Pulmonary and systemic blood flow and pulmonary vascular resistance were measured in 21 children with congenital heart disease. Blood flow was calculated by the direct Fick method, using measurements of metabolic gas exchange obtained by remote respiratory mass spectrometry. The observations showed that the administration of oxygen caused an appreciable fall in pulmonary vascular resistance in 16 of the 21 children studied and that this fall would not have been appreciated from a study of pulmonary arterial pressure alone as it was masked by a corresponding rise in blood flow. In 10 of 14 children, in whom superior vena caval blood was also sampled, the rise in flow was largely due to an increase in intracardiac left to right shunt. It was accompanied by widening of the alveolar-arterial oxygen gradient, perhaps due to imperfect gas equilibration within the lung.Pulmonary vascular resistance is conventionally calculated as the mean pressure drop across the lungs' vascular bed divided by the flow (per square metre of body surface) passing through it.' Pulmonary vascular disease is inferred from the presence of an irreversibly raised resistance, reversibility being assessed by the response of the vascular bed to oxygen or to other vasodilator agents such as tolazoline.2Use of the direct Fick principle to measure pulmonary blood flow, on which the assessment of reversibility depends, requires sampling of pulmonary arterial and pulmonary venous blood as well as measurements of metabolic gas exchange. Elegant techniques have been developed for the determination of oxygen consumption in air,3 but simple, rapid, and accurate estimation of gas exchange while the patient breathes 100% oxygen has proved more difficult to achieve. Remote mass spectrometry simplifies this problem because it permits continuous monitoring of end tidal and mixed expired gas tensions, which in turn permits the easy recognition of respiratory steady states.
MethodsMeasurements were made in 21 children referred for further study of suspected congenital heart disAddress for reprint requests: Professor DM Denison, Lung Function Unit, Brompton Hospital, London SW3 6HP.