Studies on the Cardiopulmonary Function in Tuberculosis 1. : Effects of Hypoxia on Cardiopulmonary Functions in Patients with Pulmonary Tuberculosis.

Abstract

It is established that hypoxia causes the elevation of the pulmonary arterial pressure. However, there is no definite concept sufficient to account for the mechanism of the elevation of the pressure; some investigators regard increase in amount of the cardiac output as its main reason, and the others emphasize the changes in constriction of the pulmonary artery, resulted probably from hypoxia.A series of studies on patients with pulmonary tuberculosis was carried out in an attempt to determine the effects of hypoxia in a moderate extent which may disturb the cardiopulmonary function of the patients. A possible mechanism for the elevation of the pulmonary arterial pressure will be discussed in this paper.Materials and Method A total of 25 patients with pulmonary tuberculosis were subjected to this study. Pneumonectomy was done in two cases and the remaining 23 cases were divided into the following three groups on the basis of the classification presented by American National Tuberculosis Association (1950); five being minimal cases, 11 moderately advanced cases and 6 far advanced cases (Table 6).The following measurements were made on all patients in both ambient air breathing and low oxygen breasing, 12 to 15% of O2 in N2 for 8 to 20 minutes : pulmonary wedge pressure by the technique of the right heart catheterization; oxygen and carbon-dioxide content of both blood and expired gas using Van Slyke-Neill apparatus and Rokenshiki gas analyzer, respectively; oxygen saturation of the arterial and venous blood; cardiac output by the direct Fick method. Spirometry using Collins' apparatus was also made on all cases, representing its data in percentages of predicted values calculated by Funazu's formula.Results The elevation of the pulmonary arterial pressure due to hypoxia was found in 22 cases of all 23.The pulmonary arterial pressure in the ambient air breathing was below 20 mmHg in all cases of the minimal group and it was over 20 mmHg in only two of the moderately advanced group. The average value of the pressure was lower in the former group than in the latter. The pulmonary arterial pressure in both far advanced and pneumonectomized groups was over 20 mmHg with an exception of one case, their average being over 20 mmHg. Degree and rate of elevation of the mean pulmonary arterial pressure due to the hypoxia were reduced in average in the order of minimal, moderately advanced, far advanced and pneumonectomized groups.The pulmonary arterial pressure of the patients with minimal tuberculosis showed the elevation, which appeared immediately after exposure to the hypoxia, reached the highest value after 3 to 5 minutes and continued as long as the patients were in the hypoxia. The pressure returned to the original level just after cessation of the hypoxia. The elevation was much more marked in the systolic pressure than in the diastolic.The pressure of the pulmonary artery in the hypoxic condition in several cases of the moderately advanced group showed a temporary elevation, reaching the highest value in 5 to 10 minutes, and then its gradual falling. The pressure did not return immediately after cessation of the hypoxia, but did within one hour, to the original value. Narrowing of the pulse pressure was observed in these cases in the terminal stage of the hypoxic condition. The elevation of the pressure in two cases was more intensive in the diastolic than in the systolic. The cases of the far advanced group showed the similar response of the pressure to the hypoxia to the former group was noticed, accompanied with various patterns of fluctuations of the pressure.The shape of the pulmonary arterial pressure curve showed the reduction of elastic elevation in the hypoxia and returned to the former shape after cessaiton of the hypoxia (Fig 6). [the rest omitted]