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 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. Most hemodynamically unstable patients are treated with 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. Long-term management may involve antiarrhythmic medication or curative catheter ablation.

The following are discussed in detail separately: “Management of tachycardia,” “Atrial fibrillation with rapid ventricular response” and “Atrial flutter.“

Tachycardias

• 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 originating in the following: [2][3]
    • Sinus node
    • AV node
    • Atrial myocardium
    • Bundle of His above the bifurcation
  • Includes:
    • Reentrant tachycardias: e.g., AVNRT, AVRT
    • Atrial tachycardias: focal AT, multifocal AT, Afib, Atrial flutter
    • Inappropriate sinus tachycardia
    • Junctional tachycardia
  • Paroxysmal SVT (PSVT)
    • Any SVT with a narrow QRS complex and an abrupt onset
    • Most commonly caused by AV nodal reentry

Conduction abnormalities

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 reentrant tachycardias 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

Treat unstable SVTs (except for MAT and junctional tachycardia) with electrical cardioversion.

If there is doubt about the supraventricular origin of a wide complex tachycardia, treat it as ventricular tachycardia.

• 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
  • Use of certain medications or illicit drugs [10]

Epidemiological data refers to the US, unless otherwise specified.

• 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 [2][11]
  • 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) [12]

Signs of unstable tachycardia due to SVT include acute pulmonary edema, hypotension, severe chest pain, and altered mental status.

Approach

• Confirm the rhythm with a 12-lead ECG in all patients with new or recurrent SVT.
• Investigate the underlying cause using TTE and laboratory studies in patients with new or evolving diagnoses.
• Consider ambulatory ECG for with an uncertain diagnosis of paroxysmal SVT.
• Consider EP study for uncertain diagnoses that may also require catheter ablation.
• Consider cardiac stress testing for patients with ASCVD risk factors, suspected WPW, or provoked arrythmias.

Once the diagnosis is confirmed by ECG, do not delay acute management of SVT for additional investigations.

Initial diagnostics [11]

• 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: to assess for hyperthyroidism and hypothyroidism
  • BMP: Electrolyte abnormalities (e.g., potassium disorders, calcium imbalances, hypomagnesemia) can cause arrhythmias.
• TTE [13]
  • Initial imaging modality of choice
  • Potential findings include:
    • Underlying structural or ischemic heart disease
    • Heart failure in prolonged tachycardia
    • Atrial thrombus (rare)

Additional diagnostics [11]

Consider the following tests depending on patient risk factors.

• Prolonged electrocardiography [14]
  • Indications: patients with infrequent symptoms
  • Options
    • 24-hour ambulatory 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.
• EP study: with or without catheter ablation (Gold standard for diagnosing SVT; can be used for treatment)
  • 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
• Cardiac stress testing: indicated in patients with ASCVD risk factors

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.

• Sinus tachycardia: most common differential; often secondary to physiologic stress [15]
• Other narrow complex tachycardias (NCTs): See also “Differential diagnosis of SVT.”
• Other wide complex tachycardias (WCTs): See also “SVT with aberrancy vs. Vtach.”

Patients with SVT symptoms are frequently misdiagnosed with anxiety or panic disorders. Rule out paroxysmal tachycardia before making a psychiatric diagnosis to avoid anchoring bias.

The differential diagnoses listed here are not exhaustive.

Acute management of SVT [2][8]

The underlying type of SVT is often unclear at presentation. A definitive diagnosis is not required to begin acute management of tachycardia following ACLS algorithms.

• Initiate continuous cardiac monitoring and ECG recording for all patients.
• Keep a defibrillator at the bedside in case rhythm and/or hemodynamics change (e.g., new Vfib).

Pulseless patients

• Start CPR.
• Defibrillate any WCT (i.e., possible Vtach); otherwise, treat as PEA.

Patients with unstable tachycardia with pulse

• Perform synchronized electrical cardioversion for most SVTs.
• Cardioversion will likely be ineffective for multifocal AT and junctional tachycardia.

Stable patients

Empiric management depends on QRS width and rhythm.

• SVT of unclear origin: See “Management of undifferentiated SVT.”
• Regular NCT (e.g., AVNRT, orthodromic AVRT, focal AT)
  • Typically includes vagal maneuvers and adenosine
  • See “Management of stable regular NCT.”
• Irregular NCT (e.g., multifocal AT, Afib)
  • Can include rate control, rhythm control, or management of the underlying cause.
  • See “Management of stable irregular NCT.”
• WCT (e.g., SVT with aberrancy, antidromic AVRT, Afib with WPW)
  • Usually treated with cardioversion
  • AV nodal blockers are best avoided.
  • See “Management of stable WCT”.

Avoid using AV nodal blockers to treat wide complex tachycardias, as they may precipitate Vfib. [16][17]

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 homotopy) 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, focal atrial tachycardia, 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. [18]

Modified Valsalva maneuver [18]

• 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) [19]
• 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 [20]

• Listen first to ensure there are no carotid bruits (if present, select another vagal maneuver). [21]
• 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; may cause presyncope or syncope) → 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 [22]

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

Pharmacotherapy

• See “Management of undifferentiated SVT” for a general algorithm.
• Definitive pharmacotherapy depends on the underlying rhythm.
  • See “Treatment of AVNRT.”
  • See “Treatment of AVRT.”
  • See “Treatment of WPW.”
  • See “Treatment of focal AT.”
  • See “Treatment of MAT.”
  • See “Management of Afib with RVR.”
  • See “Treatment of junctional tachycardia.”

