Title: 6 Ventilation/Perfusion Relationships in the Lungs of Children with Congenital Heart Disease
Abstract: The large increases and reductions of pulmonary blood flow (Qp) observed in congenital heart disease must challenge the lungs in their function of maintaining physiologic respiratory gas tensions in arterial blood, if ventilation (VA) and Qp arenotwell matched throughout the lung, alveolar-arterial respiratory gas tension differences result. We have examined the extent of uneven VA/QP ratio distribution by the alveolararterial O2 difference (A-aDO2) breathing air and 100 % O2; (10 subjects) and the steady-state air-breathing arterial-alveolar N2 difference (a-ADN2) (21 subjects). Arterial N2 tension was assessed by gas chromatographic determination of urine N2 tension (PuN2). Normal subjects had air breathing A-aDO2 of 10±2.7 mm Hg and 16±10 mm Hg breathing 100% O2. Those with pulmonary overperfusion had A-aDO2 of 22.4±8.6 mm Hg on room air and 135±48 mm Hg on 100 % O2 suggesting that intrapulmonary venous admixture rather than VA/QP unevenness was the major cause of lowered arterial O2 tension. Urine-alveolus N2 difference (U-ADN2) in normal subjects was 7.6±4.3 mm Hg. U-ADN2 was 3.3±6.4 mm Hg in those with overperfused lungs suggesting very even VA/QP ratio distribution. Children with underperfused lungs had U-ADN2 of 14±7.7 mm Hg indicating considerably increased VA/QP ratio unevenness. We conclude that pulmonary overperfusion is associated with rather even matching of ventilation to perfusion throughout the lung. Diminished pulmonary blood flow (with low pulmonary arterial pressure) results in poor matching of ventilation to perfusion, probably because of selective perfusion of lower lung zones and overventilation of upper zones—an exaggeration of the normal effect of gravity. (SPR)