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Supraventricular Tachyarrhythmias


Supraventricular tachycardia

Supraventricular tachycardia (SVT) is a rhythm disturbance with a rate greater than 100 that requires tissue from above the His-Purkinje system to perpetuate. SVT can be regular (e.g., atrioventricular [AV] node reentry), irregular (e.g., atrial flutter [AFL] with variable AV conduction), or irregularly irregular (e.g., multifocal atrial tachycardia [MAT], atrial fibrillation [AF]). SVT can be associated with a narrow QRS complex, a wide QRS complex, or both. When it is associated with a wide QRS complex, preexisting bundle branch block (BBB), tachycardia-dependent (phase 3) BBB (aberrancy), or an accessory pathway will be present. Intermittently wide QRS complexes caused by the Ashman phenomenon are commonly seen in AF and usually have a right bundle branch block (RBBB) pattern due to the long refractoriness of the right bundle branch that is present after long–short RR cycles. There can be a one-to-one atrial to ventricular relationship (such as is commonly seen in AV node reentry tachycardia or AV reentry tachycardia) or a two-to-one or greater relationship (commonly seen in AFL or atrial tachycardia [AT]). SVTs can be sustained, recurrent, and intermittent and/or paroxysmal.

The differential diagnosis for SVT includes sinus tachycardia (appropriate and inappropriate), AF, AFL, AV node reentry tachycardia, AV reentry tachycardia, AT (including multifocal), accelerated junctional tachycardia (JT) (junctional ectopic tachycardia), and sinoatrial (SA) reentry tachycardia. It is important to recognize the type of tachycardia because the need for and type of acute and chronic treatment vary depending on the specific rhythm ( Algorithm 5.1 ).

Algorithm 5.1, Differential diagnosis for adult narrow QRS tachycardia.

Most SVTs are not life-threatening, but they can cause potential serious hemodynamic compromise, including presyncope and syncope, tachycardia-induced cardiomyopathy, congestive heart failure (CHF), and angina; palpitations and other rather nonspecific symptoms can have significant impact on quality of life. The aggressiveness of acute and long-term therapy depends on the perceived seriousness of the problem for the patient, based mainly on hemodynamic response to the arrhythmia. Before treatment, a precise rhythm diagnosis should be actively sought.

Atrial arrhythmias

Atrial Tachycardia

Description ( Algorithm 5.2A and B )

AT ( Fig. 5.1 ) is a less common type of SVT, responsible for 5% to 10% of cases of SVT. AT is suspected when there is a narrow QRS complex SVT with a long RP interval with variable coupling of the QRS to P wave interval or evidence for SVT with AV block. A long RP tachycardia can also occur in an atrioventricular reentrant tachycardia (AVRT) mediated by a slow or decrementally conducting accessory pathway, or atypical atrioventricular nodal reentrant tachycardia (AVNRT).

Figure 5.1, (A) Long RP SVT. This 12-lead ECG with lead V 1 , II, and V 5 rhythm strip shows a regular narrow QRS complex tachycardia (rate: approximately 136 bpm) in which each QRS complex is preceded by a nonsinus P wave (P waves inverted in leads II, III, aVF). These findings are consistent with an atrial tachycardia, but included in the differential diagnosis of this “long RP” SVT is atypical AV node reentry tachycardia (with retrograde slow pathway conduction) and AVRT mediated by a slow-conducting decremental accessory pathway (permanent form of junctional reciprocating tachycardia, PJRT). (B) AT. This ECG tracing shows an AT at a rate of approximately 185 bpm. The P waves are seen just after the QRS and are positive in leads II, III, and aVF, indicating a high-to-low activation pattern.

Algorithm 5.2, (A) Acute treatment of suspected focal atrial tachycardia. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. (B) Ongoing management of focal atrial tachycardia. IV, Intravenous; Pt, patient; SHD, structural heart disease (including ischemic heart disease).

