RT Journal Article
SR Electronic
T1 Dysfunctional breathing diagnosed by cardiopulmonary exercise testing in ‘long COVID’ patients with persistent dyspnoea
JF BMJ Open Respiratory Research
JO BMJ Open Resp Res
FD British Thoracic Society
SP e001126
DO 10.1136/bmjresp-2021-001126
VO 9
IS 1
A1 Isabelle Frésard
A1 Léon Genecand
A1 Marco Altarelli
A1 Grégoire Gex
A1 Petrut Vremaroiu
A1 Andreea Vremaroiu-Coman
A1 David Lawi
A1 Pierre-Olivier Bridevaux
YR 2022
UL http://bmjopenrespres.bmj.com/content/9/1/e001126.abstract
AB Background ‘Long COVID’-associated dyspnoea may persist for months after SARS-CoV-2 infection. Among the causes of persistent dyspnoea, dysfunctional breathing (DB), defined as an erratic or inappropriate ventilation at rest or exercise, has been observed, but little is known about its occurrence and pathophysiology among individuals with ‘long COVID’. We aimed to describe the occurrence and identify clinical predictors of DB among patients following SARS-CoV-2 infection.Methods Cardiopulmonary exercise testing (CPET) was performed in 51 SARS-CoV-2 patients (median age, 64 years (IQR, 15)); male, 66.7%) living with ‘long COVID’ and persistent dyspnoea. CPET was classified into three dominant patterns: respiratory limitation with gas exchange abnormalities (RL); normal CPET or O2 delivery/utilisation impairment (D); and DB. Non-parametric and χ2 tests were applied to analyse the association between CPET dominant patterns and demographics, pulmonary function tests and SARS-CoV-2 severity.Results Among 51 patients, DB mostly without hyperventilation was found in 29.4% (n=15), RL in 54.9% (n=28) and D in 15.7% (n=8). When compared with RL individuals, patients with DB were younger, had significantly less severe initial infection, a better transfer capacity for carbon monoxide (median 85% (IQR, 28)), higher oxygen consumption (22.9 mL/min/kg (IQR, 5.5)), a better ventilatory efficiency slope (31.6 (IQR, 12.8)), and a higher SpO2 (95% (IQR, 3)).Conclusions Our findings suggest that DB without hyperventilation could be an important pathophysiological mechanism of disabling dyspnoea in younger outpatients following SARS-CoV-2 infection, which appears to be a feature of COVID-19 not described in other viral diseases.Data are available upon reasonable request.