Heart Palpitations

Heart Palpitations — scientific infographic poster
Anatomical cross-section illustrating organs affected by Heart Palpitations
Anatomical cross-section illustrating organs affected by Heart Palpitations.
Microscopic view of Heart Palpitations cellular pathology
Microscopic view of Heart Palpitations cellular pathology.
Medical visualization of Heart Palpitations clinical presentation
Medical visualization of Heart Palpitations clinical presentation.

Table of Contents

  1. Overview
  2. Types of Palpitations
  3. Common Causes
  4. Arrhythmia Causes in Detail
  5. Non-Arrhythmia Cardiac Causes
  6. Metabolic and Endocrine Causes
  7. Pharmacological and Substance Causes
  8. Psychiatric and Functional Causes
  9. Mechanisms
  10. Evaluation
  11. Management
  12. Treatment by Cause
  13. When to Seek Medical Care
  14. Connections
  15. References & Research
  16. Featured Videos

Overview

Heart palpitations are the conscious awareness of the heart beating — described as fluttering, pounding, racing, skipping, or thumping. Most palpitations are benign and reflect ordinary ectopic beats (premature atrial or ventricular contractions), caffeine, sleep deprivation, anxiety, or hormonal shifts. A meaningful minority signal a treatable arrhythmia or systemic condition. The most useful question is what the palpitations do: a few skipped beats while resting feel different from a sudden rapid run lasting minutes, and the latter requires capture on a recording device for diagnosis.

Patients describe the sensation in their own vocabulary — "my heart was jumping out of my chest," "I felt a flip-flop," "it skipped a beat and then thudded," "my heart was racing for no reason." It is felt in the chest, throat, or neck; it may last a single beat or run for minutes to hours; and it can appear at rest, during exertion, or on lying down.

Palpitations are extremely common: they account for 1–3% of all primary care visits and are among the top five presenting complaints in cardiology clinics. Because they are almost always episodic, the resting ECG is frequently normal by the time the patient reaches the clinic — which is why the history and the choice of monitoring device carry most of the diagnostic weight.

Types of Palpitations

Common Causes

Arrhythmia Causes in Detail

True arrhythmias are the most clinically important cause of palpitations. The sensation produced varies by arrhythmia type, and the patient's description alone is sometimes enough to narrow the differential.

Premature Atrial Contractions (PACs)

PACs are the single most common cause of the "skipped beat" sensation. Paradoxically, the patient does not feel the PAC itself but the compensatory pause that follows it — the heart waits, then beats with extra force (post-extrasystolic potentiation), and that forceful beat is what registers as a "thump." PACs are visible on ECG as early P waves with altered morphology. They are essentially benign in the absence of structural heart disease. Common triggers include caffeine, alcohol, fatigue, stress, and nicotine. Reassurance is the primary intervention; beta-blockers can reduce frequency if symptoms are disabling.

Premature Ventricular Contractions (PVCs)

PVCs produce the same "skipped beat" or "flip-flop" sensation as PACs but arise from ventricular ectopic foci. They appear on ECG as wide, bizarre QRS complexes without a preceding P wave, followed by a compensatory pause. PVCs occurring in a regular alternating pattern with normal beats are called bigeminy; every third beat is trigeminy. PVCs are common in the general population and are benign when the PVC burden is low (under 10% of total beats) and the heart is structurally normal. However, frequent PVCs — particularly those exceeding 10–20% of total beats — can themselves cause a reversible PVC-induced cardiomyopathy with reduced ejection fraction. This makes quantifying PVC burden on a Holter monitor important in symptomatic patients.

Atrial Fibrillation (AFib)

AFib causes palpitations described as irregular, fast, and often sustained — "my heart was going completely haywire." On ECG it is characterized by absent P waves, an irregularly irregular ventricular response, and a fibrillatory baseline. AFib is the most common sustained cardiac arrhythmia, affecting roughly 6 million Americans. Beyond symptoms, it carries substantial stroke risk from atrial thrombus formation.

