blockers with negative chronotropic effects, digoxin). Atropine can be used in emergency situations for symptomatic bradycardia. Pacing is indicated for symptomatic bradycardia, tachycardia- bradycardia syndrome, complete heart block, and for asympto- matic patients with asystolic pauses >3.0 seconds or a ventricular escape rate <40/min. Permanent pacing improves survival in patients with complete heart block, particularly if syncope has occurred.
Tachyarrhythmias
Atrial fibrillation is the most common sustained atrial tachy- arrhythmia and is associated with loss of sinus node function, lead- ing to uncoordinated atrial activity. The electrocardiogram is char- acterized by loss of P waves and irregularity of the ventricular response (Figure 2). Atrial fibrillation is classified according to its duration into acute (<48 hours), chronic (>48 hours), paroxys- mal, or indeterminate; this classification determines the nature of treatment. Symptoms may include palpitations, syncope or pre- syncope, chest pain, dyspnea, or fatigue. Eighty percent of patients with atrial fibrillation have heart disease, including hypertension with left ventricular hypertrophy, valvular heart disease, coro- nary artery disease, cardiomyopathy, congenital heart disease (especially atrial septal defect), or recent open heart surgery. Heart failure and increasing age are also strongly associated with atrial fibrillation.
Chronic atrial fibrillation leads to shortening of the atrial action potential making the arrhythmia more persistent with time. This clinical observation is the basis for the aphorism “atrial fibrillation
begets atrial fibrillation.” Even after only 24 hours of atrial fibril- lation, drug therapy becomes progressively less effective at termi- nating the arrhythmia.
Atrial flutter is characterized by regular atrial contractions (flut- ter waves or sawtooth pattern) on electrocardiography (Figure 3). Untreated, the atrial rate is 240-300/min and is usually associat- ed with a 2:1 or 3:1 atrioventricular block, resulting in a ventric- ular rate of approximately 100-150/min. Sustained atrial flutter is less common than atrial fibrillation, and flutter typically converts to atrial fibrillation over time.
For atrial fibrillation and flutter, screen for noncardiac causes including substances (alcohol, caffeine, cocaine, amphetamines, inhaled β-agonists) pulmonary disease (hypoxia, chronic obstruc- tive pulmonary disease, pulmonary embolism, pulmonary hyper- tension, obstructive sleep apnea), and hyperthyroidism. Obtain an electrocardiogram, complete blood count, electrolytes, glu- cose, serum TSH, pulse oximetry, digoxin level (if taking), base- line coagulation tests, and stool for occult blood before initiating warfarin or heparin. Obtain a transthoracic echocardiogram to evaluate for valvular heart disease and determine chamber size and function. Transesophageal echocardiography may be needed to detect or exclude the presence of intracardiac thrombi, a finding that may influence the timing of cardioversion and the initiation of anticoagulation.
The most common paroxysmal reentrant supraventricular tachycardia involves reentry within atrioventricular nodal tissue. It is a regular, narrow complex tachycardia with a ventricular rate of 160-180/min. A retrograde P wave is typically buried with- in the QRS complex but may occur shortly before or shortly
16 • Cardiovascular Medicine
Figure 2 Electrocardiogram showing two sinus beats and a slow heart rate followed by atrial fibrillation consistent with bradycardia-tachycardia syndrome.
Supraventricular Arrhythmias • 17
Figure 3 Electrocardiogram showing an irregular rate and a saw-tooth pattern in leads II, III, and aVF characteristic of atrial flutter.
Figure 4 Electrocardiogram showing a narrow complex tachycardia with P waves buried in the T wave, most easily seen in lead V2, characteristic of atri-
oventricular nodal reentrant tachycardia.
after it (Figure 4). In the absence of structural heart disease, it is a benign rhythm.
Atrial tachycardia can arise from almost any region of the right or left atrium; the most common mechanism is reentry. The P- wave morphology may be upright, biphasic, or inverted in the
inferior leads, depending on the site of origin. Reentrant atrial tachycardia is frequently associated with structural heart disease; also look for possible digitalis toxicity.
