The Christiansen-Douglas-Haldane effect, in short 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 C0₂ (P_aCO₂), must be less than that of mixed venous blood (P_{V
¯}CO₂).

During the unphysiological conditions of a ‘closed’ system, e.g. hyperoxic apnoea, i.e. continuous oxygen uptake without CO₂ delivery by the lungs, the P_aco₂ will not only approximate the P_{V
¯}CO₂ but will even exceed it. Without the Haldane effect, rapid adjustment of P_aco₂ to P_{V
¯}CO₂ would be expected during apnoea due to the lack of CO₂ excretion. If however, as undertaken in this study, ongoing oxygenation (high alveolar Po₂ (P_ACO₂) with concomitant lack of C0₂ delivery (apnoea, i. e. the C0₂ concentration remains constant) lead to a continuing sufficient oxygenation of blood during its 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 (a V ¯ DPco₂) of 2.8±1.8 mmHg. The results described substantiate for the first time the existence of the Haldane effect under clinical conditions.

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Arterial and Mixed Venous Blood Gas Status during Apnoea of Intubation — Proof of the Christiansen-Douglas-Haldane Effect in Vivo