An evaluation of exercise tests in chronic obstructive lung disease.

Shuey, C B; Pierce, Alan K.; Johnson, Rachel L.

doi:10.1152/jappl.1969.27.2.256

Cited by 33 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This observation differs from previous studies of healthy adults, athletes, and other subject groups who report a higher metabolic response during treadmill exercise 26,27 and a V O 2MAX up to 7% higher than cycle exercise. 28 The finding of a greater cardiopulmonary and metabolic response during cycling exercise in patients with IC in the present study is in agreement with an analogous study comparing cycle and treadmill exercise in patients with severe COPD. 23 These authors found that although peak V O 2 did not differ between the two forms of exercise, postexercise blood lactate levels were substantially higher after cycle exercise than after treadmill exercise (ie, 2.5 vs 1.22 mmol/L).…”

Section: Discussionsupporting

confidence: 92%

Cardiopulmonary responses to treadmill and cycle ergometry exercise in patients with peripheral vascular disease

Tuner

Easton

Wilson

et al. 2008

Journal of Vascular Surgery

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 92%

Cardiopulmonary responses to treadmill and cycle ergometry exercise in patients with peripheral vascular disease

Tuner

Easton

Wilson

et al. 2008

Journal of Vascular Surgery

View full text Add to dashboard Cite

show abstract

“…At E1, the end-exercise concentration was 3.5 mmol·L -1 for a mean workload of 76 W, and it reached 2.6 mmol·L -1 at E2 for a mean maximal workload of only 56 W. As previously shown by many authors, COPD patients produce lactic acid quite early during exercise [28][29][30]. Hypoxaemia, inappropriate cardiac output, and peripheral muscle deconditioning are some of the pathophysiologic mechanisms that have been proposed to explain this early lactic acid production.…”

Section: Discussionsupporting

confidence: 61%

Functional outcome of patients with chronic obstructive pulmonary disease and exercise hypercapnia

Simard¹,

Maltais²,

Leblanc³

1995

Eur Respir J

View full text Add to dashboard Cite

F Fu un nc ct ti io on na al l o ou ut tc co om me e o of f p pa at ti ie en nt ts s w wi it th h c ch hr ro on ni ic c o ob bs st tr ru uc ct ti iv ve e p pu ul lm mo on na ar rySixteen stable COPD patients (13 males and 3 females, aged 60±5 yrs, mean±SD) who had previously undergone pulmonary function tests and progressive exercise testing with arterial blood sampling at rest and maximal capacity, entered the study. At first evaluation (E1), subjects were normocapnic at rest (arterial carbon dioxide tension (Pa,CO 2 ): 4.9-5.7 kPa, (37-43 mmHg)) and all presented exercise-induced hypercapnia (end-exercise Pa,CO 2 >5.7 kPa (43 mmHg) with a minimal 0.5 kPa (4 mmHg) increase from resting value). The subjects were re-evaluated 24-54 months later (34±8 months) (second evaluation (E2)).At E2, forced expiratory volume in one second (FEV1) had decreased from 42±13 to 38±15% of predicted values, and mean resting Pa,CO 2 had increased from 5.2±0.3 to 5.7 + 0.4 kPa. Maximal exercise capacity (Wmax) decreased between E1 and E2 from 76±30 to 56±22 W. Even if Wmax was lower at E2, end-exercise Pa,CO 2 was higher than at E1 (6.6±0.8 vs 6.4±0.5 kPa). At E2, eight subjects presented resting hypercapnia (group H), whilst the others remained normocapnic (Group N). Group H subjects had higher Pa,CO 2 , at Wmax than Group N and lower Wmax than Group N at E2. Group H and N were not significantly different for physiological dead space/tidal volume ratio (VD/VT), FEV1, lung volumes and transfer factor of the lungs for carbon monoxide (TL,CO), both at E1 and E2.In half of the patients studied, exercise hypercapnia was a step in the progression of COPD towards resting hypercapnia, and was associated with severe exercise limitation. During exercise, patients who responded to a deterioration in their lung function by increasing minute ventilation remained normocapnic at rest, whilst those who did not increase their ventilation developed chronic hypercapnia at rest during the 2-4 year follow-up period.

show abstract

“…A probable cause of LV failure during ventilator weaning must be the associated increased LV afterload induced by the phasic decreases in ITP with each spontaneous breath with its obligatory increase in myocardial O 2 consumption. This weaning-associated LV failure may be a primary cause of failure to wean in critically ill ventilator-dependent patients (32,33).…”

Section: Left Heart and Determinants Of Afterloadmentioning

confidence: 99%

Heart-lung interactions during mechanical ventilation: the basics

Mahmood¹,

Pinsky²

2018

Ann. Transl. Med.

145

106

View full text Add to dashboard Cite

The hemodynamic effects of mechanical ventilation can be grouped into three clinically relevant concepts. First, since spontaneous ventilation is exercise. In patients increased work of breathing, initiation of mechanical ventilatory support may improve O 2 delivery because the work of breathing is reduced. Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As lung volume increases so does the pressure difference between airway and pleural pressure. When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular resistance. Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection. Anything that over distends lung units will increase their vascular resistance, and if occurring globally throughout the lung, increase pulmonary vascular resistance. Decreases in endexpiratory lung volume cause alveolar collapse increases pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers that restore alveolar oxygenation without over distention will reduce pulmonary artery pressure. Third, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, it can induce profound decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload and will augment left ventricular ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved left ventricular ejection, increased cardiac output and reduced myocardial O 2 demand. This brief review will focus primarily on mechanical ventilation and intrathoracic pressure as they affect right and left ventricular function and cardiac output.

show abstract

An evaluation of exercise tests in chronic obstructive lung disease.

Cited by 33 publications

References 0 publications

Cardiopulmonary responses to treadmill and cycle ergometry exercise in patients with peripheral vascular disease

Cardiopulmonary responses to treadmill and cycle ergometry exercise in patients with peripheral vascular disease

Functional outcome of patients with chronic obstructive pulmonary disease and exercise hypercapnia

Heart-lung interactions during mechanical ventilation: the basics

Contact Info

Product

Resources

About