Right-to-left shunt in normal man determined by the use of tritium and krypton 85

Mellemgaard, Kresten; Lassen, Niels A.; Georg, J

doi:10.1152/jappl.1962.17.5.778

Cited by 20 publications

(11 citation statements)

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“…XXII, Jmne 1968 output normally passes through true venousarterial shunts. This is in agreement with the findings of other groups (13)(14)(15).…”

Section: Discussionsupporting

confidence: 94%

“…Because of the low solubility of H2, the pulmonary venous concentrations produced by the latter process would be negligible. This argument is compatible with observed recoveries of arterial tritium following intravenous injections of dissolved tritium in man (15) and provides a reasonable basis for the inability to detect recirculation in the studies employing the H2 electrode. It may also suggest an advantage of the technique of sudden, single injection when alveoli having low V A /Q are present in increased numbers.…”

Section: Discussionsupporting

confidence: 73%

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Indicator-Dilution Measurement of Cardiac Output with Dissolved Hydrogen

Klocke

Greene

Koberstein

1968

Circulation Research

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Dissolved HL has been used as an indicator for measuring cardiac output by the techniques of constant-rate injection and sudden, single injection indicator dilution. Because of its low solubility, H 2 is eliminated essentially quantitatively in the lungs and recirculates negligibly. The constant-rate injection technique involves the gas chromatographic measurement of pulmonary (or systemic) arterial H 2 concentration during an infusion of dissolved H 2 into a vena cava (or the left atrium). Measurements in anesthetized dogs agreed well with simultaneous measurements by dye dilution, direct Fick, and direct volumetric techniques. Measurements could be repeated several times a minute, and using a linearly responding platinum electrode, intravascular H 2 concentrations could be recorded continuously. In the sudden, single injection technique, dissolved H 2 was injected into a vena cava (or the left atrium) while monitoring pulmonary (or systemic) arterial H 2 concentration with a chromatographically calibrated platinum electrode. Measurements again agreed with simultaneous measurements by dye dilution, constant-rate injection of H 2 , and the direct volumetric technique. Hydrogen curves could be repeated rapidly and integrated instantaneously. Hydrogen appears to be a useful indicator for rapidly repeated determinations of cardiac output and for measurements of output in situations in which recirculation of conventional indicators limits their usefulness. This investigation was supported by U. S. Public Health Service Grants HE-09587 from the National Heart Institute and General Research Support Grant FR-05400, and by a grant from United Health Foundations, Inc. ADDITIONAL KEY WORDSPreliminary reports of this work were presented at the April 1966 and April 1967 meetings of the American Physiological Society.Accepted for publication April 15, 1968. creted quantitatively during a single passage through the lungs. Their investigations were performed with 8B Kr, and Rochester and co-workers from the same laboratory subsequently reported the use of this agent for measuring right ventricular output by constant-rate injection (2). In addition, Cornell and associates extended the use of 8s Kr to measurements employing a modified sudden, single injection or Stewart-Hamilton technique (3). With the development of gas chromatographic techniques for measuring trace amounts of inert gases in blood (4), it has become possible to employ any of a large number of nonradioactive gases as a cardiovascular indicator. The lower the solubility of a gas, the more completely it should be eliminated from mixed venous blood during a single passage through the lungs.

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“…XXII, Jmne 1968 output normally passes through true venousarterial shunts. This is in agreement with the findings of other groups (13)(14)(15).…”

Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 73%

Indicator-Dilution Measurement of Cardiac Output with Dissolved Hydrogen

Klocke

Greene

Koberstein

1968

Circulation Research

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“…Detection of right-to-left shunts —In normal individuals the right-to-left shunt is less than 2% of the cardiac output99 100 and ascribed to “post-pulmonary” shunting due to the mixing of pulmonary venous blood with deoxygenated blood from bronchial, mediastinal, and thebesian veins. The flow through right-to-left shunts is usually expressed as a fraction of total flow (Q˙s/Q˙T) and may be calculated from the reduction in arterial oxygenation or by anatomical methods using particles 7–11 mm in diameter which normally impact in pulmonary capillaries but pass through large calibre shunt vessels.…”

Section: Pulmonary Arteriovenous Malformations and Hhtmentioning

confidence: 99%

Rare diseases bullet 4: Hereditary haemorrhagic telangiectasia and pulmonary arteriovenous malformations: issues in clinical management and review of pathogenic mechanisms

Shovlin¹,

Letarte²

1999

Thorax

358

310

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Hereditary haemorrhagic telangiectasia (HHT, Rendu-Osler-Weber syndrome) exemplifies an important group of diseases which have catalysed advances in the understanding of fundamental pathophysiological mechanisms. In this paper areas of clinical management of HHT are discussed and the molecular pathogenesis is reviewed. The first section is aimed at all clinicians and concentrates on the recognition of a disorder in which silent cerebral and pulmonary involvement may be life threatening if left untreated. Recent data concerning the diagnostic and treatment modalities for pulmonary arteriovenous malformations (PAVMs) are also reviewed, and the growing concern that many patients with HHT may have small or residual PAVMs is highlighted. The paucity of good longitudinal data on these patients and others with diVerent forms of HHT highlights the need for further clinical studies. In the second section the results of molecular research which suggests a role for receptors and ligands of the transforming growth factor (TGF)-superfamily in the pathogenesis of this vascular disease are discussed. The means by which such information may relate to the clinical heterogeneity observed in HHT are specifically addressed, and more fundamental questions such as how reduced cell surface expression of endoglin predisposes a patient to develop PAVMs are also discussed. Hereditary haemorrhagic telangiectasiaThe classical patient with the vascular disorder hereditary haemorrhagic telangiectasia (HHT) has nose bleeds, dilated blood vessels over the lips and finger tips, and gastrointestinal bleeding in later life. However, this clinical scenario represents only one of the presentation patterns of HHT.1 2 It is now recognised that, in addition to microscopic mucocutaneous telangiectases derived from post capillary venules ( fig 1A), 3 HHT leads to the development of larger abnormal vascular structures at other sites. Arteriovenous malformations in the pulmonary, cerebral, and hepatic circulations account for some of the most devastating clinical complications of the disease.The autosomal dominant inheritance pattern of HHT has enabled identification of the underlying genetic defects, prompting increased scientific interest in the disorder. Mutations in at least two genes have been shown to be associated with HHT in diVerent families: endoglin on chromosome 9, 4 and ALK-1 (activin receptor-like kinase 1) on chromosome 12.5 Both genes encode endothelial cell transmembrane proteins that can be defined as components of the receptor complexes for growth factors of the TGF-super- Figure 1 Hereditary haemorrhagic telangiectasia (HHT). (A) Mucocutaneous

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“…In normal subjects, an average T2 recovery of 1.1%o has been found (14). In studies using simultaneous iv injections of T2 and krypton85, a right-to-left shunt averaging 0.3% has been calculated (17), the remaining T2 recovery being caused by alveolar back-pressure.…”

Section: Discussionmentioning

confidence: 98%

“…As a measure of the right-to-left shunt, the T2 recovery gives an overestimation on account of the contribution to the T2 recovery caused by -"back-pressure" from the alveolar T2 tension, which builds up during the passage. This can, however, be corrected by calculation (18) or by simultaneous use of two gases with different solubilities (17).…”

Section: Cst2/cstho [2]mentioning

confidence: 99%