International Journal of Heart Rhythm

: 2021  |  Volume : 6  |  Issue : 2  |  Page : 95--97

Persistent bradycardia in post-COVID-19: Possible dysautonomia? A case report

Olivia Handayani 
 Cardiovascular Care of Mayapada Hospital Kuningan, South Jakarta, Indonesia

Correspondence Address:
Dr. Olivia Handayani
Mayapada Hospital Kuningan, HR Rasuna Said, Kav C-17, South Jakarta


The impact of coronavirus disease 2019 (COVID-19) infection is immeasurable. As we continue to learn about the presentation and complications of this infection, we begin to understand that COVID-19 is associated with multiorgan involvement. Bradycardia is one of cardiac complications that occur frequently in patients with COVID-19 infection. This clinical case is one approach to further understand the mechanism of COVID-19–induced dysautonomia causing bradycardia, through overstimulation of parasympathetic nervous system. Routine physical rehabilitation had improved the symptoms.

How to cite this article:
Handayani O. Persistent bradycardia in post-COVID-19: Possible dysautonomia? A case report.Int J Heart Rhythm 2021;6:95-97

How to cite this URL:
Handayani O. Persistent bradycardia in post-COVID-19: Possible dysautonomia? A case report. Int J Heart Rhythm [serial online] 2021 [cited 2022 Jul 2 ];6:95-97
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Full Text


The novel coronavirus disease 2019 (COVID-19) pandemic has caused unprecedented morbidity and mortality. The infection has been found to affect every organ system, including cardiovascular system. Studies have shown that there is an increase in the incidence of myocarditis, acute coronary syndrome, arrhythmia, cardiomyopathies, and coagulopathies in COVID-19 patients and also increased risk of mortality due to preexisting cardiovascular disease.[1]

Bradyarrhythmia is newly recognized in COVID-19 infection, and the pathogenesis is multifactorial. One of them is the involvement of autonomic nervous system that innervates the heart. Hu et al.[2] stated that sinus bradycardia occurred in one-third of patients with severe COVID-19 infection, all improved after treating the viral infection. Amaratunga et al.[3] reported 36% relative bradycardia cases presented in 110 hospitalized COVID-19 patients. Others also mentioned similar findings, and relative bradycardia was defined as a characteristic finding in COVID-19.[1],[4] This is a challenge for a clinician to understand the exact mechanism of bradycardia to deliver appropriate therapies.

 Case Report

A 34-year-old female with a 2-week history of COVID-19 infection was admitted to the Department of Emergency, Mayapada Hospital Kuningan with dizziness, light headedness, and slow heart rate (HR). Her blood pressure was 104/60 mmHg and HR was 45 beats/min, regular and strong. Her symptoms began during breathing training at physiotherapy, a few minutes before being transferred to the Department of Emergency. There is no hypoxia presented, oxygen saturation 98%. The electrocardiogram showed sinus bradycardia with normal axis and no ST-segment deviation. She was given 0.5 mg of sulfa atropine for this symptomatic bradycardia, and her HR increased to 82 beats/min. This patient was admitted to the intensive care unit, and our first-line approach was stabilization, hydration, and recumbent position.

She had no history of chest pain, breathing difficulties, palpitation, or leg edema. Her family history was clear. Therefore, her cardiovascular risk assessment was low. She had COVID-19 infection 2 weeks ago. Her symptoms were mild to moderate, and she received all supporting medications at the hospital for 2 weeks. She was discharged in good condition, and her polymerase chain reaction test was negative. She was advised for routine physiotherapy afterward.

At the intensive care unit, blood pressure and HR were supported by inotropic dopamine that was then stopped because it was invalid. There were no abnormalities in her laboratory results. Troponin I, creatine kinase-MB, and N-terminal-pro hormone B-type natriuretic peptide were within normal limits. The D-dimer, C-reactive protein level, electrolytes, magnesium, and calcium were normal. There was neither evolution nor conduction disturbance in her serial electrocardiogram. We have excluded other diseases that could induce bradycardia and also low blood pressure.

During her care, her HR was below 50 beats/min while sleeping and could reach 56–60 beats/min when awakened. Blood pressure was 94/55 mmHg at standing and 92/60 mmHg at rest, meaning no orthostatic hypotension. She did not experience any dizziness.