Supraventricular Tachycardia (SVT)

SVT presents as sudden-onset, sudden-offset rapid regular palpitations — often described as "the switch just flipped." Heart rates typically run 150–250 bpm. The most common mechanism is AV node re-entrant tachycardia (AVNRT), in which a re-entry circuit within the AV node causes rapid, regular conduction. SVT is generally not life-threatening in the absence of structural heart disease or WPW, but it can cause hemodynamic compromise at very high rates or with prolonged duration.

Wolff-Parkinson-White Syndrome (WPW)

WPW results from an accessory conduction pathway (the Bundle of Kent) that bypasses the AV node. On resting ECG, the signature findings are a short PR interval, a delta wave (slurred upstroke of the QRS), and a widened QRS. Most WPW patients experience SVT from re-entry involving the accessory pathway. The critical danger is atrial fibrillation in WPW: if AFib develops and conduction travels preferentially down the accessory pathway rather than the AV node, the rapid and irregular impulses can trigger ventricular fibrillation. This makes WPW with AFib a medical emergency. Critically, the standard AV node-blocking drugs — digoxin, verapamil, diltiazem, and adenosine are all contraindicated in AFib with WPW — because they preferentially block the AV node, leaving the accessory pathway unopposed and potentially accelerating conduction to dangerous rates. Treatment is IV procainamide or electrical cardioversion. Curative catheter ablation of the accessory pathway is the definitive treatment for symptomatic WPW.

Ventricular Tachycardia (VT)

VT is defined as three or more consecutive ventricular beats at a rate exceeding 100 bpm. On ECG it appears as a wide-complex tachycardia (QRS wider than 120 ms). VT in the setting of structural heart disease — post-infarction scar, dilated cardiomyopathy, hypertrophic cardiomyopathy — is potentially life-threatening and warrants aggressive evaluation, including consideration of an implantable cardioverter-defibrillator. Sustained VT can cause hemodynamic collapse and degenerate into ventricular fibrillation. Not every wide-complex tachycardia is VT (SVT with aberrant conduction is the main alternative), but in a patient with structural heart disease the safest assumption is always VT until proven otherwise.

Long QT Syndrome

Long QT syndrome (LQTS) — both congenital and acquired — predisposes to Torsades de Pointes, a distinctive polymorphic VT that can degenerate into ventricular fibrillation and sudden cardiac death. The QTc is prolonged when it exceeds 470 ms in women and 450 ms in men by the Bazett formula. Congenital LQTS involves mutations in cardiac ion channel genes (KCNQ1, KCNH2, SCN5A — LQT1, LQT2, LQT3). Acquired LQTS is commonly drug-induced, by antiarrhythmics, antipsychotics, antibiotics, and antihistamines. Hypokalemia and hypomagnesemia potentiate drug-induced QT prolongation.

Non-Arrhythmia Cardiac Causes

Sinus Tachycardia

Sinus tachycardia — a regular heart rate above 100 bpm driven by the sinus node — is the most common rapid heart rate overall. It is never a primary problem; it is always a physiological response to an underlying driver. The key clinical task is identifying the cause: pain, hypovolemia, sepsis, pulmonary embolism, heart failure, fever, anemia, hyperthyroidism, dehydration, anxiety, stimulants, or drugs. Sinus tachycardia should not be treated with rate-slowing agents in isolation — that suppresses a compensatory response without addressing the root problem. Patients typically describe a persistent "racing" feeling that builds gradually, rather than the sudden onset of SVT.

POTS (Postural Orthostatic Tachycardia Syndrome)

POTS is a form of dysautonomia defined by a heart rate increase of 30 bpm or more within 10 minutes of standing (or 40 bpm in adolescents), without orthostatic hypotension. Palpitations are a cardinal symptom — patients notice their heart racing whenever they stand up, often accompanied by lightheadedness, fatigue, brain fog, nausea, and near-syncope. POTS predominantly affects young women (female-to-male ratio approximately 5:1) and is increasingly recognized as a post-viral syndrome, including after COVID-19. Diagnosis is confirmed by an active stand test or a tilt table test.

