Some Clinical Aspects on the Blood Gas Physiology

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Special Article* Some Clinical Aspects on the Blood Gas Physiology Hiroshi Sasamoto Professor and Chairman, Department of Medicine, School of Medicine Keio University, Shinjuku, Tokyo Recent trends on the clinical hematology were mostly concentrated upon the morphological studies. In this presentation the emphasis was placed upon the physiological aspects of the blood to transport the respiratory gases as well as to maintain the homeostasis. The treatment of respiratory insufficiency was also referred to. 1) Alveolar Gas Exchange and Blood Gases: The quantitative estimation of the uneven VA/Qdistribution in the lungs was done on (1) the alveolar-arterial gas tension differences (O2 and N2), (2) the compartmental analysis based upon the inert gas elimination, (3) the lung scanning by use of the radioisotope tracers and on (4) the CO pulmonary diffusing capacity. The alveolar-arterial O2 tension differences on breathing air as well as other gas mixtures of different O2 tension and the arterial-alveolar N2 difference were measured on the anesthetized dogs or on the healthy human subjects to establish their normal values. AaDo2upon breathing O2 of 40%or higher concentration revealed somewhat smaller values than those previously expected (Table 1). Table 1. The Proposed Normal Alveolar-Arterial Gas Tension Differences (Men, Supine) The short pulmonary capillary transit time less than 0.5 sec. observed in cases with pulmonary hypertension was considered as a possible factor to increase AaDo2. * Presented at the 66th Annual Meeting of the Japanese Society of Internal Medicine, April 2, 1969, in Sendai.

148 Sasamato Jap. J. Med. 1970 It was also concluded, through some experimental observations, that the leftwards shifting of the O2 dissociation curve may cause increased AaDo2. AaDo2on 21% O2 and on 40% O2 was measured on the cases with typical chronic non-specific lung diseases. Significant increase in AaDo2 was found in diffuse pulmonary fibrosis. In cases with bronchitis AaDo2revealed increase of various degree. In emphysematous patients AaDo2 appeared larger both on different O2 levels. aadn2on 96 healthy aged demonstrated somewhat skewed frequency distribution while those on 67 healthy young revealed the normal distribution. Some aged subjects demonstrated large aadn2even though they were accompanied by FEV1% within normal limits. The author thus assumes that the uneven VA/Qdistribution may be one of the physiological features in the so-called senescence lungs. Some young bronchitic patients also revealed larger aadn2with normal FEV1%indicating the uneven VA/Qdistribution could be one of the physiological disturbances. Both AaDo2 and aadn2 exhibited reverse correlation with DLco so that the CO pulmonary diffusing capacity also considered to represent the uneven VA/Q distribution as well as the true diffusion impairment (Fig. 1). 20J By the multiple inert gas elimination method one can detect the compartment with any VA/Qby use of a pair of adequate inert gases io- x of different solubilities. On the fl.nesthp.hzph dogs the methane-ethane elimination allowed a us to evaluate the compartment having VA/Q 20 3cT less than 0.1 quantitatively. This method cannot p Fig. 1. Arterial-alveolarN2dif-.. inpoint. the geometrical u... location,. of the... spaces,, A-rc - having any abnormality as the radioisotopic terence vs. pulmonary diffusing capacity (breath-holding method). method can do. 2) Oxygen Transport: Factors to cause the leftwards shifting of the O2 dissociation curve, such as the hypothermia, alkaline infusion, or CO inhalation brought up any increase in AaDo2. In those dogs with anemia, COintoxication and with hypothermia the mixed venous oxygen tension revealed significant depression. Although VO2/Qwas increased in either acid- or alkaline infused dogs the mixed venous oxygen tension was decreased only in the alkaline infused dogs while it remained unchanged in the acid-infused dogs. Blood gas studies on anemic patients revealed decreased O2 content with normal arterial oxygen tension. The patients were also accompanied by the respiratory alkalosis due to compensatory alveolar hyperventilation. AaDo2in most of the cases remained normal. Relative high cardiac output and depressed mixed venous oxygen.

