Supraventricular tachycardia

Supraventricular tachycardias (SVTs) are a group of tachyarrhythmias arising from abnormalities in pacemaker activity and/or conduction involving myocytes of the atria and/or AV node. Types of SVT include atrioventricular nodal reentrant tachycardia (AVNRT; approx. two-thirds of cases), atrioventricular reciprocating (or reentrant) tachycardia (AVRT), focal atrial tachycardia (FAT), multifocal atrial tachycardia (MAT), and junctional tachycardia. AVNRT and AVRT are caused by abnormal conduction circuits that form an unending loop of conduction referred to as reentry. These reentry circuits can occur between parallel pathways within the AV node (as in AVNRT) or between the AV node and an accessory pathway of atrioventricular conduction (as in AVRT). Atrial tachycardias (FAT and MAT) and junctional tachycardias are usually the result of abnormal or ectopic pacemaker activity and do not involve reentry. The most common congenital accessory pathway (bundle of Kent) is seen in Wolff-Parkinson-White (WPW) syndrome and can cause ventricular preexcitation, in which supraventricular impulses bypass the AV node and are abnormally conducted to the ventricles, leading to a characteristic preexcitation pattern on ECG and a specific subset of preexcited tachyarrhythmias. SVTs have similar clinical features (typically paroxysms of tachycardia with dizziness, dyspnea, chest pain, or syncope) that may be self-limiting or progress to hemodynamic instability and sudden cardiac death. Common diagnostic steps include obtaining the patient's history and a 12-lead ECG to identify the type of SVT. The paroxysmal nature of SVTs means that continuous recording with a Holter monitor is often needed to confirm the diagnosis; in some cases, invasive electrophysiological studies (EP studies) may also be indicated. Management of SVT should be tailored to the patient. Hemodynamically unstable patients should undergo emergency cardioversion, while patients with acute SVT episodes that are hemodynamically stable may benefit from vagal maneuvers and/or antiarrhythmic medication (typically intravenous), depending on the underlying rhythm (see “Management of tachycardia”). Long-term management may involve antiarrhythmic medication or curative catheter ablation.

While atrial fibrillation and atrial flutter are types of supraventricular tachycardia, they are usually considered separately (see “Atrial fibrillation”).

General

• Paroxysmal tachycardia: an arrhythmia with an abrupt onset and termination that can last from seconds to days (e.g., AVNRT) ^[1]
• Supraventricular tachycardia (SVT)
  • A tachycardia generated in one of the following structures: ^[2][3]
    • Sinus node
    • AV node
    • Atrial myocardium
    • Bundle of His above the bifurcation
  • Includes:
    • Atrial tachycardia, including focal atrial tachycardia (FAT) and multifocal atrial tachycardia (MAT)
    • Inappropriate sinus tachycardia
    • AVRT
    • AVNRT
    • Junctional tachycardia
  • While atrial fibrillation and atrial flutter are types of supraventricular tachycardia, they are usually considered separately (see “Atrial fibrillation”).
  • Paroxysmal SVT (PSVT)
    • Any SVT with a narrow QRS complex and an abrupt onset
    • Most commonly caused by AV nodal reentry
• Reentry
  • A mechanism that causes an impulse in the heart (which would normally die out) to return via conduction circuit to reexcite the tissue, leading to an extra beat (or, if it continues, an ongoing tachyarrhythmia) ^[4][5]
  • Examples of tachyarrhythmia with underlying reentry include AVNRT and AVRT.

• Aberrant conduction ^[6][7]
  • Abnormal conduction of a myocardial impulse due to, e.g., a bundle branch block, conduction delay, or (according to some definitions) an accessory pathway
  • Results in a wide QRS complex, as the depolarization of the ventricle happens more slowly (from myocyte to myocyte) rather than through rapidly conducting Purkinje fibers
  • SVT with aberrant conduction can have a very similar appearance to ventricular tachycardia (see “Differentiating between VT and SVT” in “Management of tachycardia”).

