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Palpitations are the perception of cardiac activity. They are often described as a fluttering, racing, or skipping sensation. They are common; some patients find them unpleasant and alarming. Palpitations can occur in the absence of heart disease or can result from life-threatening heart disorders. The key to diagnosis and treatment is to “capture” the rhythm on ECG and make careful observations during the palpitations.

Pathophysiology

The mechanisms responsible for the sensation of palpitations are unknown. Ordinarily, sinus rhythm at a normal rate is not perceived, and palpitations thus usually reflect changes in cardiac rate, rhythm, or contractility. In all cases, it is the abnormal movement of the heart within the chest that is felt. In cases of isolated extrasystoles, the patient may actually perceive the augmented post-extrasystolic beat as the “skipped” beat rather than the premature beat itself, probably because the extrasystole blocks the next sinus beat and allows longer ventricular filling and thus a higher stroke volume.

The clinical perception of cardiac phenomena is highly variable. Some patients are aware of virtually every premature ventricular beat, but others are unaware of even complex atrial or ventricular tachyarrhythmias. Awareness is heightened in sedentary, anxious, or depressed patients and reduced in active, happy patients. In some cases, palpitations are perceived in the absence of any abnormal cardiac activity.

Etiology

Some patients simply have heightened awareness of normal cardiac activity, particularly when exercise, febrile illness, or anxiety increases heart rate. However, in most cases, palpitations result from arrhythmia. Arrhythmias range from benign to life threatening.

The most common arrhythmias include

• Premature atrial contractions (PACs)
• Premature ventricular contractions (PVCs)

Both of these arrhythmias usually are harmless.

Other common arrhythmias include

• Paroxysmal supraventricular tachycardia (PSVT)
• Atrioventricular nodal reentrant tachycardia
• Atrial fibrillation or flutter
• Ventricular tachycardia
• Bradyarrhythmias and heart block

Causes of arrhythmias: Some arrhythmias (eg, PACs, PVCs, PSVT) often occur spontaneously in patients without serious underlying disorders, but others are often caused by a serious cardiac disorder.

Serious cardiac causes include myocardial ischemia or other myocardial disorders, congenital heart disease, valvular heart disease, and conduction system disturbances (eg, disturbances that produce bradycardia or heart block). Patients with orthostatic hypotension commonly sense palpitations caused by sinus tachycardia upon standing.

Noncardiac disorders that increase myocardial contractility (eg, thyrotoxicosis, pheochromocytoma, anxiety) may produce palpitations.

Some drugs, including digitalis, caffeine, alcohol, nicotine Some Trade Names
COMMIT
NICORETTE
NICOTROL
Click for Drug Monograph
, and sympathomimetics (eg, albuterol Some Trade Names
PROVENTIL
VENTOLIN
Click for Drug Monograph
, amphetamines, cocaine, dobutamine Some Trade Names
DOBUTREX
Click for Drug Monograph
, epinephrine Some Trade Names
ADRENALIN
PRIMATENE MIST
Click for Drug Monograph
, ephedrine Some Trade Names
PRETZ-D
Click for Drug Monograph
, isoproterenol Some Trade Names
ISUPREL
Click for Drug Monograph
, norepinephrine Some Trade Names
LEVOPHED
Click for Drug Monograph
, and theophylline Some Trade Names
ELIXOPHYLLIN
THEO-DUR
Click for Drug Monograph
), frequently produce palpitations.

Metabolic disturbances, including anemia, hypoxia, hypovolemia, and electrolyte abnormalities (eg, diuretic-induced hypokalemia), can trigger or exacerbate palpitations.

Consequences: Many arrhythmias that cause palpitations have no adverse physiologic consequences of their own (ie, independent of the underlying disorder). However, bradyarrhythmias, tachyarrhythmias, and heart blocks can be unpredictable and may adversely affect cardiac output and cause hypotension or death. Ventricular tachycardia sometimes degenerates to ventricular fibrillation.

Evaluation

A complete history and physical examination are essential. Observations by other medical personnel or reliable observers should be sought.