P-wave morphology differs from sinus but can help to predict the origin of the tachycardia. Focal AT can be difficult to distinguish from atrial reentrant tachycardia (ART) on the surface ECG, and an electrophysiology (EP) study may be necessary to distinguish the two.

Several mechanisms can be responsible for AT; it can be difficult to differentiate one mechanism from the others. They can be macroreentrant or of focal origin.

Focal ATs may be triggered by autonomic activity (sympathetic activation), increased automaticity, or triggered automaticity or may be microreentrant. Focal tachycardias may be characterized by their location (e.g., sinus nodal or ectopic to the sinus node). Automatic AT (AAT) is a focal AT that is characterized by a gradual onset (speeding up, warm-up) and gradual offset (slowing), in contrast with ARTs that may have sudden onset after a premature beat, and sudden offset. Triggered ATs may have sudden onset and offset. If they are catecholamine dependent, they may occur with exercise.

Specific pulmonary vein ectopic-triggered tachycardias may be related to effects from the parasympathetic and sympathetic nervous system and from ganglionated plexuses to initiate AF.

Whatever the mechanism of a focal AT, the approach to treatment is similar. If the tachycardia is focal, it can be ablated. Given the difficulty in mechanism differentiation, there is no specific approach to medical therapy should ablation not be first line for a specific patient and also for treatment in the acute phase of the tachycardia.

A unique and very rare form of AT is known as sinoatrial node reentrant tachycardia (SART) ( Fig. 5.2 ). SART appears because of a reentry circuit involving the SA node. The P-wave morphology is the same as or similar to the sinus P wave. This tachycardia tends to be nonsustained and somewhat irregular with a relatively normal PR interval and a consistent P-wave morphology. The tachycardia can respond to autonomic maneuvers, as well as drugs, in particular verapamil, adenosine, digoxin, and less commonly β-adrenergic blockers and amiodarone. SART can be ablated; the ablation point may be in the inferior portion of the SA node as it exits into the crista terminalis.

Figure 5.2, Sinoatrial node reentrant tachycardia.

Reentrant ATs may be due to “macro” reentry around structural or functional barriers in the right and/or left atria, or due to microreentrant circuits. AV block can be present during AT and may result in variable or 2:1 AV conduction. It is useful to look for this because it helps to differentiate this tachycardia from AVNRT and AVRT.

Associated Conditions

Although AT may occur in normal, healthy adults, it can be associated with acute myocardial infarction (MI), acute alcohol intoxication, exacerbation of chronic obstructive pulmonary disease (COPD), electrolyte abnormalities, and digoxin toxicity (especially if accompanied by AV block); this last one is now uncommon given the doses of digoxin in current use. AT due to digoxin can occur with normal serum digoxin levels in older persons, especially if hypokalemia is present. AAT episodes are often transient in young patients but may be more persistent in older patients.

Clinical Symptoms and Presentation

As with other SVTs, symptoms range from mild palpitations to angina or symptoms of heart failure, depending on the presence and severity of underlying heart disease.

Approach to Management

AT can occur as an isolated episode related to, for example, infection and acute alcohol ingestion and does not necessarily require chronic therapy, or it may be frequent and/or recurrent, causing disabling symptoms so that long-term treatment is necessary. Chronic persistent AT can cause tachycardia-induced cardiomyopathy, a reversible form of systolic heart failure caused by chronic rapid heart rates and similar symptoms to other SVTs. Acute therapy generally consists of treating any precipitating factors and terminating with antiarrhythmic drugs. Prevention of recurrences over the long term is typically addressed with drugs or catheter ablation (success rate: 50% to 80%). Asymptomatic or minimally symptomatic patients can usually be managed as outpatients unless tachy-brady syndrome is suspected. If the P wave can be seen and is similar to that in sinus rhythm, SART could be present; the patient may respond acutely to carotid massage, adenosine, a β-adrenergic blocker, calcium channel blocker, or digoxin ( Table 5.1 ).

