Comparisons between basal metabolic rate and diet-induced thermogenesis in different types of chronic obstructive pulmonary disease

1992 ◽  
Vol 83 (1) ◽  
pp. 109-116 ◽  
Author(s):  
J. H. Green ◽  
M. F. Muers
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Metabolic Rate ◽  
Pulmonary Disease ◽  
Basal Metabolic Rate ◽  
Work Of Breathing ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Partial Pressure ◽  
Partial Pressure Of Co2 ◽  
Diet Induced Thermogenesis

1. Some patients with the emphysematous type of tobacco-related chronic obstructive pulmonary disease are hypermetabolic. Since the likely mechanism is the increased work of breathing, other groups of patients with chronic obstructive pulmonary disease should be similar. We have now measured basal metabolic rate and diet-induced thermogenesis in six patients with chronic obstructive pulmonary disease with an arterial partial pressure of CO2 of <5kPa (emphysematous), nine patients with chronic obstructive pulmonary disease with an arterial partial pressure of CO2 of >6kPa (bronchitic), eight patients with chronic obstructive pulmonary disease due to chronic asthma and seven control subjects. Diet-induced thermogenesis was measured for 4h after a meal of 87% carbohydrate, 11% protein and 2% fat as energy, with a total energy content of 40% of basal metabolic rate. 2. There was no difference between measured and predicted basal metabolic rate in the control (5541 ± 272 versus 5881 ± 245 kJ/24h) or emphysematous (5552 ± 370 versus 6239 ± 197 kJ/24 h) groups, but measured basal metabolic rate was significantly higher than predicted in the bronchitic (6126 ± 387 versus 5405 ± 250 kJ/24 h) and asthmatic (6293 ± 197 versus 5701 + 245, mean ± SEM, P<0.01) groups. All the control subjects had measured basal metabolic rates within 10% of predicted, whereas two out of six emphysematous patients, four out of nine bronchitic patients and five out of eight asthmatic patients were hypermetabolic. The contributions of fat, carbohydrate and protein oxidation rates to the overall basal metabolic rate were similar between groups. 3. Diet-induced thermogenesis was similar between groups. The postprandial fuel mix oxidized was also similar between all four groups. 4. Thus, some patients with both types of smoking-related chronic obstructive pulmonary disease and other patients with chronic asthma were hypermetabolic. This could not be predicted from detailed lung function tests, arterial blood gases or anthropometric measurements, and suggests that the increased work of breathing may not be the only cause of the hypermetabolism and weight loss seen in these patients.

Diet-induced Thermogenesis in Chronic Obstructive Pulmonary Disease

1993 ◽  
Vol 148 (6_pt_1) ◽  
pp. 1479-1483 ◽  
Author(s):  
Olivier Hugli ◽  
Philippe Frascarolo ◽  
Yves Schutz ◽  
Eric Jéquier ◽  
Philippe Leuenberger ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Diet Induced Thermogenesis

Noninvasive Ventilation and High-Flow Nasal Therapy Administration in Chronic Obstructive Pulmonary Disease Exacerbations

2020 ◽  
Vol 41 (06) ◽  
pp. 786-797
Author(s):  
Miquel Ferrer ◽  
Antoni Torres
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Respiratory Failure ◽  
Pulmonary Disease ◽  
Noninvasive Ventilation ◽  
Work Of Breathing ◽  
High Flow ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Hypercapnic Respiratory Failure ◽  
Acute Hypercapnic Respiratory Failure

AbstractNoninvasive ventilation (NIV) is considered to be the standard of care for the management of acute hypercapnic respiratory failure in patients with chronic obstructive pulmonary disease exacerbation. It can be delivered safely in any dedicated setting, from emergency rooms to high dependency or intensive care units and wards. NIV helps improving dyspnea and gas exchange, reduces the need for endotracheal intubation, and morbidity and mortality rates. It is therefore recognized as the gold standard in this condition. High-flow nasal therapy helps improving ventilatory efficiency and reducing the work of breathing in patients with severe chronic obstructive pulmonary disease. Early studies indicate that some patients with acute hypercapnic respiratory failure can be managed with high-flow nasal therapy, but more information is needed before specific recommendations for this therapy can be made. Therefore, high-flow nasal therapy use should be individualized in each particular situation and institution, taking into account resources, and local and personal experience with all respiratory support therapies.

Elevated levels of brain natriuretic peptide in acute hypoxaemic chronic obstructive pulmonary disease

1992 ◽  
Vol 83 (5) ◽  
pp. 529-533 ◽  
Author(s):  
Chim C. Lang ◽  
Wendy J. Coutie ◽  
Allan D. Struthers ◽  
D. Paul Dhillon ◽  
John H. Winter ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Pulmonary Disease ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Partial Pressure ◽  
Atrial Natriuretic

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 ± 0.4 kPa; arterial partial pressure of CO2, 6.9 ± 0.1 kPa; forced expiratory volume in 1 s, 0.6 ± 0.07 litre (27 ± 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 ± 4.1 pmol/l and 45.0 ± 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 ± 0.8 pmol/l and 8.0 ± 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = −0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide. 4. Thus, plasma levels of brain natriuretic peptide were proportionately higher than those of atrial natriuretic peptide in patients with hypoxaemic chronic obstructive pulmonary disease. Unlike those of atrial natriuretic peptide, plasma levels of brain natriuretic peptide were correlated with the degree of hypoxaemia. Further studies are required to investigate the release and clearance of brain natriuretic peptide in chronic obstructive pulmonary disease, as well as its pulmonary vasodilator activity in vivo.

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