History: History of present illness should cover the frequency and duration of palpitations and provoking or exacerbating factors (eg, emotional distress, activity, change in position, intake of caffeine or other drugs). Important associated symptoms include syncope, light-headedness, tunnel vision, dyspnea, and chest pain. Asking the patient to tap out the rate and cadence of palpitations is better than a verbal description and often allows a definitive diagnosis, as in the “missed beat” of atrial or ventricular extrasystoles or the rapid total irregularity of atrial fibrillation.

Review of systems should cover symptoms of causative disorders, including heat intolerance, weight loss, and tremor (hyperthyroidism); chest pain and dyspnea on exertion (cardiac ischemia); and fatigue, weakness, heavy vaginal bleeding, and dark tar-like stools (anemia).

Past medical history should identify known potential causes, including documented arrhythmias and heart or thyroid disorders. Family history should note occurrences of syncope or sudden death at an early age.

The drug profile should be reviewed for offending prescription drugs (eg, antiarrhythmics, digitalis, β-agonists, theophylline Some Trade Names
ELIXOPHYLLIN
THEO-DUR
Click for Drug Monograph
, and rate-limiting drugs); OTC drugs (eg, cold and sinus medications, dietary supplements containing stimulants), including alternative medicines; and illicit drugs (eg, cocaine, methamphetamines). Caffeine (eg, coffee, tea, numerous soft drinks and energy drinks), alcohol, and tobacco use should be determined.

Physical examination: The general examination should note whether an anxious demeanor or psychomotor agitation is present. Vital signs are reviewed for fever, hypertension, hypotension, tachycardia, bradycardia, tachypnea, and low O₂ saturation. Orthostatic changes in BP and heart rate should be measured.

Examination of the head and neck should note any abnormality or dyssynchrony of the jugular pulse waves compared with the carotid pulse or auscultated heart rhythm and findings of hyperthyroidism, such as thyroid enlargement or tenderness and exophthalmos. The conjunctivae, palmar creases, and buccal mucosa should be inspected for pallor.

Cardiac auscultation should note the rate and regularity of the rhythm as well as any murmurs or extra heart sounds that might indicate underlying valvular or structural heart disease.

Neurologic examination should note whether resting tremors or brisk reflexes are present (suggesting excess sympathetic stimulation). An abnormal neurologic finding suggests that seizures rather than a cardiac disorder may be the cause if syncope is one of the symptoms.

Red flags: Certain findings raise suspicion of a more serious etiology of palpitations:

• Light-headedness or syncope (particularly if injury occurs from syncope)
• Chest pain
• New onset of irregularly irregular heart rhythm
• Heart rate >120 beats/min or < 45 beats/min while at rest
• Significant underlying heart disease
• Family history of sudden death

Interpretation of findings: History (see Table 10: Approach to the Cardiac Patient: Suggestive Historical Findings with Palpitations) and, to a lesser extent, physical examination provide clues to the diagnosis.

Palpation of the arterial pulse and cardiac auscultation may reveal a rhythm disturbance. However, the examination is not always diagnostic of a specific rhythm, except when it identifies the unique irregular irregularity of some cases of rapid atrial fibrillation, the regular irregularity of coupled atrial or ventricular extrasystoles, the regular tachycardia at 150 beats/min of atrial flutter (in adults, this rate is rare with any other arrhythmia), and the regular bradycardia of < 35 beats/min of complete atrioventricular block. Careful examination of the jugular venous pulse waves simultaneously with cardiac auscultation and palpation of the carotid artery allows diagnosis of most arrhythmias if an ECG is not available, because the jugular waves will show the atrial rhythm while the auscultated sounds or the pulse in the carotids are the product of ventricular contraction.

Thyroid enlargement or tenderness with exophthalmos suggests thyrotoxicosis. Marked hypertension and regular tachycardia suggest pheochromocytoma.

