The Influence of Hydrogen Ion in the Control of Pulmonary Artery Pressures in Patients with Obstructive Disease of the Lungs

Harvey, Réjane M.

doi:10.1159/000192387

Cited by 11 publications

(4 citation statements)

References 12 publications

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“…The PA pressure changes were greatest with the highest pulmonary arterial pressures at rest during ambient air breathing. This is in agreement with the findings of most authors that oxygen has its greatest effect in decreasing the high pulmonary arterial pressures in connection with respiratory failure (1,16). Several authors (8,12,30,39,47), have observed small or no significant decrease of the pulmonary hypertension in patients exposed to high oxygen concentrations in resting conditions.…”

Section: Discussionsupporting

confidence: 91%

“…On the other hand, at an alkalotic pH the pulmonary hypertension obtained should be due mostly to hypoxia. The question of the influence of oxygen tension, pH and the role of sympathetic stimulation in pulmonary hypertension is still open though many studies have been performed on heart-lung preparations, on intact animals and on man (5,9,10,12,16,17,18,21,29,32,41).…”

Section: Discussionmentioning

confidence: 99%

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Central Haemodynamics during Hypoxia, Hyperoxia and Hypercapnoea in Severe Chronic Obstructive Lung Disease

Tammivaara-Hilty

1973

Upsala Journal of Medical Sciences

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During inhalation of four different gas mixtures, with FIo,-0.15 and -0.11 and N 0.99 and with FICO2-0.055, the central haemodynamics of 25 patients with severe chronic obstructive Lung disease and with a ventilatory capacity of Q 35 7; of predicted normal values were studied. Fourteen patients (8 male, 6 female) had previously had periods of manifest respiratory insufficiency (R-group) and 11 patients (10 male, one female) had had no such severe respiratory symptoms (comparison group C).The lowest tolerated FIoz level and the tolerated duration of the inhalation periods of different gas mixtures varied in relation to the severity of the disease. Hypoxid caused an increase in pulmonary arterial pressure and probably in vascular resistance. At the lowest attained hypoxaemic level the pulmonary arterial (PA) mean pressure was about 37 mmHg, although with large individual differences, in both groups. This PA pressure level was reached at significantly higher FIo,, arterial saturation and oxygen tension levels in the Rgroup patients. During hyperoxia there was no significant difference between PA mean pressure in R-(25 mmHg) and C-(22 mmHg) group patients. The pressure reactions during hypoxia suggest that the vascular responsiveness might have been greater in R-group patients.During induced hypercapnoea the increase in PA mean pressure (R-group 36 and C-group 33 mmHg) was mostly due to an elevation of PCV pressure, which occurred in relation to an increase in arterial blood pressure. The pulmonary vascular resistance probably did not increase during induced hypercapnoea. In a few patients latent failure of the left ventricle became manifest when the arterial blood pressure was raised due to the increased inspiratory CO,.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Central Haemodynamics during Hypoxia, Hyperoxia and Hypercapnoea in Severe Chronic Obstructive Lung Disease

Tammivaara-Hilty

1973

Upsala Journal of Medical Sciences

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“…It has been known for many years that pulmonary hypertension in patients with chronic bronchitis is due to the presence of an abnormally large pressure clifference across the pulmonary vascular bed (Dexter et al, 1951 ;Parker et al, 1966) and is significantly correlated with both arterial acidaemia and oxygen unsaturation (Harvey, 1965;Harvey et al, 1967). Other mechanisms of pulmonary hypertension in this condition have been suggested in recent years.…”

mentioning

confidence: 99%

Comparative Effects of Exercise and Isocapnic Voluntary Hyperventilation on Pulmonary Haemodynamics in Chronic Bronchitis and Emphysema

Lockhart¹,

Nader²,

Tzareva³

et al. 1970

Eur J Clin Investigation

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(1) Twelve patients with chronic bronchitis and/or pulmonary emphysema with borderline pulmonary artery Eressure and arterial blood gases have been submitted to aemodynamic studies in order to compare changes in the pulmonary circulation brought about by leg exercise and by voluntary hyperventilation with comparable breathing rate, tidal volume and arterial blood gases during both periods. (2) Minute ventilation (Exercise: 12.1 ± 1.9 l. min‐l m‐2; hyperventilation: 12.8± 1.8 1 · min‐1· m‐2), breathing rate (E: 22.6 ±3.4, H: 23.5 ±3.8), percentage arterial oxygen saturation (E: 94.7±3.3%, H: 95.9±2.7%) and carbon dioxide tension (E: 45.5 ± 5.1 mm Hg, H: 46.8 ± 5.1 mm Hg) did not differ significantly during exercise and hyperventilation, thus suggesting that both mechanical forces acting upon intrathoracic structures and pulmonary vasomotor tone were comparable. (3) During exercise pulmonary arterial mean pressure (31.4±5.7mm Hg) and pulmonary wedge pressure (13.2± 4.2 mm Hg) rose significantly (p < 0.001) and consistently. During hyperventilation pulmonary arterial mean pressure rose slightly (22.1 ± 5.5 mm Hg, p < 0.05) and the increase in average pulmonary wedge pressure was insignificant (10.0±5.4 mm Hg), although the latter rose markedly in five cases. Pulmonary vascular resistances were not consistently modified. Pulmonary wedge pressure was not correlated with minute ventilation but was positively correlated with the amplitude of respiratory variations in intrathoracic pressure. (4) Thus, our data suggested that the rise in pulmonary artery and wedge pressures during exercise was due to the combined effects of large intrathoracic pressure swings and of an increase in the haemodynamic load of the left ventricle.

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“…Vasoconstriction brought about 'by the interaction of low alveolar oxygen tension and high blood hydrogen ion concentration upon muscular pulmonary arteries of about 1 mm. in diameter (Harvey, 1965) is the most important cause of pulmonary hypertension. Of course, as in systemic hypertension, continual vasoconstriction can give rise to secondary organic changes in the vessels.…”

Section: Diseases Causing Chronic Cor Pulmonalementioning

confidence: 99%

Chronic cor Pulmonale

Towers¹

1966

Postgraduate Medical Journal

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The Influence of Hydrogen Ion in the Control of Pulmonary Artery Pressures in Patients with Obstructive Disease of the Lungs

Cited by 11 publications

References 12 publications

Central Haemodynamics during Hypoxia, Hyperoxia and Hypercapnoea in Severe Chronic Obstructive Lung Disease

Central Haemodynamics during Hypoxia, Hyperoxia and Hypercapnoea in Severe Chronic Obstructive Lung Disease

Comparative Effects of Exercise and Isocapnic Voluntary Hyperventilation on Pulmonary Haemodynamics in Chronic Bronchitis and Emphysema

Chronic cor Pulmonale

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