Hyperoxic intubation apnoea: an in vivo model for the proof of the Christiansen-Douglas-Haldane effect.

The Christiansen-Douglas-Haldane effect, commonly known as the HALDANE effect, describes the dependence of the CO2 binding of blood on the degree of oxygenation of haemoglobin. Under the physiological conditions of an "open" system between blood and alveoli the partial pressure of arterial CO2, after CO2 delivery to the alveoli for example, can only range below the value of mixed venous blood. However, during the unphysiological circumstances of a "closed" system, e.g. the state of hyperoxic apnoea, i.e. oxygen uptake and lacking CO2 delivery, the paCO2 cannot only approximate the mixed venous value but must even exceed it. Without the Haldane effect coming into force, a rapid adjustment of arterial to mixed venous pCO2 would have to be expected during apnoea, due to the lacking CO2 delivery. If however, as a consequence of adequate preoxygenation (a high alveolar pO2) and failure to eliminate CO2 (i.e. the CO2 concentration remains constant) a sufficient oxygenation of blood takes place during the passage through the lung capillaries, then this leads to a rightwards shift of the CO2 binding curve--the Haldane effect. The resulting increase in pCO2 as shown here, actually leads to an arterial-mixed venous CO2 partial pressure difference of 2.8 +/- 1.8 mmHg, where pvCO2 decreases paCO2. The results described substantiate for the first time the existence of the Haldane effect under clinical conditions, too.