ARTERIAL AND MIXED-VENOUS BLOOD-GASES DUR ING INTUBATION APNEA AND AFTER ONSET OF CONTROLLED VENTILATION - CLINICAL-EVIDENCE OF THE CHRISTIANSEN-DOUGLAS-HALDANE EFFECT

The Christiansen-Douglas-Haldane effect describes the reduced CO2 bind ing capacity of oxygenated compared to deoxygenated haemoglobin. Under the condition of a ''closed system'', for example hyperoxic apnoea af ter adequate preoxygenation (continuous O2 uptake with lack of CO2 del ivery), specific effects on the arterial and mixed venous blood gas st atus, due to the Haldane effect, are seen: within 30 s after onset of apnoe, ''paradoxical pCO2'' (paCO2 exceeds pvCO2BAR) and ''pH reversal '' (pHa falls under pHvBAR) can be observed. It was the aim of this st udy to demonstrate how fast arterial and mixed venous pCO2 and pH norm alize when a change from apnoea (''closed system'') to controlled vent ilation (''open system'') takes place. Methods. 12 patients (ASA II-IV , NYHA II-III) scheduled for coronary artery bypass grafting were stud ied. Premedication consisted of flunitrazepam 2.0 mg p.o. given the ev ening 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 contin uous pulse oximetry. Following standardized preoxygenation, induction of anaesthesia was performed with fentanyl, pancuronium and etomidate. After cessation of spontaneous respiration, controlled ventilation wa s 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 ar terial (a) and 18 mixed-venous (vBAR) blood samples were drawn simulta neously in a sequential manner immediately before and during the last 20 s of apnoea, as well as within 4 min after onset of controlled vent ilation (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 tota l decrease of 131.5 mmHg that was followed by an almost linear increas e of 29.7 mmHg/min (Fig. 1a). In the course of apnoea and controlled v entilation the pvO2BAR remained relatively stable, with values ranging from 42 to 43 mmHg (Fig. 1b). During apnoea the paCO2 showed an incre ase 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 con trolled ventilation (Fig. 2 a). With an increase of 4.2 mmHg, the pvCO 2BAR 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). C omparing the course of paCO2 and pvCO2BAR during apnoea as well as dur ing the period of controlled ventilation, pHa and pHvBAR changed in a reciprocal manner (Fig. 3a/b). The so-called normalization of pCO2 (pa CO2 falls under pvCO2BAR) and pH (pHa exceeds pHvBAR) began 18.2 s and 23.2 s respectively after the onset of controlled ventilation (Fig. 4 a, b). Conclusions. Considering the expected decrease of paO2 during h yperoxic apnoea, insufficient pulmonary N2 elimination prior to the on set of apnoea, as well as direct N2 delivery into the alveoli, due to the so-called a ventilatory mass flow, will limit unrestricted pulmona ry O2 uptake. The continuing decrease of the paCO2 after the onset of controlled ventilation can be regarded as indirect proof of a ventilat ory mass flow. The course of pCO2 and pH after the onset of controlled ventilation shows that normalization in arterial and mixed-venous blo od gas status takes place in about 18.2 s after the cessation of apnoe a.