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Overview of Arrhythmias

by L. Brent Mitchell, MD

The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial contractions. Arrhythmias and conduction disorders are caused by abnormalities in the generation or conduction of these electrical impulses or both.

Any heart disorder, including congenital abnormalities of structure (eg, accessory atrioventricular connection) or function (eg, hereditary ion channelopathies), can disturb rhythm. Systemic factors that can cause or contribute to a rhythm disturbance include electrolyte abnormalities (particularly low K or Mg), hypoxia, hormonal imbalances (eg, hypothyroidism, hyperthyroidism), and drugs and toxins (eg, alcohol, caffeine).

Anatomy

At the junction of the superior vena cava and high lateral right atrium is a cluster of cells that generates the initial electrical impulse of each normal heart beat, called the sinoatrial (SA) or sinus node. Electrical discharge of these pacemaker cells stimulates adjacent cells, leading to stimulation of successive regions of the heart in an orderly sequence. Impulses are transmitted through the atria to the atrioventricular (AV) node via preferentially conducting internodal tracts and unspecialized atrial myocytes. The AV node is located on the right side of the interatrial septum. It has a slow conduction velocity and thus delays impulse transmission. AV nodal transmission time is heart-rate–dependent and is modulated by autonomic tone and circulating catecholamines to maximize cardiac output at any given atrial rate.

The atria are electrically insulated from the ventricles by the annulus fibrosus except in the anteroseptal region. There, the bundle of His, the continuation of the AV node, enters the top of the interventricular septum, where it bifurcates into the left and right bundle branches, which terminate in Purkinje fibers. The right bundle branch conducts impulses to the anterior and apical endocardial regions of the right ventricle. The left bundle branch fans out over the left side of the interventricular septum. Its anterior portion (left anterior hemifascicle) and its posterior portion (left posterior hemifascicle) stimulate the left side of the interventricular septum, which is the first part of the ventricles to be electrically activated. Thus, the interventricular septum depolarizes left to right, followed by near-simultaneous activation of both ventricles from the endocardial surface through the ventricular walls to the epicardial surface.

Physiology

An understanding of normal cardiac physiology is essential before rhythm disturbances can be understood.

Electrophysiology

The passage of ions across the myocyte cell membrane is regulated through specific ion channels that cause cyclical depolarization and repolarization of the cell, called an action potential. The action potential of a working myocyte begins when the cell is depolarized from its diastolic 90 mV transmembrane potential to a potential of about 50 mV. At this threshold potential, voltage-dependent fast Na channels open, causing rapid depolarization mediated by Na influx down its steep concentration gradient. The fast Na channel is rapidly inactivated and Na influx stops, but other time- and voltage-dependent ion channels open, allowing Ca to enter through slow Ca channels (a depolarizing event) and K to leave through K channels (a repolarizing event). At first, these 2 processes are balanced, maintaining a positive transmembrane potential and prolonging the plateau phase of the action potential. During this phase, Ca entering the cell is responsible for electromechanical coupling and myocyte contraction. Eventually, Ca influx ceases, and K efflux increases, causing rapid repolarization of the cell back to the 90 mV resting transmembrane potential. While depolarized, the cell is resistant (refractory) to a subsequent depolarizing event. Initially, a subsequent depolarization is not possible (absolute refractory period), and after partial but incomplete repolarization, a subsequent depolarization is possible but occurs slowly (relative refractory period).

There are 2 general types of cardiac tissue:

  • Fast-channel tissues

  • Slow-channel tissues

Fast-channel tissues (working atrial and ventricular myocytes, His-Purkinje system) have a high density of fast Na channels and action potentials characterized by little or no spontaneous diastolic depolarization (and thus very slow rates of pacemaker activity), very rapid initial depolarization rates (and thus rapid conduction velocity), and loss of refractoriness coincident with repolarization (and thus short refractory periods and the ability to conduct repetitive impulses at high frequencies).

Slow-channel tissues (SA and AV nodes) have a low density of fast Na channels and action potentials characterized by more rapid spontaneous diastolic depolarization (and thus more rapid rates of pacemaker activity), slow initial depolarization rates (and thus slow conduction velocity), and loss of refractoriness that is delayed after repolarization (and thus long refractory periods and the inability to conduct repetitive impulses at high frequencies).

Normally, the SA node has the most rapid rate of spontaneous diastolic depolarization, so its cells produce spontaneous action potentials at a higher frequency than other tissues. Thus, the SA node is the dominant automatic tissue (pacemaker) in a normal heart. If the SA node does not produce impulses, tissue with the next highest automaticity rate, typically the AV node, functions as the pacemaker. Sympathetic stimulation increases the discharge frequency of pacemaker tissue, and parasympathetic stimulation decreases it.


Normal rhythm

The resting sinus heart rate in adults is usually 60 to 100 beats/min. Slower rates (sinus bradycardia) occur in young people, particularly athletes (see Athlete’s Heart : Diagnosis), and during sleep. Faster rates (sinus tachycardia) occur with exercise, illness, or emotion through sympathetic neural and circulating catecholamine drive. Normally, a marked diurnal variation in heart rate occurs, with lowest rates just before early morning awakening. A slight increase in rate during inspiration with a decrease in rate during expiration (respiratory sinus arrhythmia) is also normal; it is mediated by oscillations in vagal tone and is particularly common among healthy young people. The oscillations lessen but do not entirely disappear with age. Absolute regularity of the sinus rhythm rate is pathologic and occurs in patients with autonomic denervation (eg, in advanced diabetes) or with severe heart failure.

Most cardiac electrical activity is represented on the ECG (see Figure: Diagram of the cardiac cycle, showing pressure curves of the cardiac chambers, heart sounds, jugular pulse wave, and the ECG.), although SA node, AV node, and His-Purkinje depolarization does not involve enough tissue to be detected. The P wave represents atrial depolarization. The QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization.

The PR interval (from the beginning of the P wave to the beginning of the QRS complex) is the time from the beginning of atrial activation to the beginning of ventricular activation. Much of this interval reflects slowing of impulse transmission in the AV node. The R-R interval (time between 2 QRS complexes) represents the ventricular rate. The QT interval (from the beginning of the QRS complex to the end of the T wave) represents the duration of ventricular depolarization. Normal values for the QT interval are slightly longer in women; they are also longer with a slower heart rate. The QT interval is corrected (QTc) for influence of heart rate. The most common formula (all intervals in sec) is:

equation

Pathophysiology

Rhythm disturbances result from abnormalities of impulse formation, impulse conduction, or both. Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction, principally within the AV node or the His-Purkinje system. Most tachyarrhythmias are caused by reentry; some result from enhanced normal automaticity or from abnormal mechanisms of automaticity.

Reentry is the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods (see see Figure: Mechanism of typical reentry.).

Mechanism of typical reentry.

Atrioventricular nodal reentry is used here as an example. Two pathways connect the same points. Pathway A has slower conduction and a shorter refractory period. Pathway B conducts normally and has a longer refractory period.