Table 5.1
Atrial tachycardia therapy
Acute therapy, unstable (hypotension, angina, heart failure symptoms)

  • First line: Synchronized DCC (50-200 J with anesthesia); however, DCC may not convert AT to sinus rhythm, or if sinus rhythm is achieved, it may be transient. Using cardioversion, AT as a mechanism may be difficult to distinguish from other SVTs that respond to cardioversion (e.g., AV nodal reentrant, sinus nodal reentrant, or interatrial or intraatrial reentrant tachycardia). DCC should not be performed if digoxin toxicity is suspected because potentially lethal digoxin toxic rhythms, including VF, can be induced.

  • Second line: IV diltiazem or IV verapamil to control the ventricular response rate.

  • Third line: IV β-adrenergic blocker (e.g., esmolol or metoprolol). β-adrenergic blockers can produce some degree of AV block, thus slowing the ventricular rate, but they are not expected to terminate the atrial rhythm because the rhythm does not depend on the AV node for its maintenance.

    • Similar responses occur in response to IV adenosine but use of adenosine may be useful diagnostically by demonstration of AV block during continued AT. In addition, some focal atrial tachycardias are adenosine dependent and will terminate with this drug.

Digoxin toxicity

  • Digoxin antibody (Digibind) if the patient is unstable or the rhythm is associated with other more malignant arrhythmias such as PVCs or nonsustained or sustained VT.

  • Maintain serum K + > 4.0 mEq/L.

Stable ventricular rate < 120 bpm

  • Ventricular rate control with IV or oral β-adrenergic blockers. Alternate: diltiazem.

  • Tachy-brady or unresponsive to rate control drugs: oral flecainide or propafenone (if normal LV function and no evidence of CAD, sotalol, dofetilide, or amiodarone); if tachy-brady syndrome, permanent cardiac pacing may be required.

  • Because the long-term goal is to achieve and maintain sinus rhythm, especially if symptoms are present, catheter ablation or drug therapy may be helpful.

Stable ventricular rate > 120 bpm

  • May require hospitalization.

  • IV β-adrenergic blocker or calcium channel blocker (diltiazem or verapamil) to control rate, followed by flecainide, propafenone, sotalol, dofetilide, or catheter ablation to terminate AT. If persistent, β-adrenergic blockers can occasionally terminate the arrhythmia, especially in young patients, where AT may be exercise induced.

  • Avoid digoxin if possible.

  • Treat precipitating factors (infection, CHF, digoxin toxicity) when present.

  • Nonresponders: Amiodarone (IV or oral) or catheter ablation (of the tachycardia [first line] or AV junctional ablation and pacemaker [last line]).

Prevention (for patients with persistent risk for AT)

  • Normal heart:

    • 1.

      β-adrenergic blocker.

    • 2.

      Catheter ablation.

    • 3.

      Drug therapy (preferred: class IC; alternate: class III, IA).

  • SHD, normal or near-normal LVEF (> 40%):

    • 1.

      β-adrenergic blocker.

    • 2.

      Catheter ablation or drug therapy (preferred: sotalol; alternate: dofetilide, amiodarone, class IA).

    • 3.

      Catheter ablation.

  • SHD, poor LVEF (< 40%):

    • 1.

      Catheter ablation or drug therapy (dofetilide, amiodarone).

    • 2.

      Catheter ablation. Avoid class IC drugs due to their proarrhythmic potential.

  • Tachy-brady syndrome: Catheter ablation or antiarrhythmic drug; pacemaker implantation if needed for symptomatic bradycardia or to facilitate use of antiarrhythmic drugs.

  • Catheter ablation of the atrial focus or foci is successful in 50% to 70% of ATs, which often originate in the crista terminalis, near the right atrial appendage, near the SA or AV nodes, or near the pulmonary veins; it is the preferred treatment. If unsuccessful and tachycardia-induced cardiomyopathy is present, consider catheter ablation of the AV junction and then placement of a mode-switching dual chamber pacemaker.

MI

  • First line: β-adrenergic blocker if tolerated.

  • Second line: Sotalol or amiodarone.

