Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2, predominantly affects the respiratory system and produces a clinical spectrum ranging from asymptomatic infection to severe pneumonia, acute respiratory distress syndrome, respiratory failure, and multiorgan dysfunction. Although most patients recover from the acute infection, a considerable proportion continue to experience respiratory symptoms and functional limitations after the initial illness. The World Health Organization described post-COVID-19 condition as symptoms that usually occur within three months of probable or confirmed infection, persist for at least two months, and cannot be explained by an alternative diagnosis [1]. Common respiratory manifestations include persistent dyspnoea, cough, chest discomfort, fatigue, exercise intolerance, and exertional oxygen desaturation. The mechanisms responsible for these abnormalities are multifactorial and may include residual pulmonary inflammation, impaired alveolar repair, organizing pneumonia, microvascular injury, pulmonary fibrosis, respiratory-muscle weakness, and physical deconditioning [2].

Follow-up studies have demonstrated persistent radiological and physiological abnormalities among COVID-19 survivors, particularly those who experienced severe acute disease. Huang et al. reported fatigue, muscle weakness, sleep difficulties, diffusion impairment, and abnormal chest imaging six months after hospitalization, with greater pulmonary dysfunction among more severely affected patients [3]. A systematic review and meta-analysis by Torres-Castro et al. showed that impaired diffusing capacity was the most frequent pulmonary-function abnormality following COVID-19, followed by restrictive and obstructive ventilatory patterns [4]. Spirometry provides an accessible and non-invasive method of measuring forced vital capacity, forced expiratory volume in the first second, and their ratio, thereby identifying restrictive, obstructive, or mixed respiratory abnormalities. Functional exercise capacity and exertional desaturation can additionally be assessed using the six-minute walk test, a standardized and clinically useful measure of cardiopulmonary performance [5].

The probability of persistent respiratory impairment may be related to the severity of the initial pulmonary injury, degree of hypoxaemia, extent of pneumonia, need for oxygen or ventilatory support, and associated comorbidities. However, the magnitude and pattern of post-COVID respiratory dysfunction have varied across populations. Evaluating these abnormalities and their relationship with acute COVID-19 severity may facilitate risk-based follow-up, early pulmonary rehabilitation, and timely referral for advanced investigations.

AIM

To determine the association between acute COVID-19 disease severity and post-COVID respiratory dysfunction among adult COVID-19 survivors.

OBJECTIVES

1. To assess post-COVID respiratory function using spirometry and the six-minute walk test.
2. To determine the pattern and frequency of respiratory dysfunction among post-COVID-19 patients.
3. To examine the association of acute COVID-19 disease severity with post-COVID spirometric abnormalities and exertional oxygen desaturation.