I. A normal impulse arriving at 1 goes down both A and B pathways. Conduction through pathway A is slower and finds tissue at 2 already depolarized and thus refractory. A normal sinus beat results.

II. A premature impulse finds pathway B refractory and is blocked, but it can be conducted on pathway A because its refractory period is shorter. On arriving at 2, the impulse continues forward and retrograde up pathway B, where it is blocked by refractory tissue at 3. A premature supraventricular beat with an increased PR interval results.

III. If conduction over pathway A is sufficiently slow, a premature impulse may continue retrograde all the way up pathway B, which is now past its refractory period. If pathway A is also past its refractory period, the impulse may reenter pathway A and continue to circle, sending an impulse each cycle to the ventricle (4) and retrograde to the atrium (5), producing a sustained reentrant tachycardia.

Initiation of an atrioventricular nodal reentry tachycardia.

There is an abnormal P wave (P′) and atrioventricular nodal delay (long P′R interval) before onset of the tachycardia.

Under certain conditions, typically precipitated by a premature beat, reentry can cause continuous circulation of an activation wavefront, causing a tachyarrhythmia (see see Figure: Initiation of an atrioventricular nodal reentry tachycardia.). Normally, reentry is prevented by tissue refractoriness following stimulation. However, 3 conditions favor reentry: shortening of tissue refractoriness (eg, by sympathetic stimulation), lengthening of the conduction pathway (eg, by hypertrophy or abnormal conduction pathways), and slowing of impulse conduction (eg, by ischemia).

Symptoms and Signs

Arrhythmia and conduction disturbances may be asymptomatic or cause palpitations (sensation of skipped beats or rapid or forceful beats—see Palpitations), symptoms of hemodynamic compromise (eg, dyspnea, chest discomfort, presyncope, syncope), or cardiac arrest. Occasionally, polyuria results from release of atrial natriuretic peptide during prolonged supraventricular tachycardias (SVTs).

Palpation of pulse and cardiac auscultation can determine ventricular rate and its regularity or irregularity. Examination of the jugular venous pulse waves may help in the diagnosis of AV blocks and tachyarrhythmias. For example, in complete AV block, the atria intermittently contract when the AV valves are closed, producing large a (cannon) waves in the jugular venous pulse (see Neck veins). Other physical findings of arrhythmias are few.

Diagnosis

  • ECG

History and physical examination may detect an arrhythmia and suggest possible causes, but diagnosis requires a 12-lead ECG or, less reliably, a rhythm strip, preferably obtained during symptoms to establish the relationship between symptoms and rhythm.

The ECG is approached systematically; calipers measure intervals and identify subtle irregularities. The key diagnostic features are rate of atrial activation, rate and regularity of ventricular activation, and the relationship between the two. Irregular activation signals are classified as regularly irregular or irregularly irregular (no detectable pattern). Regular irregularity is intermittent irregularity in an otherwise regular rhythm (eg, premature beats) or a predictable pattern of irregularity (eg, recurrent relationships between groups of beats).

A narrow QRS complex (< 0.12 sec) indicates a supraventricular origin (above the His bundle bifurcation). A wide QRS complex ( 0.12 sec) indicates a ventricular origin (below the His bundle bifurcation) or a supraventricular rhythm conducted with an intraventricular conduction defect or with ventricular preexcitation in the Wolff-Parkinson-White syndrome.

Bradyarrhythmias

ECG diagnosis of bradyarrhythmias depends on the presence or absence of P waves, morphology of the P waves, and the relationship between P waves and QRS complexes.

A bradyarrhythmia with no relationship between P waves and QRS complexes indicates AV dissociation; the escape rhythm can be junctional (narrow QRS complex) or ventricular (wide QRS complex).

A regular QRS bradyarrhythmia with a 1:1 relationship between P waves and QRS complexes indicates absence of AV block. P waves preceding QRS complexes indicate sinus bradycardia (if P waves are normal) or sinus arrest with an escape atrial bradycardia (if P waves are abnormal). P waves after QRS complexes indicate sinus arrest with a junctional or ventricular escape rhythm and retrograde atrial activation. A ventricular escape rhythm results in a wide QRS complex; a junctional escape rhythm usually has a narrow QRS (or a wide QRS with bundle branch block or preexcitation).

When the QRS rhythm is irregular, P waves usually outnumber QRS complexes; some P waves produce QRS complexes, but some do not (indicating 2nd-degree AV block—see Second-degree AV block). An irregular QRS rhythm with a 1:1 relationship between P waves and the following QRS complexes usually indicates sinus arrhythmia with gradual acceleration and deceleration of the sinus rate (if P waves are normal).

Pauses in an otherwise regular QRS rhythm may be caused by blocked P waves (an abnormal P wave can usually be discerned just after the preceding T wave or distorting the morphology of the preceding T wave), sinus arrest, or sinus exit block (see Sinus Node Dysfunction), as well as by 2nd-degree AV block.


Tachyarrhythmias

Tachyarrhythmias may be divided into 4 groups, defined by being visibly regular vs irregular and by having a narrow vs wide QRS complex.

Irregular, narrow QRS complex tachyarrhythmias include atrial fibrillation (AF), atrial flutter or true atrial tachycardia with variable AV conduction, and multifocal atrial tachycardia. Differentiation is based on atrial ECG signals, which are best seen in the longer pauses between QRS complexes. Atrial ECG signals that are continuous, irregular in timing and morphology, and very rapid (> 300/min) without discrete P waves indicate AF. Discrete P waves that vary from beat to beat with at least 3 different morphologies suggest multifocal atrial tachycardia. Regular, discrete, uniform atrial signals without intervening isoelectric periods suggest atrial flutter.

Irregular, wide QRS complex tachyarrhythmias include the above 4 atrial tachyarrhythmias, conducted with either bundle branch block or ventricular preexcitation, and polymorphic ventricular tachycardia (VT). Differentiation is based on atrial ECG signals and the presence in polymorphic VT of a very rapid rate (> 250 beats/min).

Regular, narrow QRS complex tachyarrhythmias include sinus tachycardia, atrial flutter or true atrial tachycardia with a consistent AV conduction ratio, and paroxysmal SVTs (AV nodal reentrant SVT, orthodromic reciprocating AV tachycardia in the presence of an accessory AV connection, and SA nodal reentrant SVT). Vagal maneuvers or pharmacologic AV nodal blockade can help distinguish among these tachycardias. With these maneuvers, sinus tachycardia is not terminated, but it slows or AV block develops, disclosing normal P waves. Similarly, atrial flutter and true atrial tachycardia are usually not terminated, but AV block discloses flutter waves or abnormal P waves. The most common forms of paroxysmal SVT (AV nodal reentry and orthodromic reciprocating tachycardia) must terminate if AV block occurs.

Regular, wide QRS complex tachyarrhythmias include those listed for a regular, narrow QRS complex tachyarrhythmia, each with bundle branch block or ventricular preexcitation, and monomorphic VT. Vagal maneuvers can help distinguish among them. ECG criteria to distinguish between VT and SVT with an intraventricular conduction defect are often used (see Modified Brugada criteria for ventricular tachycardia.). When in doubt, the rhythm is assumed to be VT because some drugs for SVTs can worsen the clinical state if the rhythm is VT; however, the reverse is not true.

