Quantitative measurement of intrapulmonary and extrapulmonary right-to-left shunt.

We have developed a new technique that enables the shunting of blood from the right to the left side of the circulation to be partitioned into a cardiac and a lung component. The effects of recirculation are minimal, and the method does not require on-line data analysis. Quantitative estimates of these components have been made in two normal dogs and in five patients with raised pulmonary arterial pressures, some of whom were known to have a patent foramen ovale. The results were compared with oxygen shunt measured during air breathing. A poorly soluble gas, nitrogen, radiolabelled with 13N in solution is injected first into a central vein while matched samples of blood are drawn from the pulmonary artery and the aorta. A second solution containing 13N is injected into the right ventricle and sampled from the aorta only. Standardized gamma-counting techniques were used to analyze both the injected radioactivity and the radioactivity in the samples. These two measurements enable us to calculate the total right-to-left shunt, the pulmonary shunt, and by subtraction the extrapulmonary cardiac shunt

Prediction of favourable responses to long term vasodilator treatment of pulmonary hypertension by short term administration of epoprostenol (prostacyclin) or nifedipine.

Eighteen patients with moderate to severe pulmonary hypertension were studied, nine with intracardiac shunts and nine without. The effects of an incremental infusion of epoprostenol (prostacyclin) (0.5-8 ng/kg per minute) or sublingual nifedipine (20-30 mg) were compared with the response to three months' treatment with oral nifedipine. Both epoprostenol and sublingual nifedipine caused a fall in pulmonary vascular resistance and pressure and a rise in cardiac output. Patients with intracardiac shunts had higher systemic blood flows than those without shunts. Exercise in the shunt group was accompanied by systemic desaturation and hyperventilation. Analysis of individual results showed that the size of the response was inversely related to the severity of the pulmonary vascular disease. A good long term response to nifedipine seemed to be as readily predicted by the resting control values for haemodynamic variables as by values after short term treatment. A favourable response was likely if the pretreatment mean pulmonary artery pressure was less than 50 mm Hg, the ratio of total pulmonary to systemic resistance was less than 0.7, or the ratio of mean pulmonary artery pressure to systemic artery pressure was less than 0.6. Short term vasodilator protocols may do harm. If such studies are carried out, an adequate dose range must be tried before the long term efficacy of an individual drug can be forecast