Source of Data The study participants were recruited from post-COVID-19 patients attending the outpatient departments of Victoria Hospital and Bowring and Lady Curzon Hospital, Bengaluru. Patients with documented previous COVID-19 infection who satisfied the eligibility criteria and provided written informed consent constituted the source population. Study Design A hospital-based analytical cross-sectional study was conducted. Study Location The study was conducted in the Department of General Medicine at Victoria Hospital and Bowring and Lady Curzon Hospital, affiliated with Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India. Study Duration The study was conducted from February 2021 to December 2022. Sample Size The calculated sample size was approximately 205. After allowing for incomplete or technically unacceptable assessments, it was rounded to 210 participants. Inclusion Criteria 1. Patients who provided written informed consent. 2. Patients aged more than 18 years and less than 75 years. 3. Patients with previously documented COVID-19 confirmed by reverse-transcription polymerase chain reaction or rapid antigen testing. 4. Patients in whom at least six weeks had elapsed since the positive COVID-19 test. 5. Patients who were clinically stable and able to perform spirometry and the six-minute walk test. Exclusion Criteria 1. Patients who refused to provide informed consent. 2. Patients aged 18 years or younger or 75 years or older. 3. Patients with a known pre-existing respiratory disease, including bronchial asthma, chronic obstructive pulmonary disease, bronchiectasis, interstitial lung disease, or pulmonary tuberculosis with significant residual damage. 4. Patients with known clinically significant cardiac disease that could independently affect exercise capacity. 5. Patients with musculoskeletal, neurological, or mobility disorders that prevented safe performance of the six-minute walk test. 6. Patients evaluated within six weeks of the positive COVID-19 test. 7. Patients with breathlessness at rest or resting oxygen saturation below 94%. 8. Patients unable to perform technically acceptable spirometry despite repeated instructions. Data Collection Eligible patients were enrolled consecutively until the required sample size was achieved. Data were recorded in a predesigned and pretested study proforma. Information collected included age, sex, body mass index, smoking history, comorbidities, date and method of COVID-19 diagnosis, symptoms during acute infection, hospitalization, oxygen requirement, intensive-care admission, ventilatory support, and treatment received. The severity of acute COVID-19 was determined retrospectively from medical records and categorized as mild, moderate, or severe using the clinical findings, respiratory rate, oxygen saturation, and evidence of pneumonia documented during the acute illness. Available chest radiographs, high-resolution computed-tomography reports, discharge summaries, laboratory reports, and oxygen or ventilatory-support records were reviewed to improve the accuracy of severity classification. Current respiratory symptoms, including cough, dyspnoea, chest discomfort, fatigue, and exercise intolerance, were documented. A general physical examination, vital-sign assessment, pulse oximetry, and systemic examination, with particular attention to the respiratory and cardiovascular systems, were performed. Procedure and Methodology After obtaining Institutional Ethics Committee approval, potentially eligible patients were informed about the nature, purpose, procedures, benefits, and possible discomforts associated with the study. Written informed consent was obtained before enrolment. Confidentiality was maintained by assigning a unique identification number to every participant. Spirometry was performed by trained personnel using a calibrated spirometer. Participants were instructed regarding the correct technique and were tested in the sitting position with a nose clip, following appropriate infection-control precautions. At least three acceptable forced expiratory manoeuvres were attempted, and the best reproducible values were recorded. The principal parameters included forced vital capacity (FVC), forced expiratory volume in the first second (FEV₁), and FEV₁/FVC ratio. Values were expressed as absolute measurements and percentages of predicted values based on age, sex, height, and ethnicity. The spirometric pattern was classified as: • Normal: FVC ≥80% predicted and FEV₁/FVC >70%. • Obstructive: reduced FEV₁/FVC ratio (≤70%). • Restrictive: FVC <80% predicted with a preserved FEV₁/FVC ratio (>70%). • Mixed: reduced FVC and reduced FEV₁/FVC ratio. Because total lung capacity was not measured, a restrictive spirometric pattern was interpreted as suggestive of restriction rather than definitive physiological restriction. Each participant subsequently underwent a six-minute walk test on a level walking surface according to a standardized protocol. Resting pulse rate, respiratory rate, oxygen saturation, and relevant symptoms were recorded before the test. Participants were instructed to walk at their own pace for six minutes and were permitted to slow down, stop, or rest if required. Oxygen saturation and pulse rate were monitored using a fingertip pulse oximeter. Post-test oxygen saturation, distance walked, symptoms, and reasons for premature termination were recorded. The test was stopped if the participant developed severe breathlessness, chest pain, dizziness, near-syncope, marked fatigue, or clinically important oxygen desaturation. The test was considered positive for exertional hypoxaemia when the post-exercise SpO₂ was below 94% or when an absolute decline of at least three percentage points from baseline was observed. Chest radiography was reviewed for residual abnormalities such as ground-glass opacity, reticular opacity, consolidation, or fibrotic changes. High-resolution computed tomography of the thorax was considered when clinically indicated; it was not performed solely for research purposes. The primary exposure variable was the severity of acute COVID-19, while the primary outcome was post-COVID respiratory dysfunction demonstrated by an abnormal spirometric pattern and/or exertional desaturation during the six-minute walk test. Sample Processing No blood, sputum, tissue, or other biological sample was collected specifically for this study. Therefore, laboratory sample processing, preservation, and storage were not applicable. Previous RT-PCR or rapid antigen-test reports were reviewed only to confirm prior COVID-19 infection. Relevant investigations conducted as part of routine clinical care were documented from the participants’ medical records. Statistical Methods Data were entered into Microsoft Excel and analysed using IBM SPSS Statistics version 22.0. Data completeness and consistency were verified before analysis. Continuous variables were summarized using mean and standard deviation when normally distributed and median with interquartile range when non-normally distributed. Categorical variables were expressed as frequencies and percentages. Normality was assessed using the Shapiro-Wilk test, Kolmogorov-Smirnov test, and graphical methods. Mean respiratory-function values across acute-disease severity categories were compared using one-way analysis of variance, followed by Bonferroni post-hoc comparisons when statistically significant. The Kruskal-Wallis test was used for non-normally distributed continuous variables. The association between acute COVID-19 severity and categorical respiratory outcomes was assessed using the chi-square test or Fisher’s exact test, as appropriate. Effect sizes were reported as odds ratios with 95% confidence intervals. Multivariable binary logistic regression was used, where appropriate, to evaluate whether acute COVID-19 severity was independently associated with post-COVID respiratory dysfunction after adjustment for potential confounders such as age, sex, body mass index, smoking, diabetes mellitus, and hypertension. A two-sided p value <0.05 was considered statistically significant.