Pearls & Pitfalls

  • Assume a regular, wide-complex tachyarrhythmia is VT until proven otherwise.

Modified Brugada criteria for ventricular tachycardia.

* With RBBB QRS:

  • In V 1 , monophasic R, or QR, or RS

  • In V 6 , R/S < 1 or monophasic R or QR

With LBBB QRS :

  • In V 1 , R > 30 msec wide or RS > 60 msec wide

  • In V 6 , QR or QS

AV = atrioventricular; LBBB = left bundle branch block; RBBB = right bundle branch block; VT = ventricular tachycardia.


Treatment

  • Treatment of cause

  • Sometimes antiarrhythmic drugs, pacemakers, cardioversion-defibrillation, catheter ablation, or electrosurgery

The need for treatment varies; it is guided by symptoms and risks of the arrhythmia. Asymptomatic arrhythmias without serious risks do not require treatment even if they worsen. Symptomatic arrhythmias may require treatment to improve quality of life. Potentially life-threatening arrhythmias require treatment.

Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic drugs, cardioversion-defibrillation, pacemakers, or a combination, is used. Patients with arrhythmias that have caused or are likely to cause symptoms of hemodynamic compromise may have to be restricted from driving until response to treatment has been assessed.

Drugs for Arrhythmias

Most antiarrhythmic drugs are grouped into 4 main classes (Vaughan Williams classification) based on their dominant cellular electrophysiologic effect (see Antiarrhythmic Drugs (Vaughan Williams Classification)). Digoxin and adenosine are not included in the Vaughan Williams classification. Digoxin shortens atrial and ventricular refractory periods and is vagotonic, thereby prolonging AV nodal conduction and AV nodal refractory periods. Adenosine slows or blocks AV nodal conduction and can terminate tachyarrhythmias that rely upon AV nodal conduction for their perpetuation.

Antiarrhythmic Drugs (Vaughan Williams Classification)

Drug

Dosage

Target Levels

Selected Adverse Effects

Comments

Class Ia

Uses: APB and VPB suppression, SVT and VT suppression, AF or atrial flutter, and VF suppression

Disopyramide

IV: Initially, 1.5 mg/kg over > 5 min followed by an infusion of 0.4 mg/kg/h

Oral immediate-release: 100 or 150 mg q 6 h

Oral controlled-release: 200 or 300 mg q 12 h

2–7.5 μg/mL

Anticholinergic effects (urinary retention, glaucoma, dry mouth, blurred vision, intestinal upset), hypoglycemia, torsades de pointes VT; negative inotropic effects (which may worsen heart failure or hypotension)

Drug should be used cautiously in patients with impaired LV function.

Dosage should be decreased in patients with renal insufficiency.

Adverse effects may contribute to nonadherence.

If QRS interval widens (> 50% if initially < 120 msec or > 25% if initially > 120 msec) or if QTc interval is prolonged > 550 msec, infusion rate or dosage should be decreased or drug stopped.

IV form is not available in the US.

Procainamide*

IV: 10–15 mg/kg bolus at 25–50 mg/min, followed by a constant IV infusion of 1–4 mg/min

Oral: 250–625 mg (rarely, up to 1 g) q 3 or 4 h

Oral controlled-release: For patients < 55 kg, 500 mg; for patients 55–91 kg, 750 mg; or for patients > 91 kg, 1000 mg q 6 h

4–8 µg/mL

Hypotension (with IV infusion), serologic abnormalities (especially ANA) in almost 100% taking drug for > 12 mo, drug-induced lupus (arthralgia, fever, pleural effusions) in 15–20%, agranulocytosis in < 1%, torsades de pointes VT

Sustained-release preparations obviate the need for frequent dosing.

If QRS interval widens (> 50% if initially < 120 msec or > 25% if initially >120 msec) or if QTc interval is prolonged > 550 msec, infusion rate or dosage should be decreased or drug stopped.

Quinidine*

Oral: 200–400 mg q 4–6 h

2–6 μg/mL

Diarrhea, colic, flatulence, fever, thrombocytopenia, liver function abnormalities, torsades de pointes VT; overall adverse effect rate of 30%

If QRS interval widens (> 50% if initially < 120 msec or > 25% if initially > 120 msec) or if QTc interval is prolonged > 550 msec, dosage should be decreased or drug stopped.

Class Ib

Uses: Suppression of ventricular arrhythmias (VPB, VT, VF)

Lidocaine

IV: 100 mg over 2 min, followed by continuous infusion of 4 mg/min (2 mg/min in patients > 65) and 5 min after first dose, a 2nd 50-mg bolus

2–5 μg/L

Tremor, seizures; if administration is too rapid, drowsiness, delirium, paresthesias; possibly increased risk of bradyarrhythmias after acute MI

To reduce toxicity risk, clinicians should reduce dosage or infusion rate to 2 mg/min after 24 h.

Extensive first-pass hepatic metabolism occurs.

Mexiletine

Oral immediate-release: 100–250 mg q 8 h

Oral slow-release: 360 mg q 12 h

IV: 2 mg/kg at 25 mg/min, followed by 250-mg infusion over 1 h, 250-mg infusion over next 2 h, and maintenance infusion of 0.5 mg/min

0.5–2 μg/mL

Nausea, vomiting, tremor, seizures

Oral slow-release and IV forms are not available in the US.

Class Ic

Uses: APB and VPB suppression, SVT and VT suppression, AF or atrial flutter, and VF suppression

Flecainide

Oral: 100 mg q 8 or 12 h

IV: 1–2 mg/kg over 10 min

0.2–1 μg/mL

Occasionally, blurred vision and paresthesias

If QRS complex widens (> 50% if initially < 120 msec and > 25% if initially > 120 msec), dose must be decreased or drug stopped.

IV form is not available in US.

Propafenone

Oral: Initially, 150 mg tid, titrated up to 150–300 mg tid

IV: 2-mg/kg bolus, followed by 2 mg/min infusion

0.1–1.0 μg/mL

β-Blocking activity, possible worsening of reactive airway disorders; occasionally GI upset

Pharmacokinetics are nonlinear; increases in dose should not exceed 50% of previous dose.

Bioavailability and protein binding vary; drug has saturable first-pass metabolism.

IV form is not available in the US.

Class II (β-blockers)

Uses: Supraventricular tachyarrhythmias (APB, ST, SVT, AF, atrial flutter) and ventricular arrhythmias (often in a supportive role)

Acebutolol

Oral: 200 mg bid

β-Blocker levels not measured; dose adjusted to reduce heart rate by > 25%

Typically for β-blockers, GI disturbances, insomnia, nightmares, lethargy, erectile dysfunction, possible AV block in patients with AV node dysfunction

β-Blockers are contraindicated in patients with bronchospastic airway disorders.

