Cardiopulmonary exercise pattern in patients with persistent dyspnoea after recovery from COVID-19

Abstract

Cause and mechanisms of persistent dyspnoea after recovery from COVID-19 are not well described. The objective is to describe causal factors for persistent dyspnoea in patients after COVID-19. We examined patients reporting dyspnoea after recovery from COVID-19 by cardiopulmonary exercise testing. After exclusion of patients with pre-existing lung diseases, ten patients (mean age 50±13.1 years) were retrospectively analysed between May 14th and September 15th, 2020. On chest computed tomography, five patients showed residual ground glass opacities, and one patient showed streaky residua. A slight reduction of the mean diffusion capacity of the lung for carbon monoxide was noted in the cohort. Mean peak oxygen uptake was reduced with 1512±232 ml/min (72.7% predicted), while mean peakwork rate was preserved with 131±29 W (92.4% predicted). Mean alveolar-arterial oxygen gradient (AaDO2) at peak exercise was 25.6±11.8 mmHg. Mean value of lactate post exercise was 5.6±1.8 mmol/l. A gap between peak work rate in (92.4% predicted) to peak oxygen uptake (72.3% pred.) was detected in our study cohort. Mean value of lactate post exercise was high in our study population and even higher (n.s.) compared to the subgroup of patients with reduced peak oxygen uptake and other obvious reason for limitation. Both observations support the hypothesis of anaerobic metabolism. The main reason for dyspnoea may therefore be muscular.

Cardiopulmonary exercise capacity and limitations 3 months after COVID-19 hospitalisation

“…Two studies including COVID-19 patients found V′ O 2 peak 81% and 73% predicted [3,24], which is comparable to our results, whereas another study reported V′ O 2 peak 57% predicted for mechanically ventilated COVID-19 patients [12].…”

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

“…(%) 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...…”

Phenotyping long COVID

“…When grouped together thus on a total of 581 patients, mean values of FEV 1 of 97% predicted, DL CO of 83% predicted, VO 2 max of 82% predicted with an anaerobic threshold of 50% of VO 2 max, V E /VCO 2 slope of 30, preserved breathing reserve and moderately decreased max heart rate altogether offer a CPET profile of deconditioning on the recovery of an acute inflammatory process, prolonged bed rest, and post-traumatic syndrome and depression. Interestingly, there was a tight correlation with a r 2 =0.92, p<0.01 between VO 2 max (in % predicted) and length of hospital stay as calculated on a total of 298 patients from 4 studies [ 13 , 15 , 16 , 20 ]. In one of the studies, CPET was combined with exercise stress echocardiography [ 21 ].…”

“…These results are in agreement with those of 8 previous mostly smaller studies on a total of 203 patients. (15)(16)(17)(18)(19)(20)(21)(22). When grouped together thus on a total of 581 patients, mean values of FEV 1 of 97 % predicted, DL CO of 83 % predicted, VO 2 max of 82 % predicted with an anaerobic threshold of 50 % of VO 2 max, V E /VCO 2 slope of 30, preserved breathing reserve and moderately decreased max heart rate altogether offer a CPET profile of deconditioning on the recovery of an acute inflammatory process, prolonged bed rest, and post-traumatic syndrome and depression.…”