Table 1. Association between acute COVID-19 disease severity and post-COVID respiratory dysfunction (N=210)

Table 1 demonstrates a strong, graded association between the severity of acute COVID-19 and subsequent respiratory dysfunction. Overall, 93 (44.3%; 95% CI: 37.7%-51.0%) participants had an abnormal spirometric pattern, whereas 117 (55.7%) had normal spirometry. Respiratory dysfunction increased progressively from 0% among asymptomatic participants and 20.4% among those with mild disease to 56.0% among those with moderate disease and 78.9% among those with severe disease. Conversely, normal spirometry declined from 79.6% in the mild group to 44.0% and 21.1% in the moderate and severe groups, respectively. This association was statistically significant (χ²=62.84, df=3; p<0.001). Participants with severe acute COVID-19 had approximately ten times greater odds of post-COVID respiratory dysfunction than those with non-severe disease (OR=10.29; 95% CI: 5.20-20.37; p<0.001), indicating a substantial relationship between the intensity of the acute illness and persistent respiratory impairment.

Table 2. Assessment of post-COVID respiratory function using spirometry and the six-minute walk test (N=210)

1. Spirometric parameters according to acute COVID-19 severity

1. Six-minute walk-test findings

Bonferroni post-hoc comparisons:

FVC: mild versus moderate, p=0.001; mild versus severe, p<0.001; moderate versus severe, p=0.838.

FEV₁: mild versus moderate, p=0.013; mild versus severe, p<0.001; moderate versus severe, p=1.000.

†FEV₁ and FEV₁/FVC measurements were available for 209 participants.
‡The reported severe-group SD of 97.42 and maximum value of 898 suggest a probable data-entry outlier and should be checked against the original dataset.

Table 2 shows that post-COVID spirometric measurements declined with increasing severity of the acute illness. The overall mean FVC was 80.07% (SD 14.80; 95% CI: 78.06-82.09). Mean FVC decreased from 86.06% in the mild group to 75.48% in the moderate group and 72.11% in the severe group. The difference across severity groups was statistically significant (ANOVA F=16.999; p<0.001). Bonferroni analysis showed significant differences between the mild and moderate groups (p=0.001) and between the mild and severe groups (p<0.001), but not between the moderate and severe groups (p=0.838). Similarly, the overall mean FEV₁ was 79.89% (SD 17.32; 95% CI: 77.53-82.26), decreasing from 85.65% in mild disease to 75.36% in moderate disease and 71.99% in severe disease. This difference was significant (ANOVA F=11.400; p<0.001), with significant differences between mild and moderate disease (p=0.013) and between mild and severe disease (p<0.001). In contrast, the FEV₁/FVC percentage did not differ significantly across acute-severity groups (ANOVA F=0.258; p=0.855). However, the unusually large standard deviation in the severe group suggests a possible data-entry outlier that should be verified.