"Vol. 9-, No. 3 BLOOD GAS PHYSIOLOGY 14^ tension were observed. 3) Tissue Oxygen Utilization and Blood Gases: To estimate the gas tension in various tissue the author studied the gas tension in various venous blood on the anesthetized dogs. In the figure the venous points representing the pulmonary artery, the coronary-^ the jugular-, the portal- and the renal veins are demonstrated on the O2-CO2diagram (Fig. 2). The estimated renal blood flow was significantly higher than those in other organs. The subcutaneous and/or the intraperitoneal gas pockets madeon the rats were also used to estimate the tissue gas tension experimentally. The pocket gas tension on 907 subcutaneous pockets and on 394 intraperitoneal pocket was distributed, on the O2-CO2 diagram, between and around the blood R-line of 0.6 and 1.0. TheO2 tension in the intraperitoneal pocket appeared a little higher than that in the subcutaneous pockets. Upon breathing COmixture, changes in oxygen tension of the rat's pocket gas were mmhg 60 CM & 40 20-1 O2-CO2 DIAGRAM ( VENOUS BLOOD ) JUGULAR HAL 30 60 90 Bo2 120 150 mmhg Fig. 2. The venous blood gas tensions on the O2-CO2 diagram. found significant depending on the inspired COconcentration. The observation was. also performed on the rats, on which thyroid preparations were experimentally administered. Rats, which revealed significantly increased oxygen consumption,, were accompanied by any depressed O2 tension in the gas pockets. The data were suggestive to the changes of tissue gas tension to be applied on the patients with hyperthyroidism or with high fever. The rats exposed to the environment of various O2 tension revealed the symptoms of oxygen intoxication accompanied by the convulsion, hemoptysis and the death. The incidence of these symptoms was related to the inspired O2 tension as well as the duration exposed to the environment. The observation on the effect of THAM to prevent oxygen intoxication was done on the rat's subcutaneous gas pocket. THAM inhibited the prevalence of oxygen intoxication, but also produced any depression of the tissue O2 tension, which diminished the essential effects of hyperbaric O2 administration itself. 4) Acid-Base Regulation and CO2 Transport: Since it is difficult to obtain complete information on the acid-base regulation by the arterial blood analysis, the author madefurther experimental trial to estimate the intracellular ph by the DMOmethod on the excised rat's heart muscle and diaphragm. The intracellular ph was found approximately 7.00 against the extracel-

150 Sasamoto Jap. J. Med. 1970 lular ph of 7.40. The intracellular ph was found variable in terms of CO2 tension in the media while its intracellular bicarbonate concentration remained unchanged. On clinical practice, the acid-base disturbance be assessed on the arterial blood analysis although the information obtained be not perfect. The data shownare the proposed normal values for the arterial ph, CO2tension and the plasma bicarbonate concentration (Table 2). Table 2. The Proposed Normal Values for the Acid-Base Regulation ACID-BASE REGULATION ( CLINICAL CASES ) 10 20 30 40 50 60 70 80 Pto 2 mmhg Fig. 3. The plasma bicarbonate ion concentration vs. arterial CO2 tension in cases with chronic stable acid-base disturbances. The acid-base balance in cases with chronic stable hypercapnia was studied to establish the so-called significance band represented by the relationship between arterial CO2tension vs. plasma bicarbonate ion concentration. Further studies were conducted on the cases with chronic metabolic acid-base disturbance to demonstrate the relationship of the plasm bicarbonate concentration with the arterial CO2tension. The figure summarizes the findings of acid-base disturbances in cases with chronic stable acid-base impairment (Fig. 3). 5) The Respiratory Insufficiency and Its Treatment : The author proposes to define the respiratory insufficiency and the pulmonary failure as follows : the respiratory insufficiency be the condition accompanied by any abnormal blood gas (O2 and/or CO2) data so that the patient cannot perform her normal physical activities. The pulmonary failure may be defined to be the condition, under which the patient's pulmonary function be impaired to meet his physical demand. The respiratory insufficiency is defined on the physiological basis while the pulmonary failure is rather on the clinical background. The oxygen therapy for the respiratory insufficiency was discussed on three

