The haemodynamic response to exercise in chronic obstructive pulmonary disease: assessment by impedance cardiography

Bogaard, Harm-Jan; Dekker, Bianca M. den; Arntzen, B. W. G. J.; Woltjer, H. H.; Keimpema, Anton R.J. van; Postmus, Pieter E.; Vries, P. M. J. M. De

doi:10.1183/09031936.98.12020374

Cited by 17 publications

(23 citation statements)

References 42 publications

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“…During exercise there was a rapid increase in Ppa even in patients with normal resting pressures. The findings of a reduced SV response during exercise together with an increase in Ppa are consistent with those of previous studies [3,5,21] and fit with the idea that this reduced SV during exercise is caused by an increased afterload.…”

Section: Discussionsupporting

confidence: 81%

“…KEYWORDS: Chronic obstructive pulmonary disease, magnetic resonance imaging, pulmonary hypertension, sildenafil, stroke volume S everal studies have shown that stroke volume (SV) in chronic obstructive pulmonary disease (COPD) patients may be reduced at rest and frequently fails to increase during exercise [1][2][3][4][5]. Since cardiac output is proportionally related to tissue oxygen delivery, impaired SV response (when not compensated by an increased cardiac frequency) may contribute to reduced exercise capacity in COPD.…”

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confidence: 99%

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Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

et al. 2007

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In chronic obstructive pulmonary disease (COPD) patients, stroke volume response to exercise is impaired. The aim of the present study was to investigate whether 3 months of sildenafil treatment improves stroke volume and, if so, whether this improvement is related to the pulmonary artery pressure and translated into an improved exercise capacity.A total of 15 stable COPD patients (Global Initiative for Chronic Obstructive Lung Disease stage II-IV) underwent right heart catheterisation at rest and during exercise. Stroke volume was assessed by magnetic resonance imaging (MRI) at rest and during submaximal exercise in the supine position and compared with eight age-matched controls. Additionally, a cardiopulmonary exercise test and a 6-min walking distance test were performed. Exercise tests and MRI were repeated after 12 weeks of oral therapy with 50 mg sildenafil three times daily.Stroke volume in COPD patients was significantly lower than in healthy controls (62¡12 versus 81¡22 mL at rest and 70¡15 versus 101¡28 mL during exercise). Pulmonary hypertension (PH) was diagnosed in nine patients and was absent in six. Treatment with sildenafil had no effect on stroke volume or exercise capacity. Although the stroke volume was lower in COPD patients with associated PH in comparison with non-PH patients, there was no difference in treatment response between both groups.In the present group of 15 chronic obstructive pulmonary disease patients, a reduced stroke volume was found at rest and during exercise. Neither stroke volume nor exercise capacity were improved by 3 months of sildenafil therapy.

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Section: Discussionsupporting

confidence: 81%

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confidence: 99%

Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

et al. 2007

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“…Decreases in exercise cardiac output have been documented (Stewart and Lewis 1986;Bogaard et al 1998). There is a decrease in right ventricular ejection fraction (Morrison et al 1987) which fails to increase with increases in exercise workload and right ventricular end-diastolic volume (Mahler et al 1984;Uenami et al 1986).…”

Section: Relevance To Copdmentioning

confidence: 97%

Influence of expiratory flow-limitation during exercise on systemic oxygen delivery in humans

et al. 2005

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To determine the effects of exercise with expiratory flow-limitation (EFL) on systemic O(2) delivery, seven normal subjects performed incremental exercise with and without EFL at approximately 0.8 l s(-1) (imposed by a Starling resistor in the expiratory line) to determine maximal power output under control (W'(max,c)) and EFL (W'(max,e)) conditions. W'(max,e) was 62.5% of W'(max,c), and EFL exercise caused a significant fall in the ventilatory threshold. In a third test, after exercising at W'(max,e) without EFL for 4 min, EFL was imposed; exercise continued for 4 more minutes or until exhaustion. O(2) consumption (V'(O)(2)) was measured breath-by-breath for the last 90 s of control, and for the first 90 s of EFL exercise. Assuming that the arterio-mixed venous O(2) content remained constant immediately after EFL imposition, we used V'(O)(2) as a measure of cardiac output (Q'(c)). Q'(c) was also calculated by the pulse contour method with blood pressure measured continuously by a photo-plethysmographic device. Both sets of data showed a decrease of Q'(c) due to a decrease in stroke volume by 10% (p < 0.001 for V'(O)(2)) with EFL and remained decreased for the full 90 s. Concurrently, arterial O(2) saturation decreased by 5%, abdominal, pleural and alveolar pressures increased, and duty cycle decreased by 43%. We conclude that this combination of events led to a decrease in venous return secondary to high expiratory pressures, and a decreased duty cycle which decreased O(2) delivery to working muscles by approximately 15%.

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“…There appears to be considerable variability between patients. Stewart and Lewis [42]and Bogaard et al [43]both found a decrease in cardiac output during exercise in some patients with COPD and suggested that severity of expiratory flow limitation might be an important determinant of exercise cardiac output. Morrison et al [44]found strong correlations between maximal exercise oxygen consumption in COPD on the one hand and right ventricular ejection fraction, exercise stroke volume, and exercise cardiac output on the other.…”

Section: Cardiovascular Factors Limiting Exercise In Copdmentioning

confidence: 99%

“…Just as there is variability in exercise performance and exercise cardiac output among patients with COPD [42, 43], not all patients with COPD have a detectable anaerobic threshold [50, 51, 52]. Perhaps these are patients who have a true ventilatory limit to exercise.…”

Section: The Competition Between Ventilatory and Skeletal Musclesmentioning

confidence: 99%

How and Why Exercise Is Impaired in COPD

Aliverti

Macklem²

2001

Respiration

100

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Published data indicate that exercise in COPD is more often limited by leg effort than breathlessness. This casts some doubt on the classical belief that inability to ventilate limits exercise performance. In fact, symptoms limiting exercise appear to be essentially the same in COPD and in health or congestive heart failure, where exercise is limited by inadequate energy supply to locomotor muscles. In COPD, impaired O₂ delivery to locomotor muscles is suggested by: (1) the O₂ cost (v̇_O2) of breathing may be ∼50% of whole body v̇_O2; (2) decreasing the work of breathing improves performance and v̇_O2 of locomotor muscles, and (3) locomotor muscle v̇_O2 is greater when it is the only muscle exercising than during whole body exercise. Excessive expiratory pressures when expiratory flow is limited may lead to decreased venous return and contribute importantly to exercise limitation.

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The haemodynamic response to exercise in chronic obstructive pulmonary disease: assessment by impedance cardiography

Cited by 17 publications

References 42 publications

Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

Sildenafil treatment in COPD does not affect stroke volume or exercise capacity

Influence of expiratory flow-limitation during exercise on systemic oxygen delivery in humans

How and Why Exercise Is Impaired in COPD

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