Effects of increased inspired oxygen concentrations on exercise performance in chronic heart failure

Moore, D.; Weston, A.R.; Oakley, Celia M.; Cleland, John G.F.; Hughes, J.

doi:10.1016/0140-6736(92)90288-e

Cited by 86 publications

(48 citation statements)

References 18 publications

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“…Further support for this view comes from the finding that hyperoxic breathing, with resulting improvement in pulmonary gas exchange and downregulation of the peripheral chemoreceptors, improves exercise tolerance and reduces exercise ventilation, with a tendency for reduced VEVCO 2 , in CHF patients. 26 …”

Section: Discussionmentioning

confidence: 99%

Impaired Pulmonary Diffusion During Exercise in Patients With Chronic Heart Failure

et al. 1999

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Background-Pulmonary diffusion is impaired at rest in patients with chronic heart failure (CHF) and has been implicated in the generation of symptoms and exercise intolerance. The aim of this study was to determine whether pulmonary diffusion is impaired during exercise in CHF, to examine its relationship to pulmonary blood flow, and to consider its functional significance in relation to metabolic gas exchange. Methods and Results-Carbon monoxide transfer factor (TLCO) and pulmonary blood flow (Q C ) were measured by a rebreathe technique at rest and during steady-state cycling at 30 W in 24 CHF patients and 10 control subjects. Both patients and control subjects were able to raise TLCO and Q C during exercise. However, the patient group had a lower diffusion for a given blood flow (TLCO/Q C ) both at rest (3.6Ϯ0.16 and 4.8Ϯ0.23 mL ⅐ L Ϫ1 ⅐ mm Hg Ϫ1 ; PϽ0.001) and during exercise (2.8Ϯ0.16 and 3.4Ϯ0.13 mL ⅐ L Ϫ1 ⅐ mm Hg Ϫ1 for CHF patients and control subjects, respectively; PϽ0.05). TLCO/Q C was related to the ventilatory equivalent for carbon dioxide (VEVCO 2 ) production at 30 W (TLCO/Q c versus VEVCO 2 , rϭϪ0.58, PϽ0.01) and to peak exercise oxygen consumption measured during a progressive test (TLCO/Qc versus VO 2peak , rϭ0.57, PϽ0.01) in these patients. Conclusions-Patients with CHF are able to recruit reserves of TLCO and Q C during exercise. However, the TLCO/Q C ratio is consistently impaired in these patients and relates to both exercise hyperpnea and peak exercise oxygen consumption. Whether this impairment in alveolar gas exchange is reversible in CHF and therefore is a potential target for therapy has yet to be determined.

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Section: Discussionmentioning

confidence: 99%

Impaired Pulmonary Diffusion During Exercise in Patients With Chronic Heart Failure

et al. 1999

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“…Arterial oxygen content (CaO 2 ) was calculated from the venous [Hb] at rest, assuming an arterial SO 2 of 94% in HF 18,19 and 97% in CTL (commonly observed by ear oximetry). Venous oxygen content (CvO 2 ) was calculated by use of the measured [Hb] and saturation and the venous PO 2 .…”

Section: Data Acquisition and Analysismentioning

confidence: 99%

Blood Flow Dynamics in Heart Failure

et al. 1999

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Background-Exercise intolerance in heart failure (HF) may be due to inadequate vasodilation, augmented vasoconstriction, and/or altered muscle metabolic responses that lead to fatigue. Methods and Results-Vascular and metabolic responses to rhythmic forearm exercise were tested in 9 HF patients and 9 control subjects (CTL) during 2 protocols designed to examine the effect of HF on the time course of oxygen delivery versus uptake (protocol 1) and on vasoconstriction during exercise with 50 mm Hg pressure about the forearm to evoke a metaboreflex (protocol 2). In protocol 1, venous lactate and H ϩ were greater at 4 minutes of exercise in HF versus CTL (PϽ0.05) despite similar blood flow and oxygen uptake responses. In protocol 2, mean arterial pressure increased similarly in each group during ischemic exercise. In CTL, forearm blood flow and vascular conductance were similar at the end of ischemic and ambient exercise. In HF, forearm blood flow and vascular conductance were reduced during ischemic exercise compared with the ambient trial. Conclusions-Intrinsic differences in skeletal muscle metabolism, not vasodilatory dynamics, must account for the augmented glycolytic metabolic responses to moderate-intensity exercise in class II and III HF. The inability to increase forearm vascular conductance during ischemic handgrip exercise, despite a normal pressor response, suggests that enhanced vasoconstriction of strenuously exercising skeletal muscle contributes to exertional fatigue in HF.(Circulation. 1999;99:3002-3008.)