Preexcitation

• Ventricular preexcitation: the premature activation of the ventricles by an accessory pathway
• Accessory pathway: an abnormal electrical connection outside of the AV node that allows for the propagation of impulses between the myocardium of the atrium and the ventricle; usually congenital, e.g., the bundle of Kent (see “Wolff-Parkinson-White syndrome”), but also rarely acquired ^[2]
• Preexcitation syndrome: the combination of ventricular preexcitation and associated tachyarrhythmias (e.g., AVRT, atrial flutter, atrial fibrillation, focal atrial tachycardia); WPW syndrome is the most common example
• Preexcitation pattern: the typical ECG appearance of ventricular preexcitation due to abnormal conduction and depolarization of the ventricles

Epidemiology ^[2]

• Prevalence of SVT: ∼ 2.3 per 1000
• Incidence of PSVT: 36 per 100,000 per year
• Sex: ♀ > ♂ (2:1)
• Risk factors
  • Underlying structural heart disease
  • Family history of SVT or sudden cardiac death

Clinical features ^[2][8]

• Palpitations
• Fatigue
• Chest pain or discomfort
• Dyspnea
• Dizziness or presyncope
• Syncope (uncommon; occurs more frequently in older adults)
• Diaphoresis
• Additional features seen more commonly in AVNRT
  • Feeling of neck pounding/shirt flapping (thought to be due to cannon A waves)
  • Urinary urgency and polyuria
• Symptom onset and resolution are typically abrupt, in contrast to sinus tachycardia (in which onset and resolution are more gradual).
• Sudden cardiac death (rare)

For all patients with a new SVT, a 12-lead ECG, basic laboratory studies, and a TTE should be obtained. Further testing depends on patient risk factors but may include exercise tolerance testing or myocardial ischemia testing. An EP study can be used for simultaneous diagnosis and treatment. ^[8]

Initial diagnostics ^[8]

• ECG: A 12-lead ECG should be performed in every patient with suspected SVT.
  • Typical features during an episode include:
    • Regular rhythm; may be irregular in MAT or atrial fibrillation
    • Rate > 100/minute (typically exceeds > 150/minute) ^[2]
    • Narrow QRS complex (< 120 ms); a wide complex may be seen with aberrant conduction
  • If findings are inconclusive, consider recording the heart's electrical activity for 24–48 hours (e.g., Holter monitor, event recorder)
• Laboratory studies: to identify underlying conditions
  • CBC: can show signs of anemia or infection
  • TSH: investigation for hyperthyroidism or hypothyroidism
  • BMP: Electrolyte abnormalities (e.g., disorders of potassium balance or disorders of calcium balance) can cause arrhythmias.
• TTE ^[9]
  • Initial imaging modality of choice
  • Potential findings include:
    • Underlying structural or ischemic heart disease
    • Heart failure in prolonged tachycardia
    • Atrial thrombus (rare)

Additional diagnostics ^[8]

• Prolonged electrocardiography ^[10]
  • Indications: patients with infrequent symptoms
  • Options
    • 24-hour ECG: if symptoms are frequent and likely to be captured in a 24-hour period
    • Event recorder: if patients have infrequent and mild symptoms
    • Implantable loop recorder: for patients with infrequent and severe symptoms that impede their ability to activate the recorder
  • Data is downloaded from the device, allowing for an analysis of rhythm and an evaluation of whether symptoms correlate with arrhythmias.
• Electrophysiological study (EP study): with or without catheter ablation (Gold standard for diagnosing SVT)
  • Indications include: uncertain diagnosis, planned ablation, risk stratification
  • Disadvantages: invasive procedure, involves radiation
• Exercise tolerance testing: indicated in preexcitation (e.g., risk stratification in WPW syndrome) and suspected catecholamine-dependent arrhythmias
• Myocardial ischemia testing: indicated in patients at risk for coronary artery disease (e.g., men > 40 years of age, postmenopausal women)

Differential diagnoses

Although differentiating between types of SVT can be challenging and may require EP studies to confirm the diagnosis, some ECG features may help to differentiate diagnoses.

