Does lung diffusion impairment affect exercise capacity in patients with heart failure?

Abstract

Objective: To determine whether there is a relation between impairment of lung diffusion and reduced exercise capacity in chronic heart failure.

Design: 40 patients with heart failure in stable clinical condition and 40 controls participated in the study. All subjects underwent standard pulmonary function tests plus measurements of resting lung diffusion (carbon monoxide transfer, TLCO), pulmonary capillary volume (VC), and membrane resistance (DM), and maximal cardiopulmonary exercise testing. In 20 patients and controls, the following investigations were also done: (1) resting and constant work rate TLCO; (2) maximal cardiopulmonary exercise testing with inspiratory O2 fractions of 0.21 and 0.16; and (3) rest and peak exercise blood gases. The other subjects underwent TLCO, DM, and VC measurements during constant work rate exercise.

Results: In normoxia, exercise induced reductions of haemoglobin O2 saturation never occurred. With hypoxia, peak exercise uptake (peak O2) decreased from (mean (SD)) 1285 (395) to 1081 (396) ml/min (p < 0.01) in patients, and from 1861 (563) to 1771 (457) ml/min (p < 0.05) in controls. Resting TLCO correlated with peak O2 in heart failure (normoxia < hypoxia). In heart failure patients and normal subjects, TLCO and peak O2 correlated with O2 arterial content at rest and during peak exercise in both normoxia and hypoxia. TLCO, VC, and DM increased during exercise. The increase in TLCO was greater in patients who had a smaller reduction of exercise capacity with hypoxia. Alveolar-arterial O2 gradient at peak correlated with exercise capacity in heart failure during normoxia and, to a greater extent, during hypoxia.

Conclusions: Lung diffusion impairment is related to exercise capacity in heart failure.

Figure 1

Peak V̇o₂ during normoxia v resting lung transfer capacity for carbon monoxide (Tlco) (reported as per cent of predicted) in heart failure patients (upper panel, n = 40) and healthy controls (lower panel, n = 40).

Figure 2

Peak V̇o₂ during hypoxia v resting lung transfer capacity for carbon monoxide (Tlco) (both reported as per cent of predicted) in heart failure patients (upper panel, n = 20) and healthy subjects (lower panel, n = 20) (group A). In chronic heart failure, the correlation between Tlco and peak V̇o₂ increased further during hypoxia.

Figure 3

Lung transfer capacity for carbon monoxide (Tlco) at rest (on the bicycle ergometer) and at the third and fifth minute of constant workload exercise (20% of peak exercise workload). Circles, normal subjects; diamonds, chronic heart failure patients. *p < 0.01 v rest; †p < 0.01 v 3rd minute value; ‡p < 0.01 v chronic heart failure patients.

Figure 4

Reduction of exercise capacity with hypoxia. ΔW/W = [maximum workload achieved in normoxia − maximum workload achieved in hypoxia]/maximum workload achieved in normoxia. ΔTlco = differences in lung diffusing capacity for carbon monoxide between the fifth minute of exercise and rest in heart failure patients. Patients with the greatest capability to increase Tlco during exercise are those who show the smallest reduction in exercise capacity in hypoxia.

Figure 5

Correlation between alveolar–arterial O₂ differences at peak exercise divided by peak V̇o₂ (ΔP[A−ao₂]/peak V̇o₂) v resting diffusing capacity for carbon monoxide (Tlco) in normoxia (upper panel) and hypoxia (lower panel).