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Supraventricular Tachyarrhythmias

These rapid, irregular heart beats are associated with an atrial rate of a 100 or more a minute; the ventricular rate may be less when AV conduction is incomplete.

Supraventricular tachycardias (SPVT) usually have narrow QRS complexes, but they may be wide because of aberrant counduction through the intraventricular conducting tissue, participation of a bypass tract in the intraventricular depolarization pattern,or in the presence of a coexiting bundle branch block.

They originate above the bifurcation of the bundle of His. They may be sudden and brief, persistent or chronic, lasting for seconds, hours, to days or weeks (chronic).

The chronic and recurrent ones are related to underlying structural causes like atrial disease or mitral disease. Persistent episodes may be caused by drug toxicity, low potassium levels, and lung disease.

A. The paroxysmal SPVT tend to be recurrent and of short duration (seconds to hours) to days or weeks:
1. SPVT due to AV nodal reentry or WPW syndrome (figure3);

2. Paroxysmal atrial flutter or fibrillation.

B. The persistent ones (sinus tachycardia, nonparoxysmal ectopic atrial tachycardia, multifocal atrial tachycardia, longer episodes of PSVT or atrial flutter or fibrillation) may last for days to weeks and may be associated with a specific contributing pathophysiologic factor such as:

1. decompensated chronic lung disease (COPD),
2. pulmonary emboli,
3. electrolyte disturbences(low potassium levels),
4. drug toxicity (digoxin, figure 4).

C. They tend to be recucurrent when an underlying structural cause such as atrial disease or mitral disease is the dominant pathophysiologic factor.

D. They are transient when functional abnormality dominates (hypoxemia, heart failure, electrolyte abnormality).

E. The chronic or long standing PSVT'S like atrial flutter or fibrillation do not revert without treatment,often fail to revert even with attempted treatment and if reverted will often recur despite therapy.

F. The most common form of paroxysmal supraventricular tachycardia (PSVT) is AV nodal reentry due to dual pathways of excitation in the region of the AV node (see Figure 1).

G. There is a slow conduction pathway as well as a fast one. When there is a disturbance in the normal conduction through the fast pathway, the slow pathway may be activated to conduct the excitation wave to the bundle of His, as well as retrograde back to the fast one, and then back again down the slow pathway continuously to produce the PSVT (see Figure 1).

Management of PSVT due to AV nodal reentry.

1. In acute situations rest and sedation plus carotid artery (one on each side of the front of the neck) sinus massage may be adequate and effective.

2. Medications include intravenous adenosine (see figure 2), calcium- entry blockers, digoxin, beta-adrenergic blockers.

3. Long term management include medications like digoxin, propranolol (inderal) or verapamil.

Radiofrequency catheter ablation techniques are safe and effective as well, especially for patients with poor tolerance to drugs (see figure figure 3b radiofrequency ablation in WPW, as well as in the treatment of atrial flutter and fibrillation by identifying tract carrying the excitation impulse).

Reference:Zipes,D.P.,Clinical Application of the EKG,JACC Vol.36,No.6,2000

Supraventricular Tachycardia, Wolff-Parkinson-White Syndrome

Synonyms and related keywords: WPW syndrome, preexcitation syndromes, preexcitation and paroxysms of tachycardia, accessory pathway, AP

Author: Robert Hamilton, MD, Acting Chief, Division of Cardiology, Associate Professor, Department of Pediatrics, The Hospital for Sick Children and University of Toronto, Canada

Coauthor(s): Shubhayan Sanatani, MD , Consulting Staff, Division of Pediatric Cardiology, Children's and Women's Health Center of British Columbia, Assistant Professor, Department of Pediatrics, University of British Columbia at Vancouver



In 1930, Wolff, Parkinson, and White described a series of young patients who had a bundle branch block pattern on electrocardiography (ECG), a short PR interval, and paroxysms of tachycardia. Case reports began appearing in the literature in the late 1930s and early 1940s, and the term Wolff-Parkinson-White (WPW) syndrome was coined in 1940. In 1943, the existence of an accessory connection between atria and ventricles was confirmed, which is about 50 years after Kent's description of myocardial fibers that were believed to conduct from atria to ventricle.