Atenolol

Oral: 50–100 mg once/day

Betaxolol

Oral: 20 mg once/day

Bisoprolol

Oral: 5–10 mg once/day

Carvedilol

Oral: Initially, 6.25 mg bid, followed by titration to 25 mg bid

Esmolol

IV: 50–200 μg/kg/min

Metoprolol

Oral: 50–100 mg bid

IV: 5 mg q 5 min up to 15 mg

Nadolol

Oral: 60–80 mg once/day

Propranolol

Oral: 10–30 mg tid or qid

IV: 1–3 mg (may repeat once after 5 min if needed)

Timolol

Oral:10–20 mg bid

Class III (membrane-stabilizing drugs)

Uses: Any tachyarrhythmia except torsades de pointes VT

Amiodarone

Oral: 600–1200 mg/day for 7–10 days, then 400 mg/day for 3 wk, followed by a maintenance dose (ideally, 200 mg/day)

IV: 150–450 mg over 1–6 h (depending on urgency), followed by a maintenance dose of 0.5–2.0 mg/min

1–2.5 μg/mL

Pulmonary fibrosis (in up to 5% of patients treated for > 5 yr), which may be fatal; QTc prolongation; torsades de pointes VT (rare); bradycardia; gray or blue discoloration of sun-exposed skin; sun sensitivity; hepatic abnormalities; peripheral neuropathy; corneal microdeposits (in almost all treated patients), usually without serious visual effects and reversed by stopping the drug; changes in thyroid function; serum creatinine increased up to 10% without change in GFR; slow clearance possibly prolonging adverse effects

Drug has noncompetitive β-blocking, Ca channel blocking, and Na channel blocking effects, with a long delay in onset of action.

By prolonging refractoriness, drug may cause homogeneous conditions of repolarization throughout the heart.

IV form can be used for conversion.

Azimilide

Oral: 100–200 mg once/day

200–1000 ng/mL

Torsades de pointes VT

Bretylium*

IV: Initially, 5 mg/kg, followed by 1–2 mg/min as a constant infusion

IM: Initially, 5–10 mg/kg, which may be repeated to a total dose of 30 mg/kg

IM maintenance dose of 5 mg/kg q 6–8 h

0.8–2.4 μg/mL

Hypotension

Drug has class II properties.

Effects may be delayed 10–20 min.

Drug is used to treat potentially lethal refractory ventricular tachyarrhythmias (intractable VT, recurrent VF), for which it is usually effective within 30 min of injection.

Dofetilide

Oral: 500 μg bid if CrCl is > 60 mL/min; 250 μg bid if CrCl is 40–60 mL/min; 125 μg bid if CrCl is 20–40 mL/min

N/A

Torsades de pointes VT

Drug is contraindicated if QTc is > 440 msec or if CrCl is < 20 mL/min.

Dronedarone

Oral: 400 mg bid

N/A

QTc prolongation, torsades de pointes VT (rare), bradycardia, GI upset, possible hepatotoxicity (rare), serum creatinine increased up to 20% without change in GFR

Drug is a modified amiodarone molecule (including deiodination) with shorter half-life, smaller volume of distribution, fewer adverse effects, and less efficacy.

Drug should not be used in patients with history of heart failure or with permanent AF.

Ibutilide

IV: For patients 60 kg, 1 mg infusion or, for patients < 60 kg, 0.01 mg/kg over 10 min, with dose repeated after 10 min if the first infusion is unsuccessful

N/A

Torsades de pointes VT (in 2%)

Drug is used to terminate AF (success rate, about 40%) and atrial flutter (success rate, about 65%).

Sotalol

Oral: 80–160 mg q 12 h

IV: 10 mg over 1–2 min

0.5–4 μg/mL

Similar to class II; possible depressed left ventricular function and torsades de pointes VT

Racemic [ d - l ] form has class II (β-blocking) properties, [ d ] form does not. Both forms have class III activity. Only racemic sotalol is available for clinical use.

Drug should not be used in patients with renal insufficiency.

Class IV (Ca channel blockers)

Uses: Termination of SVT and slowing of rapid AF or atrial flutter

Diltiazem

Oral slow-release (diltiazem CD): 120–360 mg once/day

IV: 5–15 mg/h for up to 24 h

0.1–0.4 μg/mL

Possible precipitation of VF in patients with VT, negative inotropy

IV form is most commonly used to slow ventricular response rate to AF or atrial flutter.

Verapamil

Oral: 40–120 mg tid or, for sustained-release form, 180 mg once/day to 240 mg bid

IV: 5–15 mg over 10 min

Oral prophylaxis: 40–120 mg tid

N/A

Possible precipitation of VF in patients with VT, negative inotropy

IV form is used to terminate narrow-complex tachycardias involving the AV node (success rate, almost 100% with 5–10 mg IV over 10 min).

Other antiarrhythmics

Adenosine

6 mg rapid IV bolus, repeated twice at 12 mg if needed; flush bolus with additional 20 mL saline

N/A

Transient dyspnea, chest discomfort, and flushing (in 30–60%), transient bronchospasm

Drug slows or blocks AV nodal conduction.

Duration of action is extremely short.

Contraindications include asthma and high-grade heart block.

Dipyridamole potentiates effects.

Digoxin

IV loading dose: 0.5 mg

Oral maintenance dose: 0.125–0.25 mg/day

0.8–1.6 μg/mL

Anorexia, nausea, vomiting, and often serious arrhythmias (VPBs, VT, APBs, atrial tachycardia, 2nd-degree or 3rd-degree AV block, combinations of these arrhythmias)

Contraindications include antegrade conduction over an accessory AV connection pathway (manifest Wolff-Parkinson-White syndrome) because if AF occurs, ventricular responses may be excessive (digoxin shortens refractory periods of the accessory connection).

*Availability uncertain.

AF = atrial fibrillation; ANA = antinuclear antibody; APB = atrial premature beat; AV = atrioventricular; CrCl = creatinine clearance; LV = left ventricular; QTc = QT interval corrected for heart rate; SVT = supraventricular tachycardia; VF = ventricular fibrillation; VPB = ventricular premature beat; VT = ventricular tachycardia.

Class I

Na channel blockers (membrane-stabilizing drugs) block fast Na channels, slowing conduction in fast-channel tissues (working atrial and ventricular myocytes, His-Purkinje system). In the ECG, this effect may be reflected as widening of the P wave, widening of the QRS complex, prolongation of the PR interval, or a combination.

Class I drugs are subdivided based on the kinetics of the Na channel effects. Class Ib drugs have fast kinetics, class Ic drugs have slow kinetics, and class Ia drugs have intermediate kinetics. The kinetics of Na channel blockade determine the heart rates at which their electrophysiologic effects become manifest. Because class Ib drugs have fast kinetics, they express their electrophysiologic effects only at fast heart rates. Thus, an ECG obtained during normal rhythm at normal rates usually shows no evidence of fast-channel tissue conduction slowing. Class Ib drugs are not very potent antiarrhythmics and have minimal effects on atrial tissue. Because class Ic drugs have slow kinetics, they express their electrophysiologic effects at all heart rates. Thus, an ECG obtained during normal rhythm at normal heart rates usually shows fast-channel tissue conduction slowing. Class Ic drugs are more potent antiarrhythmics. Because class Ia drugs have intermediate kinetics, their fast-channel tissue conduction slowing effects may or may not be evident on an ECG obtained during normal rhythm at normal rates. Class Ia drugs also block repolarizing K channels, prolonging the refractory periods of fast-channel tissues. On the ECG, this effect is reflected as QT-interval prolongation even at normal rates. Class Ib drugs and class Ic drugs do not block K channels directly.

