Uncovering the mechanisms of exertional dyspnoea in combined pulmonary fibrosis and emphysema

Autor: J. Alberto Neder, Carlos Gustavo Yuji Verrastro, Camila M. Costa, Eloara M. V. Ferreira, Carlos Alberto de Castro Pereira, Roberta Pulcheri Ramos, Marcelle Paula-Ribeiro, Jaquelina S. Ota-Arakaki, Luiz Eduardo Nery, Denis E. O'Donnell
Rok vydání: 2019
Předmět:
Zdroj: European Respiratory Journal. 55:1901319
ISSN: 1399-3003
0903-1936
DOI: 10.1183/13993003.01319-2019
Popis: The prevailing view is that exertional dyspnoea in patients with combined idiopathic pulmonary fibrosis (IPF) and emphysema (CPFE) can be largely explained by severe hypoxaemia. However, there is little evidence to support these assumptions.We prospectively contrasted the sensory and physiological responses to exercise in 42 CPFE and 16 IPF patients matched by the severity of exertional hypoxaemia. Emphysema and pulmonary fibrosis were quantified using computed tomography. Inspiratory constraints were assessed in a constant work rate test: capillary blood gases were obtained in a subset of patients.CPFE patients had lower exercise capacity despite less extensive fibrosis compared to IPF (p=0.004 and 0.02, respectively). Exertional dyspnoea was the key limiting symptom in 24 CPFE patients who showed significantly lower transfer factor, arterial carbon dioxide tension and ventilatory efficiency (higher minute ventilation (V′E)/carbon dioxide output (V′CO2) ratio) compared to those with less dyspnoea. However, there were no between-group differences in the likelihood of pulmonary hypertension by echocardiography (p=0.44). High dead space/tidal volume ratio, low capillary carbon dioxide tension emphysema severity (including admixed emphysema) and traction bronchiectasis were related to a highV′E/V′CO2ratio in the more dyspnoeic group.V′E/V′CO2nadir >50 (OR 9.43, 95% CI 5.28–13.6; p=0.0001) and total emphysema extent >15% (2.25, 1.28–3.54; p=0.01) predicted a high dyspnoea burden associated with severely reduced exercise capacity in CPFEContrary to current understanding, hypoxaemiaper seis not the main determinant of exertional dyspnoea in CPFE. Poor ventilatory efficiency due to increased “wasted” ventilation in emphysematous areas and hyperventilation holds a key mechanistic role that deserves therapeutic attention.
Databáze: OpenAIRE