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  • Title: [Investigation of pulmonary hemodynamics and chest X-ray findings in patients with pulmonary tuberculosis sequelae and obstructive ventilatory impairment].
    Author: Yasuda J, Okada O, Kuriyama T, Nagao K, Yamagishi F, Hashizume I, Suzuki A.
    Journal: Kekkaku; 1999 Jan; 74(1):5-18. PubMed ID: 10067051.
    Abstract:
    We investigated pulmonary hemodynamics and chest X-ray findings to explore significance of obstructive ventilatory impairment in patients with pulmonary tuberculosis sequelae. One hundred and two patients underwent examinations of blood gases, spirometry, and right cardiac catheterization. The patients were divided into two groups, according to forced expiratory volume in one second as the percentage of forced vital capacity (FVC), which was expressed as FEV1%. Group A (n = 38) had FEV1% of 55% or lower and Group B (n = 64), FEV1% above 55%. First, the values of blood gases and hemodynamics were compared between the two groups, regarding the percent predicted value of FVC as a covariate. Secondly, between 26 of Group A and 42 of Group B, the change of pulmonary arteriolar resistance (PAR) before and after 100% oxygen breathing for 10 minutes was compared. These comparisons were made by exploratory data analysis. Lastly, we described every case with five items of chest X-ray findings and the extent of each finding we had defined. The items were emphysematous change; fibrosis, bronchiectasis and/or cavity; pulmonary resection and/or atelectasis; pleural thickening; and thoracoplasty. We explored X-ray findings influenced on airway obstruction by ridit (abbreviation for "relative to an identified distribution") analysis, taking smoking status into consideration. The results were as follows. (1) The patients of Group A tended to show severer hypoxemia and tissue hypoxia than the patients of Group B. (2) The patients of Group A tended to show worse values of pulmonary hemodynamics than the patients of Group B. Under an even level of the arterial oxygen tension that was 60 Torr or lower, pulmonary artery mean pressure was higher in Group A than in Group B. (3) PAR after oxygen breathing was less likely to decrease in Group A than in Group B. (4) As any mean ridit was standardized and adjusted to 0.5 in Group B, every mean ridit of "emphysematous change" in Group A was the largest-0.63 in non-smokers, 0.74 in ex-smokers and 0.70 in current smokers. Therefore, "emphysematous change" was more influenced on airway obstruction than any other finding because of the largest mean ridit. We conclude as follows. Pulmonary hypertension is more serious in patients suffering from severe airway obstruction with pulmonary tuberculosis sequelae, and it may be attributable to reduction in capacity of anatomical pulmonary vascular bed rather than hypoxic pulmonary vasoconstriction. Pathological changes such as "emphysematous change" on the radiograph might be considered as an important cause of obstructive ventilatory impairment.
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