Cardiopulmonary Exercise Testing in Clinical Practice

Weber, Karl T.; Janicki, Joseph S.; McElroy, Patricia A.; Maskin, Carol S.

doi:10.1159/000174177

Cited by 21 publications

(21 citation statements)

References 10 publications

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“…It is therefore possible that if exercise were limited by impaired mechanics in COPD, (submaximal) O 2 extraction might be normal, but would appear to be inappropriately blunted at peak exercise. Weber and Janicki (1986) noted that the O 2 ER is 0.55 ± 0.60 at the LT in normal subjects and patients with congestive heart failure, regardless of the O 2 at which it occurs. Although O 2 extraction at the LT could not be determined in the current study, peak exercise values were below those normally expected at the LT.…”

Section: Discussionmentioning

confidence: 96%

“…With the possible exception of the elite endurance athlete (Dempsey et al 1984), maximal exercise capacity is normally limited by cardiovascular function (Weber and Janicki 1986). Conversely, patients with COPD are thought to be limited by decreased ventilatory capacity relative to demand (Brown and Wasserman 1981;Jones et al 1971).…”

Section: Discussionmentioning

confidence: 99%

“…C a O 2 data were not available for six COPD patients. O 2 delivery and O 2 ER data were not available for one normal subject, one LVF patient, and six COPD patients 1968; Weber and Janicki 1986). It is therefore possible that if exercise were limited by impaired mechanics in COPD, (submaximal) O 2 extraction might be normal, but would appear to be inappropriately blunted at peak exercise.…”

Section: Discussionmentioning

confidence: 99%

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

Oelberg

Medoff

Markowitz

et al. 1998

European Journal of Applied Physiology

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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.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Oelberg

Medoff

Markowitz

et al. 1998

European Journal of Applied Physiology

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“…delivery or ventila tion in the face of a steady increase in O; uptake. Maxi mal O; uptake was defined as the maximal oxygen uptake reached, usually in the plateau phase of oxygen uptake [14,15].…”

Section: Cardiopulmonary Exercise Testingmentioning

confidence: 99%

Mechanisms Involved in Cardiac Enlargement and Congestive Heart Failure Development after Acute Myocardial Infarction

Kleber

Nussberger

Niemöller³

et al. 1992

Cardiology

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For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO₂max in patients with vs. without volume enlargement 24.7 ± 1.7 vs. 29.5 ± 1.9 ml O₂/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.

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“…Patients with CHF can be broken down into groups by their hemodynamic response to exercise [9]. Those with the most severe disease cannot elevate cardiac output suffi ciently to respond to dynamic exercise.…”

mentioning

confidence: 99%

Cardiac Rehabilitation for Heart Failure Patients

Dubach¹,

Froelicher²

1989

Cardiology

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Exercise tolerance in patients with normal cardiac function can improve with an exercise program. Controversy exists whether this is also true for patients with congestive heart failure (CHF). The limiting symptoms in patients with CHF are shortness of breath and fatigue. Hemodynamic parameters do not correlate well with exercise capacity in patients with CHF. These symptoms may be more related to factors that cause fatigue during exercise than to hemodynamic parameters or even to changes in pulmonary capillary pressure. The factors that cause symptoms include an increased lactate production and metabolic and blood flow abnormalities in the skeletal muscle. Exercise training can improve vasodilation and oxidation capacity, thereby reducing lactate production. Exercise programs may improve exercise capacity in the majority of patients with CHF due to coronary artery disease or idiopathic cardiomyopathy. However, certain patients with ischemia and with anterior infarctions may experience a detrimental effect on their cardiac function. Further studies are needed to better enable recognition of these patients but until this is possible, good clinical judgement must suffice.

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Cardiopulmonary Exercise Testing in Clinical Practice

Cited by 21 publications

References 10 publications

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

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

Mechanisms Involved in Cardiac Enlargement and Congestive Heart Failure Development after Acute Myocardial Infarction

Cardiac Rehabilitation for Heart Failure Patients

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