Valvular Heart Disease

Mitral valve prolapse has historically been associated with palpitations; most prolapse is benign, and the palpitations are caused by concomitant PACs and PVCs rather than by the prolapse itself. Severe aortic regurgitation can cause prominent awareness of the heartbeat because of the large stroke volume and pounding pulse (Corrigan's pulse). Any significant valvular disease can also trigger atrial fibrillation, which then produces palpitations.

Metabolic and Endocrine Causes

Hyperthyroidism

Excess thyroid hormone sensitizes cardiac tissue to catecholamines and directly increases heart rate, stroke volume, and cardiac output. Patients experience fast, regular palpitations often present even at rest, along with heat intolerance, excessive sweating, unintended weight loss despite increased appetite, tremor, anxiety, diarrhea, and insomnia. TSH is suppressed and is the appropriate first-line screening test. Causes include Graves' disease (autoimmune, the most common), toxic multinodular goiter, and thyroiditis. Atrial fibrillation complicates hyperthyroidism in roughly 10–15% of cases and is a common initial presentation in older patients with "apathetic hyperthyroidism," who may lack the classic adrenergic features entirely.

Pheochromocytoma

Pheochromocytoma — a catecholamine-secreting tumor of the adrenal medulla — classically presents with episodic palpitations, severe headache, and diaphoresis (the classic triad), often accompanied by hypertensive crises. Episodes typically last minutes to an hour and may be triggered by positional change, physical exertion, or even abdominal palpation. Sustained hypertension can also occur. Screening uses plasma free metanephrines (sensitivity above 95%) or 24-hour urine fractionated metanephrines. CT or MRI of the adrenal glands follows a positive biochemical screen. Surgical resection is curative; alpha-blockade with phenoxybenzamine or doxazosin is essential preoperatively to prevent hypertensive crisis during induction of anesthesia.

Hypoglycemia

When blood glucose falls, the body mounts a sympathoadrenal counter-regulatory response — epinephrine and norepinephrine surge — producing palpitations, tremor, diaphoresis, and anxiety. Patients often wake at night feeling clammy and panicked. This is most relevant in people with diabetes using insulin or sulfonylureas, but it also occurs in reactive hypoglycemia after high-carbohydrate meals. Checking blood glucose during an episode, by fingerstick or continuous glucose monitor, is diagnostic. Treatment addresses the underlying cause: insulin dose adjustment, dietary change, or evaluation for rare endogenous hyperinsulinism (insulinoma).

Anemia

Anemia of any cause reduces oxygen-carrying capacity, and the compensatory rise in heart rate and stroke volume produces a hyperdynamic circulation with prominent palpitations, particularly on exertion. In severe anemia the heart "pounds" even at rest. A complete blood count is the key initial test; the underlying cause — iron deficiency, B12 or folate deficiency, hemolysis, chronic disease — guides treatment, and correcting the anemia resolves the palpitations.

Electrolyte Disturbances

Hypokalemia shifts the resting membrane potential and makes cardiac cells more excitable. PVCs are common; the ECG classically shows flattened T waves and prominent U waves. Hypokalemia is frequent in patients using loop diuretics (furosemide) or thiazides, in eating disorders with purging, and in diarrheal illness. Potassium replacement corrects most hypokalemia-associated palpitations.

Hypomagnesemia frequently co-occurs with hypokalemia and independently predisposes to arrhythmias, particularly Torsades de Pointes. Magnesium is essential for cardiac ion channel function and for the Na/K-ATPase pump that maintains intracellular potassium. IV magnesium is the first-line treatment for Torsades de Pointes regardless of the measured serum magnesium level. Common causes include diuretic use, alcoholism, malabsorption, and proton pump inhibitor use, which impairs intestinal magnesium absorption.

Fever

For every 1°C rise in core body temperature, heart rate increases by approximately 10 bpm. Any febrile illness can therefore cause prominent palpitations. The clinical task is identifying and treating the infection — the palpitations resolve with defervescence.