The six-minute walk test was normal in 189 (90.0%; 95% CI: 85.2%-93.4%) participants. Exertional oxygen desaturation occurred in 14 (6.7%; 95% CI: 4.0%-10.9%), while six (2.9%) participants could not complete the test and one (0.5%) did not undergo testing. Six-minute walk-test findings were significantly associated with acute COVID-19 severity (χ²=41.330, df=9; p<0.001).

Table 3. Pattern and frequency of post-COVID respiratory dysfunction (N=210)

†Goodness-of-fit chi-square test comparing the observed distribution of the four mutually exclusive spirometric patterns with an equal expected distribution.

Table 3 presents the distribution of post-COVID spirometric patterns. Normal spirometry was observed in 117 (55.7%; 95% CI: 49.0%-62.3%) participants, whereas 93 (44.3%; 95% CI: 37.7%-51.0%) demonstrated some form of respiratory dysfunction. A restrictive pattern was the most frequent abnormality, occurring in 80 (38.1%; 95% CI: 31.8%-44.8%) participants. Obstructive and mixed patterns were comparatively uncommon, affecting six (2.9%; 95% CI: 1.3%-6.1%) and seven (3.3%; 95% CI: 1.6%-6.7%) participants, respectively. The distribution of the four mutually exclusive spirometric patterns differed significantly from an equal expected distribution (χ²=174.27, df=3; p<0.001).

Table 4. Association of acute COVID-19 severity with post-COVID spirometric abnormality and exertional oxygen desaturation (N=210)

Effect estimates

†Fisher’s exact test compared severe with non-severe COVID-19 because no exertional-desaturation events occurred in the non-severe group.

‡The conventional odds ratio was infinite because of the zero-event cell. A continuity-corrected estimate would be unstable and was therefore not presented as the principal effect measure.

Table 4 confirms that both abnormal spirometry and exertional oxygen desaturation were strongly associated with severe acute COVID-19. Abnormal spirometry increased from 20.4% among participants with mild disease to 56.0% among those with moderate disease and 78.9% among those with severe disease. The association between acute-disease severity and abnormal spirometry was statistically significant (χ²=62.84, df=3; p<0.001). Severe COVID-19 was associated with 10.29 times greater odds of an abnormal post-COVID spirometric result compared with non-severe COVID-19 (95% CI: 5.20-20.37; p<0.001).

Exertional oxygen desaturation was observed in 14 (6.7%; 95% CI: 4.0%-10.9%) participants overall. All 14 cases occurred among participants who had experienced severe acute COVID-19, corresponding to a prevalence of 19.7% (95% CI: 12.1%-30.4%) in the severe group. No desaturation was recorded in the asymptomatic, mild, or moderate groups. Fisher’s exact test demonstrated a significant association between severe acute COVID-19 and exertional desaturation (p<0.001). Because there were no events in the non-severe group, the conventional odds ratio was infinite and could not be estimated reliably. Collectively, these findings show that severe acute COVID-19 was closely associated with persistent spirometric impairment and exercise-induced hypoxaemia during the post-COVID period.

