<i>Maximal Diffusing Capacity of the Lungs</i>

Riley, Richard L.; Shepard, Richard H.; Cohn, Jerome E.; Armstrong, Bruce W.

doi:10.1152/jappl.1954.6.10.573

Cited by 100 publications

(27 citation statements)

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“…), the measured diffusing capacity for oxygen (27.6 and 15.3 ml per mmil Hg per minute, respectively), was within normal limits, but the AaD was increased. This apparent discrepancy may be related to the error in estimating diffusing capacity by this method in resting subjects with little or no impairment of diffusion (42,43). It is also possible that when relatively few alveolar units have become functionless, the increase in venous adlmixture would be apparent before any reduction in the overall diffusing capacity could be detected.…”

Section: Resultsmentioning

confidence: 99%

Venous Admixture to the Pulmonary Circulation in Human Subjects Breathing 100 Per Cent Oxygen*

Said¹,

Banerjee²

1963

J. Clin. Invest.

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At any given time, the alveolar-arterial oxygen partial pressure difference (AaD) may be due to one or more of the three following mechanisms (1-5): 1) failure of pulmonary capillary blood to come to complete equilibrium with alveolar gas; 2) uneven ventilation perfusion ratios; and 3) admixture of venous blood by direct shunting.The first mechanism causes the diffusion component of the AaD, relating to diffusion across the alveolar-capillary membrane as well as chemical reaction rates of oxygen with hemoglobin (6, 7). The second mechanism accounts for the "distribution" component, and the third is spoken of as the "true," "pure," or "anatomical" shunt, or the "direct" venous admixture component.When the inspired oxygen tension is low, as at high altitude or during breathing of hypoxic mixtures, particularly if either condition is combined with exercise, the diffusion component increases, whereas those due to direct venous admixture and to uneven ventilation-perfusion ratios diminish. These changes are used to determine the pulmonary diffusing capacity for oxygen (1-3, 8).On the other hand, breathing 100% oxygen increases the AaD due to direct venous-arterial shunting, and virtually eliminates all other components (9).The role of diffusion impairment in the causation of arterial hypoxemia has been recently reevaluated ( 10), and a number of newer approaches have permitted a more precise definition of the distribution of ventilation-perfusion ratios and of its importance in gas exchange (11)(12)(13)(14)(15).

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Section: Resultsmentioning

confidence: 99%

Venous Admixture to the Pulmonary Circulation in Human Subjects Breathing 100 Per Cent Oxygen*

Said¹,

Banerjee²

1963

J. Clin. Invest.

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“…Dead space/tidal air ratios, venous admixture and maximal diffusing capacities were determined by methods described by Riley and his associates (3,4).…”

Section: Methodsmentioning

confidence: 99%

The Physical Properties of the Lung in Chronic Obstructive Pulmonary Emphysema 1

Cherniack¹

1956

J. Clin. Invest.

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“…Thus it seems probable that the pulmonary hypertension was at least in part due to an anatomic reduction in the capacity of the pulmonary vascular bed. It is likely that such anatomic reduction was in the arteriolar or arterial branches since the normal maximum diffusing capacity suggests that the area of the pulmonary capillary surface was normal (12). It is impossible to determine with certainty whether pulmonary arterial disease resulted from long standing hypoxia or was primary.…”

Section: Measurementsmentioning

confidence: 99%

Clinical and Physiological Aspects of a Case of Obesity, Polycythemia and Alveolar Hypoventilation

Jh¹,

Cook²,

Ad³

1955

J. Clin. Invest.

150

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The occurrence of arterial hypoxia with polycythemia usually results from some known type of pulmonary disease or from an abnormal communication between the right and left sides of the circulation. Although arterial oxygen unsaturation has been observed in patients with polycythemia vera (1)(2)(3)(4) Physical examination revealed an alert, cyanotic, slightly orthopneic man who weighed 290 pounds and was 67 inches in height. A few rales were heard at the right posterior lung base. The heart was in gallop rhythm, and the pulmonic second sound was accentuated. Mild edema of the abdominal wall and marked edema of the lower extremities was present.The significant laboratory findings were as follows: red blood cells 6.77 million per cu. mm.; hemoglobin 20 gm. per cent; hematocrit 69 per cent; white blood cells 6,000 per cu. mm. with a normal differential count and normal cellular morphology; platelets 150,000 per cu. mm. The bone marrow showed hyperplasia of the erythroid series, and reticulocytes were 1 per cent of the red blood cells. The blood uric acid was 9.6 mg. per cent. The urinary 17-ketosteroid excretion was 8 mg. in twenty-four hours (normal). X-ray of the chest showed cardiac enlargement and enlargement of the pulmonary vessels. Angiocardiography showed filling of the cardiac chambers in normal sequence. The sella turcica appeared normal by X-ray. An electrocardiogram showed evidence of right ventricular hypertrophy.

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Maximal Diffusing Capacity of the Lungs

Cited by 100 publications

References 0 publications

Venous Admixture to the Pulmonary Circulation in Human Subjects Breathing 100 Per Cent Oxygen*

Venous Admixture to the Pulmonary Circulation in Human Subjects Breathing 100 Per Cent Oxygen*

The Physical Properties of the Lung in Chronic Obstructive Pulmonary Emphysema 1

Clinical and Physiological Aspects of a Case of Obesity, Polycythemia and Alveolar Hypoventilation

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