Pulmonary vascular resistance in children with congenital heart disease.

Abstract

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.

High plasma adiponectin is associated with increased pulmonary blood flow and reduced right ventricular function in patients with pulmonary hypertension

“…Subsequently, oxygen contents of the arterial and venous blood were calculated to determine the oxygen consumption (VO2). In the Fick method [12], the systemic (cardiac output, CO), pulmonary blood flow (pulmonary output, PO) and the corresponding cardiac index (CI), pulmonary index (PI) were estimated by the following equations: Pulmonary vascular resistance (PVR) was calculated by mean pulmonary arterial pressure divided by the cardiac output.…”

Does prostacyclin enhance the selective pulmonary vasodilator effect of oxygen in children with congenital heart disease?

“…The effects of any possible delay on measured blood oxygen content have been investigated and shown to be minor. 33 The oxygen content of each sample was calculated with the use of the data of Kelman34 and assuming the solubility of free oxygen in blood to be 0.003 ml/ 100 ml/mm Hg. The reasons for the use of calculation rather than direct measurement and the validity of the calculation in chronically hypoxic patients have been discussed elsewhere.33…”

Pulmonary Venous Flow Index as a Predictor of Pulmonary Vascular Resistance Variability in Congenital Heart Disease with Increased Pulmonary Flow: A Comparative Study before and after Oxygen Inhalation

“…The use of pulmonary vasodilators causes, in reversible situations, a decrease in PVR and an increase in the Qp:Qs ratio. Oxygen is the pulmonary vasodilator most frequently used, most likely due to its availability and easy monitoring . Although Qp and Qs can be reliably assessed by echocardiography, pulmonary vasodilation‐dependent variations can be difficult to determine.…”

“…Oxygen is the pulmonary vasodilator most frequently used, most likely due to its availability and easy monitoring. [14][15][16][17][18] Although Qp and Qs can be reliably assessed by echocardiography, 4-8 pulmonary vasodilationdependent variations can be difficult to determine. It is not known whether the pulmonary valve ring diameter remains constant throughout the test or if it should be measured before and after the use of a vasodilator.…”