Contribution of the Haldane Effect to the Increase in Arterial Carbon Dioxide Tension in Hypoxaemic Subjects Treated with Oxygen
Carbon dioxide retention is a well-known risk of oxygen administration to hypoxaemic patients. The classic explanation for this retention is that oxygen cuts off the hypoxic drive for ventilation leading to a decreased ventilation in patients in whom the ventilatory response to carbon dioxide is diminished. However, Aubier et al.1 found only a slight decrease in steady state minute ventilation (V̇E) in patients with chronic obstructive pulmonary disease (COPD) in whom hypoxaemia had been relieved by oxygen administration. Nevertheless, the mean rise in arterial oxygen tension (pO2(a)) of 38 to 225 mmHg and in arterial oxygen saturation (sO2(a)) of 65% to 100% in their patients was attended by a mean rise in arterial carbon dioxide tension (pCO2(a)) of 65 to 88 mmHg. The greater part of this rise is explained by an increased inhomogeneity of the ventilation/perfusion (V̇/Q̇) distribution within the lungs, which may be due to the relief by oxygen of hypoxic vasoconstriction in poorly ventilated lung units. In addition a substantial part of the rise in pCO2(a) is ascribed to the Haldane effect. Aubier et al. calculate that in their series the Haldane effect caused a rise in pCO2(a) of 7 mmHg
KeywordsDioxide Bicarbonate Posite Carbamate Haldane
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