Effect of Highly Concentrated Oxygen Inhalation (I) : CLINICAL STUDIES OF THE PULMONARY FUNCTION IN PATIENTS OF HEART DISEASE AND RESPIRATORY RESPONSE AND CIRCULATORY DYNAMICS OF PATIENTS UNDER

It has been observed by many investigators, especially by Comroe & Schmidt in 1938, that (1) Carotic body is reflexible respiratory regulation centre acting as the chemoreceptor, and (2) Hypoxemia, acidosis and accmulation of PACO2 in blood stimulated this centre. Also Lambertson & Shephard have reported on respiratory response in healthy man to the inhalation of oxygen at high atmospheric pressure.The author has examined the pulmonary function in patients of heart diseases, and also made a study of both respiratory response and circulatory dynamics under highly concentrated oxygen inhalation at 1 atmospheric pressure in both normal men and patients with heart diseases.20 patients who suffered from mitral diseases, aotric disease, myocard infarction and hypertensive heart diseases were divided into 2 groups : Group I, 12 with cardiac compensation ; Group II, 8 with cardiac decompensation.Pulmonary function was tested by Benedict-Roth's respirometer. Also, changes of Respiratory minute volume between normal cases and patients in 40-50% oxygen inhalation at 1 atmospheric pressure for 20 minutes were observed.Alveolar gases, and O2 content, CO2 content, PH, and PCO2 of arterial blood were observed, before and after 5 minutes from the beginning of oxygen inhalation.CO2 content and O2 content of the blood samples collected from puncture of femoral artery were determined manometrically by the technique of Van' slyke and Neill, alveolar gases were done routinely by gasmetry (Roken-shiki) and arterial pH by electric pH-meter.Results obtained from these experiments are as follows : (1) Disturbance of the pulmonary function in patients in most clearly seen in proportion to the degree of decompensation. In decompensated group, the obtained results revealed prominent decrease, as follows : up to 48.7% of predicted value in Vital capacity, 17.7% of p. v. in Expiratory reserve volume, 43.0% of p. v. in Maximum breathing capacity, 68.9% in Ventiratory reserve ratio, and showed 0.88 in Air velocity index. However, Respiratory minute volume showed an increase of 43.3% due mainly to increased Respiratory rate ; and the Respiratory equivalence became 4.1. So, it is presumed that secondary pulmonary congestion in the decompensated group causes the disturbance of Ventiration.(2) As to Respiratory minute volume, it was observed that after 10% initial decrease the Respiratory minute volume was increased 16% (average), followed again by depressive tendency in normal men under oxygen inhalation at 1 atmospheric pressure, while in decompensated patients, marked depression continued in proportion to the degree of decompensation.(3) As to Alveolar gases, O2 concentration in alveoli increased in all cases in both groups ; but in regard to the CO2 decrease, patients of decompensation revealed a disturbance of ventiration, mainfesting the least decrease with a rate of 9.3% as compared with cases of normal men (decrease ratio of 19.9%) and compensated patients (decrease ratio of 12%).(4) As for Arterial pH, I observed alkalosis in normal men on the average of +0.032 and in compensated patients +0.022, while acidosis averaged -0.002 in decompensated patients.(5) About PACO2 in blood, decompensated patients showed the elevated tension on the average of +2.86 mmHg compared with decrease in CO2 tension which normal men (average -4.34 mmHg) and compensated patients (average -0.61 mmHg) manifested.In conclusion, healthy men who were administered highly concentrated oxygen at 1 atmospheric pressure showed alkalosis, and a decrease in PACO2 and in CO2 content in alveoli ; while on the other hand, decompensated patients under the same conditions showed acidosis, elevation of PACO2, and the smallest precentage among the groups of decrease in alveolar CO2.