  • If recurrent episodes, treat for several months as described for chronic prevention (above).

Preoperative/postoperative

  • Stable: Ventricular rate control (see Acute therapy, stable, above).

  • Unstable: Achieve sinus rhythm (see Acute therapy, unstable, above).

  • Transient postoperative: β-adrenergic blocker.

AV, Atrioventricular; AT, atrial tachycardia; CAD, coronary artery disease; DCC, direct current cardioversion; IV, intravenous; LV, left ventricle; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PVCs, premature ventricular contraction; SHD , structural heart disease; VF, ventricular fibrillation.

Automatic Atrial Tachycardia

Description

AAT is a rare type of SVT, responsible for less than 2% to 5% of cases. P-wave morphology differs from sinus but can help to predict the origin of the tachycardia. AAT can be difficult to distinguish from ART on the surface ECG, and an EP study may be necessary to distinguish the two. AAT is characterized by a gradual onset (speeding up) and offset (slowing), in contrast with reentrant tachycardias that may have sudden onset after a premature beat and sudden offset. AV block can be present during AAT and may result in variable or 2:1 AV conduction.

Associated Conditions

Although AAT may occur in normal, healthy adults, it is more often associated with acute MI, acute alcohol intoxication, exacerbation of COPD, electrolyte abnormalities, and digoxin toxicity (especially if accompanied by AV block); this last one is now uncommon given the lower doses of digoxin in current use. AAT can occur with normal serum digoxin levels in older patients, especially if hypokalemia is present. AAT episodes are often transient in young patients but may be more persistent in older patients.

Clinical Symptoms and Presentation

As with other SVTs, symptoms range from mild palpitations to angina or symptoms of heart failure, depending on the presence and severity of underlying heart disease.

Approach to Management

AAT can occur as an isolated episode related to, for example, infection and acute alcohol ingestion and does not require chronic therapy, or it may be frequent and/or recurrent, causing disabling symptoms. Chronic persistent AAT can cause tachycardia-induced cardiomyopathy, a reversible form of systolic heart failure caused by chronic rapid heart rates. Acute therapy generally consists of treating any precipitating factors and terminating with antiarrhythmic drugs. Prevention of recurrences over the long term is typically addressed with drugs or catheter ablation (a success rate of 50%). Asymptomatic or minimally symptomatic patients can be managed as outpatients unless severe tachy-brady syndrome is suspected ( Table 5.2 ).

Table 5.2
Automatic atrial tachycardia therapy
Acute therapy, unstable (hypotension, angina, heart failure symptoms)

  • First line: Synchronized DCC (50-200 J with anesthesia). However, DCC may not convert AAT to sinus rhythm, or, if sinus rhythm is typically achieved, it may be transient. DCC should not be performed if digoxin toxicity is suspected, as potentially lethal digoxin toxic rhythms, including VF, can be induced.

  • Second line: IV diltiazem.

  • Third line: IV β-adrenergic blocker (e.g., esmolol or metoprolol). β-adrenergic blockers can produce some degree of AV block, thus slowing the ventricular rate, but they are not expected to terminate the atrial rhythm since the rhythm does not depend on the AV node for its maintenance.

    • Similar responses occur in response to IV adenosine, but response may be transient.

Digoxin toxicity

  • Digoxin antibody (Digibind) if the patient is unstable or the rhythm is associated with other, more malignant arrhythmias such as PVCs or nonsustained or sustained VT.

  • Maintain serum K + > 4.0 mEq/L.

Stable ventricular rate < 120 bpm

  • Ventricular rate control with IV or oral β-adrenergic blockers. Alternate: diltiazem.

  • If unresponsive to rate control drugs: oral flecainide or propafenone (if normal LV function and no evidence of CAD), sotalol, dofetilide, or amiodarone; if tachy-brady syndrome, permanent cardiac pacing will be required.

  • Because the long-term goal is to achieve and maintain sinus rhythm, especially if symptoms are present, catheter ablation (of the tachycardia itself) or drug therapy may be required.