Preexcitation refers to the presence of an accessory pathway that can conduct impulses from the atrium to the ventricle,
bypassing the atrioventricular node. Most patients with preexci- tation demonstrate a short PR interval and an initial slurring of the upstroke of the QRS complex (the delta wave), establishing the diagnosis of Wolff-Parkinson-White syndrome. Because the bypass tract may be capable of rapid antegrade conduction, patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation may experience a very rapid ventricular response that can degen- erate into ventricular fibrillation. The risk of sudden cardiac death in these patients is 0.15%-0.39% over 3-10 year follow-up. Table 1 summarizes a differential diagnosis of supraventricular tachy- cardia based on electrocardiographic features.
Therapy
Consider teaching patients with well-tolerated atrioventricular- nodal-dependent supraventricular tachycardia the Valsalva maneu- ver or carotid massage to help terminate episodes of arrhythmia. These maneuvers may terminate an episode of supraventricular tachycardia by increasing vagal tone, slowing atrioventricular nodal conduction, and increasing atrioventricular nodal refractoriness.
Electrical cardioversion is indicated for hemodynamically unstable patients, regardless of the tachyarrhythmia. Intravenous heparin is started immediately in patients with atrial fibrillation of unknown duration before cardioversion. Potential risks of urgent electrical cardioversion include thromboembolism (2%), tachy- arrhythmias, or bradyarrhythmias. Electrical cardioversion is an alternative to pharmacologic cardioversion of atrial fibrillation of any duration; patients are anticoagulated prior to cardioversion and for up to 4 weeks after cardioversion. Cardioversion is suc- cessful in 70%-90% of patients with atrial fibrillation of less than 48 hours duration and is effective in 50% of patients with longer duration of atrial fibrillation.
Other options to control ventricular rate include atrioventric- ular-nodal catheter ablation techniques or surgery. Pulmonary vein catheter ablation is increasingly used to treat paroxysmal atri- al fibrillation in patients with a structurally normal heart. Foci for atrial fibrillation are commonly located around the ostia of the pul- monary veins; up to 80% of patients with paroxysmal atrial fibril- lation will remain arrhythmia-free after pulmonary vein catheter ablation. Catheter ablation of the accessory bypass tract is the treatment of choice for symptomatic Wolff-Parkinson-White syn- drome. The “maze” surgical procedure consists of multiple atrial
incisions to reduce effective atrial size and prevent formation of atrial fibrillation wavelets; it is 99% effective with operative mor- tality of 1%-3%.
Consider a calcium-channel blocker (i.e., verapamil or dilti- azem) to treat patients who have atrioventricular nodal re-entrant tachycardia to terminate an acute event or to prevent recurrences. Calcium-channel blocking drugs work by slowing atrioventricu- lar conduction and increasing nodal refractoriness.
With cardiology consultation, consider using class I and class III antiarrhythmic agents (Table 2) to treat atrial tachycardia, par- ticularly re-entrant atrial tachycardia. Amiodarone has the least proarrhythmic effect and is the preferred agent in patients with left ventricular dysfunction and structural heart disease.
The stroke rate with nonrheumatic atrial fibrillation is about 5% per year. Risk factors for stroke are history of previous tran- sient ischemic attack or stroke, myocardial infarction, hyperten- sion, age >65 years, diabetes, left atrial enlargement, and left ven- tricular dysfunction. Warfarin (target INR of 2.0-3.0) reduces the risk of stroke by an average of 64% in nonvalvular atrial fibrilla- tion. Chronic anticoagulation is considered if there is high risk for recurrence of atrial fibrillation following successful conversion, current asymptomatic atrial fibrillation, evidence of intracardiac thrombus, or any known risk factors for thromboembolism.