The term preexcitation was first published by Ohnell in 1944 (the same year that the term delta wave was coined); "preexcitation indicates an additional excitatory spread in the ventricles of the heart, coupled to auricular excitation." WPW syndrome is not the only form of preexcitation, but it is the most common. Initially, through the surgical treatment of WPW syndrome and, now in the era of radiofrequency (RF) ablation, understanding of the pathophysiology of WPW syndrome has become refined in the wake of these elegant descriptions.

The first surgical division of an accessory pathway (AP) was performed at Duke University by Will C. Sealy, MD, in 1968. The first catheter ablation was reported in 1983, using DC energy; this was followed by the first successful RF ablation reported in 1987.


The underlying defect in WPW syndrome is the presence of an AP consisting of a myocardial connection at the atrioventricular (AV) junction. These are believed to be residual connections from the formation of the AV junction. The primary feature differentiating WPW syndrome from other AP-mediated supraventricular tachycardias (SVTs) is the ability of the AP to conduct antegradely (ie, from atrium to ventricles) and retrogradely. The presence of this AP allows a reentrant tachycardia circuit to be established. In orthodromic SVT, the conduction is through the AV node to the ventricles, then back to the atria via the AP. Because the AP can conduct in both directions, experiencing antidromic tachycardia is also possible, in which the conduction from atrium to ventricle occurs via the AP, resulting in a broad complex tachycardia.

The presence of an antegrade AV connection also allows atrial arrhythmias to be conducted to the ventricles without passing through the AV node. Patients with WPW syndrome can more frequently develop atrial fibrillation, which can potentially be conducted to the ventricles rapidly (see Mortality/Morbidity).

The different patterns of preexcitation have produced various classification systems. Classification by type is largely obsolete, and, currently, classification by anatomic location of the AP is used. The most common AP location is at the left free wall.



WPW syndrome refers to preexcitation and paroxysms of tachycardia. The WPW pattern refers to the ECG pattern. The incidence of the WPW pattern is unknown but is estimated to be 1-2 cases per 1000 population. This may be an underestimate because it often represents an asymptomatic ECG finding. The incidence of newly diagnosed cases of WPW syndrome is approximately 4 cases per 100,000 population per year.


The incidence of sudden cardiac death (SCD) in WPW syndrome is approximately 1 in 100 symptomatic cases when followed for up to 15 years. Although relatively uncommon, SCD may be the initial presentation in as many as 4.5% of cases. The cause of SCD in WPW syndrome is rapid conduction of atrial fibrillation (AF) to the ventricles via the AP, resulting in ventricular fibrillation (VF). AF develops in one fifth to one third of patients with WPW syndrome; the reasons for this and the effects of AP ablation on its development are unclear.

Certain factors increase the likelihood of VF, including rapidly conducting APs and multiple pathways. Cases have also been reported in association with esophageal studies, digoxin, and verapamil. A few reports document spontaneous VF in WPW syndrome, and SVT may degenerate into AF, thus leading to VF; however, both scenarios are rare in pediatric patients.

The morbidity in WPW syndrome results predominantly from AV reciprocating SVT. Even in the absence of VF, syncope is an occasional presenting symptom. However, in most patients, the SVT is well tolerated and not life threatening. If a patient experiences incessant tachycardia, cardiomyopathy may develop.


A male-to-female ratio of approximately 2:1 has been documented in some series. In other series, the syndrome was found to be more frequent in men (1.4 per 1000) than in women (0.9 per 1000). A recent Belgian study indicates a 3.5-fold higher prevalence of WPW in men than in women.


People with WPW syndrome may present at any age, with many patients presenting in infancy. A bimodal age distribution is observed in pediatric patients, with a second peak in school-aged children.



The presentations of WPW syndrome are as diverse as an incidental finding to syncope or sudden death.

Patients usually present with symptomatic orthodromic SVT. This is usually well tolerated and not a high risk, especially in the pediatric population after young infancy.

The infant is often noted to be irritable, to not tolerate feedings, or to demonstrate evidence of congestive heart failure.