Table 10
Suggestive Historical Findings with Palpitations Finding Possible Cause Occasional skipped beats PACs, PVCs Rapid, regular palpitations with sudden onset and termination Often history of recurrence PSVT, atrial flutter with 2:1 atrioventricular block, ventricular tachycardia Syncope following palpitations Sinus node dysfunction, atrioventricular bypass tract, such as in the Wolff-Parkinson-White syndrome, congenital long QT syndrome Palpitations during exercise or an emotional episode Healthy person: Sinus tachycardia History of coronary artery disease: Ventricular arrhythmia from exercise-induced ischemia Palpitations following episodic* drug use Drug-induced cause Sense of doom, anxiety, or panic Suggests (but does not confirm) a psychologic cause Postoperative patient Sinus tachycardia (eg, due to infection, bleeding, pain) Recurrent episodes since childhood Supraventricular arrhythmia (eg, atrioventricular nodal re-entrant bypass tract, Wolff-Parkinson-White syndrome) Congenital long QT syndrome (usually manifests during adolescence) Family history of syncope or sudden death Brugada syndrome, long QT syndrome, inherited dilated or hypertrophic cardiomyopathy *The role of regular use of drugs (particularly therapeutic drugs) or substances (eg, daily caffeine) can be hard to determine; sometimes a trial of withdrawal is diagnostic. All drugs with cardiovascular effects, most psychoactive drugs, and drugs capable of causing hypokalemia or hypomagnesemia must be suspected. PACs = Premature atrial contractions; PSVT = paroxysmal supraventricular tachycardia; PVCs = premature ventricular contractions.

Testing: Testing typically is done.

• ECG, sometimes with ambulatory monitoring
• Laboratory testing
• Sometimes imaging studies, stress testing, or both

ECG is done, but unless the recording is done while symptoms are occurring, it may not provide a diagnosis. Many cardiac arrhythmias are intermittent and show no fixed ECG abnormalities; exceptions include

• Wolff-Parkinson-White syndrome
• Long QT syndrome
• Arrhythmogenic right ventricular dysplasia cardiomyopathy
• Brugada syndrome and its variants

If no diagnosis is apparent and symptoms are frequent, Holter monitoring for 24 to 48 h is useful; for intermittent symptoms, an event recorder worn for longer periods and activated by the patient when symptoms are felt is better. These tests are used mainly when a sustained arrhythmia is suspected, rather than when symptoms suggest only occasional skipped beats. Patients with very infrequent symptoms that clinicians suspect represent a serious arrhythmia may have a device implanted beneath the skin of the upper chest. This device continuously records the rhythm and can be interrogated by an external machine that allows the cardiac rhythm to be printed.

Laboratory testing is needed in all patients. All patients should have measurement of CBC, serum electrolytes including Mg and Ca, and C-reactive protein (indicating inflammation that may be affecting the heart or coronary arteries). Cardiac markers (eg, troponin and CPK) should be measured in patients with ongoing arrhythmias, chest discomfort, or other symptoms suggesting active or recent coronary ischemia, myocarditis, or pericarditis.

Thyroid function tests are indicated when atrial fibrillation is newly diagnosed or there are symptoms of hyperthyroidism. Patients with paroxysms of high BP should be evaluated for pheochromocytoma.

Sometimes tilt-table testing is done in patients with postural syncope.

Imaging is often needed. Patients with findings suggesting cardiac dysfunction or structural heart disease require echocardiography and sometimes cardiac MRI. Patients with symptoms on exertion require stress testing sometimes with stress echocardiography, nuclear scanning, or PET.

Treatment

Precipitating drugs and substances are stopped. If dangerous or debilitating arrhythmias are caused by a necessary therapeutic drug, a different agent should be tried.

For isolated PACs and PVCs in patients without structural heart disease, simple reassurance is appropriate. For otherwise healthy patients in whom these phenomena are disabling, a β-blocker can be given provided efforts are made to avoid reinforcing the perception by anxious patients that they have a serious disorder.

Identified rhythm disturbances and underlying disorders are investigated and treated (see Table 11: Approach to the Cardiac Patient: Some Treatments for Arrhythmias).

