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Exercise capacity impairment after COVID-19 pneumonia is mainly caused by deconditioning


Kathleen Jahn, Mihaela Sava, Gregor Sommer, Desiree M. Schumann, Stefano Bassetti, Martin Siegemund, Manuel Battegay, Daiana Stolz, Michael Tamm, Nina Khanna, Katrin E. Hostettler

European Respiratory Journal 2022 59: 2101136; DOI: 10.1183/13993003.01136-2021

To the Editor:

The new severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) can cause severe pneumonia characterised by dry cough, dyspnoea, hypoxaemia and diffuse ground glass opacities on chest computed tomography (CT). While much has been learnt concerning diagnosis and treatment of coronavirus disease 2019 (COVID-19) during the first year of the pandemic, only scarce data is available concerning post-COVID long-term pulmonary sequelae. Data about pulmonary function in early convalescence demonstrated impaired diffusion capacity, lower respiratory muscle strength, and radiological abnormalities. Herein we report data of cardio-pulmonary exercise testing (CPET) 3 months after severe COVID-19 pneumonitis.

Between 26 February and 3 May, 2020, 221 patients with RT-PCR-confirmed SARS-CoV-2 infection were admitted to the University Hospital Basel, Switzerland. A total of 50 (22.6%) patients suffered from severe COVID-19 pneumonitis, fulfilling ≥2 of the following criteria: respiratory rate >30 breaths·min−1, peripheral oxygen saturation (SpO2) <93% while breathing ambient air, C-reactive protein (CRP) levels >75 mg·L−1 (normal <10.0 mg·L−1), ground glass opacities or diffuse infiltrates on CT scan, or progression of CT findings >50% within 24–48 h or typical CT findings ≥4 lobes. Patients were treated according to local standards at that time, and only one patient received systemic corticosteroids (cumulative dose of 80 mg prednisone); all patients were included in an observational study (NCT04351503).

During hospitalisation 5/50 (10%) patients died due to COVID-19. One further patient succumbed to pre-existing haematological disease after hospital discharge. Among the 44 COVID-19 survivors, four experienced prolonged hospitalisation with oxygen dependency. A further five patients declined to undertake CPET. All patients received physiotherapy during their hospitalisation; after discharge, 8/35 (23%) patients were transferred for further inpatient pulmonary rehabilitation, and 3/35 (9%) patients underwent outpatient pulmonary rehabilitation. In all these patients, pulmonary rehabilitation programmes were completed at the time of CPET.

In the context of this analysis, patients were followed-up, including clinical status, body plethysmography and chest CT scan 3 months after COVID-19 pneumonitis.

All 35 patients underwent an incremental CPET using a cycle ergometer (Ergoline Ergoselect 1000) in semi-recumbent position in continuous ramp mode (10–20 W·min−1). CPET parameters were systematically computed according to breath-by-breath analysis and data were displayed online (Sentry Suite Version 3.10). Arterial blood gas analysis at rest and at maximal exercise level was performed (ABL 800 Flex). The level of dyspnoea and exhaustion at peak exercise was objectified using the Borg modified scale. The evaluation of the collected data was in accordance with the Wassermann algorithm and the adaptation of Schmid et al.. Health-related quality of life (QoL) was evaluated using the St George's Respiratory Questionnaire (SGRQ) and the King's Brief Interstitial Lung Disease (K-BILD) questionnaire. Chest CT scans were conducted on a dual source CT scanner (Somatom Definition Flash, Siemens Healthineers) using dual-energy acquisition after intravenous injection of iodine contrast material in the late pulmonary arterial phase. Mann–Whitney U-test was computed to assess statistical differences; a p-value <0.05 was considered statistically significant.

Baseline characteristics, underlying comorbidities, and concomitant medication of those 35 patients who agreed to perform CPET are shown in table 1. On chest CT scan, 15/35 patients (43%) exhibited residuals only, and 6/35 patients (17%) had additional fibrotic changes. Pulmonary function values were normal (total lung capacity ≥80% predicted, diffusion capacity of the lung for carbon monoxide (DLCO) ≥80% predicted, Tiffeneau index >0.7) in 23/35 patients (66%). A normal maximal oxygen uptake (VO2max) during CPET (VO2max ≥82% predicted) was observed in 16/35 (46%) patients; 19/35 (54%) proved to have impaired VO2max (15 with mild impairment: VO2max 61–81% predicted; four with moderate impairment: VO2max 51–60% predicted). The main limiting factors in those patients with impaired VO2max were deconditioning in 9/19, cardiovascular in 5/19, and pulmonary limitations in 5/19 patients. In those patients with impaired VO2max, DLCO %pred at day 90 was significantly lower as compared to the patients with normal VO2max (p = 0.006); no other parameter differed between the two groups (table 1). Detailed variables of CPET are shown in table 1.