The CHADS2scoring system has been well validated to esti-
mate patient stroke risk. The CHADS2acronym is derived from
the individual stroke risk factors: congestive heart failure, hyper- tension, age >75 years, diabetes mellitus, and prior stroke or tran- sient ischemic attack (TIA). Patients are assigned 2 points for a previous stroke or TIA and 1 point for each of the other risk fac- tors. In patients with a CHADS2score of 0, the risk of stroke is
low and anticoagulation is not required; the risk of major bleed- ing in this category is greater than the benefit from anticoagula- tion. Those with a CHADS2score ≥ 3 and those with a prior TIA
or stroke are at high risk and anticoagulation is indicated; the ben- efit from anticoagulation exceeds the risk of major bleeding. For patients at intermediate risk for stroke (score 1 or 2) warfarin ther- apy should be assessed individually, taking into account the risk of major hemorrhage and patient preference. In these patients, and those in whom full anticoagulation with warfarin is contraindi- cated, aspirin alone decreases stroke risk by 22%.
In patients aged >65 years, heart rate control is preferred to using antiarrhythmic drugs to maintain sinus rhythm because the
18 • Cardiovascular Medicine
Table 1. Differential Diagnosis of Supraventricular Tachycardia Based on Electrocardiographic Features Disease Notes
Atrial fibrillation, atrial flutter Atrial fibrillation is an irregular rhythm with no definitive P waves. Atrial flutter typically has saw-tooth pattern flutter waves, most noticeably in the inferior leads.
Atrial tachycardia (reentrant) Long RP tachycardia.* Commonly associated with structural heart disease.
AV-nodal reentrant tachycardia In the typical variety, the atria and ventricles are simultaneously activated, and either no P wave is visible or a small pseudo r-prime deflection in lead V1 and a pseudo S-wave deflection inferiorly are seen.
AV reentrant tachycardia Short RP tachycardia.* P wave is usually located within the ST segment. Accessory AV pathways can conduct anterograde (atrium to ventricle), retrograde (ventricle to atrium), or in both directions. Only accessory pathways with anterograde conduction will show pre-excitation (Wolff-Parkinson-White pattern) on the ECG (during sinus rhythm).
* RP is the measured interval from the onset of the QRS complex to the onset of the P wave. If the RP interval is longer than the PR interval during tachycardia, the tachycardia is referred as a long-RP tachycardia, whereas if the RP interval is shorter than the PR interval, it is referred as a short-RP tachycardia.
former strategy results in fewer hospitalizations and serious drug reactions. The goal of rate control is to reduce the ventricular rate to <80/min at rest and <100/min during exercise. Calcium-chan- nel blockers (i.e., diltiazem or verapamil) or β-blocking agents (i.e., atenolol or metoprolol) are first-line therapy. Digitalis is not recommended as a single agent for rate control due to its slower onset, increased toxicity, and less efficacy of controlling the ven- tricular rate during exercise.
Rhythm control can be accomplished with Class Ia, Class Ic, and Class III antiarrhythmic agents (see Table 2). Oral or intra- venous antiarrhythmic agents result in successful cardioversion of 60%-90% of patients with atrial fibrillation of <48 hours duration but are less effective in chronic atrial fibrillation. In patients with recurrent symptomatic atrial fibrillation, the choice of an antiar- rhythmic drug depends on the presence or absence of underlying structural heart disease. Propafenone or flecainide may be initiat- ed in the absence of structural heart disease, whereas amiodarone is typically used when underlying heart disease is present. Because these drugs can be proarrhythmic, consultation with cardiology is recommended.
Follow-Up
In patients with atrial fibrillation, assess rate control by asking about easy fatigability and exertional dyspnea and observe for heart rate >100/min while walking. If rate is >100/min, increase the atrioventricular nodal blockade with higher doses of current agent or additional drugs. In patients on warfarin, check INR as often as required to achieve a stable target INR of 2.0-3.0 in non- valvular atrial fibrillation or 2.5-3.5 in valvular atrial fibrillation.