Table 11
Some Treatments for Arrhythmias Disorder Treatment* Narrow complex tachycardias Multifocal atrial extrasystoles Reassurance or β-blocker Atrial fibrillation Aspirin Some Trade Names BUFFERIN ECOTRIN GENACOTE Click for Drug Monograph , warfarin Some Trade Names COUMADIN Click for Drug Monograph , enoxaparin Some Trade Names LOVENOX Click for Drug Monograph , unfractionated heparin Some Trade Names HEPFLUSH-10 Click for Drug Monograph , DC cardioversion, flecainide Some Trade Names TAMBOCOR Click for Drug Monograph , β-blocker, digoxin Some Trade Names DIGITEK LANOXIN Click for Drug Monograph , verapamil Some Trade Names CALAN ISOPTIN Click for Drug Monograph , diltiazem Some Trade Names CARDIZEM CARTIA DILACOR Click for Drug Monograph , ibutilide Some Trade Names CORVERT Click for Drug Monograph , amiodarone Some Trade Names CORDARONE Click for Drug Monograph , radioablation, or Maze procedure depending upon clinical circumstances Atrial flutter DC cardioversion, digoxin Some Trade Names DIGITEK LANOXIN Click for Drug Monograph , β-blocker, verapamil Some Trade Names CALAN ISOPTIN Click for Drug Monograph , anticoagulation, radioablation Supraventricular tachycardia Vagotonic maneuvers, adenosine Some Trade Names ADENOCARD Click for Drug Monograph , DC cardioversion, β-blocker, verapamil Some Trade Names CALAN ISOPTIN Click for Drug Monograph , flecainide Some Trade Names TAMBOCOR Click for Drug Monograph , amiodarone Some Trade Names CORDARONE Click for Drug Monograph , digoxin Some Trade Names DIGITEK LANOXIN Click for Drug Monograph Atrioventricular nodal reentrant tachycardia β-blocker, verapamil Some Trade Names CALAN ISOPTIN Click for Drug Monograph , radioablation Broad complex tachycardias Ventricular tachycardia DC cardioversion, amiodarone Some Trade Names CORDARONE Click for Drug Monograph , sotalol Some Trade Names BETAPACE Click for Drug Monograph , lidocaine Some Trade Names XYLOCAINE Click for Drug Monograph , mexiletine Some Trade Names MEXITIL Click for Drug Monograph , flecainide Some Trade Names TAMBOCOR Click for Drug Monograph , radioablation, implanted defibrillator Torsade de pointes Mg, K, DC cardioversion, β-blocker, overdrive pacemaker, implanted defibrillator Ventricular fibrillation DC cardioversion, amiodarone Some Trade Names CORDARONE Click for Drug Monograph , lidocaine Some Trade Names XYLOCAINE Click for Drug Monograph , implanted defibrillator Brugada syndrome DC cardioversion, implanted defibrillator *Always identify and correct causes and exacerbating factors (eg, electrolyte abnormalities, hypoxemia, drugs). DC = Direct current.

Geriatric Essentials

Elderly patients are at particular risk of adverse effects of antiarrhythmics; reasons include lower GFR and concomitant use of other drugs. When drug treatment is needed, lower doses should be used to start. Subclinical conduction abnormalities may be present (recognized on ECG or other studies), which might worsen with use of antiarrhythmics; such patients may require a pacemaker to allow the use of antiarrhythmics.

Key Points

• Palpitations are a frequent but relatively nonspecific symptom.
• Palpitations are not a reliable indicator of a significant arrhythmia, but palpitations in a patient with structural heart disease or an abnormal ECG may be a sign of a serious problem and warrant investigation.
• An ECG or other recording done during symptoms is essential; a normal ECG in a symptom-free interval does not rule out significant disease.
• Most antiarrhythmics themselves can cause arrhythmias.
• If in doubt about a rapid tachyarrhythmia in a patient in hemodynamic distress, use electrocardioversion first and ask questions later.

Last full review/revision April 2009 by Paul H. Tanser, MD

Content last modified April 2009