A normal resting heart rate for an adult generally falls within the range of 60 to 100 beats per minute (bpm). A sustained resting heart rate exceeding 100 bpm is clinically defined as tachycardia, signaling the heart is beating too fast. Changes to heart rhythm and rate are a common way the body responds to the SARS-CoV-2 virus, affecting the cardiovascular system. Understanding these heart rate changes is important for patients and clinicians navigating both the acute infection and recovery period.
The Immediate Impact of COVID-19 on Heart Rate
During the active phase of a COVID-19 infection, an elevated heart rate is a frequent and often temporary finding. Studies involving hospitalized patients have documented a mean heart rate around 90 bpm upon admission, which is at the upper limit of the normal range. In fact, a significant minority of patients, around 16%, exhibit frank tachycardia with a resting rate of 100 bpm or higher.
The presence of a rapid heartbeat, often described as palpitations, can be one of the more noticeable symptoms. This elevated rate is the body’s attempt to compensate for the stress caused by the virus. Patients may experience palpitations alongside other symptoms like shortness of breath. Wearable technology data has shown that the resting heart rate is often notably higher in symptomatic patients compared to their pre-infection baseline.
This acutely increased heart rate, known as sinus tachycardia, is typically a direct physiological reaction to the systemic effects of the virus. While this response is common to many infections, its prevalence and persistence during COVID-19 have garnered particular attention.
Understanding Tachycardia Mechanisms in Acute Infection
The increase in heart rate during acute COVID-19 infection stems from a complex interplay of systemic and local biological factors. One of the primary drivers is the body’s fever response, which raises the overall metabolic rate. For every degree Celsius increase in body temperature, the heart must pump faster to circulate blood more quickly to meet the heightened oxygen demand and to help dissipate heat.
Another major contributing factor is the intense systemic inflammation triggered by the immune system’s battle against the virus. The immune response releases inflammatory signaling molecules, such as cytokines and interleukins, into the bloodstream. These markers can directly affect the cardiovascular system, potentially altering the electrical signals that regulate the heart’s rhythm. This inflammatory cascade effectively puts the heart under stress, leading to an accelerated beat.
Dehydration or volume depletion, often resulting from fever, vomiting, or reduced fluid intake, also forces the heart to work harder. When the body loses fluid volume, blood pressure can drop, requiring the heart to beat more quickly to circulate the remaining blood and maintain perfusion. In more severe cases, the virus can directly infect the heart muscle tissue, causing inflammation known as myocarditis. This direct injury compromises the heart’s function and can contribute to a rapid, abnormal rhythm.
Persistent Heart Rate Changes After Recovery
Heart rate abnormalities can persist long after the acute infection has resolved, often becoming a defining feature of post-acute COVID-19 syndrome, commonly referred to as Long COVID. These lingering effects are frequently linked to a condition known as Postural Orthostatic Tachycardia Syndrome (POTS). Individuals with POTS experience an unusually large and sustained increase in heart rate, typically 30 bpm or more, immediately upon changing posture from lying down to standing.
POTS is classified as a form of dysautonomia, meaning there is a malfunction in the Autonomic Nervous System (ANS). The ANS controls involuntary bodily functions like heart rate, blood pressure, digestion, and body temperature. The immune system’s overreaction to the initial viral infection is thought to cause this dysfunction, leaving the body’s sympathetic “fight or flight” response in an overactive state.
Unlike the acute tachycardia driven by fever and systemic stress, this chronic form is driven by a dysregulated nervous system. The sustained high heart rate upon standing, known as orthostatic intolerance, can lead to debilitating symptoms like lightheadedness, dizziness, profound fatigue, and cognitive impairment often described as “brain fog.” This post-viral syndrome is distinctly different from the acute infection in its mechanism, representing a long-term change in the body’s ability to regulate its own circulation. Patients with this persistent condition may notice that even mild activity triggers an exaggerated heart rate response.
When to Seek Medical Attention for Heart Rate Concerns
While many cases of elevated heart rate during COVID-19 are temporary, certain signs require immediate medical evaluation to rule out serious complications. Any sustained resting heart rate staying at or above 120 beats per minute is a clear threshold for concern and warrants prompt consultation with a healthcare provider. This is especially true if the rapid heart rate is a new symptom or appears unrelated to fever or exertion.
Patients should also seek immediate help if they experience new onset palpitations accompanied by more severe symptoms, such as chest pain or pressure. Signs of circulatory or respiratory distress, including fainting (syncope) or severe shortness of breath, are indications for emergency care. Monitoring tools like pulse oximeters and wearable devices can track heart rate and oxygen saturation, providing valuable data for a physician.
For symptoms that persist beyond the acute illness phase, like persistent dizziness or an exaggerated heart rate response to standing, a medical consultation is necessary. A healthcare provider can conduct a thorough cardiovascular assessment, which may include testing for conditions like POTS. While conservative home management, such as increasing fluid and salt intake, can help manage mild symptoms, receiving a medical diagnosis and guidance is best for any ongoing heart rate abnormality.