In patients on antiarrhythmic drugs, obtain a 12-lead electro- cardiogram to check QRS and QT intervals for drug toxicity.
Increases in the QRS duration or QT interval may indicate an increased risk of proarrhythmia. Monitor levels of antiarrhythmic drugs when feasible in all patients who are taking pharmacologic therapy for supraventricular tachycardia. Routinely screen patients for side effects of antiarrhythmic therapy. Obtain periodic thyroid function tests, liver chemistry tests, and pulmonary function tests (including diffusing capacity) for patients treated with amiodarone and periodic complete blood counts for patients treated with pro- cainamide. Amiodarone has several severe side effects, including pulmonary fibrosis, hyperthyroidism, hypothyroidism, and hepa- titis. Procainamide can cause agranulocytosis.
Book Enhancement
Go to www.acponline.org/essentials/cardiovascular-section.html to view the mechanism of atrioventricular nodal reentry and atri- oventricular reentry tachycardias, a description of electrocardio- graphic recording devices, and risk estimates of atrial fibrillation related stroke and to access a tutorial on electrocardiography inter- pretation. In MKSAP for Students 4, assess yourself with items 23- 29 in the Cardiovascular Medicine section.
Bibliography
Delacrétaz E.Clinical practice. Supraventricular tachycardia. N Engl J Med. 2006;354:1039-51. [PMID: 16525141]
Ferrari VA, Callans D, Wiegers S.Atrial Fibrillation. http://pier.acponline .org/physicians/diseases/d027. [Date accessed: 2008 Jan 23] In: PIER [online database]. Philadelphia: American College of Physicians; 2008.
Mangrum JM, DiMarco JP. The evaluation and management of bradycar- dia. N Engl J Med. 2000;342:703-9. [PMID: 10706901]
Supraventricular Arrhythmias • 19
Table 2. Antiarrhythmic Agents Class Ia
Procainamide Prolongs conduction and slows repolarization by blocking inward sodium flux. Recommended for Wolff-Parkinson-White syndrome. Not for use in patients with severe left ventricular dysfunction; avoid in patients with renal impairment. Quinidine gluconate Prolongs conduction and slows repolarization. Blocks fast inward sodium channel. Adjust dose in patients with
renal insufficiency.
Disopyramide Similar electrophysiologic properties to procainamide and quinidine. Rarely used.
Class Ic
Flecainide Blocks sodium channels (and fast sodium current). Not for use in patients with structurally abnormal hearts. Propafenone Blocks myocardial sodium channels. Antiarrhythmic and weak calcium channel and β-blocking properties.
Class III
Amiodarone Blocks sodium channels (affinity for inactivated channels). Noncompetitive α- and β-receptor inhibitor. Safest agent for use in patients with structural heart disease and can be used for Wolff-Parkinson-White syndrome.
Dofetilide Blocks rapid component of the delayed rectifier potassium current, prolonging refractoriness without slowing conduction. Must be strictly dosed according to renal function, body size, and age.
Ibutilide Prolongs action potential duration (and atrial and ventricular refractoriness) by blocking rapid component of delayed rectifier potassium current.
Sotalol Nonselective β-blocking properties but some positive inotropic activity. Lethal arrhythmias possible. Adjust dose in patients with renal insufficiency.
20
V
entricular tachycardia is a potentially life threatening arrhythmia due to rapid, depolarizing impulses origi- nating from the His-Purkinje system, the ventricular myocardium, or both. Ventricular tachycardia requires imme- diate evaluation and, at times, treatment as it can lead to sud- den cardiac death.The pathophysiology of ventricular tachycardia is most com- monly due to abnormalities of impulse conduction (i.e., a reentrant pathway). Once the reentrant pathway is initiated, repetitive cir- culation of the impulse over the loop can produce ventricular tachycardia. Ventricular tachycardia may also arise through abnor- mal impulse formation such as enhanced automaticity or triggered activity. Enhancement of normal automaticity in latent pacemak- er fibers or the development of abnormal automaticity due to par- tial resting membrane depolarization can serve as a nidus for ven- tricular tachycardia. Triggered activity does not occur spontaneously; it requires a change in cardiac electrical frequency as a “trigger” such as early depolarizations.
