[The status of arterial and mixed venous blood gases in the initial phase of intubation apnea. Studies on the Christiansen-Douglas-Haldane effect]

Abstract

The Christiansen-Douglas-Haldane effect describes the reduced CO2 binding capacity of oxygenated as compared to deoxygenated hemoglobin on the basis of its increased acidity. This study describes the development of the above effect during the first 2 min of hyperoxic intubation apnea. METHODS. After institutional approval 12 patients (NYHA III, ASA IV) scheduled for coronary-artery bypass grafting were studied after written informed consent. Routine monitoring measures included invasive arterial and pulmonary-arterial pressure monitoring. Pulse oximetry (Nellcor N 101) was also used during intubation apnea. Premedication consisted of flunitrazepam 2.0 mg p.o. the evening before operation and another 2.0 mg p.o. 90-120 min before induction of anesthesia. Following standardized preoxygenation induction of anesthesia was performed with 20-25 micrograms/kg fentanyl and 0.1 mg/kg pancuronium. After cessation of spontaneous respiration, controlled ventilation was continued with 100% oxygen until intubation. Thirteen arterial (a) and mixed-venous (v) blood samples were drawn sequentially immediately before and during the first 2 min of apnea and analyzed using Corning 150 pH/blood gas analyzer and a Corning 2500 CO-oximeter. RESULTS. As shown in Table 1 and Fig. 1, paO2 decreased from 485 +/- 100 mmHg before apnea to 376 +/- 68 mmHg after 2 min of apnea while pvO2 remained constant at 47-50 mmHg. Arterial oxygen saturation (saO2) showed stable values greater than 97% while svO2 slightly increased from 81.9% to 82.4% until the end of apnea. A biphasic increase was observed in paCO2 from 41.2 +/- 3.4 mmHg before to 54.5 +/- 3.9 mmHg at the end of apnea. An increase in pvO2 during apnea was linear from 45.7 +/- 3.9 mmHg to 51.9 +/- 4.0 mmHg. After 28.5 s of apnea paCO2 exceeded pvCO2 due to the Haldane effect ("pCO2 reversal"). During apnea, pHa decreased biphasically from 7.40 +/- 0.03 to 7.31 +/- 0.02. The speed of decrease was 0.106 pH units/min (5-35 s) in the 1st and 0.023 pH units/min in the 2nd min of apnea; pHv decreased almost linearly from 7.37 +/- 0.03 mmHg (5s) to 7.33 +/- 0.02 mmHg (115s). After 20.66 s of apnea pHa exceeded pHv ("pH reversal"); pH-reversal occurred earlier than pCO2 reversal (p less than = 0.05). CONCLUSIONS. During early hyperoxic apnea, venoarterial pH and pCO2 reversal can be observed due to the Christiansen-Douglas-Haldane effect. pH reversal starts earlier than pCO2 reversal. Reversal time is dependent on arterial-mixed-venous pCO2 difference (avDpCO2) before apnea, arterial-mixed-venous O2 saturation difference (avDsO2) and cardiac output. The amount of reversal is dependent on avDsO2, i.e. the pH difference of arterial and m