Long-term dyspnea, regional ventilation distribution and peripheral lung function in COVID-19 survivors: a 1 year follow up study

Gaetano Scaramuzzo, Luca Ronzoni, Gianluca Campo, Paolo Priani, Chiara Arena, Riccardo La Rosa, Cecilia Turrini, Carlo Alberto Volta, Alberto Papi, Savino Spadaro, Marco Contoli, Gaetano Scaramuzzo, Luca Ronzoni, Gianluca Campo, Paolo Priani, Chiara Arena, Riccardo La Rosa, Cecilia Turrini, Carlo Alberto Volta, Alberto Papi, Savino Spadaro, Marco Contoli

Abstract

Background: Dyspnea is common after COVID-19 pneumonia and can be characterized by a defective CO2 diffusion (DLCO) despite normal pulmonary function tests (PFT). Nevertheless, DLCO impairment tends to normalize at 1 year, with no dyspnea regression. The altered regional distribution of ventilation and a dysfunction of the peripheral lung may characterize dyspnea at 1 year after COVID-19 pneumonia. We aimed at assessing the pattern of airway resistance and inflammation and the regional ventilation inhomogeneity in COVID-19 pneumonia survivors at 12-months after hospital discharge.

Methods: We followed up at 1-year patients previously admitted to the respiratory units (intensive care or sub-intensive care unit) for COVID-19 acute respiratory failure at 1-year after hospital discharge. PFT (spirometry, DLCO), impulse oscillometry (IOS), measurements of the exhaled nitric oxide (FENO) and Electrical Impedance Tomography (EIT) were used to evaluate lung volumes, CO2 diffusion capacity, peripheral lung inflammation/resistances and the regional inhomogeneity of ventilation distribution. A full medical examination was conducted, and symptoms of new onset (not present before COVID-19) were recorded. Patients were therefore divided into two groups based on the presence/absence of dyspnea (defined as mMRC ≥1) compared to evaluate differences in the respiratory function derived parameters.

Results: Sixty-seven patients were admitted between October and December 2020. Of them, 42/67 (63%) patients were discharged alive and 33 were evaluated during the follow up. Their mean age was 64 ± 11 years and 24/33 (73%) were males. Their maximum respiratory support was in 7/33 (21%) oxygen, in 4/33 (12%) HFNC, in 14/33 (42%) NIV/CPAP and in 8/33 (24%) invasive mechanical ventilation. During the clinical examination, 15/33 (45%) reported dyspnea. When comparing the two groups, no significant differences were found in PFT, in the peripheral airway inflammation (FENO) or mechanical properties (IOS). However, EIT showed a significantly higher regional inhomogeneity in patients with dyspnea both during resting breathing (0.98[0.96-1] vs 1.1[1-1.1], p = 0.012) and during forced expiration (0.96[0.94-1] vs 1 [0.98-1.1], p = 0.045).

Conclusions: New onset dyspnea characterizes 45% of patients 1 year after COVID-19 pneumonia. In these patients, despite pulmonary function test may be normal, EIT shows a higher regional inhomogeneity both during quiet and forced breathing which may contribute to dyspnea.

Clinical trial registration: Clinicaltrials.gov NCT04343053, registration date 13/04/2020.

Keywords: COVID-19; Dyspnea; Electrical impedance tomography; Post COVID-19; Pulmonary function test; Spirometry.

Conflict of interest statement

SS and GS are associate editors for BMC pulmonary medicine. The other authors declare no competing interests related to the current work.

© 2022. The Author(s).

Figures

Fig. 1
Fig. 1
Flow chart of the study
Fig. 2
Fig. 2
Inhomogeneity index derived from Electrical Impedance tomography (EIT) in patients with and without dyspnea during resting breathing (panel A, tidal volume) and forced expiratory maneuver (panel B)
Fig. 3
Fig. 3
Example of EIT images during forced expiration maneuver (∆FEV1EIT) in two representative patients. Dynamic image of expired volume at 1 second during forced expiration (∆FEV1EIT) in two representative patients; 2A, asymptomatic patients (mMRC = 0); panel 2B: Symptomatic patient (mMRC = 2). Negative values represent the regional loss of volume (AU) in the 1st second after the start of forced expiration from vital capacity (FEV1)

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Source: PubMed

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