Infants often have a history of not behaving as usual for 1 or 2 days.

An intercurrent febrile illness is often observed.

The verbal child usually reports chest pain, palpitations, or breathing difficulty.

Most children are previously well, and a minority of children have a positive family history of this condition.

Older patients can usually describe the sudden onset of a pounding heartbeat, which is regular and "too rapid to count." This is accompanied by a concomitant change in their tolerance for activity.

Look for an irregular rhythm because this may herald the presence of AF.


During an episode of SVT, the infant is usually tachypneic and irritable; pallor is common. The pulse is very rapid and diminished in volume. The ventricular rate typically is 200-250 bpm, and the blood pressure is decreased. If the episode has been untreated for several hours, the patient often has poor perfusion, hepatomegaly, and cardiac failure. The child is usually anxious but hemodynamically stable. Tachypnea often accompanies the tachycardia.

Once the arrhythmia has been terminated, the physical examination findings are generally normal.

In several series, the incidence of associated congenital heart disease (CHD) is reported to be as high as 30%, most commonly Ebstein anomaly of the tricuspid valve and "corrected" transposition of the great arteries {S,L,L}.

A genetic locus linking hypertrophic cardiomyopathy to WPW syndrome has been found on chromosome 7.

The findings of the underlying condition often become apparent only after the SVT has been terminated, although the hemodynamic consequences may be poorly tolerated in the presence of CHD.


APs are considered congenital phenomena, which are related to a failure of insulating tissue maturation within the AV ring. A proportion of patients with preexcitation may have a genetic predisposition. One example of such a predisposition is the association of preexcitation with a certain hypertrophic cardiomyopathy locus on chromosome 7.

Preexcitation can be created surgically, such as in certain types of Bjork modifications of the Fontan procedure, if atrial tissue is flapped onto and sutured to ventricular tissue.

Certain tumors of the AV ring, such as rhabdomyomas, may also cause preexcitation.


Ventricular Tachycardia

Other Problems to be Considered:

The differential diagnosis for a narrow complex tachycardia is extensive and the term SVT is nonspecific. Automatic versus reentrant mechanisms may be differentiated by the presence of a warm-up or cool-down period. A regular tachycardia, allowing for some cycle length oscillation, favors a reentrant mechanism. The most common mechanism in pediatrics is AP-mediated SVT. The main differential during SVT is whether the AP is concealed (ie, conducts only from ventricle to atrium).

Few entities involve paroxysms of SVT with a WPW ECG in sinus rhythm. Occasionally, a low atrial focus produces the appearance of a short PR interval. The preexcitation associated with atriofascicular APs (so-called Mahaim) is associated with a normal PR interval. Patients with so-called Lown-Ganong-Levine syndrome demonstrate a short PR interval but not a broad QRS morphology. This terminology is currently out of favor but is historically relevant.

Aberrantly conducting orthodromic SVT must be differentiated from VT. Antidromic tachycardia must also be differentiated from VT or Mahaim fiber tachycardia..


Lab Studies:

The extent of the workup is determined by the acuity of the patient’s illness. In the patient who has cardiogenic shock or is unconscious, direct current (DC) cardioversion is indicated as soon as an arrhythmia is identified to be causative. Once the patient is hemodynamically stable or in the context of assessment following an arrest, measuring blood gases, electrolytes, lactate levels, and drug screening may be appropriate.

Imaging Studies:

Perform echocardiography, focusing on cardiac function and dimensions to rule out cardiomyopathy and associated CHD (eg, hypertrophic cardiomyopathy, Ebstein anomaly, L-transposition of the great vessels). Significantly depressed function may be observed in the setting of an acute arrhythmia but should typically normalize in the absence of an incessant tachycardia.

Other Tests:

Obtaining a 12-lead ECG is necessary in stable patients. The characteristic features are a short PR interval, often with no isoelectric line between the end of the P wave and the beginning of the QRS complex. The QRS is usually broad and has accompanying ST changes. In patients demonstrating intermittent preexcitation, ECG findings may appear normal or even demonstrate 2 distinct QRS patterns. Several algorithms are available to predict the location of the AP, which assists in planning an ablation and in counseling about the risks of the procedure. During orthodromic tachycardia, a narrow complex QRS is evident with the P wave often detectable as a subtle deflection within the T wave.

