Pathogenesis of pulmonary hypertension in tuberculosis.

The pathogenic factors involved in the increase of pressure in the pulmonary artery in 55 tuberculous patients with manifest, and 50 patients with latent pulmonary hypertension were examinated and analyzed in detail. The authors consider decisive the restriction of pulmonary blood bed together with the decrease of functional parenchyma. In the increase of arterial pressure also the functional vasoconstriction participates. An important role plays here hypoxemia adversely affecting the cardiac function. Hypoxemia, of all pathogenic factors, represents the most serious limitation of pulmonary diffusion, though other agents may not be primarily important for the onset and development of pulmonary hypertension. The originating pulmonary hypertension in tuberculosis does not necessitate compensating mechanisms such as polyglobulia, hypervolemia, or increase of the minute cardiac volume normally present in severe and protracted hypoxemia. The prognosis of patients with the mean pulmonary artery pressure higher than 30 mmHg (3.33 kPa) is very bad, the median survival being about 10 months. Contrarily, a low-grade pulmonary hypertension may not, per se, provide sinister prognostic outlooks. Here rather some other agents capable of influencing the perspectives seen to be of major importance.