No abstract

In an attempt to clarify further the mechanisms underlying labile rise in pulmonary vascular resistance, the effects of administering high oxygen concentrations, briefvoluntary hyperventilation, and correction of acidosis were studied in 16 patients in whom congenital heart disease was associated with pulmonary vascular disease. On breathing 100 per cent oxygen thele was a significant fall in pulmonary vascular resistance from 21 8 ± 4.6 to 12.9 3-6 units/M2 (P < 0.001), with a rise in pulmonary blood flow from 4-4 ± 0-6 to 8-8 ± 2-0 1/min per m2 (P < 0 025) and a fall in pulmonary artery pressure from #67.8 ± 2.8 to 61 8 ± 4 0 mmHg (P < 0 025). The changes occurring on sodium bicarbonate adninistra-;tion in 6 patients did not reach levels of significance, but the size of each individual response was closely correlated with the response to oxygen administration. No significant changes occurred either on voluntary hyperventilation or, in the systemic circulation, with any intervention. However, systemic vascular resistance was positively correlated with pulmonary vascular resistance (P < 0.01). As a result of this, though age was correlated positively with both pulmonary artery mean pressure (P < 0 025) and vascular resistance (P < 0.025), it was not correlated with the ratio of pulmonary to systemic resistance. Since pulmonary vascular disease is progressive, these results cast some doubt on the validity ofresistance ratio as a measure of its severity.

No abstract

It is well known on the basis of acute experiments that changes in systemic arterial oxygen saturation, haemoglobin concentration and acid-base state produce changes in systemic vascular resistance. However, it is not known whether the same changes occur in the chronic state. In order to investigate this problem, we measured systemic vascular resistance in a population in whom chronic changes in these variables are common, namely 195 subjects with congenital heart disease. The significance of these factors was assessed by their ability to predict systemic vascular resistance in a multiple regression equation which also took account of the size of the patient. No matter how the size of the patient was allowed for, haemoglobin concentration, systemic arterial pH (or non-respiratory pH) and systemic arterial oxygen saturation were significantly (P less than 0.025) and positively correlated with systemic vascular resistance. We conclude that, as far as these factors are concerned, the mechanisms operating in the acute state continue to function in the chronic state.