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)

Further management and disposition [23]

• Successful cardioversion: Consider discharge after a period of monitoring if clinically stable and no other acute medical issues.
• Unsuccessful cardioversion
  • Urgent cardiology consult for specialist treatment, e.g., a second dose of cardioversion, antiarrhythmic infusion
  • Admit to critical care unit for further management.
• Other indications for hospital admission
  • Possible ischemic event
  • Any VT or unstable rhythm (even if terminated)
  • Any LOC
  • Possible preexcitation syndrome

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 [24][25]

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

• Unstable tachycardia with a pulse: electrical cardioversion
• Stable with narrow QRS complex: See “Management of stable regular NCT.”
  • 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)
• Stable with wide QRS complex (suspected aberrant conduction): See “Management of stable WCT.”
  • Established diagnosis of AVNRT: AV nodal blocking agents are generally safe. [26]
  • 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][27]
• 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) [28]
    • Propranolol PLUS diltiazem [28]
    • OR flecainide [2][28]

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. [11]

Pathophysiology [11][29]

• Orthodromic AVRT (most common; 90–95%) [30]
  • 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][31]
• Antidromic AVRT (rare; 5–10%) [32]
  • 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

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

• Unstable tachycardia with a pulse: electrical cardioversion
• Stable orthodromic AVRT: See “Management of stable regular NCT.”
  • 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)
• Stable antidromic AVRT (wide QRS complex): See “Management of stable WCT.”
  • 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
• Pharmacotherapy 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 [35]

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 [36]
• ∼ 10% of patients have multiple accessory pathways (more common with coexisting structural heart disease). [35][37]
• May be asymptomatic (WPW pattern) or associated with arrhythmias (WPW syndrome), including: [36]
  • AVRT (most common; 80%)
  • Atrial fibrillation (15–35%; incidence increases with age)
  • Atrial flutter (5%)
  • Others (rare): MAT, focal atrial tachycardia, ventricular fibrillation

Epidemiology

• The prevalence of WPW pattern is 0.1–0.2% in the general population and 0.55% in first-degree relatives. [38]
• A proportion of these cases is due to familial WPW syndrome, a rare autosomal-dominant genetic disorder that causes conduction abnormalities and hypertrophic cardiomyopathy. [39]
• ♂ > ♀ [40]
• Symptoms typically develop at 20–40 years of age. [36]

ECG findings in WPW

• While in sinus rhythm, a preexcitation pattern may be present. [9]
  • 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 [36]
  • See “ECG findings in AVRT.”
  • See “WPW with atrial fibrillation.”

Treatment of WPW [8]

Acute episodes

• Unstable tachycardia with a pulse: electrical cardioversion
• Stable: Assess underlying rhythm.
  • Regular NCT (i.e., orthodromic AVRT): vagal maneuvers, adenosine; see “Management of stable regular NCT”
  • WCT: irregular (e.g., underlying Afib or multifocal AT) OR regular (underlying Aflut or focal AT) [8]
    • Avoid AV nodal blocking agents and vagal maneuvers (may precipitate Vtach or Vfib)
    • Rhythm control measures (i.e., cardioversion or IV procainamide) are the safest treatment option.
    • See “Management of stable WCT” and ”Management of preexcited Afib.”

Avoid AV nodal blocking agents and vagal maneuvers for the following preexcited tachycardias: Afib, Aflut, focal AT, and MAT.

Long-term management of WPW [2][40]

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

Risk stratification in WPW syndrome [41]

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 [42]
• 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 [41]

High-risk patients

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

Low-risk patients [2]

• Asymptomatic: usually no treatment required
• Symptomatic
  • First-line: catheter ablation
  • Second-line (e.g., ablation contraindicated or declined): long-term antiarrhythmics in consultation with a cardiologist
    • No structural heart disease: Consider flecainide OR propafenone. [2]
    • Structural heart disease
      • Consider dofetilide OR sotalol
      • Use AV nodal blockers with caution.

Definition

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

Etiology [15]

• Idiopathic: most common
• Chronic conditions: hypertension, heart disease, cardiomyopathy
• Acute conditions: myocardial infarction, infection, alcohol poisoning
• Drug toxicity
  • Digoxin (most common)
  • Theophylline
  • Cocaine

Pathophysiology [43][44]

• Possible mechanisms [45]
  • 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 [46]
• Key features
  • Originates outside of the SA node
  • Abrupt onset
  • Can be sustained or nonsustained
  • Worsened by adrenergic activity

ECG findings in focal AT [2][46]

• Heart rate 100–250/minute [46]
• 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. [8]

Treatment of focal AT [2]

Acute episodes

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

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

Avoid AV nodal blockers in patients with preexcited focal atrial tachycardia (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, focal atrial tachycardia-induced cardiomyopathy) or those who prefer it as an alternative to pharmacotherapy [47][48]
• Pharmacotherapy
  • 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 [49]
• Other
  • Management of underlying conditions (see “Etiology”)
  • Anticoagulation: not indicated in the absence of coexisting arrhythmia.

Definition

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

Etiology [50][51]

• Severe underlying conditions (e.g., heart failure and pulmonary diseases, such as COPD or pneumonia)
• Drugs (e.g., theophylline, isoproterenol) [52]
• Electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia)
• Other: hypoxia, hypercapnia, acidosis, dysautonomia

Pathophysiology [53]

• Multifocal origin of pacemaker activity
• Mechanism remains unclear [50]
• Often associated with right atrial enlargement

ECG findings in MAT [50]

• 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][11][54]

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 [55]
  • 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. [17]
• 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][54]

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 [11]
  • Digoxin toxicity
  • Catecholamine use [56]
  • COPD
  • Hypokalemia

Pathophysiology [2][11]

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

ECG findings in junctional tachycardia [2][57]

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 QRS 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 pharmacotherapy
  • 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.