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“…Recently, the DLCO has been reported to be an independent predictor of exercise tolerance, measured as peak oxygen consumption [7,8]. Further, Moore et al [9] found the increase in oxygen diffusion through the alveolar-capillary membrane, obtained by higher inspired oxygen concentration on exercise, to induce a prolongation of exercise duration, an increase in SaO 2 , and a reduction in breathlessness. The potential to modulate the diffusing capacity by pharmacological agents and its effects on exercise performance in CHF should be further investigated.…”

Section: Introductionmentioning

confidence: 99%

Effects of Body Position on the Carbon Monoxide Diffusing Capacity in Patients with Chronic Heart Failure: Relation to Hemodynamic Changes

Faggiano¹,

D’Aloia²,

Simoni

et al. 1997

Cardiology

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Objective: Pulmonary diffusion has been found to be reduced in patients with congestive heart failure. The effects of postural changes on the diffusing capacity had been evaluated in healthy subjects, but not in patients with heart failure. The aim of this study was to evaluate the posture-induced changes in diffusing capacity in patients with chronic heart failure and their relation to the hemodynamic profile. Methods: The pulmonary carbon monoxide diffusing capacity (DLCO) was measured in the supine position, with 20° passive head elevation, and in the sitting position, both postures maintained for 10 min, in a group of 32 male patients with mild to moderate chronic heart failure due to left ventricular systolic dysfunction (ejection fraction <35%). On a separate day, in the absence of any changes in clinical status and therapy, the hemodynamic parameters were measured by right-heart catheterization. The sequence of postures was assigned randomly. Results: The mean values of DLCO were slightly reduced and did not differ in the two positions (20.3 ± 5.7 vs. 19.4 ± 5.6 ml/min/mm Hg, 77 ± 23 vs. 75 ± 20% of predicted, respectively). The patients were then subdivided according to changes in DLCO from the supine to the sitting position: DLCO increased (+23%) in 9 patients (28%, group 1), decreased (–17.5%) in 17 patients (53%, group 2), and remained within the coefficient of reproducibility (±5%) in 6 patients (group 3). As compared with group 2, group 1 patients showed a significant increase in mean pulmonary artery pressure (+7 vs. –15%, p < 0.01) and pulmonary capillary wedge pressure (+8 vs. –22%, p < 0.005) from the supine to the sitting position, while the cardiac index showed a smaller – but not significant – decrease in group 1 (–5 vs. –12%). The percent changes in DLCO significantly correlated with changes in pulmonary capillary wedge (r = 0.54, p < 0.0005) and mean pulmonary artery (r = 0.47, p < 0.005) pressures. Conclusions: In chronic heart failure postural changes may induce different responses in diffusing capacity. To a greater extent than in healthy subjects, the most common response is a decrease in DLCO in the sitting as compared with the supine position. The DLCO changes correlate with variations in pulmonary circulation pressure, probably due to changes in pulmonary vascular recruitment and pulmonary capillary blood volume.

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Effects of increased inspired oxygen concentrations on exercise performance in chronic heart failure

Cited by 86 publications

References 18 publications

Impaired Pulmonary Diffusion During Exercise in Patients With Chronic Heart Failure

Impaired Pulmonary Diffusion During Exercise in Patients With Chronic Heart Failure

Blood Flow Dynamics in Heart Failure

Effects of Body Position on the Carbon Monoxide Diffusing Capacity in Patients with Chronic Heart Failure: Relation to Hemodynamic Changes

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