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The Christiansen-Douglas-Haldane effect, in short the Haldane effect, describes the dependence of the CO 2  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 C0 2  (P a CO 2 ), must be less than that of mixed venous blood (P [Formula: see text] CO 2 ).    During the unphysiological conditions of a ‘closed’ system, e.g. hyperoxic apnoea, i.e. continuous oxygen uptake without CO 2  delivery by the lungs, the P a co 2  will not only approximate the P [Formula: see text] CO 2  but will even exceed it. Without the Haldane effect, rapid adjustment of P a co 2  to P [Formula: see text] CO 2  would be expected during apnoea due to the lack of CO 2  excretion. If however, as undertaken in this study, ongoing oxygenation (high alveolar Po 2  (P A CO 2 ) with concomitant lack of C0 2  delivery (apnoea, i. e. the C0 2  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 CO 2  binding curve — the Haldane effect.    The resulting increase in Pco 2  as shown here actually leads to an arterial-mixed venous CO 2  partial pressure difference (a[Formula: see text]DPco 2 ) of 2.8±1.8 mmHg. The results described substantiate for the first time the existence of the Haldane effect under clinical conditions.

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