Singh I; Joseph P; Heerdt PM; Cullinan M; Lutchmansingh D; Gulati M; Possick JD; Systrom DM; Waxman AB;
Chest [Chest] 2021 Aug 10. Date of Electronic Publication: 2021 Aug 10.
Background: Some Coronavirus disease 2019 (COVID-19) patients who have recovered from their acute infection after experiencing only mild symptoms continue to exhibit persistent exertional limitation that is often unexplained by conventional investigative studies.
Research Question: What is the patho-physiological mechanism of exercise intolerance that underlies the post-COVID-19 long haul syndrome following COVID-19 in patients without cardio-pulmonary disease?
Study Design and Methods: This study examined the systemic and pulmonary hemodynamics, ventilation, and gas exchange in 10 post-COVID-19 patients without cardio-pulmonary disease during invasive cardiopulmonary exercise testing (iCPET) and compared the results to 10 age- and sex matched controls. These data were then used to define potential reasons for exertional limitation in the post-COVID-19 cohort.
Results: Post-COVID-19 patients exhibited markedly reduced peak exercise aerobic capacity (VO 2 ) compared to controls (70±11%predicted vs. 131±45%predicted; p<0.0001). This reduction in peak VO 2 was associated with impaired systemic oxygen extraction (i.e., narrow CaVO 2 /CaO 2 ) compared to controls (0.49±0.1 vs. 0.78±0.1, p<0.0001) despite a preserved peak cardiac index (7.8±3.1 vs. 8.4±2.3 L/min, p>0.05). Additionally, post-COVID-19 patients demonstrated greater ventilatory inefficiency (i.e., abnormal VE/VCO 2 slope: 35±5 vs. 27±5, p=0.01) compared to controls without an increase in dead space ventilation.
Interpretation: Post-COVID-19 patients without cardiopulmonary disease demonstrate a marked reduction in peak VO 2 from a peripheral rather than a central cardiac limit along with an exaggerated hyper-ventilatory response during exercise.