Pharmacological and Substance Causes

Caffeine

Caffeine is the most common dietary trigger. It blocks adenosine receptors, increasing sympathetic tone and directly exciting cardiac tissue, precipitating PACs and PVCs in susceptible individuals. The relationship is dose-dependent: moderate intake of up to 300–400 mg/day is generally tolerated, but individual sensitivity varies widely. Sources include coffee, tea, energy drinks, cola sodas, and dark chocolate.

Alcohol

Alcohol triggers palpitations through two distinct mechanisms. Acutely, even moderate intake can precipitate PACs and AFib in susceptible individuals. More dramatically, "Holiday Heart Syndrome" — first described by Ettinger in 1978 — refers to AFib or other atrial arrhythmias that develop after binge drinking in otherwise healthy young adults with no structural heart disease; the arrhythmia typically converts to sinus rhythm spontaneously as blood alcohol clears. Chronic heavy use causes alcoholic cardiomyopathy and its associated arrhythmias. Any patient with recurrent unexplained AFib should be asked carefully about alcohol intake.

Stimulant Medications

Multiple over-the-counter and prescription drugs contain sympathomimetic agents that raise heart rate:

Nicotine

Nicotine stimulates nicotinic acetylcholine receptors, acutely increasing heart rate and blood pressure through catecholamine release. Both cigarette smoking and nicotine replacement products — patch, gum, vaping — can trigger palpitations, particularly during a transition to higher-dose replacement.

Thyroid Hormone Over-Replacement

Patients on levothyroxine who are supraphysiologically dosed develop the palpitation pattern of hyperthyroidism: fast, regular, and present at rest. A TSH suppressed below 0.1 mIU/L on thyroid supplementation should prompt dose reduction. This is commonly seen after empiric dose increases without TSH follow-up.

Beta-Agonist Bronchodilators

Albuterol, salmeterol, and other beta-2 agonists used in asthma and COPD also stimulate cardiac beta-1 receptors — they are not perfectly selective — causing sinus tachycardia and palpitations. The effect is dose-dependent and worsens with overuse of rescue inhalers.

Antiarrhythmic Proarrhythmia

A paradoxical risk of antiarrhythmic drugs is that they can cause the very arrhythmias they are meant to treat. Class IC agents — flecainide and propafenone — are particularly notable: used for AFib, they can organize the fibrillation into atrial flutter that then conducts 1:1 to the ventricle at rates of 200–250 bpm. This is why class IC drugs for AFib are routinely combined with an AV node blocker. The CAST trial demonstrated that class IC agents increased mortality in post-infarction patients; they are contraindicated in structural heart disease.

Digoxin Toxicity

Digoxin has a narrow therapeutic window, with a target level of 0.5–0.9 ng/mL in heart failure. Toxicity — from accumulation, drug interactions with amiodarone or verapamil, or renal impairment — causes a wide range of arrhythmias: accelerated junctional rhythm, bidirectional VT (pathognomonic), and various degrees of AV block. Hypokalemia worsens digoxin toxicity. Management includes holding the drug, correcting electrolytes, and digoxin-immune Fab antibodies for severe toxicity.

Recreational Drugs

Psychiatric and Functional Causes

Panic Disorder and Panic Attacks

Panic disorder is a major cause of palpitations and one of the most important diagnoses to consider once cardiac causes have been excluded. A panic attack produces a sudden surge of autonomic activation — palpitations, shortness of breath, chest pain, dizziness, tingling, sweating, and an overwhelming sense of impending doom. Attacks peak at roughly 10 minutes and then subside. They can occur during the day or wake the patient from sleep as nocturnal panic attacks. Because the physical symptoms so closely mimic cardiac events, patients often present to emergency departments believing they are having a heart attack. An important diagnostic principle: panic disorder should be diagnosed only after arrhythmias have been adequately excluded — some patients have both a genuine arrhythmia and panic, and finding one does not rule out the other.

