous values have been developed that are practical for routine use but consistent performance remains a problem; an extra-arterial device that provides intermittent values has been shown to be consistent but is not yet available for routine use. The transfer of blood gas measurements from laboratory analysers to the combination of point-of-care analysers and monitors should have as profound an impact on acute respiratory care as did the introduction of laboratory-based blood gas analysers over 30 years ago. However, we must be sure these devices are reliable, consistent and cost beneficial in order to avoid widespread adoption of yet another technology that provides more data, more cost, and questionable patient benefit.     

PCO2 electrodes at the surface of the kidney detect ischaemia

Background: Under ischaemic (anaerobic) conditions there will be an accumulation of CO₂ in the tissue secondary to a build up of protons that is buffered by HCO₃^-. We reasoned that CO₂ could be measured at the surface of the kidney by PCO₂ electrodes to detect ischaemic conditions. Methods: Anaesthetized, mechanically ventilated pigs (25–30 kg) were investigated. Two acute porcine models, one of haemorrhagic shock and one of renal artery stenosis were used. Renal blood flow was gradually decreased, either by successive episodes of bleeding through the arterial cannula or by successive snaring of the renal artery. Results: In both models we found that with decreased blood flow but maintained aerobic metabolism (supply independence) PCO₂ both at the surface of the kidney and in the renal vein increased by 2–3 kPa. Thus, the tissue-venous PCO₂ difference did not change much. At DO_2crit, i.e., at the transition to supply-dependent O₂ consumption, the tissue PCO₂ started to increase rapidly, as did the tissue-venous PCO₂ difference. This is compatible with the notion that a hallmark of ischaemia is decreased ability of the blood to transport away waste products because the contact between large parts of tissue and blood is virtually non-existent. In the renal artery stenosis model kidney surface PCO₂ values rose from a baseline of 6.6±0.6 kPa (mean±SEM) to a value near DO_2crit of 10.6±0.8 kPa, reaching a final value of 29.9±3.5 kPa at no flow. PCO₂ in the renal vein, however, reached a maximum of only 8.2±0.6 kPa. Numbers very similar to these were also found in the haemorrhagic model. The urine production decreased before the onset of ischaemia. When surface PCO₂ values increased sharply indicating ischaemia, the urine production was zero. Lactate production by the kidney correlated very well with increasing tissue PCO₂ values further corroborating that anaerobic metabolism was detected with the electrodes. Conclusion: We conclude that PCO₂ electrodes placed at the surface of the kidney detect renal cortical ischaemia.     

Pulmonary ventilation, CO2 response and inspiratory drive in spontaneously breathing young infants during halothane anaesthesia

Pulmonary ventilation, CO2 response and inspiratory drive were studied during halothane anaesthesia prior to surgery in 13 spontaneously breathing infants less than 6 months of age. Pneumotachography and capnography were used. Airway and oesophageal pressures were measured and occlusion tests were performed at functional residual capacity. Measurements were made before and during 8 min of 4% CO2 stimulation. Inspiratory drive increased significantly (P less than 0.001) at CO2 stimulation. This resulted in increased minute ventilation (P less than 0.001) and tidal volume (P less than 0.001) while respiratory rate was unchanged. As VBohrD/VT ratios were the same, the net effect was increased alveolar ventilation (P less than 0.001). CO2 elimination was unpredictable in these young infants and decreased during CO2 stimulation (P less than 0.05), while mean end-tidal CO2 concentration only increased from 5.2 to 6.3% (P less than 0.001). The ventilatory response to 4% CO2 could therefore be deemed to be adequate during the short period (8 min) of CO2 breathing. However, this was achieved at the cost of increased work as witnessed by the increased ratio between minute ventilation and CO2 elimination (P less than 0.01). Stabilisation of end-tidal CO2 concentrations during CO2 inhalation took only 10 s while the maximal increase in ventilation volumes was not achieved until after 150 s. It is concluded that young spontaneously breathing infants anaesthetized with halothane (MAC 1.3) have an increased respiratory drive with greater tidal volumes during CO2 stimulations. Respiratory timing, dynamic compliance and total pulmonary resistance were, however, uninfluenced by 4% CO2 stimulation. Increased monitoring of CO2 output in anaesthetized infants is suggested.     

Perioperative gastric tonometric PCO2 and intramucosal pH in patients undergoing liver transplantation

BACKGROUND: Extensive research has focused on the role of insufficient gastro-intestinal perfusion and inflammatory activation in the development of organ dysfunction during critical illness. In patients undergoing liver transplantation, portal and caval vein clamping leads to gastro-intestinal and lower extremity venous congestion during the anhepatic phase, and studies suggest that gastro-intestinal perfusion may be compromised. This study was performed to investigate gastro-intestinal perfusion in patients undergoing liver transplantation. METHODS: In 16 patients undergoing liver transplantation, perioperative gastric tonometry with determination of tonometric PCO2, tonometric-arterial PCO2 gradient and intramucosal pH were performed. Blood gases were obtained simultaneously from the arterial and portal vein blood. RESULTS: Tonometric PCO2 was 4.6 (4.2/5.3) kPa preoperatively and increased to 5.6 (4.5/6.0) kPa during the anhepatic phase (P<0.01), while the tonometric-arterial PCO2 gradient increased from -0.3 (-0.5/0.0) kPa preoperatively to 0.7 (0.3/1.2) kPa during the anhepatic phase (P<0.01). Intramucosal pH decreased to 7.27 (7.21/7.32) u during the anhepatic phase (P<0.01, compared to preoperatively). The portal vein PCO2 was not significantly different from arterial PCO2 or tonometric PCO2 at any measurement point. CONCLUSION: This study demonstrates that clinical liver transplantation is associated with gastro-intestinal perfusion in the range of aerobic metabolism. The results do not support the presence of gastro-intestinal perfusion in the range of anaerobic metabolism.     

Respiratory Depressant Action of Tilidine during N2O+O2, Anaesthesia

The respiratory depressant actions of pethidine and tilidine during anaesthesia were compared in 18 surgical patients anaesthetized with N₂O + O₂ after thiopental induction. Five minutes after thiopental, 0.5 mg/kg pethidine or 1.5 mg/kg tilidine were each given intravenously to six patients, the remaining six patients serving as controls.
Minute ventilation, respiratory rate, end-tidal CO₂ and Pco₂ from arterialized venous blood were measured up to 30 min. Pethidine caused the following maximal changes: 0–0.98±0.24 (s.e. mean) 1/min, rate -.5.5 ± 0.7/min, C0_2ET+0.7±0.1 vol % and Pco₂ + 5.7±1.1 mm Hg. These changes occurred within 10 xnin of the injection.
In terms of the above parameters, tilidine caused at least as pronounced a respiratory depression as pethidine. The peak effect of tilidine, however, could not be measured with certainty, since the respiratory depression first became apparent 15 min after the injection, and then increased throughout the study period. The long onset time of tilidine explains our previous failure to demonstrate tilidine-induced respiratory depression.     

Single breath end-tidal Pco2, measurement during high frequency jet ventilation in critical care patients

The relationship between arterial and end-tidal carbon dioxide tensions following a single large breath was investigated in seven critically ill patients receiving high frequency jet ventilation. There was a close correlation (r = 0.989) between arterial and end-tidal carbon dioxide tensions over a wide range (3.29-8.95 kPa). Measurement of the end-tidal carbon dioxide tension following a single large breath may be useful in monitoring the efficiency of high frequency jet ventilation in the elimination of carbon dioxide.