Syncope, or fainting, is a temporary loss of consciousness caused by a sudden decrease in blood flow to the brain (cerebral hypoperfusion). Recovery is rapid and complete. Following infection with the SARS-CoV-2 virus, episodes of fainting or near-fainting (presyncope) have become recognized complications. These episodes can occur during the initial, active phase of the illness or months later as part of the post-COVID-19 syndrome. The underlying causes differ significantly based on timing, ranging from temporary systemic stress to persistent dysfunction of the body’s regulatory systems.
Acute Causes of Syncope During Active COVID-19
Syncope during the acute phase of COVID-19 often stems from temporary physiological stress. A primary mechanism involves systemic inflammation, where the immune response releases cytokines that affect vascular tone. This inflammatory state leads to vasodilation (the widening of blood vessels), effectively dropping systemic blood pressure. Reduced systemic vascular resistance makes it harder to maintain adequate blood pressure, particularly when standing or changing positions.
Fever, a common symptom of acute infection, also contributes by promoting vasodilation and increasing fluid loss through sweating. When combined with reduced fluid intake due to illness, this can lead to dehydration and low blood volume (hypovolemia). Both hypovolemia and vasodilation compromise the body’s ability to pump enough blood to the brain, triggering a fainting episode.
The virus can also directly or indirectly affect the heart, causing temporary cardiac complications. These include transient myocarditis (inflammation of the heart muscle) or new-onset cardiac rhythm disturbances (arrhythmias). These cardiac events can severely impair the heart’s pumping function, leading to a sudden and profound drop in cerebral blood flow. In acute illness, a careful medical assessment is important to differentiate between benign reflex syncope and these potentially serious cardiac causes.
Long-Term Post-COVID Syndromes Leading to Fainting
Fainting that occurs weeks or months after the initial infection is often linked to a disruption in the Autonomic Nervous System (ANS). The ANS regulates involuntary functions, such as heart rate, blood pressure, and digestion. When the ANS malfunctions, dysautonomia occurs, which is a frequent complication reported by people experiencing long-term symptoms after COVID-19.
A prevalent form of dysautonomia observed in post-COVID patients is Postural Orthostatic Tachycardia Syndrome (POTS). POTS is characterized by an excessive increase in heart rate when moving from a lying or sitting position to standing, without a significant drop in blood pressure. Diagnosis requires the heart rate to increase by at least 30 beats per minute within the first 10 minutes of standing (or 40 beats per minute for adolescents).
When a person with POTS stands up, gravity pulls blood toward the lower body, but the dysfunctional ANS fails to properly constrict blood vessels. To compensate for the resulting drop in blood return to the heart, the heart rate inappropriately speeds up. This rapid heart rate does not always maintain sufficient blood flow to the brain, leading to symptoms like lightheadedness, dizziness, and sometimes syncope.
The exact trigger for this long-term ANS dysfunction is not fully understood, but hypotheses point to an autoimmune response. The viral infection may cause the immune system to mistakenly create autoantibodies that attack components of the nervous system, including the small nerves controlling blood vessel constriction. Chronic inflammation following the infection may also damage neurons and impair ANS signaling. Many people with persistent symptoms after COVID-19 report features of dysautonomia, highlighting this neuro-cardiac connection.
Medical Evaluation for COVID-Related Syncope
The evaluation of syncope, whether acute or long-term, begins with a thorough medical history and physical examination. If a fainting episode occurs, especially if accompanied by chest pain, palpitations, or injury, emergency medical attention is necessary to rule out life-threatening causes. Initial testing includes an electrocardiogram (EKG) to check for underlying heart rhythm problems or signs of heart muscle damage.
Blood tests are performed to exclude non-COVID-related causes of syncope, such as anemia, electrolyte imbalances, or thyroid dysfunction. If an underlying cardiac cause is suspected, continuous heart monitoring, such as a Holter monitor, may be used over several days to detect intermittent arrhythmias that do not appear on a single EKG.
For suspected post-COVID dysautonomia, specific testing is required to confirm a diagnosis like POTS. The “poor man’s tilt test” or orthostatic vital signs involve monitoring heart rate and blood pressure while the patient lies down, sits, and then stands. The definitive diagnostic tool is the Tilt-Table Test. During this test, the patient is secured to a table that gradually tilts them upright while heart rate and blood pressure are continuously recorded. Observing the exaggerated heart rate response confirms the presence of POTS.
Fainting episodes associated with COVID-19 can arise from temporary systemic stresses during active infection or persistent autonomic dysfunction in the post-viral phase. Differentiating between these two mechanisms is crucial, and a proper medical evaluation is required to identify the underlying cause and guide management.