Anorexia Nervosa (AN) is a psychiatric disorder defined by an intense fear of weight gain, a distorted body image, and energy restriction leading to significantly low body weight. A serious medical complication is the impact on the cardiovascular system, which can result in tachycardia, defined as a heart rate exceeding 100 beats per minute. While chronic malnutrition is typically associated with a slow heart rate (bradycardia), the presence of tachycardia signals acute physiological distress. Understanding the mechanisms that cause this high heart rate is important, as it often indicates life-threatening instability.
The Core Cardiac Paradox in Anorexia
The cardiovascular system in chronic malnutrition adapts by slowing down to conserve energy, leading to the cardiac paradox. The body reduces its basal metabolic rate against starvation, resulting in a low resting heart rate, often below 60 beats per minute. This adaptive bradycardia is usually accompanied by low blood pressure, reflecting a reduction in workload and muscle mass. The heart shrinks, undergoing atrophy that reduces the size of the left ventricle and makes the muscle less efficient.
Tachycardia represents a failure of this adaptive mechanism or the introduction of an acute stressor that overrides the body’s slowed state. The atrophied heart muscle becomes hypersensitive and weak, making it highly reactive to sudden demands. Tachycardia can be triggered by external factors like dehydration, which reduces blood volume and forces the heart to beat faster to maintain circulation. Stimulants, such as excessive caffeine or diet pills, can also directly overexcite the fragile cardiac electrical system.
A resting high heart rate can also signal an underlying acute medical issue, such as an infection. Individuals with AN are often immunocompromised due to chronic nutritional deficiencies, making them susceptible to illnesses that accelerate the heart rate. In a patient whose heart is compromised by malnutrition, this sudden acceleration can quickly lead to cardiac decompensation.
Electrolyte Disruption and Heart Rhythm Instability
Anorexia Nervosa causes acute cardiac instability through the disruption of electrolytes, the charged minerals that regulate the heart’s electrical impulses. The heart relies on precise concentrations of minerals like Potassium (K+) and Magnesium (Mg2+) to maintain its rhythm. Potassium is important for the repolarization phase of the cardiac cycle, allowing the heart muscle to relax after a contraction.
Behaviors associated with AN, such as chronic vomiting or the misuse of laxatives and diuretics, lead to the rapid depletion of these electrolytes. This loss results in conditions like hypokalemia (low potassium) and hypomagnesemia (low magnesium). A deficit in these minerals creates an unstable electrical environment within the heart muscle cells.
This electrical instability can manifest on an electrocardiogram (ECG) as a prolonged QT interval, which is the time it takes for the heart’s ventricles to repolarize. A prolonged QT interval increases the risk of developing life-threatening ventricular tachyarrhythmias, such as Torsades de Pointes. Magnesium deficiency can make potassium replacement ineffective, complicating heart rhythm stabilization and increasing the risk of sudden cardiac death.
Refeeding Syndrome and Heart Rate Fluctuations
A distinct cause of sudden tachycardia is Refeeding Syndrome, a metabolic complication that occurs when nutritional support is initiated in a malnourished patient. During prolonged starvation, the body switches its primary energy source from carbohydrates to fat and protein, maintaining a catabolic state with low insulin levels. The reintroduction of food, particularly carbohydrates, causes a rapid surge of insulin secretion.
Insulin drives glucose, phosphate, potassium, and magnesium from the bloodstream into the cells to begin the synthesis of glycogen, protein, and fat. This sudden intracellular shift depletes the serum levels of these electrolytes, creating hypophosphatemia, hypokalemia, and hypomagnesemia in the blood. This acute extracellular deficit triggers the complications of refeeding.
The drop in serum electrolytes, coupled with rapid fluid retention caused by the influx of sodium and water, places stress on the already atrophied heart. The heart muscle, deprived of necessary minerals and overwhelmed by fluid volume, can fail. This acute strain commonly results in congestive heart failure and arrhythmias, often presenting initially as sustained tachycardia.
Recognizing and Responding to Cardiac Danger Signs
Recognizing the signs of cardiac distress is important for anyone struggling with AN, as an elevated heart rate is a red flag for medical instability. Symptoms indicating potentially dangerous tachycardia or other cardiac complications include:
- Persistent palpitations (feelings of a racing or pounding heart).
- Unexplained fainting or syncope.
- Dizziness and near-fainting episodes.
- Shortness of breath, particularly when lying flat.
- Chest pain, which can signal acute heart failure or an arrhythmia.
- Swelling in the legs, ankles, or feet (peripheral edema), suggesting the heart is struggling to manage fluid volume.
Any of these symptoms warrant immediate medical evaluation, often requiring a visit to the emergency department.
In a clinical setting, diagnosis and intervention focus on immediate stabilization using tools like an electrocardiogram (ECG) to identify rhythm disturbances and measure the QT interval. Blood tests are conducted to obtain an electrolyte panel, focusing on potassium, magnesium, and phosphate levels. Continuous vital sign monitoring and cardiac telemetry track heart rate and rhythm fluctuations, allowing clinicians to manage the underlying metabolic or infectious cause of the tachycardia.