Anorexia Nervosa and Bradycardia: Mechanisms, Risks, and Treatment

Bradycardia (HR <60 bpm; often <50 in AN) is a cardinal sign of anorexia nervosa (AN), reflecting profound metabolic adaptation to starvation.

Mechanisms

• Energy conservation: ↓ BMR up to 30–50%; heart reduces work via ↓ HR, contractility, cardiac mass.
• Vagal dominance: Enhanced parasympathetic tone (protective vs. arrhythmia?); ↓ sympathetic drive.
• Electrolyte disturbances: Hypokalemia, hypomagnesemia → arrhythmia risk despite bradycardia.
• Structural changes: Left ventricular atrophy, reduced wall thickness, pericardial effusion.
• Hormonal: Low T3 (euthyroid sick), leptin, insulin, sex steroids.

Clinical Consequences

• Orthostatic hypotension, syncope, exercise intolerance.
• Risk of lethal arrhythmia (QT prolongation from hypokalemia + bradycardia).
• Refeeding syndrome: insulin surge → hypophosphatemia, heart failure, arrhythmia.

Monitoring and Treatment

• Vitals: HR, BP (supine/standing), ECG (QTc), electrolytes daily in acute refeeding.
• Refeeding protocol: Start low (1200–1500 kcal), advance slowly; phosphate, thiamine, magnesium supplementation.
• Cardiology consult: If HR <40, syncope, arrhythmia, QTc >450 ms, or pericardial effusion.
• Weight restoration: HR normalizes with nutritional rehabilitation; cardiac mass recovers.

Prognosis

Bradycardia is largely reversible with sustained recovery. Persistent arrhythmia or structural damage increases mortality risk (AN has highest mortality of psychiatric disorders).

Early intervention by eating disorder specialists saves lives.