Abstract

The arterial-alveolar tension gradient for CO2 has been investigated in 17 normal new born infants and in 15 with some degree of respiratory distress. Whereas the normal infants had virtually no Pco2 gradient from pulmonary capillary to alveolus, an average difference of 13.9 mm Hg was detected in sick infants. This gradient for Pco2 is caused by increased alveolar (and total physiological dead space, the relative amount of which closely parallels the clinical course of the disease. The data obtained indicate the increase in alveolar dead space to be largely due to poor perfusion of ventilated alveoli. In severely ill infants more than 60% of ventilated alveoli appear to be under-perfused.

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