Alveolar-arterial Oxygen Tension Gradient Research Articles

The Effects of Time-Varying Blood Flow on Diffusional Resistance to Oxygen Transfer in the Pulmonary Capillaries

The effects of the persistence of pulsatile blood flow in the pulmonary capillaries on the over-all diffusing capacity and alveolar-arterial oxygen tension gradient were studied. A mathematical analysis was made of the oxygen transfer process using an undamped cardiac flow pulse in the capillaries and taking into account the finite rate of reaction of oxygen with hemoglobin.In five cases of both normal and low oxygen atmospheres, combined with varying degree of exercise, it was found that the alveolar-arterial oxygen tension gradients were not affected by the time-varying blood flow, while in cases of breathing air the over-all diffusing capacity of the lung increased 10-15% over the diffusing capacity obtained with constant blood flow rate in the pulmonary capillaries.

Mechanism of postural hypoxemia in asymptomatic smokers.

Ventilatory function, lung volumes, flow-volume curves, and alveolar-arterial oxygen tension gradients were measured in 24 smokers and nonsmokers by standard methods. Ventilatory tests and lung volumes were normal in both groups. As compared to nonsmokers, the smokers had a slightly smaller residual volume and functional residual capacity, (FRC), particularly in the supine position, and their flow-volume curves were less favorable. As a result, the forced expiratory flow rate at FRC in the supine position was significantly less in smokers than in nonsmokers. Alveolar-arterial oxygen tension gradients while breathing room air were larger in smokers than in nonsmokers, more so in the supine (P < 0.01) than in the erect position. When pure oxygen or 14 per cent oxygen was breathed, the alveolar-arterial oxygen tension gradients were identical in both groups; this indicates that maldistribution caused postural hypoxemia. Alveolar-arterial oxygen tension gradients, measured while the subjects were breathing ro...

Pulmonary Function in Convalescents of High Altitude Pulmonary Edema

Pulmonary function in 14 high altitude pulmonary edema convalescents were statistically compared to those of 27 control subjects. The convalescents showed significant hypoxemia and widening of alveolar-arterial oxygen tension gradient. The resting DLCo was moderately increased. The results suggest persistence of pulmonary dysfunction for more than 9 to 12 weeks after apparent clinical recovery from high altitude pulmonary edema.

Pulmonary complications and water retention in prolonged mechanical ventilation.

Abstract In a retrospective study of 100 patients treated with prolonged mechanical ventilation, water retention without evidence of cardiac failure developed in 19. This was associated with radiologic evidence of pulmonary edema and with the following significant changes: a mean gain in weight of 2.6 kg; a mean increase in the alveolar-arterial oxygen tension gradient of 127 mm of mercury; a decrease in vital capacity of 29 per cent; a reduction in estimated compliance of 31 per cent; a fall in hematocrit of.13 percent; and a decrease in serum sodium of 5.80 mEq per liter. These changes were reversed after the institution of a negative water balance by restriction of water intake and by diuretic therapy. Radiologic improvement was usually prompt. The appearance of pulmonary edema may be related to a relative water overload, a rise in antidiuretic hormone production or subclinical cardiac failure.

Bronchodilators, pulmonary function, and asthma.

Editorial Notes1 April 1968Bronchodilators, Pulmonary Function, and AsthmaMAURICIO J. DULFANO, M.D.MAURICIO J. DULFANO, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-68-4-955 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe previously undisputed benefits of isoproterenol, epinephrine, and aminophylline in treatment of bronchial asthma have recently come under critical review. For decades pulmonary physiologists characterized the asthmatic disturbance primarily in terms of increased work of breathing resulting from augmented airway resistance and uneven distribution of ventilation throughout the lung, while little attention was directed to the characteristics of pulmonary blood flow (Q) distribution, and the resultant effects on alveolar ventilation-perfusion ratios (VA/QT), "physiological" shunt (QS/QT), and the alveolar-arterial oxygen tension gradient (A-ao2D). The concept that hypoxemia and hypercapnia are infrequent in asthma (1) went unchallenged for years until convincing evidence...

Response of blood gas tensions to aminophylline and isoprenaline in patients with asthma.