Association between acute COVID-19 severity and post-COVID respiratory dysfunction The present study demonstrated a clear severity-response relationship between acute COVID-19 illness and subsequent respiratory dysfunction. Although respiratory dysfunction was found in 44.3% of the total cohort, its prevalence increased from 20.4% in patients with mild disease to 56.0% in those with moderate disease and 78.9% in those with severe disease. Patients who had experienced severe COVID-19 had approximately tenfold greater odds of an abnormal post-COVID spirometric result than those with non-severe illness (OR=10.29; 95% CI: 5.20-20.37). Mo et al. (2020)[1] similarly found that pulmonary-function abnormalities at discharge were more frequent among patients with severe COVID-19, with impairment of diffusing capacity followed by restrictive ventilatory defects being the predominant findings. Zhao et al. (2020)[2] reported pulmonary-function abnormalities three months after recovery in approximately one-quarter of COVID-19 survivors and observed that abnormal chest imaging during acute illness was associated with subsequent physiological impairment. Frija-Masson et al. (2020)[3] also reported that patients recovering from SARS-CoV-2 pneumonia frequently exhibited restrictive functional changes and reduced diffusion capacity within 30 days of infection. The observed severity gradient is biologically plausible because severe acute COVID-19 is associated with more extensive alveolar and interstitial injury, hypoxaemia, endothelial dysfunction, microvascular thrombosis and fibroproliferative repair. Huang et al. (2020)[4] found that impaired diffusing capacity, decreased respiratory-muscle strength and residual radiological abnormalities were common after hospitalization, particularly among patients with severe pneumonia. Daher et al. (2020)[5] documented persistent functional limitations and reduced exercise capacity approximately six weeks after severe COVID-19, even when conventional pulmonary-function measurements had substantially improved. Collectively, these findings support the present observation that the severity of the initial pulmonary insult was an important marker of post-acute respiratory impairment. The histopathological findings described by Xu et al. (2020)[6] provide a pathological explanation for this relationship. Their examination of COVID-19-associated acute respiratory distress syndrome showed diffuse alveolar damage, inflammatory cellular infiltration, hyaline-membrane formation and interstitial thickening. Carsana et al. (2020)[7] likewise demonstrated diffuse alveolar damage, capillary congestion, pneumocyte hyperplasia and platelet-fibrin thrombi in the lungs of patients with fatal COVID-19. Ackermann et al. (2020)[8] further identified severe endothelial injury, widespread thrombosis with microangiopathy and intussusceptive angiogenesis. These pulmonary parenchymal and vascular injuries may persist beyond viral clearance and manifest clinically as reduced lung volumes, impaired gas exchange and exercise-induced hypoxaemia. Spirometric parameters and the six-minute walk test In the present study, mean FVC and FEV₁ decreased progressively with increasing acute COVID-19 severity. Mean FVC declined from 86.06% predicted in the mild group to 75.48% in the moderate group and 72.11% in the severe group, while mean FEV₁ decreased from 85.65% to 75.36% and 71.99%, respectively. Both trends were statistically significant. Mo et al. (2020)[1] observed a comparable relationship, reporting lower FVC, total lung capacity and diffusing capacity in patients with more severe acute disease. Frija-Masson et al. (2020)[3] also found reductions in FVC and gas-transfer measurements among patients evaluated after SARS-CoV-2 pneumonia. Huang et al. (2020)[4] reported impaired pulmonary diffusion in 52.6% of their post-discharge cohort and showed that diffusion impairment was associated with disease severity. By contrast, the FEV₁/FVC percentage did not differ significantly across severity groups in the present study (F=0.258; p=0.855). The simultaneous decline in FVC and FEV₁ with relative preservation of their ratio was consistent with a predominantly restrictive rather than obstructive physiological pattern. This agrees with the findings of Mo et al. (2020)[1], who identified restrictive and diffusion abnormalities more frequently than airflow obstruction. However, the extremely high variability and implausible maximum FEV₁/FVC value reported in the severe group indicate a probable data-entry outlier. This variable should be rechecked in the original dataset before publication because the reported standard deviation of 97.42 could have distorted the ANOVA result. The six-minute walk test was normal in 90.0% of participants; nevertheless, 6.7% developed exertional oxygen desaturation and 2.9% could not complete the test. The findings were significantly associated with acute COVID-19 severity. Daher et al. (2020)[5] similarly found that many survivors of severe COVID-19 had reduced six-minute walking distance six weeks after discharge, although marked oxygen desaturation was less common. Liu et al. (2020)[9] demonstrated that respiratory rehabilitation significantly improved FEV₁, FVC, FEV₁/FVC and six-minute walking distance among elderly COVID-19 survivors, suggesting that part of the functional deficit may be reversible. Curci et al. (2020)[10] also documented considerable limitations in walking and physical performance during early post-acute rehabilitation, particularly among patients who had required prolonged hospitalization or ventilatory assistance. Interpretation of the six-minute walk test should consider that performance is influenced by