Stable ventricular rate > 120 bpm

  • May require hospitalization.

  • IV β-adrenergic blocker or calcium channel blocker (diltiazem or verapamil) to control rate, followed by flecainide, propafenone, sotalol, dofetilide, or catheter ablation to terminate AAT. If persistent, β-adrenergic blockers can occasionally terminate the arrhythmia, especially in young patients, where AAT may be exercise induced.

  • Avoid digoxin, if possible.

  • Treat precipitating factors (infection, CHF, digoxin toxicity) when present.

  • Nonresponders: Amiodarone (IV or oral) or catheter ablation (of the tachycardia [first line] or AV junctional ablation and pacemaker [last line]).

Prevention (for patients with persistent risk for AAT)

  • Normal heart:

    • 1.

      β-adrenergic blocker.

    • 2.

      Catheter ablation.

    • 3.

      Drug therapy (preferred: class IC; alternate: class III, IA).

  • SHD, normal or near-normal LVEF (> 40%):

    • 1.

      β-adrenergic blocker.

    • 2.

      Catheter ablation or drug therapy (preferred: sotalol; alternate: dofetilide, amiodarone, class IA).

    • 3.

      Catheter ablation.

  • SHD, poor LVEF (< 40%):

    • 1.

      Catheter ablation or drug therapy (dofetilide, amiodarone).

    • 2.

      Catheter ablation. Avoid class IC drugs due to their proarrhythmic potential.

  • Tachy-brady syndrome: Catheter ablation or antiarrhythmic drug; pacemaker implantation if needed for symptomatic bradycardia or to facilitate use of antiarrhythmic drugs.

  • Catheter ablation of the atrial focus or foci is successful in 50% to 70% of AATs, which often originate in the crista terminalis, near the SA or AV nodes, or near the pulmonary veins; it is the preferred treatment. If unsuccessful and tachycardia-induced cardiomyopathy is present, consider catheter ablation of the AV junction and then placement of a mode-switching dual chamber pacemaker.

MI

  • First line: β-adrenergic blocker if tolerated.

  • Second line: Sotalol or amiodarone.

  • If recurrent episodes, treat for several months as described for chronic prevention (above).

Preoperative/postoperative

  • Stable: Ventricular rate control (see Acute therapy, stable, above).

  • Unstable: Achieve sinus rhythm (see Acute therapy, unstable, above).

  • Transient postoperative: β-adrenergic blocker.

AAT, Automatic AT; AV, atrioventricular; CAD, coronary artery disease; CHF, congestive heart failure; DCC, direct current cardioversion; IV, intravenous; LV, left ventricle; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PVCs, premature ventricular contraction; SA, sinoatrial; SHD , structural heart disease; VF, ventricular fibrillation.

Atrial Reentrant Tachycardia

Description

ART ( Fig. 5.3 ) is an SVT that can be due to macroreentry (using large portions of the left or right atria) or microreentry. Macroreentrant ATs tend to occur around areas of scarring, including incisional scars from prior cardiac surgery, corrected congenital heart disease (“incisional or scar-related ART”), or trauma. ART causes 5% to 10% of SVTs. ART can be distinguished from AFL by discrete (nonsinus) P waves (which may be buried in the QRS complexes or T waves) and by their slower rate (170 to 220 bpm), but can be considered a slow atrial flutter. It can be distinguished from sinus tachycardia by its abrupt onset, persistence, and nonsinus P-wave morphology. Adenosine terminates ART in only approximately 15% of cases but can be used for diagnostic purposes because it causes transient AV block, uncovering the underlying P-wave rate and morphology. ART can be difficult to distinguish from AAT; an EP study may be needed.

Figure 5.3, Macroreentrant atrial tachycardia.

Associated Conditions

ART is generally associated with structural heart disease. If ART is persistent, it can cause tachycardia-mediated cardiomyopathy or hemodynamic deterioration.

Clinical Symptoms and Presentation

Symptoms are similar to other SVTs but are also dependent on underlying heart disease.

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