Exertional dyspnoea in interstitial lung diseases: the clinical utility of cardiopulmonary exercise testing

Abstract

Interstitial lung diseases (ILDs) represent a heterogeneous group of pathologies characterised by alveolar and interstitial damage, pulmonary inflammation (usually associated with fibrosis), decreased lung function and impaired gas exchange, which can be attributed to either a known or an unknown aetiology. Dyspnoea is one of the most common and disabling symptoms in patients with ILD, significantly impacting quality of life. The mechanisms causing dyspnoea are complex and not yet fully understood. However, it is recognised that dyspnoea occurs when there is an imbalance between the central respiratory efferent drive and the response of the respiratory musculature. The respiratory derangement observed in ILD patients at rest is even more evident during exercise. Pathophysiological mechanisms responsible for exertional dyspnoea and reduced exercise tolerance include altered respiratory mechanics, impaired gas exchange, cardiovascular abnormalities and peripheral muscle dysfunction.This review describes the respiratory physiology of ILD, both at rest and during exercise, and aims to provide comprehensive and updated evidence on the clinical utility of the cardiopulmonary exercise test in the assessment and management of these pathological entities. In addition, the role of exercise training and pulmonary rehabilitation programmes in the ILD population is addressed.

Ventilation efficiency to exercise in patients with cystic fibrosis

“…By providing breath‐by‐breath data on several indices such as oxygen uptake, CO 2 output, minute ventilation, and various others, CPET can help assess which system fails to respond first and thus provide focused treatment and rehabilitation in various conditions . CPET has been recognized as the preferred examination to evaluate exertional dyspnea in both COPD and interstitial lung diseases as well as exploring underlying pathophysiological mechanisms that contribute and lead to respiratory deterioration . Upon maximal exercise in these diseases a shallow breathing pattern is noted with elevated minute ventilation (VE) and increased ventilatory equivalents for CO 2 and ventilation efficiency index .…”

“…CPET has been recognized as the preferred examination to evaluate exertional dyspnea in both COPD and interstitial lung diseases as well as exploring underlying pathophysiological mechanisms that contribute and lead to respiratory deterioration . Upon maximal exercise in these diseases a shallow breathing pattern is noted with elevated minute ventilation (VE) and increased ventilatory equivalents for CO 2 and ventilation efficiency index . V′E/V′CO 2 is also elevated in COPD as Neder et al point, however no data exist on the structural correlates of the ΔVE/ΔVCO 2 slope with further studies in this direction needed both in COPD and other disease entities.…”

Mandibular advancement reveals long-term suppression of breathing discomfort in patients with obstructive sleep apnea syndrome

“…Increased inspiratory load due to abnormal upper airways mechanics, increased neural ventilatory drive, and respiratory-related cortical activation are generally associated with breathing discomfort or dyspnea. This has been verified experimentally Raux et al, 2007) and in various clinical contexts, like chronic obstructive pulmonary disease (COPD) (Jolley et al, 2015), idiopathic pulmonary fibrosis (Bonini and Fiorenzano, 2017), cystic fibrosis (Reilly et al, 2011), laryngeal obstruction (Walsted et al, 2018), or amyotrophic lateral sclerosis (Georges et al, 2016). Yet OSAS patients typically do not complain spontaneously from breathing discomfort at rest.…”

Markers of Heart, Lung and Dorsal Aorta Damage of Mother Rats and Their Neonates Post Therapeutic Treatment with Doxorubicin, Cisplatin and 5-Flurouracil

“…The hypoxic stress in lung tissues and disorganized pulmonary vascular peds reproduced myocardial damage [47]. The lung dysfunction may lead to decrease respiratory mechanics, impaired gas exchange and cardiovascular abnormalities [48], increased arterial stiffness, the marker of heart failure [49].…”