Further workup generally consists of Holter monitoring to detect intermittent preexcitation and occult episodes of SVT.

An exercise test may also be helpful in studying the behavior of the AP at higher heart rates; however, this test has limited predictive value.

In the presence of WPW syndrome without documented SVT and in the presence of symptoms, a transtelephonic transient cardiac event monitor or a longer-term monitoring system may be appropriate.


An esophageal electrophysiology study can be used to assess the behavior of the AP, the inducibility of SVT, and the response to drug therapy. This procedure can be performed safely as an outpatient procedure requiring only sedation. An invasive electrophysiology study can also be performed for these risk-stratification indications, but this is usually reserved for patients undergoing RF ablation.

Histologic Findings:

An extremely detailed postmortem assessment of histology from multiple sections around the AV ring may identify APs, but this approach is impractical for assessment of every patient with unexplained sudden death.


Medical Care:

Short-term management of WPW syndrome

Patients presenting in cardiac arrest or with hemodynamic compromise require management of the airway, breathing, and circulation, as is standard; this includes having a defibrillator available and providing appropriate monitoring. Once the patient is determined to be experiencing an arrhythmia, DC cardioversion is indicated.

In the stable patient, a variety of vagal maneuvers may be attempted. A bag of ice slurry to the face is very effective in infants. Older children may be able to perform a Valsalva maneuver. Creative alternatives abound, such as having a patient blow with his thumb in his mouth. Unilateral carotid sinus massage may also be attempted. Ocular compression should not be performed because it has been associated with retinal injury.

When conservative measures fail, intravenous access is necessary. Adenosine is the first-line agent and is effective in approximately 90% of reentrant narrow complex tachycardias. Adenosine must be administered as a rapid bolus because of its short half-life. Most adenosine failure is caused by inadequate administration of the drug. A defibrillator must be available in the event that new arrhythmias emerge, particularly atrial fibrillation postadenosine.

Procainamide or esmolol are available in the resistant cases but should only be administered by physicians familiar with these medications. Do not administer verapamil to infants; this drug has also been reported to accelerate the ventricular rate in AF, leading to rapid conduction that results in VF.

Long-term management of WPW syndrome

Treatment must be individualized for each patient and should include individual risk assessment. Despite the importance of risk stratification to assess the risk of sudden death, few reliable noninvasive markers exist. The adult literature has focussed on preexcited R-R intervals in AF as an indicator of the ability to rapidly conduct. In a series of 60 pediatric patients, a preexcited R-R interval of less than 220 milliseconds identified patients at high risk for cardiac arrest; thus, if an AP can conduct impulses at a rate of 4 per second, it can be considered a high-risk pathway. Ambulatory monitoring and treadmill testing can provide additional noninvasive information if the preexcitation disappears suddenly at a discrete heart rate. However, be careful when interpreting these noninvasive test results. Perform invasive risk assessment in patients presenting with syncope or aborted SCD.

Long-term oral medication is the mainstay of therapy in patients not undergoing RF ablation. Some of the drugs available are listed below. Note that digoxin and verapamil are contraindicated in the long-term therapy of WPW syndrome.

Surgical Care: In the era of RF ablation, eradicating AP function in almost any patient with the WPW pattern on ECG is feasible. However, because RF ablation is not without its risks, perform an assessment of the risk-to-benefit ratio for all patients. Individuals with low-risk APs, such as adults who have never had symptoms and who do not participate in extremes of competition, are not usually considered candidates for RF ablation of an AP. Patient preference is the most common indication for RF ablation in symptomatic patients not at high risk. The procedure is relatively safe, with a complication rate of approximately 1% in most centers. Success rates range from approximately 85-95%, with a 5% recurrence risk.


Patients with appropriately evaluated and treated WPW syndrome should be able to participate in all activities, assuming that patients with high-risk pathways receive treatment with RF ablation or a pathway-specific antiarrhythmic agent. Generally, if a patient is significantly altering his or her lifestyle because of the disease, he or she is probably not receiving adequate or appropriate therapy.