Aminophylline and isoprenaline, two drugs widely used in the management of asthma, have a pulmonary vasodilator action as well as a bronchodilator action. If regional pulmonary vasoconstriction in poorly ventilated parts of the lungs is a significant compensatory phenomenon in asthma, the effects of administration of these agents on gas exchange would depend on the relative magnitudes of bronchodilator action and pulmonary vasodilator action in the individual patient. If vasodilator action were greater than bronchodilator action in significant portions of the lungs, maldistribution of ventilation-blood flow ratios would increase and arterial oxygen tension might fall. In 40 patients with chronic asthma, arterial blood gas tensions, minute ventilation, alveolar-arterial oxygen tension gradient, physiological dead space/tidal volume ratio, and oxygen consumption were measured before and at intervals up to 20 to 40 minutes after the administration of various agents: in 13 patients, 250 mg. of aminophylline intravenously; in 16 patients, six deep inhalations of 1% isoprenaline aerosol; in 11 patients, after various control procedures. There were no significant changes following the control procedures. Administration of both aminophylline and isoprenaline was followed by increases of F.E.V._1·0 and increases of minute ventilation. Despite these changes, five patients in each group showed a fall of arterial Po₂ of 5 mm. Hg or more. This was accompanied by an increase of alveolar-arterial oxygen tension gradient. It was concluded that the decreases of arterial blood Po₂ resulted from reversal of pre-existing, compensatory, regional pulmonary vasoconstriction by the pulmonary vasodilator action of each drug in some subjects.

Alveolar-arterial oxygen tension gradients in cirrhosis of the liver: Further evidence of existing pulmonary arteriovenous shunting

Alveolar-arterial oxygen tension gradients in cirrhosis of the liver: Further evidence of existing pulmonary arteriovenous shunting

ARTERIAL OXYGENATION DURING HYPOTHERMIA.

The aims of this stady were: to investigate a possible significant relation between the size of the tidal volume during constant volume ventilation and the rate of change of the alveolar-arterial oxygen tension gradient (AaDO2): to determine whether hypothermia significantly affects this relationship; and to test the accuracy of correction factors previously proposed for the effect of temperature on the oxygen tension of fully saturated blood. Ten patients were surface cooled to 30° C. for over 24 hours. Anesthesia consisted of pentobarbital sodium and d-tubocurarine. Constant volume pulmonary ventilation with 100 per cent oxygen was provided by a piston pump. A significant relationship (P < 0.01) was found between the size of the constant tidal volume and the rate of increase or decrease of the AaDO2. This relation showed little evidence of being affected by hypothermia per se. The accuracy of previously determined temperature correction factors for oxygen tension was confirmed.

Cardiorespiratory Studies in Hamman-Rich Syndrome

SUMMARY Two cases of Hamman-Rich Syndrome, representing extremes of the clinical spectrum, are presented. Special emphasis has been directed to the results of the simultaneous studies of alveolo-respiratory and hemodynamic function which were carried out. The first patient, his diagnosis having been established by lung biopsy, was studied initially shortly after clinical onset of the disease. He was found to have a normal pulmonary artery pressure at rest, but pulmonary hypertension during exercise. Coincident with the development of pulmonary hypertension, a diffusion insufficiency for oxygen appeared. This latter state was defined by development of an abnormally wide alveolararterial oxygen tension gradient, in the absence of any fixed intrapulmonary right to left shunt. The same patient was restudied after six months of steroid therapy, at which time he had attained improvement both in subjective clinical symptoms and the radiologic extent of the pulmonary infiltrate. Despite such apparent amelioration of the process, the repeat cardiopulmonary evaluation revealed no alteration of the initial physiologic deficits. The second patient, whose diagnosis was established at autopsy, was studied in the terminal phase of her illness, one month prior to death. In this instance, pulmonary hypertension and a severe diffusion insufficiency for oxygen were present in the resting state. Both defects were improved when pulmonary blood flow was decreased by the carefully-monitored infusion of a ganglionic blocking agent, hexamethonium. In both cases, the pulmonary vascular resistance was found to be fixed and elevated. These findings have led to the conclusion that pulmonary hypertension and diffusion insufficiency for oxygen are a consequence of the same primary disorder; namely, extensive destruction of the pulmonary capillaries, which is reflected by the elevated and fixed pulmonary vascular resistance. In the face of this abnormality, the degree of pulmonary hypertension and diffusion insufficiency for oxygen are directly related to the pulmonary blood flow which the diminished vascular bed is called upon to accept. Both of these functional defects are heightened by increased blood flow and ameliorated when flow is lowered.

Pulmonary blood distribution and oxygen diffusion in mitral stenosis

1. 1. In thirteen patients with mitral stenosis, a study was made of the relative contributions of venous admixture and pulmonary oxygen diffusing capacity to the alveolar-arterial oxygen tension gradient. 2. 2. In this group, five subjects had an increase in venous admixture, and six had an increase in respiratory dead space. Of those with increase in dead space, three had an increase in venous admixture. These abnormalities did not show good association with the clinical state of the patient, or with the height of the pulmonary vascular pressures at rest. 3. 3. Five subjects demonstrated a diminution in the oxygen diffusing capacity of the lungs. Four of these were dyspneic and had high pulmonary vascular pressures. One had a very small calculated mitral valve orifice area with little elevation in pulmonary arterial pressure at rest. 4. 4. Direct measurement of pulmonary “capillary” oxygen tension was made in seven subjects. In three there was good agreement with the calculated pulmonary capillary tension. Possible explanations for the discrepancy in the other four cases are given.