Generalized Anxiety Disorder

Patients with generalized anxiety disorder develop chronic autonomic hyperarousal — persistently elevated sympathetic tone producing resting tachycardia, palpitations, muscle tension, fatigue, and difficulty concentrating. Unlike the discrete episodes of panic, this causes more continuous background somatic symptoms, noticed particularly during periods of heightened worry, and somatic hypervigilance amplifies awareness of normal beats. Beta-blockers such as propranolol 10–20 mg as needed can interrupt the feedback loop in which noticing a palpitation causes anxiety, which causes more palpitations.

Somatic Symptom Disorder and Cardiac Anxiety

A subset of patients with palpitations have objectively normal Holter monitor findings — including during symptom episodes — with no correlation whatsoever between symptoms and rhythm. These patients often have high levels of health anxiety focused on the heart, amplified by hypervigilance to normal cardiac sensations. Central sensitization, in which the perception threshold for interoceptive signals is lowered, likely plays a role. Treatment focuses on cognitive behavioral therapy targeting cardiac anxiety, psychoeducation, and low-dose beta-blockers to reduce the peripheral somatic signals that feed the anxiety loop. Avoiding repeated cardiac testing, which reinforces illness beliefs, is part of the therapeutic approach.

Mechanisms

Evaluation

Reading the Description

The character of the sensation maps onto the differential more reliably than any other single piece of information:

What to Look For on the Resting ECG

A 12-lead ECG should be obtained in every patient presenting with palpitations, even if the episode has already resolved — several findings visible at rest fundamentally redirect the workup: WPW pre-excitation (delta wave with a PR interval under 120 ms), a prolonged QTc, ST-segment changes suggesting ischemia, pathological Q waves from prior infarction, a Brugada pattern (coved ST elevation in V1–V2), left ventricular hypertrophy suggesting hypertrophic cardiomyopathy, and PVCs present at rest.

Choosing an Ambulatory Monitor

The goal of ambulatory monitoring is a symptom-rhythm correlation — recording the rhythm during an episode to establish whether the patient's symptoms coincide with a documented arrhythmia or with a normal rhythm. Device choice follows episode frequency:

When to Order an Echocardiogram

Transthoracic echocardiography is indicated for palpitations accompanied by exertional symptoms or syncope, for any suggestion of structural heart disease on history, examination, or ECG, and whenever a sustained arrhythmia has been documented. It measures left ventricular ejection fraction, wall thickness (for hypertrophic cardiomyopathy), valvular function, and diastolic function.

Management

Treatment by Cause

Supraventricular Tachycardia (AVNRT)

Acute termination proceeds stepwise. The modified Valsalva maneuver is the most effective vagal technique: the patient strains for 15 seconds, then the legs are passively elevated to 45° for 15 seconds while supine. The REVERT randomized trial found this approach roughly doubled the success rate of the standard Valsalva — 43% versus 17%. Ice-water facial immersion stimulates the diving reflex and is useful in children. Carotid sinus massage is an option but is contraindicated with a carotid bruit, recent stroke, or known carotid stenosis. If vagal maneuvers fail, IV adenosine 6 mg by rapid push with an immediate saline flush, repeated at 12 mg if the first dose fails, terminates most SVT by transiently blocking AV node conduction. For recurrent symptomatic SVT, catheter ablation of the re-entrant circuit achieves cure rates above 95% and is preferred over lifelong antiarrhythmic therapy in most guidelines.

Atrial Fibrillation

Three considerations run in parallel. Rate control aims for a resting ventricular rate below 110 bpm. Rhythm control restores and maintains sinus rhythm — flecainide or propafenone when there is no structural disease, amiodarone or dofetilide more broadly, or catheter ablation by pulmonary vein isolation; the EAST-AFNET 4 trial showed that early rhythm control reduces major cardiovascular events compared with rate control alone in newly diagnosed AFib. Stroke prevention follows the CHA2DS2-VASc score, and direct oral anticoagulants — rivaroxaban, apixaban, dabigatran, edoxaban — are preferred over warfarin in non-valvular AFib for their better safety profile.

