Abstract
The acute hemodynamic effect of low-flow oxygen (1-3L/min) and sublingual administration of 10mg nifedipine was investigated in 10 patients with chronic respiratory failure and secondary pulmonary hypertension (chronic pulmonary emphysema (CPE): n=5, chronic lung tuberculosis (TB): n=5). All patients showed hypoxemia with arterial oxygen tension of about 60torr (room air) and pulmonary hypertension (mean pulmonary arterial pressure >20torr).
Oxygen significantly reduced the mean pulmonary arterial pressure and pulmonary vascular resistance index in both groups without change of other hemodynamic parameters, but the degree tended to be greater in the CPE group than in the TB group.
Nifedipine significantly reduced the pulmonary and systemic vascular resistance index, and lowered mean arterial pressure. Cardiac output and the coefficient of oxygen delivery increased significantly, but mean pulmonary arterial pressure, heart rate and oxygen consumption apparently did not change. Although these responses were common in both groups, the additional administration of oxygen significantly reduced the mean pulmonary arterial pressure in the CPE group, in contrast to no change in the TB group. Furthermore, the relationship between pulmonary driving pressure and cardiac index in nifedipine-plus-oxygen shifted to a right lower position in the CPE group, and a right upper position in the TB group.
These differences between the two groups are considered to be based on the difference in the mechanism of development of pulmonary hypertension and the duration of the course of the disease. In the TB group, the reduction of the pulmonary vascular bed to respond to vasodilators and/or the decrease of reactivity to vasodilating agents should be considered.
We conclude that the hemodynamic responses to oxygen and nifedipine in secondary pulmonary hypertension may represent the diference in the mechanism of development of pulmonary hypertension.