The primary indications are SVTs for class Ia and Ic drugs and VTs for all class I drugs. The most worrisome adverse effect is proarrhythmia, a drug-related arrhythmia worse than the arrhythmia being treated. Class Ia drugs may cause torsades de pointes VT; class Ia and class Ic drugs may organize and slow atrial tachyarrhythmias enough to permit 1:1 AV conduction with marked acceleration of the ventricular response rate. All class I drugs may worsen VTs. They also tend to depress ventricular contractility. Because these adverse effects are more likely to occur in patients with a structural heart disorder, class I drugs are not generally recommended for such patients. Thus, these drugs are usually used only in patients who do not have a structural heart disorder or in patients who have a structural heart disorder but who have no other therapeutic alternatives.


Class II

Class II drugs are β-blockers, which affect predominantly slow-channel tissues (SA and AV nodes), where they decrease rate of automaticity, slow conduction velocity, and prolong refractoriness. Thus, heart rate is slowed, the PR interval is lengthened, and the AV node transmits rapid atrial depolarizations at a lower frequency. Class II drugs are used primarily to treat SVTs, including sinus tachycardia, AV nodal reentry, AF, and atrial flutter. These drugs are also used to treat VTs to raise the threshold for ventricular fibrillation (VF) and reduce the ventricular proarrhythmic effects of β-adrenoceptor stimulation. β-Blockers are generally well tolerated; adverse effects include lassitude, sleep disturbance, and GI upset. These drugs are contraindicated in patients with asthma.


Class III

Class III drugs are primarily K channel blockers, which prolong action potential duration and refractoriness in slow- and fast-channel tissues. Thus, the capacity of all cardiac tissues to transmit impulses at high frequencies is reduced, but conduction velocity is not significantly affected. Because the action potential is prolonged, rate of automaticity is reduced. The predominant effect on the ECG is QT-interval prolongation. These drugs are used to treat SVTs and VTs. Class III drugs have a risk of ventricular proarrhythmia, particularly torsades de pointes VT.


Class IV

Class IV drugs are the nondihydropyridine Ca channel blockers, which depress Ca-dependent action potentials in slow-channel tissues and thus decrease the rate of automaticity, slow conduction velocity, and prolong refractoriness. Heart rate is slowed, the PR interval is lengthened, and the AV node transmits rapid atrial depolarizations at a lower frequency. These drugs are used primarily to treat SVTs; however, one form of VT (left septal or Belhassen VT) can be treated with verapamil.


Devices and Procedures

Direct-current (DC) cardioversion-defibrillation

A transthoracic DC shock of sufficient magnitude depolarizes the entire myocardium, rendering the entire heart momentarily refractory to repeat depolarization. Thereafter, the most rapid intrinsic pacemaker, usually the SA node, reassumes control of heart rhythm. Thus, DC cardioversion-defibrillation very effectively terminates tachyarrhythmias that result from reentry. However, it is less effective for terminating tachyarrhythmias that result from automaticity because the return rhythm is likely to be the automatic tachyarrhythmia. For tachyarrhythmias other than VF, the DC shock must be synchronized to the QRS complex (called DC cardioversion) because a shock that falls during the vulnerable period (near the peak of the T wave) can induce VF. In VF, synchronization of a shock to the QRS complex is neither necessary nor possible. A DC shock applied without synchronization to a QRS complex is DC defibrillation.

When DC cardioversion is elective, patients should fast for 6 to 8 h to avoid the possibility of aspiration. Because the procedure is frightening and painful, brief general anesthesia or IV analgesia and sedation (eg, fentanyl 1 mcg/kg, then midazolam 1 to 2 mg q 2 min to a maximum of 5 mg) is necessary. Equipment and personnel to maintain the airways must be present.

The electrodes (pads or paddles) used for cardioversion may be placed anteroposteriorly (along the left sternal border over the 3rd and 4th intercostal spaces and in the left infrascapular region) or anterolaterally (between the clavicle and the 2nd intercostal space along the right sternal border and over the 5th and 6th intercostal spaces at the apex of the heart). After synchronization to the QRS complex is confirmed on the monitor, a shock is given. The most appropriate energy level varies with the tachyarrhythmia being treated. Cardioversion efficacy increases with use of biphasic shocks, in which the current polarity is reversed part way through the shock waveform. Complications are usually minor and include atrial and ventricular premature beats and muscle soreness. Less commonly, but more likely if patients have marginal left ventricular function or multiple shocks are used, cardioversion precipitates myocyte damage and electromechanical dissociation.

DC cardioversion-defibrillation can also be applied directly to the heart during a thoracotomy or through use of an intracardiac electrode catheter; then, much lower energy levels are required.


Pacemakers

Pacemakers sense electrical events and respond when necessary by delivering electrical stimuli to the heart. Permanent pacemaker leads are placed via thoracotomy or transvenously, but some temporary emergency pacemaker leads can be placed on the chest wall.

Indications are numerous (see Indications for Permanent Pacemakers) but generally involve symptomatic bradycardia or high-grade AV block. Some tachyarrhythmias may be terminated by overdrive pacing with a brief period of pacing at a faster rate; the pacemaker is then slowed to the desired rate. Nevertheless, ventricular tachyarrhythmias are better treated with devices that can cardiovert and defibrillate as well as pace (implantable cardioverter defibrillators).

Indications for Permanent Pacemakers

Arrhythmia

Indicated (Established by Evidence)

Possibly Indicated and Supported by Bulk of Evidence

Possibly Indicated But Less Well Supported by Evidence

Not Indicated

Sinus node dysfunction

Symptomatic bradycardia, including symptomatic frequent sinus pauses and bradycardia due to essential drugs (alternatives contraindicated)

Symptomatic chronotropic incompetence (heart rate cannot meet physiologic demands)

Heart rate of < 40 beats/min when symptoms have not been clearly associated with the bradycardia

Syncope of unexplained origin with significant sinus node dysfunction seen on ECG or triggered in an electrophysiologic study

Heart rate of < 40 beats/min in minimally symptomatic patients

Asymptomatic bradycardia

Symptoms consistent with bradycardia but clearly shown not to be associated with it

Symptomatic bradycardia due to nonessential drugs

AV block

Any 3rd-degree or 2nd-degree AV block associated symptomatic bradycardia or ventricular arrhythmia

Third-degree or advanced 2nd-degree AV block at any anatomic level if associated with one of the following:

  • Arrhythmias and other disorders requiring drugs that cause symptomatic bradycardia

  • Documented asystole 3.0 sec (≥ 5.0 sec in atrial fibrillation), any escape rate of < 40 beats/min, or escape rhythm below the AV node in awake, asymptomatic patients

