Respiratory failure

Roussos, C.; Koutsoukou, A.

doi:10.1183/09031936.03.00038503

Cited by 374 publications

(223 citation statements)

References 60 publications

(103 reference statements)

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“…P 0.1 /P Imax ratio reflects a balance between the magnitude of the respiratory load and the muscle strength available to meet the load. 23 When Figure 1 Mouth occlusion pressure (P 0.1 at rest and at different levels of maximal exercise (%W max ) in obese (black circles) (n ¼ 17) and control subjects (white circles) (n ¼ 14). *Po0.05; **Po0.01; ***Po0.001.…”

Section: Discussionmentioning

confidence: 99%

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Inspiratory muscle activity during incremental exercise in obese men

Chlif¹,

Keochkerian²,

Feki

et al. 2007

Int J Obes

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Objective: The aim of this study was to assess overall inspiratory muscle activity during incremental exercise in obese men and healthy controls using the non-invasive, inspiratory muscle tension-time index (T T0.1 ). We studied 17 obese subjects (mean age7s.d.; 49713 years) and 14 control subjects (42716) during an incremental, maximal exercise test. Methods: Measurements included anthropometric parameters, spirometry, breathing patterns and inspiratory muscle activity. T T0.1 was calculated using the equation T T0.1 ¼ P 0.1 /P Imax Â T I /T TOT (where P 0.1 is mouth occlusion pressure, P Imax is maximal inspiratory pressure and T I /T TOT is the duty cycle). Results: At same levels of maximal exercise (%W max ) (20, 40, 60, 80, 100% W max ), obese subjects showed higher P 0.1 (Po0.001) and P 0.1 /P Imax (Po0.001) values than controls. T T0.1 was thus higher in obese subjects for each workload increment and at maximal exercise (Po0.001). Conclusions: During exercise, patients with obesity show alterations in inspiratory muscle activity as a result of both reduced inspiratory strength (as measured by maximal inspiratory pressure) and increased ventilatory drive (as reflected by mouth occlusion pressure), which prone obese subject to respiratory muscle weakness. Our results suggest that impaired respiratory muscle activity could contribute to a decrease in exercise capacity. T T0.1 may be useful in our understanding concerning the benefits of endurance training.

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Section: Discussionmentioning

confidence: 99%

“…It follows that energy demands (VO 2resp ) increase when the efficiency is reduced, for a given work output ( Figure 6). 23 …”

Section: Discussionmentioning

confidence: 99%

Inspiratory muscle activity during incremental exercise in obese men

Chlif¹,

Keochkerian²,

Feki

et al. 2007

Int J Obes

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“…In practice, a subject would need to increase their ventilation very substantially to overcome the wasted ventilation in high ventilation/perfusion ratio units, but their inability to do so despite the respiratory stimulus that a rising CO 2 tension provides has been the subject of much debate [13]. One useful analysis has been provided by MOXHAM [14], who placed the respiratory muscle pump in the central role, being affected to some extent by the load that it has to overcome, e.g.…”

Section: Physiological Basis Of Respiratory Therapy In Chronic Obstrumentioning

confidence: 99%

Respiratory failure in chronic obstructive pulmonary disease

Calverley¹

2003

European Respiratory Journal

104

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Respiratory failure in chronic obstructive pulmonary disease. P.M.A. Calverley. #ERS Journals Ltd 2003. ABSTRACT: Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality.The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness.Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients.Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse. Eur Respir J 2003; 22: Suppl. 47, 26s-30s.

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“…In fact, respiratory acidosis was associated with metabolic acidosis in the IRG-SS, as shown by the levels of PaCO 2 . The reduced V E and the lack of respiratory compensation of metabolic acidosis reflect acute respiratory failure with fatigue of the respiratory muscles (40).…”

Section: Discussionmentioning

confidence: 99%

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

Amorim¹,

Pinheiro²,

Beppu³

et al. 2007

Braz J Med Biol Res

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We analyzed the effects of saline infusion for the maintenance of blood volume on pulmonary gas exchange in ischemia-reperfusion syndrome during temporary abdominal aortic occlusion in dogs. We studied 20 adult mongrel dogs weighing 12 to 23 kg divided into two groups: ischemia-reperfusion group (IRG, N = 10) and IRG submitted to saline infusion for the maintenance of mean pulmonary arterial wedge pressure between 10 and 20 mmHg (IRG-SS, N = 10). All animals were anesthetized and maintained on spontaneous ventilation. After obtaining baseline measurements, occlusion of the supraceliac aorta was performed by the inflation of a Fogarty catheter. After 60 min of ischemia, the balloon was deflated and the animals were observed for another 60 min of reperfusion. The measurements were made at 10 and 45 min of ischemia, and 5, 30, and 60 min of reperfusion. Pulmonary gas exchange was impaired in the IRG-SS group as demonstrated by the increase of the alveolar-arterial oxygen difference (21 ± 14 in IRG-SS vs 11 ± 8 in IRG after 60 min of reperfusion, P = 0.004 in IRG-SS in relation to baseline values) and the decrease of oxygen partial pressure in arterial blood (58 ± 15 in IRG-SS vs 76 ± 15 in IRG after 60 min of reperfusion, P = 0.001 in IRG-SS in relation to baseline values), which was correlated with the highest degree of pulmonary edema in morphometric analysis (0.16 ± 0.06 in IRG-SS vs 0.09 ± 0.04 in IRG, P = 0.03 between groups). There was also a smaller ventilatory compensation of metabolic acidosis after the reperfusion. We conclude that infusion of normal saline worsened the gas exchange induced by pulmonary reperfusion injury in this experimental model. Correspondence

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Respiratory failure

Cited by 374 publications

References 60 publications

Inspiratory muscle activity during incremental exercise in obese men

Inspiratory muscle activity during incremental exercise in obese men

Respiratory failure in chronic obstructive pulmonary disease

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

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