High incidence of hyperventilation syndrome after COVID-19

Taverne, J.; Salvator, Hélène; Leboulch, Cécile; Barizien, Nicolas; Ballester, Marie; Imhaus, Etienne; Chabi-Charvillat, Marie-Laure; Boulin, A.; Goyard, C.; Chabrol, A.; Catherinot, Émilie; Givel, C.; Couderc, Louis‐Jean; Tchérakian, Colas

doi:10.21037/jtd-20-2753

Cited by 39 publications

(37 citation statements)

References 9 publications

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“…However, ambulatory access to diagnosis was highly limited in the early beginning of the current pandemic and recent guidelines support including in Covid-19 cohorts patients in which diagnosis was based on clinical symptoms [ 25 ]. Characteristics of our population are nevertheless consistent with data recently reported by Trinkmann et al and Sonnweber et al in patients presenting with long-lasting Covid-19 symptoms [ 6 , 13 , [26] , [27] , [28] ].…”

Section: Discussionsupporting

confidence: 92%

“…Another component which may explain persistence of symptoms in our population, and especially dyspnoea-related functional limitation, is the presence of hyperventilation syndrome as previously suggested by Motiejunaite et al [ 6 , 14 , 27 , 28 ]. In our study, 41% of patients with PFS presented with both positive Nijmegen score and positive provocation test.…”

Section: Discussionmentioning

confidence: 51%

“…Out of the whole cohort, 29(74%) patients had PFS ( Table 1 ). They were younger (43±14 vs. 60±10yr, p=0.002), had a non-significantly lower rate of initial hospital admission (28% vs. 60%, p=0.123), a later rehabilitation referral (107[56-240] vs. 32[ [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] ] days, p<.001) and a longer rehabilitation duration (94[63-142] vs. 24[ [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] ] days, p<.001) than those without PFS. PFS were associated with more severe rest and exertional dyspnoea (respectively, Börg scale at rest: 2±2 vs. 0±0; p=0.002, mMRC: 2±1 vs. 1±1, p=0.051).…”

Section: Resultsmentioning

confidence: 99%

“…(%) 6(15%) 5(17%) 1(10%) 1 Initial hospitalisation > 48h; no. (%) 14(36%) 8(28%) 6(60%) 0.123 Time before rehabilitation (d); (median[IQR]) 73[34-178] 107[56-240] 32[ [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] ] <.001 Rehabilitation duration (d); (median[IQR]) 66[26-110] 94[63-142] 24[ [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] ] <.001 PCR+ diagnos...…”

Section: Methodsmentioning

confidence: 99%

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Respiratory rehabilitation for Covid-19 related persistent dyspnoea: A one-year experience

Bouteleux¹,

Henrot

Ernst³

et al. 2021

Respiratory Medicine

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Background Growing consideration is emerging regarding the burden of persisting sequelae after SARS-CoV-2 infection. Out-patients exhibiting long Covid may benefit from ambulatory rehabilitation which is, to date, poorly documented. Methods A longitudinal follow-up over a one-year period was conducted in two ambulatory rehabilitation structures in order to describe the characteristics of real-life patients referred with Covid-19 sequelae and their evolution over the course of rehabilitation. Results 39 consecutive patients were included from April 1 st 2020 to April 1 st 2021. Patients were middle-aged (48±15yr), without comorbidities, and mostly mild to moderate SARS-CoV-2 infection (25(64%) not requiring hospitalisation). Rehabilitation referral was considered with a median delay of 73[34-178] days after disease onset. Most prevalent symptoms were dyspnoea (n=35(90%)) and fatigue (n=30(77%)). Hyperventilation syndrome was highly frequent (n=12(34%)). 29(74%) patients presented with prolonged functional sequelae, which was associated with younger age (43±14 vs . 50±10yr; p=0.002), greater prevalence of hyperventilation syndrome (n=12(41%) vs . 0(0%); p=0.255) and poorer quality of life (VQ-11; 31±10 vs . 23±9; p=0.030). Over the course of rehabilitation, exertional dyspnoea, 6-minutes walking distance, 3-minutes sit-to-stand test, hyperventilation syndrome prevalence and quality of life significantly improved. Conclusion Hyperventilation is frequent in long Covid and may explain persistent dyspnoea as well as altered quality of life. Our data support screening of hyperventilation syndrome and functional impairment in mild Covid-19 out-patients as both of these components may improve with ambulatory rehabilitation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 51%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Respiratory rehabilitation for Covid-19 related persistent dyspnoea: A one-year experience

Bouteleux¹,

Henrot

Ernst³

et al. 2021

Respiratory Medicine

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“…The presence of dyspnea and cough is easily comprehensible in patients with severe acute COVID-19 infections, due to the organ damage in patients, affecting the lung, heart, and vessels. However, it is surprising to see that dyspnea also occurs in patients with only mild infections [ 1 , 2 , 3 , 12 ]. Due to the absence of abnormalities in pulmonary function tests or imaging, the causes of dyspnea and cough are enigmatic in contrast to severe COVID, in which persistent dyspnea due to lung damage and restricted function can be well explained.…”

Section: Introductionmentioning

confidence: 99%

Dyspnea in Post-COVID Syndrome following Mild Acute COVID-19 Infections: Potential Causes and Consequences for a Therapeutic Approach

Wirth

Scheibenbogen

2022

Medicina

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Dyspnea, shortness of breath, and chest pain are frequent symptoms of post-COVID syndrome (PCS). These symptoms are unrelated to organ damage in most patients after mild acute COVID infection. Hyperventilation has been identified as a cause of exercise-induced dyspnea in PCS. Since there is a broad overlap in symptomatology with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), causes for dyspnea and potential consequences can be deduced by a stringent application of assumptions made for ME/CFS in our recent review papers. One of the first stimuli of respiration in exercise is caused by metabolic feedback via skeletal muscle afferents. Hyperventilation in PCS, which occurs early on during exercise, can arise from a combined disturbance of a poor skeletal muscle energetic situation and autonomic dysfunction (overshooting respiratory response), both found in ME/CFS. The exaggerated respiratory response aggravating dyspnea does not only limit the ability to exercise but further impairs the muscular energetic situation: one of the buffering mechanisms to respiratory alkalosis is a proton shift from intracellular to extracellular space via the sodium–proton-exchanger subtype 1 (NHE1), thereby loading cells with sodium. This adds to two other sodium loading mechanisms already operative, namely glycolytic metabolism (intracellular acidosis) and impaired Na+/K+ATPase activity. High intracellular sodium has unfavorable effects on mitochondrial calcium and metabolism via sodium–calcium-exchangers (NCX). Mitochondrial calcium overload by high intracellular sodium reversing the transport mode of NCX to import calcium is a key driver for fatigue and chronification. Prevention of hyperventilation has a therapeutic potential by keeping intracellular sodium below the threshold where calcium overload occurs.

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