The volume of the dead space in breathing and the mixing of gases in the lungs of man

Krogh, August; Lindhard, J.

doi:10.1113/jphysiol.1917.sp001785

Cited by 112 publications

(38 citation statements)

References 2 publications

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“…The development of a method to sample multiple within-breath samples of CO 2 [2] demonstrated modest variability in partial pressures within an exhaled breath in normal subjects, leading to the recognition that a gas sample captured within a breath would not necessarily reflect the true mean alveolar gas composition. While that effect was minor in normal subjects, it became a substantial source of variability in patients with significant underlying lung disease.…”

Section: Bohr Dead Spacementioning

confidence: 99%

Dead space: the physiology of wasted ventilation

Robertson

2014

Eur Respir J

128

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An elevated physiological dead space, calculated from measurements of arterial CO 2 and mixed expired CO 2 , has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V′A/Q′) heterogeneity has been the most important pathophysiological mechanism. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V′A/Q′ ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces. @ERSpublications A review of current understanding of factors accounting for abnormal physiological dead space measurements in disease

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Section: Bohr Dead Spacementioning

confidence: 99%

Dead space: the physiology of wasted ventilation

Robertson

2014

Eur Respir J

128

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“…It is well known that the 'physiological' dead space, calculated from the alveolar gas tensions, when these are measured directly, increases considerably during exercise. However, Krogh & Lindhard (1913a, 1917 measured it by an independent method and found that it changed very little. The calculated alveolar gas tensions which resulted from their values for the dead space were practically the same as those prevailing during rest.…”

Section: Discussionmentioning

confidence: 99%

“…Krogh & Lindhard (1917) criticized the Haldane-Priestley method because of the uncertainties underlying the assumption that the mean of the two samples was the mean for the alveolar air. DuBois, Britt & Fenn (1952) have recently investigated this point.…”

Section: Appendixmentioning

confidence: 99%

“…In view of this uncertainty we decided to re-investigate the changes in alveolar C02 during heavy exercise, together with some factors which might modify the response of the respiratory centre to CO2. The current views are partly based on the contention of Krogh & Lindhard (1913c, 1917 that the directly measured alveolar gas tensions do not reflect the gas tensions in the arterial blood during exercise. It is therefore important to the argument presented in this paper that the old controversy between the Danish and Oxford schools of physiology should be re-examined in the light of recent evidence on the alveolar air-arterial blood gas relationships.…”

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confidence: 99%

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The carbon dioxide stimulus to breathing in severe exercise

Bannister¹,

Cunningham²,

Douglas³

1954

The Journal of Physiology

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There has been much speculation for a long time as to the causes of the increased breathing during exercise. In 1905, Haldane & Priestley put forward the theory that it was due to a slight increase in the alveolar CO2 tension (pCO2) and therefore of the arterial pCO2, just as similar increases in alveolar PCO2 induced by CO2 inhalation at rest produced hyperpnoea. Further work showed that whatever might be true for mild exercise, as the work became harder the increase in pCO2 was certainly insufficient to account for the hyperpnoea, and it was clear that some additional factors must come into play. The theory that hydrogen-ion concentration rather than CO2 as such was the stimulus to respiration was more satisfactory since it was known that severe exercise was associated with the accumulation of an excess of lactic acid in the body. Since then, this view has been challenged by many physiologists, and at present there is no agreement as to the main causes of the hyperpnoea. In view of this uncertainty we decided to re-investigate the changes in alveolar C02 during heavy exercise, together with some factors which might modify the response of the respiratory centre to CO2. The current views are partly based on the contention of Krogh & Lindhard (1913c, 1917) that the directly measured alveolar gas tensions do not reflect the gas tensions in the arterial blood during exercise. It is therefore important to the argument presented in this paper that the old controversy between the Danish and Oxford schools of physiology should be re-examined in the light of recent evidence on the alveolar air-arterial blood gas relationships. The arguments used to justify the use of the directly measured alveolar pCO2 as a guide to the arterial pCO2 in exercise are long and intricate and are therefore presented in an appendix to this paper. The conclusions reached are summarized in the main text. METHODSAlveolar air. At rest, alveolar air samples were taken by the Haldane-Priestley method. The values presented in this paper were the means of end-inspiratory and end-expiratory samples.Automatic alveolar air sample8. In exercise, a modification of the method described by Lindhard (1911), and modified by Rahn & Otis (1949), was used (Fig. 1). In this method the last few c.c. of

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“…In 1917, August Krogh and Johannes Lindhard (Krogh and Lindhard, 1917) published a paper where they speculated that pulmonary perfusion through each lung lobe should be in proportion to its ventilation. The modern era of understanding ventilation-perfusion relationships began Introduction 3 compliance in the lung.…”

Section: Introductionmentioning

confidence: 99%

Gas Exchange in the Normal Lung : Experimental studies on the effects of positive end-expiratory pressure and body position

Johansson¹

2014

Linköping University Medical Dissertations

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BACKGROUND:The principal function of the lung is gas exchange requiring adequate ventilation and perfusion at the level of the alveoli. The efficiency of gas exchange is depending on the distributions of regional ventilation (V) and pulmonary blood flow (Q) and their correlation. AIMS:To validate a high-resolution method to quantify regional V and to investigate the Radioactive microspheres, 15 m in diameter, were used for determining regional Q. Nitric oxide synthase (NOS) was inhibited with Nω-nitro-L-arginine methyl ester (L-NAME) to evaluate the role of NO on regional V/Q matching. The right lung was dried at total lung capacity and diced in approx. 1000 regions tracking the spatial location of each region. CONCLUSION: There were marked differences in redistribution of regional ventilation and regional pulmonary blood flow between prone and supine position when PEEP was applied. RESULTS:NO was not an active mechanism for V/Q matching in normal sheep lungs. VII List of original papershis thesis is based on the following four papers, which will be referred to by their Roman numerals: I.Positive end-expiratory pressure affects regional redistribution of ventilation differently in prone and supine sheep.

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The volume of the dead space in breathing and the mixing of gases in the lungs of man

Cited by 112 publications

References 2 publications

Dead space: the physiology of wasted ventilation

Dead space: the physiology of wasted ventilation

The carbon dioxide stimulus to breathing in severe exercise

Gas Exchange in the Normal Lung : Experimental studies on the effects of positive end-expiratory pressure and body position

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