Vol. 9, No. 3 BLOOD GAS PHYSIOLOGY 151 different conditions. (1) patients with the alveolar hypoventilation, (2) patients accompanied by severe hypoxemia due to uneven ventilation-per fusion ratio distribution and/or diffusion impairment, (3) patients with acute CO intoxication. Excepting for the type (3) the oxygen therapy may be given aiming to maintain the arterial O2 tension of 100-150mm.Hgif the CO2accumulation could be avoided. The author is to emphasize the importance to secure the alveolar ventilation during the treatment in parallel to give any intensive correction on the acid-base disturbance. 40% O2 may be sufficient to maintain the necessary arterial O2 tension. The patients accompanied by significant arterial O2 desaturation due to uneven ventilation-per fusion-ratio distribution and/or diffusion impairment should receive oxygen of high concentration. The patients with acute COintoxication should especially be treated by the intensive O2 administration, possibly by the hyperbaric oxygenation. Upon treatment on the cases with hypercapnia the sudden correction for the impaired acid-base regulation should be avoided. Acetazole amide or THAMmay be administered to overcome the severe CO2 retention if the proper ventilation be sufficiently maintained. 6) Conclusion: The physiological significance of the blood gases was discussed on the experimental as well as on the clinical basis. The abnormal blood gases may be brought up on variety of diseases. The discussion included not only on the patients with pulmonary diseases, but also on other patients with blood diseases, metabolic diseases, etc. The physiological significance of the venous blood gas tensions was discussed with regard to the tissue gas tension. The criteria of respiratory insufficiency and of pulmonary failure was proposed and the treatment of respiratory insufficiency was discussed basing upon three types of respiratory insufficiency. The discussion was also extended to the correction of acid-base disturbances. References Date, T. and Okuda, M.: Kokyuu to Junkan, 16: 636, 1968. Ohta, Y., Nakayama, H. and Yokoyama, T.: Kokyuu to Junkan, 14: 877 1966. Rahn, H., and Farhi, L.E. : Handbook of Physiology, Section III, vol. 1, pp. 735 (edited by W. 0. Fenn and H. Rahn), American Physiological Society, Washington D. C, 1963. Sasamoto, H.: Japanese J. of Thoracic Dis., 6: 1, 1968. Sasamoto, H. and Ohta, Y.: Nihon Rinshoo, 25: 1933, 1967. Sasamoto, H. and Kunieda, T. : Nihon Kyoobu Rinshoo, 26: 193, 1967. Sasamoto, H.: Kokyuu to Junkan, 15: 187, 1967. Sasamoto, H. and Yokoyama, T.: Kokyuu to Junkan, 17: 4, 1969. Sato, S., Okuda, M. and Date, T.: Kokyuu to Junkan, 16: 871, 1968.

152 Sasamoto Jap. J. Med. 1970 Yokoyama, T., Yamaoka, S. and Date, T.: Jap. J. Int. Med., 57: 1092, 1968. Yokoyama, T. and Ohtsuka, H.: Kokyuu to Junkan, 15: 861, 1967. Yokoyama, T.: Japanese J. Thoracic Dis., 6: 34, 1968. Yokoyama, T. : 17th Convention of Japanese Medical Association, Proceedings of Scientific Papers, 1967, IV: 903, 1967. Farhi, L.E. and Yokoyama, T. : Respiration Physiology, 3 : 12, 1967. Yokoyama, T. and Farhi, L.E. : Respiration Physiology, 3 : 166, 1967.