In many jurisdictions, the presence of preexcitation excludes patients from participating in the armed services and piloting commercial flights.


Emergency treatment in patients with hemodynamic instability is directed to convert the rhythm to sinus through a brief episode of AV block. Adenosine is the drug of choice for immediate conversion of narrow complex SVT, but it should not be used and is contraindicated for preexcited atrial fibrillation. Esmolol has also been used with some success.

Beta-blockers are probably the most common medication used to treat SVT in the presence of preexcitation. They are moderately effective and have frequent, but rarely life-threatening, adverse effects (except in the presence of reactive airway disease). The efficacy of beta-blockers in reducing the risk of accelerated conduction of atrial fibrillation in patients with WPW syndrome is unclear. More potent medications, such as flecainide, propafenone, sotalol, or amiodarone, may have more effect on AP conduction or refractoriness than beta-blockers, and they are preferred by some. The use of digoxin or verapamil for long-term therapy appears to be contraindicated for many WPW patients because these medications may shorten the refractory period of an AP.

Drug Category:

Antiarrhythmic agents -- These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Category 1 Adenosine (Adenocard)
Drug Name Adenosine (Adenocard) -- Slows conduction time through the AV node. Can interrupt reentry pathways through AV node and restore normal sinus rhythm in paroxysmal supraventricular tachycardia (PSVT).
Adult Dose

6 mg rapid IV bolus over 1-2 s initial; if no response within 1-2 min, administer 12 mg rapid IV bolus; repeat once with 12 mg/dose IV prn

Pediatric Dose Infants and children: 0.1 mg/kg IV; repeat with 0.2 mg/kg IV if first dose not effective; not to exceed 12 mg/dose; alternatively, 0.05 mg/kg IV; if not effective within 2 min, increase by 0.05-mg/kg increments q2min; not to exceed 0.25 mg/kg or 12 mg/dose
Contraindications Documented hypersensitivity; heart transplant patients (known to be hypersensitive to adenosine); second- or third-degree AV block; bradycardia; sick sinus syndrome (except in patients with functioning artificial pacemaker)
Interactions Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects; methylxanthines (eg, theophylline) may antagonize effects
Pregnancy C -Safety for use during pregnancy has not been established.


Proper administration technique (ie, thoroughly flushing IV line after rapid infusion) is essential to obtain adequate results; adenosine-induced bronchoconstriction in patients with asthma may occur; heart block, including transient asystole may occur, proarrhythmia such as atrial or ventricular fibrillation may rarely occur; cardioversion must be available during adenosine administration

Drug Name

Esmolol (Brevibloc) -- Excellent for patients at risk of complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Category 2 Esmolol (Brevibloc)
Adult Dose 250-500 mcg/kg/min IV loading dose for 1 min; followed by a 4-min maintenance infusion of 50 mcg/kg/min IV; if adequate therapeutic effect (decreased HR and BP) not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 100 mcg/kg/min (for 4 min); sequence may be repeated q5-10min, increasing maintenance infusion by 50 mcg/kg/min with each sequence; not to exceed 200 mcg/kg/min
Pediatric Dose Infants and children: Limited information is available; suggested dose is 100-500 mcg/kg IV administered over 1 min initial; followed by 200 mcg/kg/min IV; titrate upward by 50-100 mcg/kg/min q5-10min until HR or BP decreases by >10%; usual dose is 550 mcg/kg/min (range is 300-1000 mcg/kg/min)
Contraindications Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities; significant reactive airways disease
Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn (withdraw drug slowly and monitor patient closely)

Drug Name

Propranolol (Inderal) -- Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

Category 3 Propranolol (Inderal)
Adult Dose 1-3 mg IV (under careful monitoring); not to exceed 1 mg/min to avoid lowering of blood pressure and causing cardiac standstill
Allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn; thereafter, do not administered additional drug in <4 h
Do not continue doses after desired alteration in rate or rhythm achieved; switch to PO as soon as possible; 10-30 mg PO tid/qid (usual); alternatively, administer total daily dose as SR product qd
Pediatric Dose 0.5-1 mg/kg/d PO divided q6-8h initial; titrate upward q3-5d prn; typical dose is 2.5-5 mg/kg/d; not to exceed 16 mg/kg/d or 60 mg/d; in older children, total daily PO dose may be administered as SR product qd
0.01-0.1 mg/kg IV administered over 10 min; not to exceed 1 mg (infants) and 3 mg (children)
Contraindications Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
Interactions Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

C - Safety for use during pregnancy has not been established.

