Ventilation and respiratory gas transfer was studied in 44 infants; 13 of whom had pulmonary overperfusion without pulmonary edema or transposed great arteries. In order to assess the evenness of ventilation/perfusion ratios throughout the lung, (VA/Q distribution) measurements were made of the urine-alveolar nitrogen tension difference (U-Ā)DN2 in a separate group of six normal children and seven children with pulmonary overperfusion.
Infants with pulmonary overperfusion (left-to-right shunts) had normal alveolar ventilation (149.6±18.2 ml/minute/kg). Respiratory rate (38.1±10.2) was slightly increased and tidal volume (6.0±1.3 ml/kg) was diminished, possibly due to reduced lung compliance. Measurements of dead space, dead space/tidal volume ratio, and alveolar ventilation/oxygen consumption ratio were unremarkable.
No significant arterial-alveolar CO2 difference was detected in either normal subjects or those with heart disease, but a significantly increased alveolar-arterial O2 tension difference (A-a)DO2 of 22.4±8.6 mm Hg was found in infants with overperfused lungs.
Measurements of (A-a)DO2 during 100% oxygen breathing and measurements of (U-Ā)DN2 in the air-breathing subjects both suggested that intrapulmonary venous admixture rather than VA/Q unevenness was the principal factor causing lowered oxygen tensions in the arterial blood of infants with overperfused lungs.
Lowered arterial oxygen tension was associated with only trivial arterial unsaturation (92.8±2.4%) due to the high affinity of hemoglobin for oxygen.