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BACKGROUND: The novel coronavirus (SARS-CoV-2) has negatively impacted the health and economy of the world. While most patients recover, many are suffering from symptoms several months after resolution of the acute illness (“Post-Acute Sequalae of COVID-19” [PASC]). Symptoms include fatigue, light-headedness, and tachycardia/palpitations, similar to symptoms of cardiovascular autonomic disorders such as Postural Orthostatic Tachycardia Syndrome (POTS), Initial Orthostatic Hypotension (IOH), Orthostatic Hypotension (OH), and Inappropriate Sinus Tachycardia (IST). We have previously shown a high prevalence of autonomic abnormalities among PASC patients. We currently do not know if these autonomic abnormalities are chronic and persist in PASC patients over time. OBJECTIVE: We aimed to determine if the autonomic abnormalities seen in patients after COVID-19 infection are persistent or transient, by comparing hemodynamic criterion between baseline and follow-up visits. We hypothesize that patients will recover, and abnormalities will not persist between the visits. METHODS: PASC patients (n=64; F=51; 46±12y) completed baseline visits 411±133 days after their initial COVID-19 infection and follow-up visits 97±9 days later. Patients underwent autonomic function testing with beat-to-beat hemodynamics during 10min supine rest followed by a 10min active stand. Patients were evaluated for hemodynamic criterion for POTS (­­­­↑HR≥30bpm within 10min), IOH (transient ↓SBP≥40mmHg within 15s), OH (↓SBP≥20mmHg within 3min), and IST (supine HR>100bpm). Categorical data were analyzed with a McNemar’s test. RESULTS: 19 (30%) participants met POTS criterion at baseline vs. 15 (23%) at follow-up (p=0.1). 43 (67%) participants met IOH criterion at baseline vs. 37 (58%) at follow-up (p=0.08). The OH criterion was seen in 2 (3.1%) vs 5 (7.8%) patients (p=0.2) and IST was seen in 1 patient at both visits (1.6%). Overall, 48 (75%) patients met the hemodynamic criterion for at least one autonomic disorder at baseline and 43 (67%) patients met at least one criterion at follow-up (p=0.09). CONCLUSION: Many patients with PASC have evidence of cardiovascular autonomic abnormalities, most commonly IOH, followed by POTS. The prevalence of these abnormalities does not decrease over time. These findings suggest patients with PASC are not recovering from autonomic complications due to their COVID-19 infections. Treatment and management strategies for autonomic abnormalities are needed to improve the quality of life for these patients. Funding: Canadian Institutes of Health Research (CIHR) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Background: Postural Orthostatic Tachycardia Syndrome (POTS) is characterized by chronic orthostatic intolerance and significantly impacts quality of life of patients. POTS predominantly affects women of child-bearing age with an estimated prevalence of up to 1%. POTS is defined by an excessive increase in heart rate (HR) of ≥30 bpm within 10 minutes of upright posture, in the absence of orthostatic hypotension. POTS is associated with chronic symptoms (≥6 months) including hyperventilation (HV) in the form of hyperpnea. HV reduces arterial CO2 (hypocapnia) and worsens tachycardia in POTS. Whether it is hypocapnia that increases HR in these patients is unclear. Studies have not investigated the effects of CO2 on HR due to the confounding effects of posture and ventilation. Objective: We aimed to determine if hypocapnia exacerbates tachycardia in POTS patients. Hypothesis: We hypothesize that hypocapnia will increase HR in POTS. Methods: We conducted a randomized crossover trial of hypocapnic HV vs. eucapnic HV in 13 female POTS patients (34±9 y). Participants completed the supine breathing protocol: 1) HV with resultant hypocapnia, and 2) HV (with end-tidal CO2 (ETCO2) clamped at baseline). Breath-by-breath respiratory (ventilation (VE), tidal volume (VT), ETCO2, end-tidal O2 (ETO2)) and beat-to-beat hemodynamics (HR, stroke volume (SV), cardiac output (CO)) were measured. Data are reported as mean±SD. Paired t-tests were used to compare respiratory and hemodynamic parameters between hypocapnic HV vs. eucapnic HV. Results: During HV, ETCO2 was significantly lower during hypocapnia vs. eucapnia (19.6±3.7 mmHg vs. 37.4±3.5 mmHg; p<0.0001). ETO2 was greater during hypocapnia vs eucapnia (117.4±4.7 mmHg vs. 114.6±3.1 mmHg; p<0.001). There was no difference in VE (22.2±6.5 L/min vs. 22.0±5.1 L/min; p=0.8) or VT (1.4±0.4 L vs. 1.4±0.3 L; p=0.9) between hypocapnia and eucapnia. HR was significantly greater during hypocapnia vs. eucapnia (99±12 bpm vs 82±10 bpm; p<0.001); SV was significantly lower during hypocapnia vs. eucapnia (66±14 mL vs. 74±13 mL; p=0.02); and there was no difference in CO between hypocapnia and eucapnia (6.4±1.3 L/min vs. 6.1±1.6 L/min; p=0.3). Conclusion: Independent of ventilation, hypocapnia increases HR in patients with POTS. Our findings suggests that hypocapnia causes a reduction in SV, perhaps due to increased blood pooling in the capacitance vessels leading to reduced venous return. This work was supported by Standing up to POTS. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.