  • Escape ventricular rates of > 40 beats/min in patients with cardiomegaly or LV dysfunction

  • Catheter ablation of the AV junction

  • Postoperative block not expected to resolve after surgery

  • Neuromuscular disorders with AV block (eg, myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's [limb-girdle] dystrophy, Charcot-Marie-Tooth disease [peroneal atrophy])

  • Exercise (ie, occurring during) in patients without myocardial ischemia

Asymptomatic 3rd-degree AV block at any anatomic level when average ventricular rates during waking are 40 beats/min in patients without cardiomegaly

Asymptomatic type II 2nd-degree AV block with narrow QRS complex (pacemaker is indicated if QRS complex is wide)

Asymptomatic 2nd-degree AV block within or below His bundle level, detected during an electrophysiologic study done for other reasons

First- or 2nd-degree AV block with symptoms suggesting pacemaker syndrome

AV block in patients who are taking a causative drug or have drug toxicity if block is expected to recur even after drug is withdrawn

AV block of any degree (including 1st) associated with neuromuscular disorders in which conduction abnormalities may progress unpredictably (eg, myotonic muscular dystrophy, Erb’s [limb-girdle] dystrophy, Charcot-Marie-Tooth disease [peroneal atrophy] with or without symptoms)

Asymptomatic 1st-degree AV block

Asymptomatic type I 2nd-degree AV block at the AV node level or not known to be within or below His bundle level

AV block expected to resolve or unlikely to recur (eg, due to drug toxicity or Lyme disease or occurring asymptomatically during transient increases in vagal tone or during hypoxia in sleep apnea syndrome)

Tachyarrhythmias

Sustained, pause-dependent VT, with or without prolonged QT interval

High-risk patients with congenital long QT syndrome

Symptomatic recurrent SVT reproducibly terminated by pacing when ablation and/or drugs fail (except when there is an accessory AV connection capable of high-frequency antegrade conduction)

Prevention of symptomatic, recurrent atrial fibrillation refractory to drugs when sinus node dysfunction coexists

Frequent or complex ventricular ectopy without sustained VT when long QT syndrome is absent

Torsades de pointes VT with reversible causes

After acute MI

Persistent 2nd-degree AV block in the His-Purkinje system with bilateral BBB or 3rd-degree AV block within or below the His-Purkinje system

Transient advanced 2nd- or 3rd-degree AV block below the AV node level and associated with BBB

Persistent symptomatic 2nd- or 3rd-degree AV block

None

Persistent 2nd- or 3rd-degree AV block at the AV node level

Transient AV block without intraventricular conduction defects

Transient AV block with isolated left anterior fascicular block

Acquired BBB or fascicular block without AV block

Persistent 1st-degree AV block with BBB or fascicular block

Multifascicular block

Advanced 2nd-degree or intermittent 3rd-degree AV block

Type II 2nd-degree AV block

Alternating BBB

Syncope not shown to be due to AV block after other likely causes (especially VT) are excluded

Very prolonged HV interval (100 msec) in asymptomatic patients, detected incidentally during an electrophysiologic study

Nonphysiologic, infra-His block induced by pacing, detected incidentally during an electrophysiologic study

Neuromuscular disorders in which conduction abnormalities may progress unpredictably (eg, myotonic muscular dystrophy, Erb’s [limb-girdle] dystrophy, Charcot-Marie-Tooth disease [peroneal atrophy] with or without symptoms)

Fascicular block without AV block or symptoms

Fascicular block with 1st-degree AV block and without symptoms

Congenital heart disorders

Advanced 2nd- or 3rd-degree AV block causing symptomatic bradycardia, ventricular dysfunction, or low cardiac output

Sinus node dysfunction correlated with symptoms during age-inappropriate bradycardia

Postoperative high-grade 2nd- or 3rd-degree AV block that is not expected to resolve or that persists 7 days after surgery

Congenital 3rd-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction

Congenital 3rd-degree AV block in infants with a ventricular rate of < 55 beats/min or with a congenital heart disorder and a ventricular rate of < 70 beats/min

Sustained pause-dependent VT, with or without prolonged QT, when pacing has been documented as effective

Congenital heart disorder and sinus bradycardia to prevent recurrent episodes of intra-atrial reentrant tachycardia

Congenital 3rd-degree AV block persisting after age 1 yr if average heart rate is < 50 beats/min, ventricular rate pauses abruptly for 2 or 3 times the basic cycle length, or associated symptoms due to chronotropic incompetence occur

Asymptomatic sinus bradycardia in children with a complex congenital heart disorder and resting heart rate of < 40 beats/min or pauses in ventricular rate of > 3 sec

Patients with a congenital heart disorder and impaired hemodynamics due to sinus bradycardia or loss of AV synchrony

Unexplained syncope in patients who have had congenital heart disorder surgery that was complicated by transient 3rd-degree AV block with residual fascicular block

Transient postoperative 3rd-degree AV block that converts to sinus rhythm with residual bifascicular block

Congenital 3rd-degree AV block in asymptomatic infants, children, adolescents, or young adults with an acceptable ventricular rate, a narrow QRS complex, and normal ventricular function

Asymptomatic sinus bradycardia after biventricular repair of a congenital heart disorder in patients with resting heart rate of < 40 beats/min or pauses in ventricular rate of > 3 sec

Transient postoperative AV block when AV conduction returns to normal

Asymptomatic postoperative bifascicular block with or without 1st-degree AV block and without prior transient 3rd-degree AV block

Asymptomatic type I 2nd-degree AV block

Asymptomatic sinus bradycardia when the longest RR interval is < 3 sec and minimum heart rate is > 40 beats/min

Hypersensitive carotid sinus syndrome and neurocardiogenic syncope

Recurrent syncope due to spontaneously occurring carotid sinus stimulation or to carotid sinus pressure that induces asystole of > 3 sec

Recurrent syncope without obvious triggering events and with a hypersensitive cardioinhibitory response (i.e. carotid sinus pressure induces asystole of > 3 sec)

Significantly symptomatic neurocardiogenic syncope associated with bradycardia documented clinically or during tilt-table testing

Hyperactive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms (eg, dizziness, light-headedness)

Situational vasovagal syncope that can be averted by avoidance

Postcardiac transplantation

Persistent inappropriate or symptomatic bradycardia expected to persist

Other established indications for permanent pacing

None

Prolonged or recurrent relative bradycardia limiting rehabilitation or discharge after postoperative recovery

Syncope after transplantation even when bradyarrhythmia has not been demonstrated

None

Hypertrophic cardiomyopathy

Same as established indications for sinus node dysfunction or AV block

None

Medically refractory, symptomatic hypertrophic cardiomyopathy when resting or induced LV outflow is significantly obstructed

Asymptomatic or medically controlled hypertrophic cardiomyopathy

Symptomatic hypertrophic cardiomyopathy with no evidence of LV outflow obstruction

Cardiac resynchronization therapy (CRT) for patients with severe systolic heart failure