Ventricular tachycardia often accompanies structural heart dis- ease, most commonly ischemic heart disease, and is associated with electrolyte disorders (e.g., hypokalemia and hypomagnesemia), drug toxicity, prolonged QT syndrome, valvular heart disease, and nonischemic cardiomyopathy.
Ventricular tachycardia is typically subdivided into sustained
ventricular tachycardia (persists >30 seconds or requires termina-
tion due to hemodynamic collapse) and nonsustained ventricular
tachycardia (≥3 beats and ≤30 seconds). Ventricular tachycardia is
also categorized by the morphology of the QRS complexes; ven- tricular tachycardia is monomorphic if QRS complexes in the same leads do not vary in contour (Figure 1) or polymorphic if the QRS complexes in the same leads do vary in contour (Figure 2). Proper use of these terms and the patient context in which ventricular tachycardia occurs are essential for accurate diagnosis and thera- py. It is also imperative to determine the underlying cause of ven- tricular tachycardia.
Prevention
Because ventricular tachycardia often occurs in the setting of ischemic heart disease, identification and reduction of risk factors for coronary artery disease is indicated.
Screening
Routine screening for ventricular tachycardia in asymptomatic per- sons is not recommended. Asymptomatic patients with a family
history of sudden cardiac death may have long QT syndrome, arrhythmogenic right ventricular dysplasia, or Brugada syndrome (an ion channel disorder associated with incomplete right bun- dle branch block). A screening electrocardiogram is reasonable in these patients.
Diagnosis
Symptoms are dependent upon several factors, including the ven- tricular rate, the duration of tachycardia, and the presence of underlying heart disease. Patients with nonsustained ventricular
tachycardia usually are asymptomatic but may experience palpita-
tions. Patients with sustained ventricular tachycardia usually present with syncope or near syncope and can also present with sudden cardiac death.
Ventricular tachyarrhythmias consist of ventricular tachycar- dia, ventricular fibrillation, and torsades de pointes (a special sub- set of polymorphic ventricular tachycardia). Ventricular tach- yarrhythmias are characterized by wide complex QRS morphology (QRS >0.12 sec) and ventricular rate >100/min. In ventricular tachycardia, the ventricular rate typically ranges from 140- 250/min, ventricular fibrillation rate is typically >300/min, and torsades is characterized by a ventricular rate of 200-300/min.
Premature ventricular contractions and other ventricular arrhythmias increase in both prevalence and complexity as the pop- ulation ages. Although premature ventricular contractions appear to be more frequent in patients with heart disease, they have min- imal prognostic significance if left ventricular function is preserved. Among persons with a depressed ejection fraction, frequent pre- mature ventricular contractions are associated with increased mor- tality, but suppression of premature ventricular contractions with antiarrhythmic drugs does not improve clinical outcome.
Supraventricular tachycardia with a wide QRS complex, usu-
ally due to coexisting bundle-branch block or pre-excitation syn- drome (Wolff-Parkinson-White), can mimic ventricular tachycar- dia. Differentiating ventricular tachycardia from supraventricular
tachycardia with aberrant conduction is important because the
treatment differs markedly. Ventricular tachycardia is more com- mon than supraventricular tachycardia with aberrancy, particularly in individuals with structural heart disease. A key point is that any wide QRS tachycardia should be considered to be ventricular tachy- cardia until proven otherwise (Figure 3). The most important dif- ferentiating point is the history of ischemic heart disease. In the presence of known structural heart disease, especially a prior myocardial infarction, the diagnosis of ventricular tachycardia is almost certain. Other clues include more profound hemodynamic