Etiology

Palpitations can be caused by cardiac disorders or noncardiac disorders.[3][4][5][6][7]​​​​​​​ Cardiac etiologies are classified by site of origin and include supraventricular tachycardias (SVTs) and ventricular tachycardias (VTs), as well as premature atrial and ventricular depolarizations. Cardiac arrhythmias are also common in the setting of structural heart disease.​[8]

Noncardiac causes include panic attacks, anxiety disorder, anemia, fever, hyperthyroidism, hypoglycemia, and electrolyte imbalance.[9]​​ Panic disorder may cause palpitations in 20% of patients.[7] In addition, many patients with palpitations have a history of panic attacks.[10] However, psychiatric diagnoses such as panic attack or anxiety disorder should not be accepted as the sole etiologies of palpitations until true arrhythmic causes have been excluded.[11][12]

Primary cardiac arrhythmias

SVTs

  • Sinus tachycardia: the most common etiology of palpitations, defined as a heart rate >100 bpm with an identifiable cause such as exercise, stress, or some pathologic state e.g., anemia.

  • Inappropriate sinus tachycardia: defined as a resting heart rate >100 bpm, or an exaggerated heart response to exercise, without an identifiable etiology for the tachycardia such as pregnancy, anemia, or hyperthyroidism. Etiology is unknown but may be due to autonomic nervous system dysfunction or sinus node abnormality. A related syndrome is the postural orthostatic syndrome where inappropriate tachycardia is demonstrated in response to posture on a tilt-table test.

  • Atrial tachycardia: frequently seen in patients with structural heart disease or in the setting of an acute illness, such as infection. It is much more common in older people. Alternatively, it can be described as incessant with symptoms that are less specific such as fatigue and shortness of breath. Incessant atrial tachycardia can sometimes lead to a tachycardia-induced cardiomyopathy.

  • Atrial flutter: commonly seen in patients with atrial fibrillation.[13][14]

  • Atrial fibrillation: frequently seen in the setting of congestive heart failure, valvular heart disease, hypertrophic cardiomyopathy, thyroid disease, and pulmonary disease. Prevalence increases with older age.[13][15][16][17]​​​​​ Tall stature and high aerobic fitness level, alone and in combination, are associated with increased risk.[18][19][20][21]

  • Atrioventricular nodal reentrant tachycardia: can occur at any age, although most commonly presents in the late 20s or early 30s.[22] Palpitations typically have an abrupt initiation and termination.

  • Atrioventricular reentrant tachycardia: a reentrant SVT using an anomalous bypass tract between the atria and ventricles. When evidence of this bypass tract is seen as a delta wave on the ECG, and the patient has palpitations, it is referred to as Wolff-Parkinson-White syndrome. It is important to note that this condition can be present without visible delta waves on the baseline ECG, due to what is referred to as a “concealed” bypass tract; where the bypass does not conduct in the antegrade direction, and the ventricle is not preexcited. However, the bypass tract has retrograde conduction that will support an orthodromic reciprocating tachycardia. Wolff-Parkinson-White syndrome is more frequently seen in males in the late teens or early twenties, and is associated with a slight increase in incidence of sudden cardiac death.[23][24]

VTs

  • Reentrant VT due to cardiomyopathy (most often due to coronary artery disease with prior infarction).

  • Brugada syndrome: a familial syndrome that has an associated risk of sudden cardiac death.[2]

  • Long QT syndrome (LQTS): palpitations are due to episodes of nonsustained polymorphic VT, often with associated syncope.[2]​ LQTS increases predisposition to sudden cardiac death and may be congenital or acquired. Classic triggers exist for episodes in familial syndromes; triggers depend on the underlying genotype. In LQTS 1, episodes occur during exercise. In LQTS 2, they often occur with arousal from sleep or during emotional stress. A number of pharmacotherapeutic agents have been implicated in acquired LQTS; it is essential to evaluate the patient's medications for drugs that may prolong the QT interval, such as macrolide and fluoroquinolone antibiotics, or certain antipsychotics.