• Tachycardias can be categorized as regular and irregular as well as narrow complex and wide complex (see “Differential diagnosis of tachycardia”).
• If the ECG shows a narrow complex regular tachycardia, see “Differential diagnosis of SVT.”
• If there is a wide complex tachycardia with suspicion for an SVT with aberrancy, see “Brugada criteria” to help distinguish SVT with aberrancy from ventricular tachycardia.

Patients with SVT symptoms are frequently misdiagnosed with anxiety or panic disorders. Paroxysmal tachycardia should be ruled out before making a psychiatric diagnosis to avoid anchoring bias.

For clinically oriented algorithms of acute management of tachycardia see “Management of unstable tachycardia with a pulse” and “Management of undifferentiated SVT”. This section provides an overview of the management of SVT. The dedicated sections of this article (e.g., AVNRT) contain more specific information.

General principles

• Pulseless patients require CPR.
• Patients with unstable tachycardia with pulse require emergency electrical cardioversion.
• Stable, regular narrow-complex tachycardia
  • Vagal maneuvers are the initial procedure in many SVTs.
  • Medical therapy is important for acute and longterm treatment
  • Catheter ablation is a curative treatment option.
• Stable wide-complex tachycardia
  • Differentiation between ventricular and supraventricular tachycardia with aberrancy can be difficult
  • Follow the algorithm of management of stable wide-complex tachycardia
• ECG should be recorded throughout acute management because treatment for SVT may unmask an alternative diagnosis.
• A defibrillator should be at hand in case new dysrhythmias emerge (e.g., V-fib).

Vagal maneuvers

• Definition: a set of actions performed to decrease the heart rate through physical stimulation of the vagus nerve
• Physiology: slows the conduction through the AV node (negative dromotropy) and may terminate the arrhythmia
• Clinical application
  • An important first step in acute management of most SVTs
  • Avoid in ventricular preexcitation (due to an accessory pathway) with any of the following underlying tachyarrhythmias: atrial flutter, atrial fibrillation, FAT, and MAT.

Valsalva maneuver

• Definition: forceful exhalation against a closed airway
• Technique: four phases
  • Phase 1 (start strain) and phase 2 (continued strain): ↑ intrathoracic pressure → ↓ venous return/ventricular preload → ↓ cardiac output
  • Phase 3 (release of strain) & phase 4 (recovery phase): ↓ intrathoracic pressure → ↓ afterload → ↑ stroke volume → ↑ cardiac output
• Applications
  • Treatment of supraventricular tachycardia (e.g., AVNRT)
  • Evaluate conditions of the heart
    • Augments heart sounds on physical exam (e.g., earlier click in mitral valve prolapse and louder murmur in hypertrophic obstructive cardiomyopathy)
    • Decreases heart sounds intensity (most valve stenosis or regurgitation murmurs)
  • Test for hernia or varicocele (increased intraabdominal pressure → bulging)
  • Diagnosis of urinary stress incontinence (urine leakage during the maneuver)
  • Measure to normalize middle-ear pressure (e.g., in diving)
• Contraindications: include recent myocardial infarction, aortic stenosis, and glaucoma. ^[11]

Modified Valsalva maneuver ^[11]

• Patient sits in a semirecumbent position
• Blows into a 10 mL syringe for 15 seconds (moving the plunger up achieves a strain of ∼ 40 mm Hg) ^[12]
• Afterwards the patient is laid supine and the legs are passively elevated to 45° for 15 seconds.
• Return to the semirecumbent position for 45 seconds before reassessing rhythm

Carotid sinus massage ^[13]

• Listen first to ensure there are no carotid bruits (if present, select another vagal maneuver). ^[14]
• Apply steady pressure at the level of the carotid bifurcation on one side for 10–15 seconds.
• If there is no response, the process can be repeated using the contralateral carotid sinus.
• Carotid sinus massage stimulates the baroreceptors → stimulates CN IX (specifically the branch of the glossopharyngeal nerve to the carotid sinus) → nerve impulse transmission to the medulla (nucleus tractus solitarius) → efferent signals from the medulla to the myocardium via the vagus nerve (parasympathetic supply) → ↓ AVN conduction, ↓ heart rate, ↓ contractility, and vasodilation (↓ blood pressure) → termination of arrhythmia

Diving reflex

• Traditionally involves immersing the head in cold water, which is uncomfortable for most patients
• Can be limited to applying a bag of ice water to the face (particularly the forehead and nasal area) for ∼ 10 seconds ^[15]

Do not simultaneously apply bilateral carotid artery pressure because this can impede cerebral blood flow.