Precautions Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm (withdraw drug slowly and monitor closely)

Drug Name

Sotalol (Betapace) -- Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Category 4 Sotalol (Betapace)
Adult Dose 80 mg PO bid; gradually increase dose q2-3d to 240-320 mg/d
Pediatric Dose Not established; the following doses have been suggested:
Initial: 200 mg/m2/d PO divided bid/tid; not to exceed 160 mg/d
Maintenance: 2-8 mg/kg/d (40-350 mg/m2/d) PO divided bid/tid


Documented hypersensitivity; sinus bradycardia; second- and third-degree AV block; prolonged QT

Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm (withdraw drug slowly and monitor patient closely); caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and congestive heart failure; slower dose titration and lower maintenance doses required in renal impairment

Drug Name

Atenolol (Tenormin) -- Selectively blocks beta1-receptors with little or no effect on beta2 types.

Category 5 Atenolol (Tenormin)
Adult Dose
50 mg PO qd; increase to 100 mg/d, if necessary
Pediatric Dose 0.8-1.5 mg/kg PO qd; not to exceed 2 mg/kg/d
Contraindications Documented hypersensitivity; congestive heart failure; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)
Interactions Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol
Pregnancy D - Unsafe in pregnancy
Precautions Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during an IV, carefully monitor BP, heart rate, and ECG

Drug Name

Amiodarone (Cordarone) -- May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.

Category 6 Amiodarone (Cordarone)
Adult Dose Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk; then decrease to 600-800 mg/d in 1-2 doses for 1 mo; alternatively, 150 mg (10 mL) IV over first 10 min; followed by 360 mg (200 mL) IV over next 6 h; then 540 mg IV over next 18 h
Maintenance dose: 400 mg/d PO
Pediatric Dose Loading dose: 10-15 mg/kg/d PO or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained; reduce to 5 mg/kg/d or 200-400 mg/1.73 m2/d for several wk
Limited data available for IV loading dose
Maintenance dose: 2.5 mg/kg/d PO or lowest effective dose following loading
Contraindications Documented hypersensitivity; complete AV block; intraventricular conduction defects
Interactions Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in breastfeeding women, thyroid disease, or liver disease; may cause proarrhythmic effect, optic neuritis, CNS toxicity, hypothyroidism, hepatotoxicity, interstitial pneumonitis, or pulmonary fibrosis

Drug Name

Flecainide (Tambocor) -- Treats life-threatening ventricular arrhythmias. Causes a prolongation of refractory periods and decreases action potential without affecting duration. Blocks sodium channels, producing a dose-related decrease of intracardiac conduction in all parts of the heart with greatest effect on the His-Purkinje system (H-V conduction). Effects upon AV nodal conduction time and intraatrial conduction times, although present, are less pronounced than on ventricular conduction velocity.

Category 7 Flecainide (Tambocor)
Adult Dose 100 mg PO q12h; may increase by 100 mg/d q4d until adequate response achieved; not to exceed 400 mg/d
Pediatric Dose Initial dose: 1-3 mg/kg/d PO or 50-100 mg/m2/d PO divided tid; may increase gradually by 50 mg/m2/d q5d until adequate response achieved; not to exceed 8 mg/kg/d (200 mg/m2/d)
<6 months: Initiate at lowest dose
Maintenance dose: Usually 3-6 mg/kg/d PO or 100-150 mg/m2/d PO divided tid
Contraindications Documented hypersensitivity; third-degree AV block; right bundle branch block when associated with left hemiblock (bifascicular block) unless a pacemaker is present; cardiogenic shock
Interactions Beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; may increase digoxin serum levels; CYP2D6 inhibitors (eg, ritonavir, amiodarone, cimetidine) may increase serum levels and cardiotoxicity
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Because of proarrhythmic effect and associated deaths, should only be used for life-threatening arrhythmias, caution in renal or hepatic impairment (adjust dose), CHF, and post-MI

Drug Name

Verapamil (Calan) -- Interrupts reentry at AV node. Restores normal sinus rhythm in patients with PSVT. Used for short-term treatment only in children >2 y. Not intended for long-term treatment because of shortened refractory period. Do not use in children <2 y because of severe hypotension.

