Impaired systemic oxygen extraction long after mild COVID-19: potential perioperative implications, 2021, Paul M Heerdt et al

While the morbidity and mortality associated with severe COVID-19 has appropriately received considerable attention, most SARS-CoV-2 infections result in relatively mild, self-limited symptoms not requiring hospitalization. Nonetheless, some of these patients subsequently experience persistent fatigue and reduced exercise capacity that is not attributable to cardiopulmonary impairment diagnosed by conventional means

. Several mechanisms have been proposed including anaemia, deconditioning, and red blood cell abnormalities.

. However, many of the studies describing these mechanisms were conducted in patients following hospitalization and/or within a few months of recovery.

Recently published data indicates that this may well be the case. Singh and colleagues performed invasive cardiopulmonary exercise testing (iCPET) on 10 patients (mean age 48 yr, range: 28 to 79 yr, 9/10 female) with persistent exertional limitation 11 (1) months following mild COVID-19. None of the patients had abnormalities evident on chest computed tomographic imaging, pulmonary function testing, or resting echocardiogram, and all had normal haemoglobin levels.

Study results were compared to a matched control group of 10 patients with normal exercise capacity and no history of COVID-19. As shown in table 1, relative to control patients at rest, DO2 was the same for post-COVID-19 patients but VO2 and systemic EO2 were modestly reduced. At peak exercise, when functional reserve mechanisms normally increase both DO2 and EO2, the difference in VO2 and EO2 between control and post-COVID-19 patients was more profound. Importantly, this disparity occurred despite a peak exercise response for heart rate and DO2 that was similar for both groups. These results indicate that exercise capacity was primarily limited by impaired systemic EO2 of such severity that what should have been an adequate increase in DO2 was insufficient to allow for an increase in VO2. While patients who are deconditioned can exhibit impaired EO2 with exercise, preservation of the capacity to increase heart rate and cardiac output adequately at peak exercise in post-COVID-19 patients makes deconditioning a less likely singular explanation for their exercise limitation. In fact, several patients included in the study had already completed supervised exercise rehabilitation programs by the time of their iCPET.

The lack of objective evidence for the presence of other factors such as anaemia, impaired cardiac or pulmonary function, or superimposed non-COVID infection suggests a possible microvascular/molecular abnormality. It is worth noting the overlap between the clinical presentations of patients with post-COVID-19 exercise limitation and patients with myalgic encephalitis/chronic fatigue syndrome.

The causal hypothesis of myalgic encephalitis/chronic fatigue syndrome has also been linked to preceding infection including human herpes virus, enterovirus, influenzae, Epstein-Barr virus (EBV), and Borrelia burgdorferi



https://www.bjanaesthesia.org/article/S0007-0912(21)00856-4/fulltext