Medical therapy

See “Management of undifferentiated SVT” for a clinically oriented algorithmic approach and the dedicated sections of this article (e.g., “Treatment of AVNRT”) for more specific information.

Catheter ablation

• Description
  • Radiofrequency or cryothermal energy is applied via a cardiac catheter to eliminate aberrant pathways or impulses from arrhythmogenic foci.
  • Usually performed in conjunction with an EP study
• Indications ^[2]
  • Curative therapy in AVNRT, AVRT with concealed pathway, or drug-refractory AT
  • Symptomatic patients who want to avoid long-term drug therapy (especially younger patients)
  • Asymptomatic patients with special lifestyle considerations (e.g., pilots)

Definition

• A tachyarrhythmia caused by a dysfunctional AV node that contains two electrical pathways, which form a reentry circuit

Pathophysiology

• The AV node contains two electrical pathways, one fast and one slow → the electrical impulse circles around the AV node within both pathways → a continuous circuit conducts impulses to the ventricles → tachycardia
• Approx. 90% of cases are due to anterograde conduction across the slow-conducting pathway and retrograde conduction in the fast pathway (although the reverse is possible).

ECG findings in AVNRT ^[16][17]

• ECG may be normal between episodes of tachycardia. Findings may be indistinguishable from those of orthodromic AVRT and include:
  • Heart rate typically 150–220/minute
  • Typically narrow QRS complexes (a wide QRS complex may be seen if there is aberrant conduction)
  • Regular rhythm
  • P wave is typically not visible (it falls in or is "buried" in the QRS complex)

Treatment of AVNRT

Acute management

• Pulseless: Start CPR (see “ACLS”).
• Hemodynamically unstable: electrical cardioversion (see “Management of unstable tachycardia with a pulse” for details)
• Hemodynamically stable with narrow QRS complex (see “Management of undifferentiated SVT” for details)
  • First step: vagal maneuvers
  • If SVT persists: intravenous medical therapy
    • First-line: adenosine (if no contraindications to adenosine present)
    • Other options: calcium channel blockers (e.g., verapamil, diltiazem) or beta blockers (e.g., metoprolol)
• Hemodynamically stable with wide QRS complex (suspected aberrant conduction): See “Management of stable, wide-complex tachycardia”
  • Established diagnosis of AVNRT: AV nodal blocking agents are generally safe. ^[18]
  • Uncertain diagnosis of AVNRT: Avoid AV nodal blocking agents.

Long-term management

• Infrequent and mild episodes may be managed with self-guided vagal maneuvers.
• First line: percutaneous catheter ablation of the slow pathway ^[2][19]
• Second line: pharmacological therapy ^[2]
  • Daily medication options
    • Beta blockers, e.g., propranolol ^[2]
    • Verapamil ^[2]
    • Diltiazem ^[2]
  • Pill-in-the-pocket regimens (off-label) ^[20]
    • Propranolol PLUS diltiazem ^[20]
    • OR flecainide ^[2][20]

Definition

• A tachyarrhythmia caused by an accessory pathway that creates a reentrant circuit with the AV node
• Wolff-Parkinson-White syndrome is a common cause of AVRT but they are not synonymous. ^[8]

