OVERVIEW: What every practitioner needs to know
Are you sure your patient has a supraventricular tachyarrhythmia? What are the typical findings for this disease?
The most common symptom is an elevated heart rate above the norm for the patient’s age group.
The next most common symptom may or may not be that of hemodynamic compromise. An infant may demonstrate feeding intolerance and tachypnea, while the older child may complain of palpitations, nausea and lightheadedness. Syncope or seizures are typically signs of a hemodynamically unstable rhythm that requires immediate treatment.
Normal conduction and heart rates
To understand the different types of tachycardia, you must understand the normal conduction system and its correlates to the surface electrocardiogram (PQRST). The “heartbeat” originates in the sinus node and propagates through the right and left atria, producing the p-wave on the surface ECG. Because the atria and ventricles are “insulated” from each other, the impulse must travel across the AV node. This produces a delay of 0.1-0.2 seconds, allowing the atrial contraction to eject blood into the ventricles. This activation time through the atria and the conduction delay that occurs at the AV node produces the PR interval on the ECG. The impulse then travels rapidly across the His-Purkinje system, resulting in the simultaneous contraction of both ventricles, producing the QRS complex. The ventricles then repolarizes, (“re-charges”), producing the T-wave.
Supraventricular tachycardia (SVT) is the most common type of tachydysrhythmia in pediatrics, occurring in approximately 1 out of every 1,000 children. Therefore, it is important for the physician to have a good understanding of this disease. This review will provide a basic understanding of the pathophysiology, management strategies, and clinical presentations of SVT.
Supraventricular tachycardia is differentiated from ventricular tachycardia in that the atria and/or the AV node are essential for it to be sustained. Most SVTs have a “narrow” QRS that is identical to the baseline QRS, reflecting conduction over the normal His-Purkinje system. In some cases, there may be preferential conduction, or frequently a delay, in one of the bundle branches that produces a “wide” QRS, mimicking ventricular tachycardia. Because the conduction properties of the bundle branches are related to the baseline rate, many SVTs begin with a wide QRS that then narrows to the baseline QRS. This is known as Ashman’s phenomenon.
PEARL: All SVTs do not have a narrow complex, and all ventricular tachycardias do not have a wide QRS complex (especially in infants).
Patients with SVT generally present in a bimodal distribution. SVT most commonly occurs between 0-3 months of age, with the second most common age of diagnosis between 1-3 years of age. SVT in the infant may have several manifestations, from feeding intolerance to congestive heart failure, while the older verbal child might complain of their heart “beeping” fast.
There are three types of SVT with multiple different subtypes. For illustrative purposes we will discuss the two most common types: focal and reentrant.
Focal supraventricular tachycardias
Focal supraventricular tachycardia arises from an ectopic site or “focus” within the atrium or AV node. Like the sinus node, an ectopic focus can generate its own heartbeat that accelerates (“warms up”) and decelerates (“cools down”). In general, focal tachycardias are not as fast as reentrant tachycardias, only occasionally exceeding 200 bpm. Some focal tachycardias may become “chronic” tachycardias because they are slower and may go unrecognized, resulting in congestive heart failure. The two most common sub-types are: (1) atrial ectopic tachycardia and (2) junctional ectopic tachycardia.
Atrial ectopic tachycardia
Atrial ectopic tachycardia (AET or EAT) may arise anywhere in the atrium. Some of the more common sites include the pulmonary veins, atrial appendage, crista terminalis, and prior suture sites. In older patients, AET may be seen with chronic pulmonary disease.
Usually, AET occurs as a result of a single focus; however, some patients may have a multifocal tachycardia. In general, single site atrial ectopic tachycardia is best approached with transcatheter radiofrequency ablation that has a cure rate well over 90% in most centers. In the past, it was felt that multifocal tachycardia could only be treated with medications; however, recent data suggests that multifocal tachycardia may represent a single focus with different exit points within the atrium. Thus, multifocal atrial tachycardia has also been successfully approached with ablation.
Electrocardiographically, patients with AET have a narrow QRS tachycardia with a p-wave preceding all QRS complexes. Usually the ectopic p-wave will be noticeably different on a 12- or 15- lead electrocardiogram. In some cases there will be 2-to-1 or greater AV block (Figure 1). In patients with multifocal tachycardia, there are at least 3-5 different p-waves detected on an electrocardiogram (Figure 2).
Junctional ectopic tachycardia
Junctional ectopic tachycardia (JET) may be either congenital or postoperative.
Congenital JET is a chronic tachycardia that may present with a tachycardia-induced cardiomyopathy in adolescents and teenagers. These patients may be approached with transcatheter radiofrequency ablation, with an increased risk of AV node injury.
Postoperative JET is commonly seen following congenital heart surgeries that require large muscle resection or ventricular septal defect (VSD) repair (e.g., with tetralogy of Fallot). Recent evidence suggests that post-op JET may be the result of hemorrhage or edema at or near the AV node. The ensuing inflammation results in junctional acceleration to rates as high as 200 bpm. Because the postoperative congenital heart is dependent upon the atrial contraction to fill the ventricle and maintain cardiac output, patients with post-op JET can develop hypotension and poor urine output, prolonging the postoperative course. In these patients IV amiodarone has been lifesaving.