CRT (with or without an ICD) for patients with LVEF ≤ 35%, QRS duration ≥ 0.12 sec, sinus rhythm, and NYHA class III or ambulatory class IV heart failure symptoms during optimal medical therapy

CRT (with or without an ICD) for patients with LVEF ≤ 35%, QRS duration ≥ 0.12 sec, atrial fibrillation, and NYHA class III or ambulatory class IV heart failure symptoms during optimal medical therapy

CRT for patients with LVEF ≤ 35%, QRS duration ≥ 0.12 sec, frequent dependence on ventricular pacing, and NYHA class III or ambulatory class IV heart failure symptoms during optimal medical therapy

LVEF ≤ 35% and NYHA class I or class II heart failure symptoms during optimal medical therapy in patients who are undergoing implantation of a permanent pacemaker and/or ICD with anticipated frequent ventricular pacing

Asymptomatic dilated cardiomyopathy with reduced LVEF alone and no other indications for pacing

Functional status and life expectancy that are limited predominantly by chronic noncardiac conditions

AV = atrioventricular; BBB = bundle branch block; EF = ejection fraction; HV interval = interval from the start of the HIS signal to the beginning of the 1st ventricular signal; ICD = implantable cardioverter-defibrillator; LV = left ventricular; NYHA = New York Heart Association; VT = ventricular tachycardia.

Data from Epstein AE, DiMarco JP, Ellenbogen KA, et al: ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. Circulation 117(21):e350–e408, 2008.

Types of pacemakers are designated by 3 to 5 letters (see Pacemaker Codes), representing which cardiac chambers are paced, which chambers are sensed, how the pacemaker responds to a sensed event (inhibits or triggers pacing), whether it can increase heart rate during exercise (rate-modulating), and whether pacing is multisite (in both atria, both ventricles, or more than one pacing lead in a single chamber). For example, a VVIR pacemaker paces (V) and senses (V) events in the ventricle, inhibits pacing in response to sensed event (I), and can increase its rate during exercise (R).

VVI and DDD pacemakers are the devices most commonly used. They offer equivalent survival benefits. Compared with VVI pacemakers, physiologic pacemakers (AAI, DDD, VDD) appear to reduce risk of AF and heart failure and slightly improve quality of life.

Advances in pacemaker design include lower-energy circuitry, new battery designs, and corticosteroid-eluting leads (which reduce pacing threshold), all of which increase pacemaker longevity. Mode switching refers to an automatic change in the mode of pacing in response to sensed events (eg, from DDDR to VVIR during AF).

Pacemakers may malfunction by oversensing or undersensing events, failing to pace or capture, or pacing at an abnormal rate. Tachycardias are an especially common complication. Rate-modulating pacemakers may increase stimuli in response to vibration, muscle activity, or voltage induced by magnetic fields during MRI. In pacemaker-mediated tachycardia, a normally functioning dual-chamber pacemaker senses a ventricular premature or paced beat transmitted to the atrium through the AV node or a retrograde-conducting accessory pathway, which triggers ventricular stimulation in a rapid, repeating cycle.

Additional complications associated with normally functioning devices include cross-talk inhibition, in which sensing of the atrial pacing impulse by the ventricular channel of a dual-chamber pacemaker leads to inhibition of ventricular pacing, and pacemaker syndrome, in which AV asynchrony induced by ventricular pacing causes fluctuating, vague cerebral (eg, light-headedness), cervical (eg, neck pulsations), or respiratory (eg, dyspnea) symptoms. Pacemaker syndrome is managed by restoring AV synchrony by atrial pacing (AAI), single-lead atrial sensing ventricular pacing (VDD), or dual-chamber pacing (DDD), most commonly the latter.

Environmental interference comes from electromagnetic sources such as surgical electrocautery and MRI, although MRI may be safe when the pacemaker generator and leads are not inside the magnet. Cellular telephones and electronic security devices are a potential source of interference; telephones should not be placed close to the device but are not a problem when used normally for talking. Walking through metal detectors does not cause pacemaker malfunction as long as patients do not linger.

Pacemaker Codes

I

II

III

IV

V

Chamber Paced

Chamber Sensed

Response to Sensed Event

Rate Modulation

Multisite Pacing

A = Atrium

A = Atrium

O = None

O = Not programmable

O = None

V = Ventricle

V = Ventricle

I = Inhibits pacemaker

A = Atrium

D = Dual (both)

D = Dual (both)

T = Triggers pacemaker to stimulate ventricles

R = Rate-modulated

V = Ventricle

D = Dual (both): For events sensed in ventricles, inhibits; for events sensed in atria, triggers

D = Dual (both)


Cardiac resynchronization therapy

In some patients, the normal, orderly, sequential relationship between contraction of the cardiac chambers is disrupted (becomes dyssynchronous). Dyssynchrony may be present between atrial and ventricular contraction (atrioventricular dyssynchrony), between left and right ventricular contraction (interventricular dyssynchrony), and between different segments of left ventricular contraction (intraventricular dyssynchrony).

Patients at risk for dyssynchrony include those with the following:

  • Ischemic or nonischemic dilated cardiomyopathy

  • Prolonged QRS interval (≥ 130 msec)

  • Left ventricular end-diastolic dimension ≥ 55 mm

  • Left ventricular ejection fraction ≤ 35% in sinus rhythm

Cardiac resynchronization therapy (CRT) involves use of a pacing system to resynchronize cardiac contraction. Such systems usually include a right atrial lead, right ventricular lead, and left ventricular lead. Leads may be placed transvenously or surgically via thoracotomy. In heart failure patients with New York Heart Association (NYHA) class II, III, and IV symptoms, CRT can reduce hospitalization for heart failure and reduce all-cause mortality. However, there is little to no benefit in patients with permanent atrial fibrillation, right bundle branch block, intraventricular conduction delay, or only mild prolongation of QRS duration (<150 msec).


Implantable cardioverter-defibrillators (ICDs)

ICDs cardiovert or defibrillate the heart in response to VT or VF. Contemporary tiered-therapy ICDs also provide antibradycardia pacing and antitachycardia pacing (to terminate responsive atrial or ventricular tachycardias) and store intracardiac electrograms. ICDs are implanted subcutaneously or subpectorally, with electrodes inserted transvenously into the right ventricle and sometimes also the right atrium. A biventricular ICD also has a left ventricular epicardial lead placed via the coronary sinus venous system or via thoracotomy.

ICDs are the preferred treatment for patients who have had an episode of VF or hemodynamically significant VT not due to reversible or transient conditions (eg, electrolyte disturbance, antiarrhythmic drug proarrhythmia, acute MI). ICDs may also be indicated for patients with VT or VF inducible during an electrophysiologic study and for patients with idiopathic or ischemic cardiomyopathy, a left ventricular ejection fraction of < 35%, and a high risk of VT or VF. Other indications are less clear (see Indications for Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular Fibrillation).

Because ICDs treat rather than prevent VT or VF, patients prone to these arrhythmias may require both an ICD and antiarrhythmic drugs to reduce the number of episodes and need for uncomfortable shocks; this approach also prolongs the life of the ICD.