Pathophysiology

• Accessory pathways may be manifest or concealed. ^[8][21]
  • Manifest pathways
    • Can conduct in both anterograde (atrium to ventricle) and retrograde (ventricle to atrium) directions
    • Anterograde conduction is more common and leads to preexcitation seen on the ECG in sinus rhythm. ^[21]
  • Concealed pathways
    • Can conduct only in a retrograde direction
    • Not visible on ECG in sinus rhythm
• There are two types of atrioventricular reciprocating tachycardia; the direction of the impulses help distinguish between them.
  • Orthodromic AVRT: most common (90–95%) ^[22]
    • Antegrade conduction (atrium → ventricle) through AV node (narrow QRS complex); retrograde conduction (ventricle → atrium) through accessory pathway
    • Can occur with a concealed or manifest pathway
    • On rare occasions, occurs almost incessantly as a result of a concealed, posteroseptal pathway (permanent junctional reciprocating tachycardia; PJRT) ^[2][23]
  • Antidromic AVRT: rare (5–10%) ^[24]
    • Antegrade conduction (atrium → ventricle) through accessory pathway; retrograde conduction (ventricle → atrium) through AV node
    • Wide QRS complex, as ventricular depolarization happens slowly from myocyte to myocyte rather than through the rapid His-Purkinje system
    • Only occurs with a manifest pathway

Do not confuse atrioventricular reentrant (or reciprocating) tachycardia (AVRT) with atrioventricular nodal reentrant tachycardia (AVNRT)! AVRT is caused by an accessory pathway, whereas in AVNRT there are two functional pathways within the AV node.

ECG findings

Treatment of AVRT

Acute episodes

• Pulseless: Start CPR (see “ACLS”).
• Hemodynamically unstable: electrical cardioversion (see “Management of unstable tachycardia with a pulse”)
• Hemodynamically stable orthodromic AVRT (see “Management of stable, regular narrow-complex tachycardia”)
  • First step: vagal maneuvers
  • If SVT persists: intravenous medical therapy
    • First-line: adenosine (if there are no contraindications to adenosine)
    • Other options: calcium channel blockers (e.g., verapamil, diltiazem) or beta blockers (e.g., metoprolol)
• Hemodynamically stable antidromic AVRT (wide QRS complex): See “Stable, wide-complex tachycardia”
  • Established diagnosis of AVRT: AV nodal blocking agents are safe.
  • Uncertain diagnosis of AVRT: Avoid AV nodal blocking agents.

Long-term management ^[2]

• First-line: catheter ablation
• Medical therapy for AVRT: for patients who are not candidates for ablation or who prefer medication
  • Treatment depends on whether a preexcitation pattern is seen on ECG (options include sotalol, flecainide; , and propafenone). ^[2]
  • Preexcitation pattern is visible.
    • Known heart disease: sotalol OR dofetilide
    • No known heart disease: flecainide OR propafenone
  • Preexcitation pattern is not visible.
    • CCBs: verapamil OR diltiazem
    • Beta blockers: propranolol OR metoprolol
• Alternative: : Consider amiodarone if no other treatments are effective or if all are contraindicated.

Definitions

• Wolff-Parkinson-White syndrome: (WPW): a congenital condition characterized by intermittent tachycardias and signs of ventricular preexcitation on ECG, both of which arise from an accessory pathway known as the bundle of Kent
• Wolff-Parkinson-White pattern: characteristic signs of ventricular preexcitation on ECG with no evidence of arrhythmia and no reported symptoms ^[27]

Pathophysiology

• A congenital accessory pathway, the bundle of Kent, connects the atria and ventricles, bypassing the AV node and leading to ventricular preexcitation.
• May be associated with structural abnormalities of the heart, in particular Ebstein anomaly ^[28]
• ∼ 10% of patients have multiple accessory pathways (more common with coexisting structural heart disease). ^[27][29]
• May be asymptomatic (WPW pattern) or associated with arrhythmias (WPW syndrome), including: ^[28]
  • AVRT (most common; 80%)
  • Atrial fibrillation (15–35%; incidence increases with age)
  • Atrial flutter (5%)
  • Others (rare): MAT, FAT, ventricular fibrillation

