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Haemodynamic effects of proportional assist ventilation during high‐intensity exercise in patients with chronic obstructive pulmonary disease
Author(s) -
CARRASCOSSA Cláudia R.,
OLIVEIRA Cristino C.,
BORGHISILVA Audrey,
FERREIRA Eloara M.V.,
MAYA Joyce,
QUEIROGA Fernando,
BERTON Danilo C.,
NERY Luiz E.,
NEDER J. Alberto
Publication year - 2010
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2010.01846.x
Subject(s) - medicine , ventilation (architecture) , cardiology , copd , hemodynamics , stroke volume , impedance cardiography , respiratory minute volume , heart rate , cardiac output , anaerobic exercise , respiratory system , physical therapy , blood pressure , mechanical engineering , engineering
Background and objective: Proportional assist ventilation (PAV) has been proposed as a more physiological modality of non‐invasive ventilation, thereby reducing the potential for deleterious cardio‐circulatory effects during exercise, in patients with COPD. We therefore evaluated whether PAV modulates the kinetic and ‘steady‐state’ haemodynamic responses to exercise in patients with moderate‐to‐severe COPD. Methods: Twenty patients underwent constant‐load (75–80% peak work rate) cycle ergometer exercise testing to the limit of tolerance (T lim ), while receiving PAV or breathing spontaneously. Stroke volume (SV), heart rate (HR) and cardiac output (CO) were monitored by impedance cardiography. Results: Compared with unassisted breathing, PAV increased T lim in 8/20 patients (median improvement 113% (range 8 to 212) vs −20% (range −40 to −9)). PAV had no significant effects on ‘steady‐state’ haemodynamic responses either in patients with or those without increased T lim ( P > 0.05). However, at the onset of exercise, SV kinetics were slowed with PAV, in 13/15 patients with analysable data. HR dynamics remained unaltered or failed to accelerate sufficiently in nine of these patients, thereby slowing CO kinetics (T 1/2 61 s (range 81–30) vs 89 s (range 100–47)). These deleterious effects were not, however, associated with PAV‐induced changes in T lim ( P > 0.05). Conclusions: PAV slowed the SV and CO kinetics at the onset of high‐intensity exercise in selected patients with moderate‐to‐severe COPD. However, these adverse effects of PAV disappeared during the stable phase of exercise, and were not related to the ergogenic potential of PAV in this patient population.