BACKGROUND: The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation. METHODS: To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived. RESULTS: There was a fall in fractional dead space ventilation (0.43 to 0.28; P < 0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P < 0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension. CONCLUSIONS: The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.
BACKGROUND: The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation. METHODS: To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived. RESULTS: There was a fall in fractional dead space ventilation (0.43 to 0.28; P < 0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P < 0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension. CONCLUSIONS: The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.
Authors: Bryce N Balmain; Andrew R Tomlinson; James P MacNamara; Satyam Sarma; Benjamin D Levine; Linda S Hynan; Tony G Babb Journal: J Appl Physiol (1985) Date: 2021-11-11
Authors: Bryce N Balmain; Andrew R Tomlinson; James P MacNamara; Satyam Sarma; Benjamin D Levine; Linda S Hynan; Tony G Babb Journal: J Appl Physiol (1985) Date: 2022-02-03