Category 8 Verapamil (Calan)
Adult Dose 240-480 mg/d ER PO qd or IR divided q6-8h
Alternatively, 5-10 mg IV followed by a second dose 15-30 min later if patient does not satisfactorily respond to initial dose
Pediatric Dose <2 years or <15 kilograms: Contraindicated
>2 years or >15 kilograms: 1-3 mg/kg PO q8h or for rapid treatment, 0.1-0.3 mg/kg IV administered over 2 min; may repeat q30min prn if hemodynamically stable; not to exceed 10 mg/dose
Contraindications Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic); IV administration in children <2 y (deaths reported)
Interactions May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers may increase cardiac depression; cimetidine may increase verapamil levels; verapamil may increase theophylline levels
Pregnancy C - Safety for use during pregnancy has not been established.

Precautions: Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment), monitor liver function periodically.

Drug Name

Propafenone (Rythmol) -- Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging the refractory period.

Category 9 Verapamil (Calan)

Category 10 Propafenone (Rythmol)

Adult Dose 150 mg PO q8h initial; may increase at q3-4d; not to exceed 300 mg q8h
Pediatric Dose Infants and children: Not established; the following doses have been suggested:
150-400 mg/m2/d PO divided tid/qid; may increase by 100 mg/m2/d q2-3d to achieve adequate control; not to exceed 600 mg/m2 /d; alternatively, 8-10 mg/kg/d PO divided tid/qid; may increase by 2 mg/kg/d to achieve adequate control; not to exceed 20 mg/kg/d
Contraindications Documented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure; coadministration with ritonavir or amprenavir
Interactions Inhibits CYP2D6 and may decrease serum levels of isoenzyme substrates (eg, rifampin, cimetidine, quinidine, warfarin); inhibitors of CYP2D6 (eg, beta-blockers, amiodarone, paroxetine, fluoxetine, ritonavir), CYP1A2 (eg, cimetidine, ritonavir), or CYP3A4 (eg, amprenavir, ritonavir, erythromycin, amiodarone, fluoxetine) may increase blood levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Only use for life-threatening arrhythmias; caution in patients with congestive heart failure, myocardial infarction, or hepatic dysfunction (adjust dose)


Further Outpatient Care:

Follow-up care with a cardiologist is indicated for patients with WPW syndrome.

Asymptomatic patients who have a low-risk pathway and no SVT can be monitored expectantly.

Symptomatic individuals should undergo risk assessment and should be offered therapy according to their symptoms. RF ablation can be curative and carried out with a high degree of success, a low complication rate, and a low recurrence rate.


Ideally, if transfer of patients with WPW syndrome and other causes of SVT is indicated, they undergo conversion of their rhythm in the referring institution and are transferred in sinus rhythm.


Screening of school-aged children or athletes through preparticipation evaluation has been suggested but, so far, has not been considered cost-effective.


Once identified and appropriately treated, WPW syndrome is associated with an excellent prognosis, including the potential for permanent cure through RF catheter ablation.


Medical/Legal Pitfalls:

Failure to recognize this disorder or incorrect treatment resulting in deterioration can result in medicolegal vulnerability.

Controversies exist regarding athletes with WPW syndrome. Risk-stratification testing has false-negative results, with potential for adverse outcomes despite test results in patients deemed at low risk.

Special Concerns:

Patients interested in certain professions (eg, professional athlete, pilot) may be excluded based on WPW syndrome.



The above drawing on the left depicts normal conduction of the electrical impulse from the sinus node throuigh the atrioventricular nodal (AV) His-Purkinje system down into bundle branches, with the normal ECG pattern illustrated.