  • Idiopathic VT: several different types of idiopathic VT exist, classified by site of origin. These include right ventricular outflow tract VT, left ventricular outflow tract VT, and left ventricular idiopathic VT, sometimes referred to as Belhassen VT or verapamil-sensitive VT, which originates from the left ventricular myocardium.

Other cardiac causes

  • Premature ventricular contractions: one of the most common etiologies of palpitations; can be seen in normal hearts as well as in patients with structural heart disease.

  • Premature atrial contractions: one of the most common etiologies of palpitations; can be seen in normal hearts as well as in patients with structural heart disease.

Structural cardiac disorders

  • Myocardial infarction: VT is often seen in the acute setting. A myocardial scar from a previous infarction predisposes a patient to VT due to reentry, causing palpitations. Patients with prior myocardial infarction, especially those that develop congestive heart failure, are also especially prone to developing atrial fibrillation and flutter.[1][25][26][27]​​​​

  • Dilated cardiomyopathy: associated with increased frequency of VT and atrial fibrillation.[1][28][29]​​​

  • Hypertrophic obstructive cardiomyopathy: may be familial, marked by left ventricular hypertrophy that can present with a variety of arrhythmias that lead to palpitations, as well as dyspnea on exertion, near-syncope, and syncope.[30]​ The arrhythmias can be supraventricular such as atrial fibrillation, premature ventricular contractions, or ventricular (typically nonsustained VT).​[1]​​

  • Arrhythmogenic right ventricular cardiomyopathy: although rare, frequently presents with palpitations as the initial symptom.​​[1]​​[31][32]

  • Mitral valve prolapse: palpitations (often due to SVTs), and premature ventricular contractions are frequently seen in this disorder, particularly when significant mitral regurgitation is present.[1]​​[33][34]​​​[35][36]

  • Ebstein anomaly (congenital malformation of the tricuspid valve annulus): atrioventricular bypass tracts are associated with this condition, frequently resulting in atrioventricular reentry tachycardia.[1][37]​​​​

  • Valvular abnormalities (stenotic or regurgitant): commonly lead to atrial enlargement, which predisposes to atrial fibrillation and flutter.​​[1][13][25]

  • Congenital heart defects: repaired or unrepaired atrial septal defects, ventricular septal defects, and tetralogy of Fallot can lead to VT by reentry around surgical scars or atrial tachyarrhythmias due to significant atrial enlargement.[1]​​[38]​​[39]

  • Pericarditis: atrial fibrillation can be precipitated, especially after cardiac surgery.​[1][40][41]​​​

  • Cardiac surgery: any cardiac surgery that involves an incision, such as cannulation of the atria for initiation of cardiopulmonary bypass, or exposure of the mitral valve, results in scarring that may become a substrate for a reentrant tachycardia.

Noncardiac causes

Include the following:[9]​​[42]​​

  • Panic disorder

  • Anxiety disorder

  • Anemia

  • Fever

  • Hyperthyroidism: can cause sinus tachycardia or atrial fibrillation

  • Pheochromocytoma: palpitations associated with sweating and headache​

  • Alcohol use: even modest alcohol consumption has been found to increase the risk of atrial fibrillation[43]

  • Medication: drugs that prolong the QT interval may precipitate polymorphic VT; drugs that contain omega-3-acid ethyl esters, particularly at high doses, increase the risk of atrial fibrillation in patients being treated for hypertriglyceridemia[44][45]​​[46][47]

  • Caffeine use: although many patients experience increased palpitations following caffeine consumption, the epidemiology and physiology behind this are unclear[48]

  • Electrolyte imbalance: electrolyte abnormalities (particularly hypokalemia and hypomagnesemia) predispose patients to many arrhythmias from premature atrial contractions and premature ventricular contractions to atrial fibrillation, and often incite and/or contribute to VT

Use of this content is subject to our disclaimer