Echocardiography showed normal left ventricle ejection fraction 62%, normal right ventricle contractility, no chamber dilatation, and mild tricuspid regurgitation. 24-h Holter electrocardiogram recording showed sinus rhythm, minimal HR 41 beats/min, maximum HR 125 beats/min, with an average HR of 60 beats/min [Figure 1]. There was one occasional premature ventricular beat while sleeping. She was advised to continue physiotherapy and improve her physical activity. She was discharged in a very stable condition. Her symptoms improved after several physical rehabilitation.{Figure 1}


COVID-19 infection could be responsible for the invasion of the central nervous system by direct hematogenous and neural propagation, therefore causing dysautonomia. Dysautonomia is characterized by the increase of sympathetic and parasympathetic activities.[5] Some studies have shown that dysautonomia in long COVID-19 may be due to neurotropism, hypoxia, and inflammation. It remains unclear, however, whether it is associated with direct viral attack or autoimmune postimmune-mediated responses.[5],[6]

There are two proposed neurological mechanisms affecting both the peripheral and central nervous systems. The cytokine storm and hyperinflammation result in demyelination and apoptosis of neuronal cells due to the virus and hypercoagulability. In the peripheral nervous system, there is the destruction of postganglionic sympathetic neurons which may precipitate increased sympathetic tone of the heart, resulting in symptoms similar to postural orthostatic tachycardia syndrome.[7] In the central nervous system, damage to the brainstem may also precipitate sympathetic outflow to the heart.[6],[7] Postural orthostatic tachycardia syndrome is characterized by a sustained HR increment of above 30 beats/min within 10 min of standing or head-up tilt; and orthostatic hypotension is defined as a fall of >20 mmHg systolic and >10 mmHg diastolic after standing for 3 min.[6]

A study by Goldstein[8] showed abnormalities on autonomic testing in the majority of patients with a history of COVID-19 infection. The most common clinical case was orthostatic symptoms without tachycardia or hypotension, postural orthostatic tachycardia syndrome, and borderline orthostatic intolerance.[9] One clinical presentation by Suresh et al.[10] about dysautonomia presented as orthostatic hypotension in COVID-19 infection, which was successfully treated with midodrine and fludrocortisone.

In regard to bradycardia, although its mechanism remains unclear, some studies have reported a significant incidence of developing bradycardia in hospitalized patients. One hypothesis from Dani et al.[6] mentioned in orthostatic intolerance, very high catecholamine release can lead to paradoxical vasodilation, withdrawal of sympathetic activity, and activating the vagus nerve, resulting in hypotension, dizziness, and ultimately syncope. This can be triggered by hypovolemia because of systemic infections or prolonged bed rest.

Our patient had an episode of tachycardia when she was awake and moved around; this might be due to overstimulation of the sympathetic nervous system. She also had bradycardia while sleeping with HR 41 beats/min and possibly because of overstimulation of parasympathetic modulation. This might represent cardiac dysautonomia. We suggested a regular exercise program with aerobic training to improve cardiac autonomic balance. The exercise training was expected to improve the submaximal performance that is correlated with parasympathetic activity.[11],[12] Sloan et al.[13] reported that aerobic conditioning improves autonomic control of the heart, as training will induce HR reduction or improve RR interval variability.

HR variability (HRV) is the fluctuation on the time interval between consecutive heartbeats using a noninvasive method for assessing the autonomic nervous system. Autonomic nervous system plays an important role in physiological situations and in various pathological processes, including cardiovascular diseases and viral infections.[14],[15] It has been used to assess the risk of cardiac death, postinfarction syndrome, and diabetic neuropathy. Recently, HRV can act as a predictor of COVID-19 severity and outcome.[16],[17] Pan et al.[18] used HRV to monitor COVID-19 progression and to assess treatment effects. It can be combined with other biomarkers and clinical predictors to monitor patients' conditions and estimate their prognosis. In our case, the measurement of HRV was used to evaluate if there was any pause or other arrhythmias that occurred [Figure 2]. It also helped to evaluate the course of long COVID-19 disease, including the risk for cardiopulmonary complications.[19] Further studies are required to understand further the mechanism of dysautonomia post-COVID-19 infection so that more appropriate treatment can be delivered.{Figure 2}

Bradycardia is a newly recognized finding that still has unknown mechanisms, and is strongly possible to be one characteristic of dysautonomia. This shall describe the multiorgan involvement of COVID-19 infection.

Institutional review board statement

The ethical approval was waived by the Institutional Ethical Committee of our hospital owing to the retrospective nature of the study and routine treatments performed on this patient in clinical practice.

Declaration of patient consent

The author certifies that she has obtained the appropriate patient consent form. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published, and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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