But the diagram on right shows the abnormal preexcitation conduction (in the WPW syndrome) from the sinus node through the accessory pathway (AP) with the shorter refractory period, reaching the ventricles earlier with a short PR interval (less than 120msec.). As a result, the onset of the QRS ECG complex has a slurred upstroke (illustrated), causing a wide QRS and secondary T wave inversion.
(From Jin-Ho Choi's Beginner's Guide to Electrocardiography, Goto heartkorea.com // Index)


The next diagram above shows how the AP can be concealed if the electrical impulse is conducted retrograde through the pathway and antegrade through the AV His-Purkinje tissue to reach the ventricles, and cause a narrow QRS tachycardia (Orthodromic supraventricular tachycardia, SVT) as shown in the next drawings:

- svt-fig3

- svt-fig4

But if the impulse is conducted antegrade through the AP and retrograde through the AV His-Purkinje tissue a wide QRS complex tachycardia (Antidromic SVT) occurs (see diagram above).
From Jin-Ho Choi's Beginner's Guide to Electrocardiography, Goto heartkorea.com // Index.

- svt-fig5

- svt-fig6

Also, a very rapid, irregulary irregular wide QRS tachycardia called atrial fibrillation (AF) may occur, and can deteriorate into ventricular fibrillation VF) illustrated above.

Steps in Location of the AP or Bypass Tract

From Jin-Ho Choi's Beginner's Guide to Electrocardiography, Goto heartkorea.com // Index.

1. As shown in the illustration above, check for the delta wave and QRS position in ECG lead V-1.

2. If the delta wave is negative at lead V-1, the bypass tract (AP) is located in the right ventricle (RV). See figure svt-fig4 .

a). AP is located in posteroseptal area, if delta wave and QRS in Leads II, III, and AVF leads negative. See figure svt-fig4 .
b). AP is in the anteroseptal area if the delta wave is in the inferior axis.

c). If the delta wave is in the left axis, AP is in the RV free wall.

3. If the delta wave is positive at lead V-1, AP is in the left ventricle (LV).

a). If the delta wave and the QRS in leads II, III, and AVF negative, the AP is in the left posteroseptal area. See figure svt-fig3 .

b). The AP is in the lateral LV, if isoelectric or negative delta and QRS in leftward leads I, AVL,V-5, and V-6.

Approach to the Adult Patient with Supraventricular Tachycardia

by Adam Zivin, MD, Best Practice of Medicine. July 2001.

Figure 1. Possible origins of tachycardia

Re-entry in the sinoatrial node (SANRT), atrioventricular node (AVNRT), and atrial myocardium (atrial tachycardia): right anterior oblique view.

Figure 2. Possible origins of tachycardia

Orthodromic reciprocating tachycardia (ORT) in which accessory pathway is used for retrograde conduction: sagittal view.

Figure 3. Normal conduction and origin of pre-excitation

A, activation originating from the sinoatrial node and normally conducted to the ventricles via the atrioventricular node and the His-Purkinje system: sagittal view. B, activation originating from the sinoatrial node and conducted to the ventricles by both the AV node and the accessory pathway, resulting in a fusion beat with a delta wave: sagittal view.

Figure 4. Orthodromic reciprocating tachycardia using an accessory pathway

A, circuit of orthodromic reciprocating tachycardia (ORT) causing narrow-complex tachycardia. B, limb-lead recording from a patient with ORT owing to a concealed left-lateral accessory pathway. Note the retrograde P wave visible ~80 msec after the end of the QRS complex.

Figure 5. Antidromic reciprocating tachycardia

A, circuit of antidromic reciprocating tachycardia (ART). B, recording of ART in a patient with a left-sided accessory pathway.

Figure 6. Limb lead recording from a patient with AVNRT

Note the retrograde P wave buried in the terminal portion of the QRS wave.

Figure 7. SVT diagnosis algorithm

AF, atrial fibrillation; AVNRT, atrioventricular nodal re-entry tachycardia; AVRT, atrioventricular re-entry tachycardia; EAT, ectopic atrial tachycardia; ECG, electrocardiogram; MAT, multifocal atrial tachycardia; SNRT, sinus-node re-entrant tachycardia.