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After laparoscopic cholecystectomy, carbon dioxide (CO2) must be exhaled after resorption from the abdominal cavity. There is controversy about the amount and relevance of postoperative CO2 resorption. Without continuous postoperative monitoring, after laparoscopic cholecystectomy a certain risk may consist in unnoticed hypercapnia due to CO2 resorption. Studies exist on the course of end-expiratory CO2 (Pe-CO2) alone over a longer postoperative period of time in extubated patients during spontaneous breathing. The goal of this prospective study was to investigate the amount of CO2 resorbed from the abdominal cavity in the postoperative period by means of CO2 metabolism. METHODS. After giving informed consent to the study, which was approved by the local ethics committee, 20 patients underwent laparoscopic cholecystectomy. All patients received general endotracheal anaesthesia. After induction, total IV anaesthesia was maintained using fentanyl, propofol, and atracurium. Patients were ventilated with oxygen in air (FiO2 0.4). The intra-abdominal pressure during the surgical procedure ranged from 12 to 14 mm Hg. Thirty minutes after releasing the capnoperitoneum (KP), CO2 elimination (VCO2), oxygen uptake (VO2), and respiratory quotient (RQ) were measured every minute for 1 h by indirect calorimetry using the metabolic monitor Deltatrac according to the principle of Canopy. Assuming an unchanged metabolism, the CO2 resorption (delta VCO2) at any given time (t) can be calculated from delta VCO2 (t) = VCO2 (t)-RQ(preop) VO2 (t). It was thus necessary to define the patient's metabolism on the day of operation. The first data were collected before surgery and after introduction of the arterial and venous cannulae for a 15-min period. Measuring point 0 was determined after exsufflation of the KP and emptying of the remaining CO2 via manual compression by the surgeon at the end of surgery. Patient's tracheas were extubated and metabolic monitoring started 30 min after release of the KP for 60 min. Simultaneously, a nasal side-stream capnometry probe was placed and the PeCO2 and respiratory frequency (RF) were obtained by the Capnomac Ultima (Datex) and registered every minute as well. Values were averaged over four periods of 15 min each. An arterial blood gas sample was drawn at the end of every 15-min period. Postoperative pain was scored by a visual analog scale and completed by a subjective index questionnaire on general well-being. All data were analysed by the Friedman or Wilcoxon test; P < 0.05 was considered significant. RESULTS. The findings do not indicate CO2 resorption in the postoperative period after laparoscopic cholecystectomy (Tables 2 and 3, Fig. 1). Arterial CO2 as well as PeCO2 were elevated postoperatively (45 mm Hg vs. 36 mm Hg intraoperatively), while VCO2 and VO2 were unchanged when compared to the preoperative measuring period. The postoperative RF was comparable to preoperative values. Calculated delta CO2 was lower than 10 ml/min and within accuracy of measurements. The post-operative pain index ranged between 3 and 4, and 3.75-15 mg piritramid was administered. All patients felt tired immediately after the operation, but scores improved slightly at the end of the 60-min period of metabolic monitoring. CONCLUSIONS. There is no significant resorption of CO2 from the abdominal cavity later than 30 min after releasing the KP. Up to this time, any CO2 remaining in the abdominal cavity after careful emptying by the surgeon has been resorbed and exhaled. An increased PeCO2 as late as 30 to 90 min postoperatively should rather be considered a consequence of residual anaesthetics and narcotics than of CO2 resorption.

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.

Hypoxia and the hypercapnia were produced in anesthetized dogs by artificial respiration with appropriate gas mixtures, and a study was conducted of the effects of these conditions on various metabolic parameters, viz. catecholamines, renin activity, lactate, pyruvate, cortisol, non-esterified free fatty acids (FFA), and ammonia, in the plasma of the arterial blood. Hypercapnia caused a distinct increase in catecholamine concentrations, renin activity and ammonia, and a decrease in lactate and pyruvate; cortisol and FFA levels were only slightly altered. Hypoxia increased lactate, pyruvate and--though only to a slight extent--FFA, cortisol and NH3. The changes induced by hypercapnia were chiefly attributable to activation of the sympathico-adrenal system; those induced by hypoxia were not.