[The behavior of arterial and mixed venous oxygen and carbon dioxide partial pressure and the pH value during and following intubation apnoea. Studies on the occurrence of the Christiansen-Douglas-Haldane effect].

The Christiansen-Douglas-Haldane effect describes the reduced CO2 binding capacity of oxygenated compared to deoxygenated haemoglobin. Under the condition of a "closed system", for example hyperoxic apnoea after adequate preoxygenation (continuous O2 uptake with lack of CO2 delivery), specific effects on the arterial and mixed venous blood gas status, due to the Haldane effect, are seen: within 30 s after onset of apnoea, "paradoxical pCO2" (paCO2 exceeds pvCO2) and "pH reversal" (pHa falls under pHv) can be observed. It was the aim of this study to demonstrate how fast arterial and mixed venous pCO2 and pH normalize when a change from apnoea ("closed system") to controlled ventilation ("open system") takes place. METHODS. 12 patients (ASA II-IV, NYHA II-III) scheduled for coronary artery bypass grafting were studied. Premedication consisted of flunitrazepam 2.0 mg p.o. given the evening before operation and another 2.0 mg p.o. given 90-120 min before induction of anaesthesia. Routine preparation for induction consisted of venous and arterial cannulas, pulmonary artery catheter and continuous pulse oximetry. Following standardized preoxygenation, induction of anaesthesia was performed with fentanyl, pancuronium and etomidate. After cessation of spontaneous respiration, controlled ventilation was continued with 100% O2 until intubation. Intubation and insertion of stomach tube and oesophageal temperature probe were undertaken after exactly 2 min. After reconnection to the semi-closed circle breathing system, controlled ventilation was continued with 100% O2. Eighteen arterial (a) and 18 mixed-venous (v) blood samples were drawn simultaneously in a sequential manner immediately before and during the last 20 s of apnoea, as well as within 4 min after onset of controlled ventilation (Table 1). The pO2 (mmHg), pCO2 (mmHg) and pH were determined using a Stat Profile 5 blood gas analyser. RESULTS. During apnoea and within the first 35 s of controlled ventilation the paO2 showed a total decrease of 131.5 mmHg that was followed by an almost linear increase of 29.7 mmHg/min (Fig. 1a). In the course of apnoea and controlled ventilation the pvO2 remained relatively stable, with values ranging from 42 to 43 mmHg (Fig. 1b). During apnoea the paCO2 showed an increase of 12.5 mmHg that was followed by a biphasic decrease (first 13.8 mmHg/min and then 0.75 mmHg/min) beginning 15 s after the onset of controlled ventilation (Fig. 2a). With an increase of 4.2 mmHg, the pvCO2 showed about a third of the increase of the paCO2 during apnoea, reaching a maximum 45 s after the onset of controlled ventilation and then being followed by a linear decrease of 0.86 mmHg/min (Fig.2b). Comparing the course of paCO2 and pvCO2 during apnoea as well as during the period of controlled ventilation, pHa and pHv changed in a reciprocal manner (Fig. 3a/b). The so-called normalization of pCO2 (paCO2 falls under pvCO2) and pH (pHa exceeds pHv) began 18.2 s and 23.2 s respectively after the onset of controlled ventilation (Fig. 4a, b). CONCLUSION. Considering the expected decrease of paO2 during hyperoxic apnoea, insufficient pulmonary N2 elimination prior to the onset of apnoea, as well as direct N2 delivery into the alveoli, due to the so-called a ventilatory mass flow, will limit unrestricted pulmonary O2 uptake. The continuing decrease of the paCO2 after the onset of controlled ventilation can be regarded as indirect proof of a ventilatory mass flow. The course of pCO2 and pH after the onset of controlled ventilation shows that normalization in arterial and mixed-venous blood gas status takes place in about 18.2 s after the cessation of apnoea.