Syncope, the medical term for fainting, is a sudden, temporary loss of consciousness that occurs when there is insufficient blood flow to the brain. Researchers have documented a significant link between infection with the SARS-CoV-2 virus, which causes COVID-19, and episodes of syncope. This connection is observed both during the acute phase of the illness and in the months following recovery.
Mechanisms of Syncope During Acute COVID-19 Infection
During the active infection phase of COVID-19, fainting is often triggered by temporary, systemic factors that place acute stress on the body’s circulatory system. A high fever, for instance, can cause blood vessels to widen (vasodilation), which lowers overall blood pressure and reduces the volume of blood returning to the heart. This leads to a temporary reduction in cerebral blood flow.
Fluid loss plays a substantial role, as symptoms like high fever, vomiting, or diarrhea can cause significant dehydration and volume depletion. When the body lacks adequate fluid volume, blood pressure becomes more difficult to maintain, particularly when changing position, increasing the risk of fainting.
Severe and prolonged coughing fits, a common symptom of the illness, can also induce a vasovagal response known as cough syncope. This occurs when forceful coughing dramatically increases pressure within the chest cavity, temporarily reducing the amount of blood returning to the heart. The resulting drop in cardiac output decreases blood flow to the brain, causing a brief loss of consciousness.
Another contributing factor in more severe cases is hypoxia, or low blood oxygen levels. This has been observed in some patients even without them reporting difficulty breathing, a phenomenon called “silent hypoxemia.” When oxygen delivery to the brain is compromised, it can disrupt the neurological function necessary to maintain consciousness and proper circulatory control.
Fainting and Post-Viral Autonomic Dysfunction
For many individuals, fainting or near-fainting episodes persist long after the virus has been cleared, often attributed to post-viral autonomic dysfunction, or dysautonomia. The Autonomic Nervous System (ANS) is the body’s involuntary control center, regulating functions like heart rate, breathing, digestion, and blood pressure. When the virus or the resulting immune response disrupts the ANS, the body struggles to maintain stable blood flow.
One of the most recognized forms of dysautonomia following COVID-19 is Postural Orthostatic Tachycardia Syndrome (POTS). POTS is characterized by orthostatic intolerance, meaning a person experiences dizziness, lightheadedness, or presyncope when transitioning to standing upright. The core issue is an atypical response to gravity, where the heart rate increases significantly—by at least 30 beats per minute—within ten minutes of standing.
In a healthy person, standing causes blood to pool in the lower body, which the ANS quickly corrects by narrowing blood vessels and slightly increasing heart rate. In POTS, this response is exaggerated or ineffective, causing the heart to race excessively to compensate for poor blood vessel regulation. The underlying cause may involve direct viral invasion of autonomic centers, persistent inflammation, or autoantibodies attacking nerve fibers.
This persistent miscommunication between the nervous system and the circulatory system leads to symptoms that severely affect daily life, including fatigue, “brain fog,” and recurrent episodes of presyncope or syncope. The resulting fainting is a consequence of the body’s failure to regulate blood flow effectively against gravity, which is a functional issue distinct from structural heart damage.
Cardiovascular Links to Syncope
Beyond problems with the nervous system’s regulatory function, syncope after a COVID-19 infection can be linked to direct damage or inflammation of the heart itself. The virus can cause myocarditis, which is inflammation of the heart muscle. When the myocardium is inflamed, its ability to pump blood efficiently is compromised, potentially leading to a sharp drop in cardiac output and subsequent loss of consciousness.
Inflammation or scarring within the heart tissue can also disrupt the organ’s electrical system, causing arrhythmias, or irregular heart rhythms. These electrical disturbances can manifest as tachyarrhythmias (abnormally fast heart rates) or bradyarrhythmias (abnormally slow heart rates), such as atrioventricular (AV) block. An arrhythmia causes syncope when the heart’s rhythm becomes so disorganized that it cannot effectively fill or eject blood, leading to a sudden reduction in blood flow to the brain.
This type of cardiac syncope is concerning because it represents a structural or electrical problem with the heart. Structural heart complications can sometimes arise weeks or months after the initial infection.
When to Seek Emergency Medical Attention
While many fainting episodes are benign, syncope occurring during or after a COVID-19 infection can signal a serious underlying condition requiring immediate medical evaluation. Seek emergency medical attention if a fainting spell is accompanied by persistent chest pain or pressure, or significant shortness of breath. These symptoms may indicate a serious cardiac event, such as an arrhythmia or myocarditis.
Immediate care is necessary if the fainting episode occurs without any warning signs, as cardiac syncope often lacks pre-syncopal symptoms like lightheadedness or nausea. Emergency services should also be called if the loss of consciousness results in a significant injury, such as head trauma, or if the person remains confused or unresponsive for more than a minute.
Other red flags include a change in mental status, extreme difficulty staying awake, or a pale, gray, or blue discoloration of the lips or skin. If you feel the warning signs of presyncope, immediately lying down and raising your legs above heart level can help restore blood flow to the brain and prevent full loss of consciousness.