Epidemiology

• The prevalence of WPW pattern is 0.1–0.2% in the general population and 0.55% in first-degree relatives. ^[30]
• A proportion of these cases is due to familial WPW syndrome, a rare autosomal-dominant genetic disorder that causes conduction abnormalities and hypertrophic cardiomyopathy. ^[31]
• ♂ > ♀ ^[32]
• Symptoms typically develop at 20–40 years of age. ^[28]

ECG findings in WPW

• While in sinus rhythm, a preexcitation pattern may be present. ^[33]
  • Short PR interval
  • ECG delta wave: a slurred upstroke at the start of the QRS complex, secondary to preexcitation
  • Widened QRS
• Can show any of the arrhythmias associated with WPW ^[28]
  • See “ECG findings in AVRT.”
  • WPW with atrial fibrillation or flutter
    • Heart rate may be very high (> 200–250/minute) because impulses from the atria are transmitted via the accessory pathway directly to the ventricles, bypassing the AV node. ^[34]
    • Wide QRS complexes are commonly seen because of ventricular preexcitation.
    • Appearance may be very similar to that of polymorphic ventricular tachycardia ^[35]

Treatment of WPW

Acute episodes

• Pulseless: Start CPR (see “ACLS”).
• Hemodynamically unstable: electrical cardioversion (see “Management of unstable tachycardia with a pulse”)
• Stable: Assess underlying rhythm.
  • Narrow-complex tachycardia (i.e., orthodromic AVRT associated with WPW, including Afib, atrial flutter, FAT, and MAT):
    • AV nodal blocking agents and vagal maneuvers are contraindicated (may precipitate ventricular tachycardia or V-fib)
    • Rhythm control measures (i.e., cardioversion or IV procainamide) are the safest treatment option.
    • See “Management of stable, regular narrow-complex tachycardia” for more details on specific management.
  • Wide-complex regular or irregular tachycardia: See “Management of stable, wide-complex tachycardia.”

AV nodal blocking agents and vagal maneuvers are contraindicated in patients with ventricular preexcitation and the following underlying tachyarrhythmias: Afib, atrial flutter, FAT, and MAT.

Long-term management ^[2][32]

Management of WPW pattern and WPW syndrome depends on underlying risk factors and patient preference.

Risk stratification in WPW syndrome ^[36]

Risk stratification is determined by a cardiologist based on clinical, ECG, and electrophysiological parameters.

• Concerning clinical features
  • Syncope
  • Associated atrial fibrillation, atrial flutter, or atrial tachycardia
  • Aborted sudden cardiac death
• Dynamic ECG testing: e.g., ambulatory Holter monitoring or exercise stress testing to assess for evidence of intermittency or loss of preexcitation ^[37]
• EP studies
  • Indicated in patients with:
    • Concerning clinical features
    • No evidence of intermittency or loss of preexcitation signs
    • High-risk occupations (e.g., pilots, athletes)
  • Allows the length of the refractory period to be determined ^[36]

High-risk patients

Catheter ablation of the accessory pathway should be offered to all patients. ^[2]

Low-risk patients ^[2]

• Asymptomatic patients: usually no treatment required
• First-line treatment for symptomatic patients: catheter ablation
• Second-line treatment for symptomatic patients: long-term pharmacotherapy ^[2]
  • Known structural heart disease
    • Nondihydropyridine CCBs: verapamil OR diltiazem ^[2]
    • OR beta blockers: metoprolol tartrate OR propranolol ^[2]
    • OR class III antiarrhythmics: amiodarone OR sotalol ^[2]
  • If there is no associated heart disease, class IC antiarrhythmics can be used: flecainide OR propafenone. ^[2]

Definition

• Focal atrial tachycardia (FAT): a supraventricular tachycardia that arises from a localized atrial focus outside of the SA node ^[2]
• Atrial tachycardia (AT): an umbrella term for FAT and multifocal atrial tachycardia (MAT) that is often used synonymously with FAT

Etiology ^[38]

