Overview of dysrhythmias (cardiac)

Last reviewed: 30 Oct 2023
Last updated: 18 Mar 2021

This page compiles our content related to dysrhythmias (cardiac). For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.



Characterized as a rapid regular rhythm arising from a discrete area within the atria. It occurs in a wide range of clinical conditions, including catecholamine excess, digoxin toxicity, pediatric congenital heart disease, and cardiomyopathy. On ECG, P waves are visible before every QRS, and different from the P waves in sinus rhythm. Onset and termination of arrhythmia are abrupt. Response to vagal maneuvers and adenosine may be evaluated to exclude alternative diagnoses.[1]

Typical atrial flutter (counterclockwise cavotricuspid isthmus-dependent atrial flutter) is a macroreentrant atrial tachycardia with atrial rates from 250 to 320 bpm. Ventricular rates range from 120 to 160 bpm, and associated 2:1 atrioventricular block is common. ECG shows negatively directed saw-tooth atrial deflections (f waves) seen in leads II, III and aVF, with positively directed deflections in lead V1. This rhythm is closely related to atrial fibrillation.[2][3][4]

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation and variable ventricular response. Acute AF is defined as a new onset or a first detectable episode of AF, whether symptomatic or not. ECG shows absent P waves; presence of rapidly oscillating fibrillatory waves that vary in amplitude, shape and timing; and irregularly irregular QRS complexes.[4][5]

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation and variable ventricular response. Chronic AF may be paroxysmal (defined as recurrent AF >1 episode ≥30 seconds in duration that terminates spontaneously within 7 days), persistent (AF that is sustained >7 days or lasts <7 days but necessitates pharmacologic or electrical cardioversion), longstanding persistent (a subgroup of persistent AF, defined as continuous AF >1 year in duration), or permanent (refractory to cardioversion or accepted as a final rhythm).

ECG shows P waves are absent and are replaced by rapid fibrillatory waves that vary in size, shape and timing, leading to an irregular ventricular response when atrioventricular conduction is intact.

The term "lone AF" applies to patients younger than 60 years of age without echocardiographic or clinical evidence of cardiac, pulmonary, or circulatory disease. However, because definitions are variable, and all patients with AF have some form of pathophysiological basis, the term “lone AF” is potentially confusing and should not be used. [5]

The most common arrhythmias diagnosed in Wolff-Parkinson-White syndrome are atrioventricular reentrant tachycardia, atrial flutter and atrial fibrillation. Typically the heart rate varies between 150 and 240 bpm. Congenital cardiac abnormalities are strong risk factors (especially Ebstein anomaly).

Ectopic ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination earlier due to hemodynamic instability. Ventricular tachycardia (VT) is defined on ECG by the presence of a wide complex tachycardia (QRS ≥120 msec) at a rate ≥100 bpm. Usually observed in ischemic and non-ischemic cardiomyopathy, but idiopathic VT may also be observed in patients without structural heart disease.[6]

Ectopic ventricular rhythm with wide QRS complex (≥120 milliseconds), rate faster than 100 bpm lasting for at least 3 consecutive beats but terminating spontaneously in less than 30 seconds.[6] ECG shows nonsustained ventricular tachycardia with a single QRS (monomorphic) or changing QRS (polymorphic) morphology at cycle length between 600 and 180 ms. It may occur in the absence of any underlying heart disease, but is more commonly associated with ischemic and non-ischemic heart disease; known genetic disorders such as long QT syndrome, Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy; congenital heart disease; metabolic problems, including drug toxicity; or electrolyte imbalance.[7]

Characterized by a prolonged QT interval on ECG and may be congenital or acquired. In congenital LQTS, mutations within 15 identified genes result in a variety of channelopathies affecting myocardial repolarization, thus prolonging the QT interval. Acquired LQTS may occur secondary to ingestion of QT interval-prolonging drugs, electrolyte imbalances, or bradyarrhythmias. ECG shows a prolonged QT interval and abnormal T-wave morphology.[8] Patients are at increased risk for syncope, ventricular arrhythmias (e.g., torsade de pointes) and sudden cardiac death. Unless there is an identifiable reversible cause, treatment primarily involves lifestyle modification and beta-blocker therapy with the implantation of a cardioverter-defibrillator (ICD) in selected cases.

Sudden cardiac arrest is a sudden state of circulatory failure due to a loss of cardiac systolic function. Can result from 4 specific cardiac rhythm disturbances: ventricular fibrillation, pulseless ventricular tachycardia, pulseless electrical activity (electrical activity and no cardiac output) and asystole.

Any heart rhythm slower than 50 bpm, even if transient. Some consider bradycardia to be a heart rate <60 bpm; however, this is in dispute and most consider rates of <50 bpm to represent bradycardia. [9] Some patients, even if asymptomatic, may require interventions (e.g., pacemaker) to prevent life-threatening complications. Rhythm disturbances responsible may be acute, chronic or paroxysmal long-standing. They include: sinus node dysfunction (sinus bradycardia, sinoatrial nodal pauses/arrest, sinoatrial nodal exit block); atrioventricular (AV) conduction disturbance (first degree AV-block, second degree AV-block [Mobitz I, Mobitz II, 2:1 block, high degree AV-block], third degree AV-block); and AV dissociation (isorhythmic dissociation, interference dissociation).

Impaired conduction from the atria to the ventricles, with various degrees of severity. Some patients may be asymptomatic. Signs and symptoms include heart rate <40 bpm, high (or, less commonly, low) blood pressure, cannon A waves, nausea or vomiting, and hypoxemia. May be classified by degree of atrioventricular block, and the severity of symptoms are not necessarily directly related. Strong risk factors include AV-nodal blocking and antiarrhythmic medications, and increased vagal tone. May occur in patients with Lyme disease.[9][10]

Palpitations are defined as the abnormal awareness of one's own heartbeat.[11] May present in non-life-threatening cardiac conditions (e.g., ventricular and atrial premature contractions, and supraventricular tachycardias) and potentially life-threatening conditions (e.g., ventricular tachycardia, hypertrophic cardiomyopathy, Brugada syndrome, and long QT syndrome[12]). Detailed evaluation of palpitations (e.g., rate and degree of regularity, association with position, presence on awakening) can help diagnose the type of arrhythmia present.[12]

Tachycardia, generally defined as a heart rate ≥100 bpm, can be a normal physiological response to a systemic process or a manifestation of underlying pathology. Several methods of classification of tachyarrhythmia are helpful in organising and assessing tachycardias. These include: sinus versus non-sinus causes; atrial versus ventricular arrhythmias; narrow- versus wide-complex tachycardias; regular versus irregular arrhythmias; and classification based on the site of origin of the arrhythmia.

Typically presents with components of gastrointestinal, constitutional and/or cardiovascular symptoms. Paroxysmal atrial tachycardia is a classic arrhythmogenic toxic manifestation of digoxin overdose. Initial workup should focus on determining whether the patient is hemodynamically compromised from the rhythm itself, and if so, consideration of digoxin immune antibody fragments (Fab) therapy if the patient is found to be digoxin toxic.[13]



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