Role of exercise ventilation in the limitation of functional capacity in patients with congestive heart failure.
Patients with heart failure have, compared with normal subjects, an increased minute ventilation (VE) at matched workloads. This heightened ventilatory drive may contribute to their limitation of functional capacity through an increase in the work of breathing and further worsening in the lung ventilation-perfusion mismatch. To measure the ventilatory response to exercise, VE should not be assessed in absolute units but be related to one of its main determinants, e.g., carbon dioxide production (VCO2). Particularly, as VE is closely related to VCO2 during exercise, the ventilatory response to exercise has been assessed using the slope of the relation of VE versus VCO2. This slope is significantly increased in heart failure patients compared with normal subjects and is inversely related to other parameters of maximal exercise capacity, namely peak VO2. The mechanisms of exercise hyperpnea in heart failure patients are still unsettled. A first possibility is that it is a compensatory response to the abnormal exercise hemodynamics with secondary increase of the pulmonary dead space to tidal volume ratio. This mechanism should be aimed to maintain constancy of the arterial gas composition and acid-base balance. However, exercise-induced hypoxemia and/or hypercapnia do not generally develop in heart failure patients. This might imply that other mechanisms, such as an increased sensitivity of the arterial chemoreceptors and/or the activation of reflexes by the abnormal skeletal muscles, stimulate the ventilatory response in heart failure patients. Regardless of its mechanisms, exercise hyperpnea may be clinically relevant in the assessment of patients with chronic heart failure. In fact, it is inversely related with peak exercise capacity, and interventions known to improve peak functional capacity such as therapy with ACE inhibitors, physical training and heart transplantation, also tend to normalize exercise hyperpnea.
Cattedra di Cardiologia Università di Brescia, Italy.
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D015444:Exercise / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D012123:Pulmonary Ventilation / Q000502:physiology*