Exercise limitation in chronic heart failure
Author(s)
Clark, Andrew Lawrence
Type
Thesis
Abstract
The pathophysiology underlying the symptoms of breathlessness and fatigue in chronic stable heart failure are incompletely understood. A key observation is the relationship between ventilation (VE) and carbon dioxide production (VCO2), described by a linear regression function. The slope of the relationship becomes steeper with increasing severity of heart failure. A widely held view is that the stimulus to increased ventilation on exercise is carbon dioxide production, and that increased ventilatory dead space underlies the increased VE/VCO2 slope. This thesis describes a series of experiments using mass spectrometric techniques to determine ventilation and metabolic gas exchange. I have shown: (1) a fall in arterial carbon dioxide tension in patients at peak exercise; (2) that the VE/VCO2 slope deviated significantly from being a straight line relationship. Thus carbon dioxide production is unlikely to be a physiological stimulus to ventilation. I have demonstrated that the increase in the VE/VCO2 may arise from hyperventilation. Direct measurement of dead space and the alveolar-arterial oxygen difference suggest that ventilation-perfusion mismatch dose not determine the increased VE/VCO2 slope. Arterial potassium has been suggested as a possible ventilatory stimulus; measurement of potassium on exercise shows this to be unlikely. Experiments in normal subjects have (1) demonstrated a ventilatory signal arising in skeletal muscle, neurally mediated, and enhanced by ischaemia. (2) This signal is related to the bulk of muscle exercising at a given work load. Patients with heart failure lose muscle mass. In experiments relating muscle quality and quantity, the two main factors predicting exercise capacity were thigh muscle cross sectional area and quadriceps muscle strength. I have demonstrated the presence of a neurally transmitted ventilatory stimulus arising from exercising muscle. In heart failure, exercise capacity is related to muscle quantity and quality, suggesting a link between the skeletal muscle abnormalities and the excessive ventilatory response.
Version
Open Access
Date Issued
1994
Date Acceptance
1994
Copyright Statement
Attribution NoDerivatives 4.0 International Licence (CC BY-ND)