Causes of Tachycardia
Tachycardia results from either physiological responses to identifiable stressors or pathological conditions affecting cardiac rhythm, with the most critical step being to distinguish reversible secondary causes from primary cardiac arrhythmias. 1, 2
Physiological (Secondary) Causes
These represent appropriate compensatory responses where tachycardia resolves once the underlying trigger is corrected:
Metabolic and Systemic Conditions
- Fever and infection trigger increased metabolic demands 1, 2
- Dehydration reduces preload and necessitates compensatory heart rate increase 1, 2
- Anemia decreases oxygen-carrying capacity, requiring increased cardiac output 1, 2
- Hyperthyroidism increases metabolic rate and direct cardiac stimulation 1, 2
- Heart failure produces compensatory tachycardia to maintain cardiac output 1, 2
- Pain activates sympathetic nervous system 1, 2
- Acid-base disturbances alter cardiac electrophysiology 2
Exogenous Substances
- Caffeine (though epidemiologic studies show no clear connection to arrhythmia development in most patients) 2, 3
- Beta-agonist medications (albuterol, salmeterol) directly stimulate cardiac receptors 1, 2
- Illicit stimulants (amphetamines, cocaine) cause catecholamine surge 1, 2
- Alcohol particularly with binge use ("holiday heart syndrome") 2, 3
- Nicotine stimulates sympathetic activity 2
- Energy drinks contain high caffeine plus other cardiac stimulants and warrant caution 3
- Medications: aminophylline, atropine, catecholamines, anticancer agents (especially anthracyclines) 2
Physiological States
- Physical activity or exercise appropriately increases heart rate 2
- Emotional stress or anxiety activates sympathetic nervous system 1, 2
Primary Cardiac Arrhythmias
Supraventricular Tachycardias
These originate above the ventricles and include:
- Atrioventricular nodal re-entrant tachycardia (AVNRT) 2
- Atrioventricular re-entrant tachycardia (AVRT) including Wolff-Parkinson-White syndrome 2, 4
- Atrial tachycardia 2
- Atrial flutter 2
- Sinus node reentry tachycardia 2
Inappropriate Sinus Tachycardia (IST)
This is a diagnosis of exclusion after ruling out all secondary causes. 1
- Defined as resting heart rate >100 bpm with average 24-hour rate >90 bpm unexplained by physiological demands 1, 2
- Proposed mechanisms include dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity 1, 2
- Associated symptoms: weakness, fatigue, lightheadedness, uncomfortable heart racing sensations 1, 2
- Anxiety disorders commonly coexist and may trigger episodes 1
Autonomic Dysfunction
Postural Orthostatic Tachycardia Syndrome (POTS)
- Heart rate increase ≥30 bpm in adults (≥40 bpm in adolescents) within 10 minutes of standing, or heart rate ≥120 bpm 5, 6
- Symptoms predominantly worsen with postural changes and improve when lying down 5
- Results from central hypovolemia, reduced plasma volume, and secondary cardiac atrophy 5
- Critical distinction: IST must be differentiated from POTS because treating POTS with rate-lowering agents can cause severe orthostatic hypotension 1
Deconditioning
- Creates vicious cycle of reduced activity → plasma volume reduction → cardiac atrophy → compensatory tachycardia 5
Structural Heart Disease
- Cardiomyopathies can precipitate tachyarrhythmias 2
- Most supraventricular tachycardias occur without structural heart abnormalities 4
Critical Clinical Pitfalls
Always systematically exclude secondary causes before diagnosing primary arrhythmias. 1, 2 The ACC/AHA guidelines emphasize that evaluation and treatment of reversible causes is a Class I recommendation. 1
Do not assume caffeine is the culprit - large epidemiologic studies fail to demonstrate a connection between caffeine consumption and arrhythmia development, even in patients post-myocardial infarction. 3 However, energy drinks warrant more caution due to additional stimulant compounds. 3
Distinguish anxiety from primary arrhythmia - anxiety can both trigger and mimic tachycardia, and patients with IST frequently have comorbid anxiety disorders. 1, 2 Diagnosis often requires objective documentation with Holter monitoring or event recorders. 4
Recognize that moderate to heavy alcohol use associates with atrial fibrillation development, making alcohol limitation reasonable in patients with arrhythmias. 3