• Most commonly occurs in the absence of underlying disease (idiopathic)
• Chronic conditions: hypertension, heart disease, cardiomyopathy
• Acute conditions: myocardial infarction, infection, alcohol poisoning
• Drug toxicity
  • Digoxin (most common)
  • Theophylline
  • Cocaine

Pathophysiology ^[39][40]

• Mechanisms ^[41]
  • Triggered activity: a result of early afterdepolarizations (EAD) or delayed afterdepolarization (DAD)
  • Microreentry: slow conduction at discrete regions of fibrotic cardiac tissue
  • Enhanced automaticity: acceleration of a normal automatic pacemaker ^[42]
• Key features
  • Originates outside of the SA node
  • Abrupt onset
  • Can be sustained or nonsustained
  • Worsened by adrenergic activity

ECG findings ^[2][42]

• Heart rate 100–250/minute ^[42]
• Regular rhythm
• Can have 1:1 or 2:1 AV conduction
• P wave
  • Typically visible in 2:1 AT
  • May be hidden by the QRS complex or T wave in 1:1 AT
  • The morphology depends on the site of origin but remains constant.
  • An isoelectric baseline is present between P waves.
• QRS complex: morphology does not vary
  • Narrow complex: most common
  • Wide QRS complex may be present in SVT with aberrant conduction.

An isoelectric baseline between P waves can help distinguish focal AT from atrial flutter. ^[43]

Treatment ^[2]

Acute episodes

Episodes of FAT are most commonly self-limiting and asymptomatic, in which case they do not require treatment.

• Pulseless: Start CPR (see “ACLS”).
• Hemodynamically unstable: electrical cardioversion (see “Management of unstable tachycardia with a pulse” for details)
• Hemodynamically stable with narrow QRS complex (see “Management of undifferentiated SVT” for details)
  • First step: vagal maneuvers
  • If SVT persists: intravenous medical therapy
    • First-line if there are no contraindications to adenosine and diagnosis of FAT is not established: adenosine
    • First-line if diagnosis of FAT is established: calcium channel blockers (e.g., verapamil, diltiazem) or beta blockers (e.g., metoprolol)
• Hemodynamically stable with wide QRS complex (suspected aberrant conduction): See “Stable, wide-complex tachycardia”
  • Preexcited FAT ruled out: AV nodal blocking agents are generally safe.
  • Preexcited FAT possible: Avoid AV nodal blocking agents.
• Identify and treat acute reversible underlying conditions (see “Etiology” above).

Avoid AV nodal blockers in patients with preexcited FAT (e.g., due to WPW) because they can trigger ventricular arrhythmias.

Long-term management

• Catheter ablation: for symptomatic patients who are candidates (e.g., refractory AT, younger age, FAT-induced cardiomyopathy) or those who prefer it as an alternative to pharmacotherapy ^[44][45]
• Medical therapy
  • Beta blockers: e.g., metoprolol
  • CCBs: verapamil OR diltiazem
• A cardiology consultation is required if the following medications are being considered:
  • Class Ic antiarrhythmic drugs : flecainide OR propafenone
  • Class III antiarrhythmic drugs : amiodarone OR sotalol
• Pacemaker implantation: Consider for patients with refractory symptoms after unsuccessful invasive and medical therapy.
• Surgery (e.g., left atrial isolation): less common since the advancement of catheter ablation ^[46]
• Management of underlying conditions (see “Etiology” above)
• Anticoagulation is not indicated in the absence of coexisting arrhythmia.

Definition

• An irregular SVT featuring ≥ 3 morphologies of P waves ^[2]

Etiology ^[47][48]

• Severe underlying conditions (e.g., pulmonary diseases like COPD)
• Drugs (e.g., theophylline, isoproterenol) ^[49]
• Electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia)
• Other: hypoxia, hypercapnia, acidosis, dysautonomia

Pathophysiology ^[50]

• Multifocal origin of pacemaker activity
• Mechanism remains unclear ^[47]
• Often associated with right atrial enlargement

ECG findings ^[47]

• Heart rate 100–200/minute
• Irregularly irregular rhythm
• P waves
  • Three or more varying morphologies
  • Separated by an isoelectric baseline
• Variable PR interval
• QRS complex: morphology does not vary
  • Narrow QRS complex: most common
  • Wide QRS complex may be present in aberrant conduction
• May progress to atrial fibrillation

Do not confuse MAT with atrial fibrillation. In Afib, there are no distinct or organized P waves, whereas in MAT there are distinct P waves with varying morphologies.

