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.
Introduction
Relevant conditions
Focal atrial tachycardia | go to our full topic on Focal atrial tachycardia 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] |
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Atrial flutter | go to our full topic on Atrial flutter 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. Characteristic features on ECG are 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] |
New-onset atrial fibrillation | go to our full topic on New-onset atrial fibrillation Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation and variable ventricular response and consequently ineffective atrial contraction.[4][5] New-onset AF is a new or first detectable episode of a chaotic and irregular atrial arrhythmia. ECG characteristics include: irregularly irregular R-R intervals (where atrioventricular conduction is not impaired); absence of distinct repeating P waves; irregular atrial activations.[4][5] |
Chronic atrial fibrillation | go to our full topic on Chronic atrial fibrillation Chronic AF is a longstanding chaotic and irregular atrial arrhythmia. It is primarily defined based on duration and frequency of episodes; therefore, chronic AF could be paroxysmal, persistent, or permanent. AF causes significant morbidity (e.g., palpitations, dyspnea, angina, dizziness or syncope, and features of heart failure, tachycardia-induced cardiomyopathy, or stroke) and death.[6][7] Many patients are asymptomatic or have symptoms that are less specific for cardiac arrhythmias, such as mild dementia or silent strokes. |
Wolff-Parkinson-White syndrome | go to our full topic on Wolff-Parkinson-White syndrome Occurs when myocardial fibers connect the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus (accessory pathway), pre-exciting the ventricle.[8] 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). |
Sustained ventricular tachycardias | go to our full topic on Sustained ventricular tachycardias A 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 milliseconds) 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. |
Nonsustained ventricular tachycardia | go to our full topic on Nonsustained ventricular tachycardia 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.[9][10] 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.[11] |
Long QT syndrome (LQTS) | go to our full topic on Long QT syndrome (LQTS) Characterized by a prolonged QT interval on ECG and may be congenital or acquired. In congenital LQTS, genetic mutations affect ion channels important in myocardial repolarization.[12] Acquired LQTS may occur secondary to ingestion of QT interval-prolonging drugs, electrolyte imbalances, or bradyarrhythmias. An ECG should be undertaken in all suspected cases. Patients are at increased risk for syncope, ventricular arrhythmias (e.g., torsade de pointes), and sudden cardiac death. |
Cardiac arrest | go to our full topic on Cardiac arrest 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. The most common underlying causes are ischemic heart disease and myocardial infarction.[13] Presentation is usually sudden and manifests as loss of consciousness but can be preceded by chest pain or dyspnea. |
Bradycardia | go to our full topic on Bradycardia Any heart rhythm slower than 50 bpm, even if transient, owing to sinus node dysfunction and/or atrioventricular (AV) conduction abnormalities. 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.[14][15] Causes include intrinsic sinus node, AV nodal, and His-Purkinje disease, or extrinsic influences, which may be reversible. Some patients, even if asymptomatic, may require interventions to prevent life-threatening complications. |
Atrioventricular (AV) block | go to our full topic on Atrioventricular (AV) block Impaired conduction from the atria to the ventricles, with various degrees of severity. Signs and symptoms include heart rate <40 bpm, high (or, less commonly, low) blood pressure, cannon A waves, chest pain, palpitations, and nausea or vomiting, and hypoxemia. Some patients may be asymptomatic. The degree of AV block or anatomical level of block does not necessarily correlate with the severity of subsequent symptoms. Strong risk factors include increased vagal tone, use of AV nodal blocking agents, underlying cardiovascular disease, acid-base disturbance, neuromuscular disorders, and recent cardiac surgery.[16][17] |
Postural orthostatic tachycardia syndrome | go to our full topic on Postural orthostatic tachycardia syndrome A chronic, multisystem disorder that is thought to be due to an autoimmune process. It is characterized by symptoms of orthostatic intolerance and an increase in heart rate (without orthostatic hypotension) on standing, in the absence of other causes. It is also associated with comorbidities such as migraine headaches, irritable bowel syndrome, Ehlers-Danlos syndrome, chronic fatigue syndrome, and autoimmune diseases such as Hashimoto thyroiditis and celiac disease.[18] |
Evaluation of palpitations | go to our full topic on Evaluation of palpitations Palpitations are defined as the abnormal awareness of one's own heartbeat. 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).[19][20] 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.[19] |
Evaluation of tachycardia | go to our full topic on Evaluation of tachycardia 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 organizing 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. |
Digoxin overdose | go to our full topic on Digoxin overdose Typically presents with components of gastrointestinal, constitutional and/or cardiovascular symptoms. Patients with acute digoxin toxicity classically have dysrhythmias, which are associated with increased automaticity and decreased atrioventricular conduction (e.g., atrial flutter and atrial fibrillation with high-degree AV block, nonparoxysmal atrial tachycardia with block, accelerated junctional rhythms, and/or bidirectional ventricular tachycardia).[21] |
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