PubMed Health⌕ Search

PubMed · 9720997

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease.

Abstract

To determine if decreased systemic oxygen (O2) extraction contributes to the exercise limit in severe chronic obstructive pulmonary disease (COPD), 40 consecutive incremental cycle ergometer exercise tests performed by such patients, from which a "log-log" lactate threshold (LT) was identified, were compared to those of 8 patients with left ventricular failure (LVF) and 10 normal controls. Pulmonary gas exchange and minute ventilation were measured continuously and arterial blood gas tensions, pH, and lactate concentrations were sampled each minute. Cardiac output (Qc) was measured by first-pass radionuclide ventriculography. The systemic O2 extraction ratio (O2ER) was calculated as arterial - mixed venous O2 content difference (CaO2 - CvO2)/CaO2. Peak exercise O2 uptake (VO2peak) was markedly reduced in both COPD and LVF [41 (3) and 42 (3)% predicted, respectively], compared to controls [89 (2)% predicted, P < 0.0001 for each]. Similarly, the LT occurred at a low percentage of predicted maximal oxygen consumption in both COPD and LVF [25 (2) and 27 (3)%] compared to normals [46 (3)%, P < 0.0001 for each]. The systemic O2ER at peak exercise was severely reduced in COPD [0.36 (0.02)] compared to the other groups [P < 0.0001 for each], for whom it was nearly identical [0.58 (0.03) vs 0.63 (0.04), LVF vs control, P > 0.05]. In the COPD group, an early LT correlated with reduced systemic O2ER at peak exercise (r = 0.64, P < 0.0001), but not with any index of systemic O2 delivery. These data suggest that lactic acidemia during exercise in patients with severe COPD is better related to abnormal systemic O2 extraction than to its delivery and contributes to the exercise limit.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D A Oelberg, B D Medoff, D H Markowitz, P P Pappagianopoulos, L C Ginns, D M Systrom. 1998. Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease.. https://doi.org/10.1007/s004210050408

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A previously undescribed leukodystrophy in Leigh syndrome associated with T9176C mutation of the mitochondrial ATPase 6 gene.

We report two male Taiwanese siblings in whom the T-->C point mutation at nucleotide 9176 of the mitochondrial ATPase 6 gene (m.9176T>C mutation) was associated with early onset hypotonia, lactic acidosis, and death due to respiratory arrest at 7 and 10 months old. Brain MRI showed lesions over diffuse white matter and the bilateral posterior limbs of the internal capsule. The m.9176T>C mutation is suggested as the cause of the bilateral striatal necrosis and Leigh syndrome. However, leukodystrophy in Leigh syndrome associated with m.9176T>C mutation has never been reported before. We suggest that m.9176T>C mutation could be a new aetiology for leukodystrophy in children with Leigh syndrome.

Acidosis, Lactic↗

Lactic acidosis in children with acute exacerbation of severe asthma.

This is a retrospective case series reporting lactic acidosis in four pediatric patients with acute severe asthma treated with nebulized beta2-agonists in a pediatric intensive care unit of a tertiary care teaching facility. During treatment with beta2-agonists, these patients developed lactic acidosis with a peak concentration of 5.2 to 13 mmol/l. Lactic acidosis improved within 24 h after discontinuation or decrease in the dosage of beta2-agonists. We conclude that the intensive use of beta2-agonists for acute severe asthma in children may be the primary and significant cause of lactic acidosis.

Acidosis, Lactic↗