TABLE 1

Baseline characteristics, underlying comorbidities, concomitant medication, disease severity at hospital admission, pulmonary function, radiological outcome, quality of life and cardiopulmonary exercise testing data 3 months after severe COVID-19 pneumonitis

Contrary to our expectations, both in patients with and without lung function impairment, the most common main limiting factor of VO2max was not of a pulmonary nature, but general deconditioning. Of note, maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) were normal in those patients with deconditioning (mean MIP 99.4% predicted, mean MEP 79.9% predicted), making it unlikely that neuromuscular impairment caused the limitation. Three of the nine patients with deconditioning were obese. In 14% of the patients (5/35), cardiovascular limitation of CPET was observed. From those, three had previous cardiovascular disease. Only one of the five patients with pulmonary limitation had a pre-existing respiratory disease, i.e. severe obstructive sleep apnoea. Health-related QoL was not better in those with normal VO2max compared to those with impaired VO2max. However, this finding is limited by the fact that 40% of patients did not complete the questionnaires, though these were equally distributed in both groups (42% versus 37.5%).

Our data on pulmonary function impairment after COVID-19 pneumonitis are in line with previous publications. The low prevalence of respiratory comorbidities and active smoking in our population might partially explain the finding of 66% normal pulmonary function tests 3 months after severe COVID-19. Impairment of physical performance in patients recovering from COVID-19 pneumonia has been described before. To date, there are accumulating data on CPET after SARS-CoV-2 infection, but only limited respective information on patients surviving severe COVID-19 pneumonitis. In our well-characterised patient group, almost half (46%) had normal VO2max on CPET. In those patients with impaired VO2max, the majority (47%) was limited by deconditioning. Thus, despite the severity of the acute COVID-19 pneumonitis, only 14% of survivors exhibited pulmonary limitation in CPET 3 months later, demonstrating a surprisingly good pulmonary recovery. This applies even more in the light of the predominant lung pathology observed in patients with severe COVID-19, i.e. diffuse alveolar damage, endothelitis and pulmonary immunothrombosis.

In a previous issue of the European Respiratory Journal, Skjørten et al. reported a reduced VO2max in one-third of COVID-19 patients 3 months after hospital discharge, with deconditioning being the major cause of exercise limitation. Compared to these findings, we observed a higher proportion of patients with impaired peak oxygen uptake (54%), which is likely due to the more severe disease course in our patient group, as depicted by the longer length of hospital stay (median 14 day versus median 6 days) . The study by Rinaldo et al. reported CPET data in a mixed group of patients with critical, severe and mild-moderate COVID-19. Even though we included only patients with severe COVID-19 pneumonia, the mean VO2max of 82% predicted in our study population is surprisingly similar to the one reported by Rinaldo et al. (83%). A striking disparity between the two patient groups is the portion of active smokers, being only 2.9% in our population, as compared to 19% in the group studied by Rinaldo et al.. This might, at least partially, explain the good outcome in our patients. Finally, in line with our data, Rinaldo et al. found muscle deconditioning to be the main cause of reduced exercise capacity . In a very small group of 10 moderate and severe COVID-19 patients, Gao et al. performed CPET 1 month post-discharge. In contrast to our data, Gao et al. found reduced peak oxygen uptake in all cases, an apparent contradiction which might be explained by the 2 months later follow-up time-point of our study. However, similar to us, Gao et al. showed that extrapulmonary factors were the main reason for exercise limitation. Notably, our findings are in line with CPET data from survivors of the 2002 coronavirus-induced SARS outbreak: 3 months after SARS, 41% of the patients showed reduced VO2max; none of these patients had pulmonary limitation, but extrapulmonary disease, mainly impaired muscle function, caused reduced VO2max. Furthermore, similar data were found in survivors of severe acute respiratory distress syndrome (ARDS) caused by various aetiologies. By performing CPET 3 months after severe COVID-19, a time point by which most radiological abnormalities related to the acute infection had vanished, we were able to demonstrate that half of the patients have reduced exercise capacity, yet, only a minority of patients have pulmonary limitation. Thus, CPET is a helpful tool to further dissect reduced exercise tolerance and interpret exertional dyspnoea. With similar previous findings in survivors of SARS, physical deconditioning seems to be the main cause of impaired exercise capacity after severe coronavirus infections, and might even represent the natural course after severe lung injury with critical illness in general.

In summary, we demonstrate that physical deconditioning is the most common cause of impaired VO2max in patients after severe COVID-19 pneumonitis. Whether these findings are specific to SARS-CoV-2 infection or conversely depict the common sequelae after ARDS caused by any insult has to be further explored. Finally, our findings underscore the importance of an early rehabilitative intervention in survivors of severe COVID-19 pneumonitis.

Footnotes

  • Conflict of interest: S. Bassetti participated on an advisory board for Pharming Technologies BV, outside the submitted work. All other authors have nothing to disclose.

  • Received April 23, 2021.
  • Accepted October 10, 2021.
  • Copyright ©The authors 2022

sumber : https://erj.ersjournals.com/content/59/1/2101136

 
 

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