Premature Ventricular Contractions

Low-burden PVCs in a structurally normal heart need only reassurance and trigger avoidance. For symptomatic PVCs not responding to conservative measures, beta-blockers reduce both frequency and symptoms. Once the burden passes the threshold described above — especially with a reduced ejection fraction — catheter ablation of the PVC focus can dramatically reduce burden and may reverse the associated cardiomyopathy.

Long QT Syndrome

Core management: avoid every QTc-prolonging medication (the CredibleMeds QTDrugs list is the authoritative reference and should be checked before prescribing any new drug); correct potassium and magnesium; use nadolol or propranolol specifically — not cardioselective beta-blockers — as first-line therapy for LQT1 and LQT2; avoid competitive sports in LQT1 and LQT2, where adrenergic surges are the trigger; and implant an ICD for patients with prior cardiac arrest, syncope despite beta-blockade, or high-risk genetic variants.

POTS

Non-pharmacological measures are foundational: aggressive salt loading of 8–10 g NaCl/day, fluid intake of 2–3 L/day, waist-high compression garments of at least 20–30 mmHg, and a structured exercise reconditioning program that begins with recumbent work — swimming or rowing — to avoid the orthostatic challenge of upright exercise. Drug options include fludrocortisone for volume expansion, low-dose propranolol at 10–20 mg for symptom relief, ivabradine off-label as a sinus-node If current inhibitor that lowers heart rate without impairing contractility or causing the fatigue common with beta-blockers, and midodrine, an alpha-1 agonist vasoconstrictor that reduces venous pooling.

Panic Disorder

First-line treatment combines an SSRI — sertraline, escitalopram, or paroxetine, the last carrying a higher discontinuation-syndrome risk — with cognitive behavioral therapy built around interoceptive exposure, in which palpitation-like sensations are deliberately induced to decondition the fear response. The combination achieves remission in 70–80% of patients. Short-acting benzodiazepines such as lorazepam 0.5–1 mg are appropriate as needed for acute severe attacks but should not anchor maintenance therapy, because of dependence risk. Beta-blockers help situational performance anxiety but are not effective maintenance treatment for panic disorder — they block the peripheral symptoms without touching the central fear circuitry.

Caffeine and Alcohol

A structured 2- to 4-week elimination trial of caffeine, alcohol, or both is simultaneously diagnostic and therapeutic: if the palpitations resolve with abstinence, the cause is identified. Where a trigger is confirmed, sustained avoidance is the most effective long-term intervention. For alcohol-associated AFib, randomized data show a substantial reduction in AFib burden and recurrence with abstinence in regular drinkers.

Metabolic Causes

Beta-blockers give rapid relief of the adrenergic symptoms of hyperthyroidism while definitive therapy takes effect, and palpitations plus AFib resolve on return to a euthyroid state. Potassium is repleted orally for mild to moderate hypokalemia and intravenously when severe or symptomatic; significant hypomagnesemia is repleted intravenously. Anemia is treated according to its etiology.

When to Seek Medical Care

Connections

References & Research

Historical Background

Awareness of the heartbeat has been recorded since antiquity, but Holter's 1949 invention of the portable ECG monitor made systematic study of palpitations possible. The 21st century has produced increasingly sophisticated wearables, from patch monitors to consumer smartwatches that detect atrial fibrillation, transforming an occasionally elusive symptom into one frequently caught on tape before the doctor visit.

Key Research Papers

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PubMed Topic Searches

  1. Evaluation of palpitations
  2. Atrial fibrillation screening with wearables
  3. Premature ventricular contractions: benign or pathologic?
  4. Hyperthyroidism and atrial fibrillation
  5. POTS and inappropriate sinus tachycardia
  6. Panic disorder and palpitations
  7. Pheochromocytoma, palpitations, and plasma metanephrines
  8. Wolff-Parkinson-White with atrial fibrillation: management

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