A rapid heart rate, medically known as tachycardia, is a frequently reported symptom in people with both acute and long-term COVID-19 illness. This cardiac symptom, often felt as palpitations, highlights the virus’s ability to affect the cardiovascular system. Understanding the mechanisms behind this dysregulation, both during the initial illness and in the recovery period, is helpful for managing post-infection health.
Defining Tachycardia and the Acute COVID Link
Tachycardia is defined as a resting heart rate exceeding 100 beats per minute (bpm). This threshold indicates a heart that is working harder than usual when the body is at rest. In the context of an active COVID-19 infection, this rapid heart rate is a common and often temporary manifestation of the body’s response to the viral assault.
During the acute phase of illness, tachycardia is frequently a result of generalized physical stress. Factors such as high fever, dehydration, and the body’s systemic inflammatory response all contribute to an elevated heart rate. The heart attempts to compensate for lower blood volume or meet the increased metabolic demand caused by the fever.
This type of acute tachycardia is transient and is expected to resolve as the person recovers. However, the presence of tachycardia during the acute phase has been identified as a factor associated with a higher probability of developing chronic symptoms later on.
Biological Mechanisms of Cardiac Dysregulation
The SARS-CoV-2 virus affects the heart through a complex interplay of direct and indirect biological mechanisms. One primary mechanism is the widespread systemic inflammation triggered by the infection. These inflammatory markers can directly stress the heart muscle and disrupt the electrical signaling that regulates heart rhythm, leading to various arrhythmias, including tachycardia.
Another pathway involves the direct viral invasion of cardiac cells, though this is less common. The virus can bind to the Angiotensin-Converting Enzyme 2 (ACE2) receptors found on heart muscle cells, causing direct damage and inflammation called myocarditis. Myocarditis weakens the heart’s function and can lead to an elevated heart rate as the organ tries to maintain sufficient blood flow.
The third significant mechanism is the disruption of the Autonomic Nervous System (ANS). The ANS controls involuntary bodily functions, including heart rate, blood pressure, and digestion. COVID-19 can interfere with this system, causing autonomic dysfunction, or dysautonomia.
This dysregulation leads to an imbalance where the sympathetic “fight or flight” system is overactive, resulting in an inappropriately fast heart rate even at rest or with minimal activity. This neurological dysregulation may be caused by the body’s autoimmune response following the infection, laying the groundwork for persistent heart rate issues.
Post-Acute Sequelae and Sustained Tachycardia
For many people, a rapid heart rate can persist long after the initial infection has cleared, becoming a feature of Post-Acute Sequelae of COVID-19 (PASC), widely known as Long COVID. This sustained tachycardia is characterized by symptoms that continue for four weeks or more past the acute phase, representing a chronic issue.
A specific condition linked to this sustained tachycardia is Postural Orthostatic Tachycardia Syndrome (POTS). POTS is a form of dysautonomia characterized by orthostatic intolerance, meaning the body struggles to regulate heart rate and blood pressure when changing posture.
The defining feature of POTS is a disproportionately large increase in heart rate—usually 30 bpm or more—within ten minutes of standing up from a lying or sitting position, without a significant drop in blood pressure. Symptoms include lightheadedness, dizziness, fatigue, and a racing heart, which are worsened by standing.
This post-COVID POTS is one of the most common forms of autonomic dysfunction seen in those with PASC. The condition is a persistent neurological issue that often develops weeks to months after the infection. It is believed that the viral infection acts as a catalyst, possibly through an autoimmune mechanism that attacks autonomic nerve fibers.
When to Seek Medical Attention and Management Strategies
Any new or persistent rapid heart rate or palpitations following a COVID-19 infection warrants a medical evaluation. Seek immediate medical attention if the rapid heart rate is accompanied by alarming symptoms. These warning signs include new or worsening chest pain, severe shortness of breath, or fainting, which may indicate a severe heart issue, such as myocarditis or a clotting event.
If persistent symptoms like a racing heart, dizziness upon standing, or chronic fatigue last for more than four weeks, consult a healthcare provider, ideally a cardiologist or an autonomic specialist. They will likely use tests like an electrocardiogram (ECG) or a Holter monitor to evaluate the heart’s electrical activity. A tilt table test may also be performed to formally diagnose POTS.
Management strategies for post-COVID tachycardia and POTS focus on non-medical, lifestyle modifications designed to increase blood volume and manage symptoms. These lifestyle changes are foundational for managing the persistent symptoms of dysautonomia.
Lifestyle Management
Simple yet effective steps include:
- Aggressive fluid intake, aiming for two to three liters of water daily.
- Increasing salt consumption, unless otherwise advised by a doctor, to help expand blood volume.
- Wearing compression stockings or garments to prevent blood from pooling in the lower extremities.
- Practicing slow and deliberate position changes when moving from lying down to standing, to mitigate dizziness.