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- cardiovascular physiological phenomena
- dyspnea
- exercise test
- inspiratory capacity
- positive-pressure respiration
- pulmonary disease
- chronic obstructive.
Introduction
Dynamic lung hyperinflation is an important cause of morbidity and mortality in patients with COPD.1 Indeed, the use of expiratory positive airway pressure (EPAP) at rest causes acute lung deflation in COPD.2 However, its application has led to a progressive reduction in exercise tolerance in this population,3-5 and a recent meta-analysis showed no overall benefit from its use in this context.6 The justification for this disappointing effect lies in 2 possible mechanisms: (1) increased recruitment of expiratory muscles, leading to reduced venous return,3 which would be especially harmful in presence of left ventricular diastolic dysfunction4; and (2) progressive increase in inspiratory resistance (IR) caused by the diaphragm of the inspiratory branch of the 2-way valve without rebreathing.3,7 It is important to note that a higher IR model (Hans Rudolph 2700 model; resistance values 0.8/1.8 cm H2O at flows of 100/200 L/min) has recently been shown to reduce time to exhaustion compared to a lower IR model (Daniel type; resistance values 0/0.1 cm H2O at the same flows) in healthy subjects.7
To assess the impact of EPAP without IR on high-intensity exercise tolerance and metabolic/ventilatory measurements, this study was designed with the inspiratory limb connected to a continuous pressure source (4 cm H2O), maintaining the diaphragm in the inspiratory branch, and the expiratory flow against a resistance of 7 cm H2O (EPAP), a system called I-EPAP. The main hypothesis of the present study was that the combination of low-level EPAP with the absence of IR could improve the global effects on tolerance to high-intensity exercise, with better physiological adjustments.
Methods
Study Design
This was a prospective, randomized controlled and single-blind study, 4 visits, carried out at the Laboratory of Respiratory Pathophysiology of the …
Correspondence: Paulo T Müller DSc, Laboratory of Respiratory Pathophysiology, Respiratory Division of University Hospital, Federal University of Mato Grosso do Sul, Rua Filinto Müller S/N, Vila Ipiranga, CEP:79080-090, Campo Grande, Brazil. E-mail: paulo.muller{at}ufms.br
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