Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383973
Title: Right ventricular function in chronic bronchitis and emphysema
Author: MacNee, William
ISNI:       0000 0001 3615 9038
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1985
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Abstract:
A reproducible method of measuring right ventricular ejection fraction was devised using the technique of equilibrium radionuclide ventriculography. In an assessment of ventricular function, in a population of 100 patients with chronic bronchitis and emphysema, the right ventricular ejection fraction was, on average, lower than in normal subjects, but was still relatively well preserved in most, as was the left ventricular ejection fraction. However, the range of values of ejection fractions in patients with chronic bronchitis and emphysema was wide, and low values occurred mainly in patients with oedema, indicative of decompensated pulmonary heart disease. The right ventricular ejection fraction was lower in those patients with lower arterial oxygen and higher carbon dioxide tensions, but was not related to the level of simultaneous measurements of pulmonary arterial pressure. Right ventricular ejection fraction was, however, related to right ventricular afterload as measured by the pulmonary vascular resistance. Occult right ventricular dysfunction could be demonstrated during exercise in patients with chronic bronchitis and emphysema. The change in right ventricular ejection fraction was related to the fall in oxygen saturation which occurred in such patients during exercise. In 20 patients with chronic bronchitis and emphysema and pulmonary hypertension, the right ventricular end-systolic pressure/volume relation was calculated from combined measurements of right ventricular pressure, ejection fraction and cardiac output, in order to assess right ventricular contractility. Analysis of the pressure/volume relation indicated normal or enhanced right ventricular contractility in these patients, despite the presence of pulmonary hypertension. The right ventricular end-systolic pressure/volume ratio was unchanged when right ventricular systolic pressure was reduced by an infusion of sodium nitroprusside. Oxygen (3 litres/minute, nasal prongs) both when given acutely and over a period of 6 months (15 hours/24 hour day) to patients with chronic respiratory failure reduced pulmonary arterial pressure, but did not result in any change in right ventricular ejection fraction, nor in right ventricular contractility as assessed by the pressure/volume relation. From these results there was little to suggest that the effect of domiciliary oxygen in improving survival in patients with respiratory failure was mediated through a direct effect on the right ventricle. However, oxygen did improve right ventricular function during exercise in such patients although the mechanism remains obscure. The beta-agonist Pirbuterol produced pulmonary vasodilatation in patients with hypoxic chronic bronchitis and emphysema. Moreover, the right ventricular end-systolic pressure/volume ratio increased, suggesting that this drug had an additional inotropic effect. In order to determine if patients with acutely decompensated pulmonary heart disease truly had 'heart failure', haemodynamic measurements were made in 6 patients with respiratory failure and pulmonary hypertension, who presented acutely with oedema. Measurements of right ventricular ejection fraction and analysis of the right ventricular end-systolic pressure/volume relation, suggested that right ventricular contractility was depressed. However, right ventricular function, as measured by the cardiac index or stroke work index, was normal as a result of an adaptive mechanism involving large increases in right ventricular end-diastolic volume, as predicted by Starling's Law. In those patients who presented with oedema, these haemodynamic changes did not seem to result from an increase in pulmonary arterial pressure. Moreover, the relief of hypoxaemia by breathing oxygen had no consistent effect on right ventricular performance, despite a small reduction in pulmonary arterial pressure. The measurement of right ventricular ejection fraction in patients with chronic bronchitis and emphysema when measured in isolation, may give little information as to the cause of right ventricular dysfunction in such patients, but when combined with haemodynamic measurements obtained during right heart catheterisation, allows assessment of the right ventricular pressure/volume relation. This measurement is useful in assessing the mechanism of right ventricular dysfunction and in measuring the effects of therapeutic interventions in patients with pulmonary heart disease.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.383973  DOI: Not available
Keywords: Medicine
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