Impulse generators for ICDs typically last about 5 yr. ICDs may malfunction by delivering inappropriate pacing or shocks in response to sinus rhythm, SVTs, or nonphysiologically generated impulses (eg. due to lead fracture). They also may malfunction by not delivering appropriate pacing or shocks when needed because of factors such as lead or impulse generator migration, undersensing, an increase in pacing threshold due to fibrosis at the site of prior shocks, and battery depletion.

In patients who report that the ICD has discharged but that no associated symptoms of syncope, dyspnea, chest pain or persistent palpitations occurred, follow up with the ICD clinic and/or the electrophysiologist within the week is appropriate. The ICD can then be electronically interrogated to determine the reason for discharge. If such associated symptoms were present, or the patient received multiple shocks, emergency department referral is indicated to look for a treatable cause (eg, coronary ischemia, electrolyte abnormality) or device malfunction.

Indications for Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular Fibrillation

Level of Evidence

Specific Indications

Indicated (established by evidence)

Hemodynamically unstable VT or VF when there is no transient or reversible cause

Hemodynamically stable sustained VT in patients with a structural heart disorder

Syncope of undetermined origin with hemodynamically significant sustained VT or VF induced during an electrophysiologic study

Ischemic cardiomyopathy, NYHA class II or III heart failure symptoms during optimal medical therapy, and LV ejection fraction 0.35 measured at least 40 days post-MI

Ischemic cardiomyopathy, NYHA class I heart failure symptoms during optimal medical therapy, and LV ejection fraction ≤ 30% measured at least 40 days post-MI

Nonischemic dilated cardiomyopathy, NYHA class II or III heart failure symptoms during optimal medical therapy, and LV ejection fraction 0. 35

Ischemic cardiomyopathy, nonsustained VT, LV ejection fraction ≤ 40% measured at least 40 days post-MI, and inducible VF or sustained VT detected during an electrophysiologic study

Possibly indicated and supported by bulk of evidence

Patients with idiopathic dilated cardiomyopathy, significant LV dysfunction during optimal medical therapy, with unexplained syncope

Patients with sustained VT and normal or near-normal ventricular function

Patients with HCM with one or more high risk factors other than sustained VT/VF (family history of premature sudden death, unexplained syncope, LV thickness 30 mm, abnormal exercise BP response, nonsustained VT)

Patients with ARVC with one or more high risk factors other than sustained VT/VF (extensive RV disease, affected family member with sudden death, undiagnosed syncope, nonsustained VT, inducible VT detected during an electrophysiologic study)

Long QT syndrome, syncope or VT while receiving a β-blocker

Nonhospitalized patients awaiting cardiac transplantation

Brugada syndrome and syncope or documented VT that has not resulted in cardiac arrest

Patients with catecholaminergic polymorphic VT with syncope and/or documented sustained VT while receiving a β-blocker

Patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas' disease

Possibly indicated but less well supported by evidence

Patients with idiopathic dilated cardiomyopathy, NYHA class I heart failure symptoms during optimal medical therapy, LV ejection fraction 0.35

Patients with long QT syndrome, without syncope or VT and with one or more high risk factors (QTc > 0.5 sec, LQT1 with 2 abnormal copies of the abnormal gene and deafness [formerly Jervell and Lange-Neilsen syndrome], LQT2, LQT3)

Patients with syncope and an advanced structural heart disorder if invasive and noninvasive investigations have not identified a cause

Patients with familial cardiomyopathy associated with sudden death

Patients with LV noncompaction

Not indicated

Syncope of unknown etiology in absence of inducible VT or VF or a structural heart disorder

Incessant VT or VF

VT or VF with mechanisms amenable to catheter or surgical ablation

VT or VF due to transient or reversible disorders when correction is feasible and likely to prevent recurrence

Psychiatric disorders that may worsen with ICD implantation or that preclude follow-up

Patients with no reasonable expectation of survival and with an acceptable functional status for ≥ 1 yr

Patients with NYHA class IV drug-refractory heart failure symptoms who are not candidates for cardiac transplantation or a CRT ICD

ARVC = arrhythmogenic right ventricular cardiomyopathy; CRT = cardiac resynchronization therapy; HCM = hypertrophic cardiomyopathy; ICD = implantable cardioverter defibrillator; LQT1 = long QT syndrome type 1; LQT2 = long QT syndrome type 2; LQT3 = long QT syndrome type 3; LV = left ventricular; NYHA = New York Heart Association; QTc = corrected QT interval; RV = right ventricular; VF = ventricular fibrillation; VT = ventricular tachycardia.

Data modified from Epstein AE, DiMarco JP, Ellenbogen KA, et al: ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. Circulation 117:e350–408, 2008.


Radiofrequency (RF) ablation

If a tachyarrhythmia depends on a specific pathway or ectopic site of automaticity, the site can be ablated by low-voltage, high-frequency (300 to 750 MHz) electrical energy, applied through an electrode catheter. This energy heats and necroses an area < 1 cm in diameter and up to 1 cm deep. Before energy can be applied, the target site or sites must be mapped during an electrophysiologic study (see Electrophysiologic Studies (EPS)).

Success rate is > 90% for reentrant supraventricular tachycardias (via the AV node or an accessory pathway), focal atrial tachycardia and flutter, and focal idiopathic VTs (right ventricular outflow tract, left septal, or bundle branch reentrant VT). Because AF often originates or is maintained by an arrhythmogenic site in the pulmonary veins, this source can be electrically isolated by ablations at the pulmonary vein–left atrial junction or in the left atrium. Alternatively, in patients with refractory AF and rapid ventricular rates, the AV node may be ablated after permanent pacemaker implantation. RF ablation is sometimes successful in patients with VT refractory to drugs particularly when ischemic heart disease is present.

RF ablation is safe; mortality is < 1/2000. Complications include valvular damage, pulmonary vein stenosis or occlusion (if used to treat atrial fibrillation), stroke or other embolism, cardiac perforation, tamponade (1%), and unintended AV node ablation.


Surgery

Surgery to remove a focus of a tachyarrhythmia is becoming less necessary as the less invasive RF ablation techniques evolve. But it is still indicated when an arrhythmia is refractory to RF ablation or when another indication requires a cardiac surgical procedure, most commonly when patients with AF require valve replacement or repair or when patients with VT require revascularization or resection of a left ventricular aneurysm.


Resources In This Article

Drugs Mentioned In This Article

  • Drug Name
    Select Trade
  • TIKOSYN
  • RYTHMOL
  • MULTAQ
  • BETAPACE
  • LANOXIN
  • ADENOCARD
  • NORPACE
  • No US brand name
  • ZEBETA
  • PERSANTINE
  • CARDIZEM, CARTIA XT, DILACOR XR
  • CALAN
  • BETOPTIC
  • LOPRESSOR, TOPROL-XL
  • TENORMIN
  • XYLOCAINE
  • CORDARONE
  • INDERAL
  • TIMOPTIC
  • CORGARD
  • SECTRAL
  • COREG
  • CORVERT
  • BREVIBLOC
  • ACTIQ, DURAGESIC, SUBLIMAZE

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