pulmonary gas exchange, cardiovascular fitness, peripheral-muscle strength, neurological status, motivation and deconditioning. Holland et al. (2014)[11] emphasized that field-walking tests provide an integrated assessment of cardiopulmonary and musculoskeletal function rather than an isolated measurement of lung function. Consequently, inability to complete the test should not automatically be attributed to pulmonary dysfunction. Nevertheless, exertional oxygen desaturation is more suggestive of impaired pulmonary gas exchange, especially when accompanied by an abnormal restrictive pattern. Pattern and frequency of respiratory dysfunction Any spirometric dysfunction was observed in 44.3% of the present cohort. The restrictive pattern was by far the most frequent abnormality, affecting 38.1% of all participants and accounting for 86.0% of abnormal spirometric results. Obstructive and mixed patterns were uncommon, at 2.9% and 3.3%, respectively. These findings are consistent with Mo et al. (2020)[1], who reported that impaired diffusing capacity was the most frequent abnormality at discharge, followed by a restrictive ventilatory defect. Zhao et al. (2020)[2] reported abnormalities of FVC, FEV₁, FEV₁/FVC, total lung capacity and diffusing capacity three months after recovery, with diffusion impairment being the most persistent defect. Frija-Masson et al. (2020)[3] also demonstrated a predominance of restrictive and gas-transfer impairment following COVID-19 pneumonia. The predominance of restriction may reflect residual interstitial inflammation, organizing pneumonia, atelectatic change, pulmonary fibrosis or respiratory-muscle weakness. George et al. (2020)[12] proposed that extensive alveolar epithelial injury, cytokine-mediated inflammation, mechanical ventilation and abnormal wound repair could promote progressive pulmonary fibrosis after severe COVID-19. Salehi et al. (2020)[13] found that ground-glass opacities and bilateral peripheral lung involvement were the most common computed-tomography abnormalities, while reticular changes became more prominent during later disease stages. Shi et al. (2020)[14] similarly reported evolution of CT abnormalities over the clinical course, with extensive pulmonary involvement around the second week of illness. Wang et al. (2020)[15] observed that pulmonary abnormalities initially progressed and subsequently resolved gradually, although residual linear opacities and parenchymal changes persisted in some patients. Such residual radiological alterations could explain the reduction in FVC seen during post-COVID follow-up. However, spirometry alone cannot definitively establish a restrictive ventilatory defect. Graham et al. (2019)[16] stated that a reduced FVC with a preserved FEV₁/FVC ratio suggests restriction but requires confirmation by measurement of total lung capacity. Therefore, the 38.1% prevalence in the present study should technically be described as a “restrictive spirometric pattern” rather than confirmed restrictive lung disease. The absence of total lung-capacity and diffusing-capacity measurements may also have underestimated isolated gas-transfer impairment, which was the most common abnormality in several earlier investigations. Spirometric abnormality and exertional desaturation according to severity The final analysis showed that abnormal spirometry increased from 20.4% after mild COVID-19 to 56.0% after moderate and 78.9% after severe illness. Moreover, all 14 participants with exertional desaturation belonged to the severe group, giving a desaturation frequency of 19.7% among severe cases compared with no events among non-severe cases. This concentration of abnormalities among severe survivors is compatible with the acute clinical patterns described by Guan et al. (2020)[17], who showed that severe COVID-19 was associated with more extensive radiological disease, hypoxaemia and complications. Zhou et al. (2020)[18] similarly found that severe systemic inflammation, respiratory failure and acute respiratory distress syndrome characterized patients with the poorest acute outcomes. The Berlin definition described by Ranieri et al. (2012)[19] recognizes the severity of hypoxaemia as a central measure of acute respiratory distress syndrome. Patients with severe COVID-19 who developed profound hypoxaemia or ARDS would therefore be expected to sustain greater alveolar-capillary injury and have a higher probability of later gas-exchange abnormalities. Long-term evidence from other coronavirus infections also supports this interpretation. Park et al. (2018)[20] reported that survivors of Middle East respiratory syndrome continued to demonstrate pulmonary-function impairment one year after infection, and that the degree of impairment was related to the severity of the preceding pneumonia. The absence of exertional-desaturation events in the non-severe groups produced a zero cell, preventing stable estimation of the conventional odds ratio. Nevertheless, Fisher’s exact test confirmed a statistically significant association (p<0.001). This result should be interpreted alongside the relatively small moderate group, the inclusion of only one asymptomatic participant and the hospital-based nature of the sample. Because the study was cross-sectional and lacked pre-COVID spirometry, it cannot prove that all detected abnormalities were caused exclusively by COVID-19. Despite these limitations, the consistent severity gradient across spirometry and exercise testing strongly suggests that survivors of severe acute COVID-19 represent a high-risk group who may benefit from structured respiratory follow-up, complete pulmonary-function testing—including lung volumes and DLCO—and pulmonary rehabilitation.

