BLOOD-GAS DISEQUILIBRIUM THEORY

Disequilibria [in mammals] in blood while it is in the lungs, and probably acid-base changes across or along pulmonary vessel walls, seem to stimulate chemoreceptors which ensure that lung ventilation is in proportion to total pulmonary blood flow. After blood leaves the lungs, pH, PCO2 [CO2 tension] and PO2 [O2 tension] probably all rise at rates and by amounts not yet determined. The strongest evidence that the PCO2 rises can be derived from dead space calculations. The notion that PCO2 measured at equilibrium in an arterial sample represents alveolar PCO2 should probably be abandoned along with the ideal PA[arterial O2 tension]O2 and the AaDO2 [alveolar-arterial O2 tension difference] as conventionally calculated. Disequilibrium theory suggests a unified scheme whereby many diverse and confusing features of the immediate respiro-vascular response to sudden metabolic stress can be explained.