Unlike in atrial flutter, in MAT there are distinct isoelectric intervals between P waves.

Treatment of multifocal atrial tachycardia ^[2][8][51]

Treatment of MAT is challenging and specialists should be involved early. Patients often have severe underlying conditions and rhythm control and electrical cardioversion are not effective. For clinically-oriented management algorithms for patients with tachycardia, see “Management of tachycardia”.

• First-line treatment: management of underlying causes ^[52]
  • Manage exacerbations of chronic diseases (see “Etiology” above).
  • Correct reversible conditions, e.g., hypoxemia, acidosis, electrolyte abnormalities.
    • See “Potassium replacement” and “Magnesium replacement.”
    • Discontinue potential offending medications.
  • IV magnesium may be helpful even in patients with normal magnesium levels. ^[53]
• Rate control
  • Beta blockers: e.g., metoprolol
  • Calcium channel blockers : verapamil
• AV node radiofrequency ablation: Consider in refractory MAT.

Avoid AV nodal blockers in patients with preexcited MAT (e.g., due to WPW) because of the risk of ventricular arrhythmias.

Avoid electrical cardioversion and antiarrhythmic drugs (e.g., procainamide, lidocaine, phenytoin), as they are not effective in treating MAT. ^[2][51]

Definition

• A tachyarrhythmia caused by abnormal automaticity of myocytes in the AV node and bundle of His
• There are two possible presentations.
  • Paroxysmal junctional tachycardia (PJT): sudden onset, rapid tachycardia (heart rate > 100/minute)
  • Accelerated AV junctional rhythm (nonparoxysmal junctional tachycardia): gradual onset (and termination) rhythm, which can cause a mild tachycardia (heart rate ∼ 60–100/minute)

Etiology ^[2]

• Paroxysmal junctional tachycardia
  • Most commonly seen in infants with congenital heart disease
  • Following myocardial infarction
  • Transiently during slow pathway ablation in AVNRT
• Accelerated AV junctional rhythm ^[8]
  • Digoxin toxicity
  • Catecholamine use ^[54]
  • COPD
  • Hypokalemia

Pathophysiology ^[2][8]

• Caused by an ectopic focus of abnormal automaticity in the AV node or the proximal bundle of His

ECG findings ^[2][55]

While the rate varies between paroxysmal junctional tachycardia and accelerated AV junctional rhythm, the ECG appearance is otherwise similar.

• Heart rate
  • PJT: > 100/minute
  • Accelerated AV junctional rhythm: typically ∼ 60–100/minute
• Narrow complex
• Regular (occasionally may be irregular)
• P wave is inverted in lead II and can be:
  • Hidden within the QRS complex
  • Immediately before the QRS complex
  • Immediately after the QRS complex
• Short PR interval

Treatment of junctional tachycardia ^[2]

These recommendations are for confirmed junctional tachycardia. For clinically-oriented management algorithms for patients with tachycardia, see “Management of tachycardia.”

• Acute episodes: intravenous medical therapy
  • Beta blockers (e.g., metoprolol )
  • Nondihydropyridine CCBs (e.g., verapamil )
• Long-term management ^[2]
  • Accelerated AV junctional rhythm: Identify and treat the underlying cause (e.g., digoxin toxicity).
  • Paroxysmal junctional tachycardia: medical therapy (e.g., nondihydropyridine CCBs, beta blockers)
    • If there is no structural heart disease, consider flecainide OR propafenone. ^[2]
    • Nondihydropyridine CCBs: verapamil OR diltiazem ^[2]
    • Beta blockers: propranolol OR metoprolol ^[2]
  • Catheter ablation: Consider in selected patients with PJT.