Abstract
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 CO2 (PaCO2), must be less than that of mixed venous blood (PvCO2). During the unphysiological conditions of a 'closed' system, e.g. hyperoxic apnoea, i.e. continuous oxygen uptake without CO2 delivery by the lungs, the PaCO2 will not only approximate the PvCO2 but will even exceed it. Without the Haldane effect, rapid adjustment of PaCO2 to PvCO2 would be expected during apnoea due to the lack of CO2 excretion. If, however, as undertaken in this study, ongoing oxygenation (high alveolar PO2 (PACO2) with concomitant lack of CO2 delivery (apnoea, i.e. the CO2 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 (avDPCO2) 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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