The study demonstrated a significant association between the severity of acute COVID-19 and post-COVID respiratory dysfunction. Respiratory dysfunction increased progressively from 20.4% following mild disease to 56.0% following moderate disease and 78.9% following severe disease. Patients with severe acute COVID-19 had approximately tenfold greater odds of abnormal post-COVID spirometry compared with those with non-severe disease. A restrictive spirometric pattern was the predominant abnormality, while obstructive and mixed patterns were relatively uncommon. Mean FVC and FEV₁ declined significantly with increasing acute-disease severity, whereas the FEV₁/FVC percentage did not differ significantly. Exertional oxygen desaturation was observed exclusively among survivors of severe COVID-19. These findings support prioritizing patients who experienced severe acute illness for structured respiratory follow-up, complete pulmonary-function testing and appropriate pulmonary rehabilitation.

Limitations

This study had several limitations. Its cross-sectional design established an association but could not confirm a causal or temporal relationship between acute COVID-19 severity and respiratory dysfunction. The study was conducted at two tertiary-care hospitals, which may limit the generalizability of the findings to community-managed, asymptomatic or predominantly mild cases. The severity groups were unequal, with only one asymptomatic participant and relatively few participants with moderate disease. Selection and referral bias were therefore possible.

Pre-COVID pulmonary-function measurements were unavailable, making it impossible to exclude unrecognized pre-existing physiological abnormalities completely. Restriction was identified using spirometry alone and was not confirmed by total lung-capacity measurement. Diffusing capacity for carbon monoxide, which may be the most sensitive indicator of post-COVID gas-transfer impairment, was not measured. High-resolution computed tomography was not performed systematically in every participant, preventing detailed correlation between physiological and radiological abnormalities.

The interval between acute infection and respiratory assessment may not have been uniform, and changes resulting from spontaneous recovery could not be evaluated. The six-minute walk test was affected by factors such as motivation, physical deconditioning, obesity and peripheral-muscle weakness. Important potential confounders—including the extent of pneumonia, duration of hospitalization, oxygen exposure, intensive-care admission and mechanical ventilation—were not comprehensively adjusted for. The FEV₁/FVC data contained a probable extreme outlier, which should be verified against the original records. Finally, the absence of longitudinal follow-up prevented assessment of whether the identified abnormalities resolved, persisted or progressed over time.

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