Electrocardiographically, patients with JET have a narrow QRS tachycardia with no preceding p-wave. Because the impulse arises in the AV node, there may be retrograde conduction to the atrium, producing a negative p-wave that follows the QRS complex. In other patients, there may be no retrograde AV node conduction, resulting in V-A dissociation (Figure 3).
Reentrant tachycardias involve reentry of an impulse around a circuit. Classically, the reentry circuit includes the atria, AV node, ventricles, and an accessory pathway. Because the impulse travels from the atria to the ventricles and back to the atria again, it is said to be reciprocating.
Orthodromic (AV) reciprocating tachycardia
In orthodromic reciprocating tachycardia, the impulse travels from the atria down the AV node to the ventricles and returns up an accessory pathway (Figure 4).
Wolff-Parkinson-White syndrome (WPW)
The most recognized type of accessory-pathway mediated tachycardia is that seen with Wolff-Parkinson-White syndrome (WPW). In WPW, the baseline electrocardiogram demonstrates a widened QRS, indicating preexcitation of the ventricle. The syndrome was first described in 1930 and consists of (Figure 4):
a) short PR interval
b) slurred upstroke of the initial QRS complex (delta wave), giving a pseudo-bundle branch block pattern in sinus rhythm
c) occurrence of paroxysmal (sudden onset) tachycardias
Permanent Junctional Reciprocating tachycardia (PJRT)
PJRT is classically a slower narrow QRS tachycardia that occurs during childhood and is often refractory to medical therapy. It is caused by a slowly conducting accessory pathway that allows only retrograde (upward) conduction. Because there is no antegrade (downward) conduction as in WPW, there is preexcitation on the surface ECG. The slow conduction of this accessory pathway allows for AV node recovery such that every heartbeat that returns up the accessory pathway can reenter down the AV node, resulting in an incessant (or permanent) tachycardia.
The ECG features of PJRT are (Figure 5):
-Narrow QRS complex
-Retrograde negative ‘P’ wave in the inferior leads (II,II, aVF)
-Long R-P interval (slow conduction from the ventricle (R) to atrium (P))
Atrioventricular nodal reentrant tachycardia
In AVNRT, the anatomic substrate or abnormality is the presence of dual AV node pathways (designated slow and fast, respectively), each with slightly different conduction properties (A). A premature atrial contraction blocks in the fast pathway and conducts down the slow pathway (B). The fast pathway recovers and permits retrograde conduction (reentry), often initiating tachycardia (C). During AVNRT, the atria are depolarized retrogade simultaneously with antegrade ventricular depolarization so that the retrograde P waves are buried in the QRS complex. Blocking AV node conduction by changing autonomic tone or using pharmacologic agents will terminate the tachycardia.
Antidromic (VA) reciprocating tachycardia
In antidromic reciprocating tachycardia, the impulse travels from the atria down an accessory pathway to the ventricles and up the AV node (Figures 4).
Atriofascicular ("Mahaim") tachycardia
The most common type of antidromic reciprocating tachycardia is that seen with the Mahaim or atrio-fascicular fiber. This is a special fiber that permits conduction only in the antegrade (downward) direction, producing a wide QRS preexcited tachycardia. This type of tachycardia is very difficult to distinguish from ventricular tachycardia, and in the presence of hypotension should be treated aggressively (Figure 6).
Intra-atrial reentrant tachycardias
Intra-atrial reentrant tachycardias comprise a group of tachycardias in which the reentrant circuit is confined within the atria.
Atrial flutter (AFL)/ Atrial fibrillation (AF)
In the case of atrial flutter, the circuit reenters around the tricuspid valve annulus in either a counterclockwise (“typical” atrial flutter) or clockwise (“atypical” atrial flutter) direction. These macroentrant (large circuit) flutters give the classic sawtooth pattern that is commonly seen (Figure 7). In patients who have undergone surgery for repair of a congenital heart disease, there may be an atrial scar that permits reentry. This is usually associated with a lower amplitude p-wave and a slower rate of tachycardia.
Atrial fibrillation is the most common arrhythmia in the world; however, it is relatively uncommon in children with structurally normal hearts. There is a higher incidence among patients with structurally abnormal hearts, e.g., Ebstein’s anomaly, hypertrophic cardiomyopathy or Eisenmenger complex, and postoperative congenital heart disease, e.g., Fontan procedure, due to chronic atrial stretching.
Paroxysmal (sudden-onset) atrial fibrillation may occur in patients with structurally normal hearts. Recent evidence has shown that these patients may have focal atrial tachycardia arising in the pulmonary veins that induce into AF. Radiofrequency ablation of the atrial tachycardia can “cure” AF.
Patients with WPW are also at an increased risk of developing atrial fibrillation. Atrial fibrillation in the presence of a normal conduction system is not usually a life-threatening arrhythmia, because the ventricles (pumps of the heart) are protected by the AV node. However, in patients with WPW and atrial fibrillation, conduction may be rapid across the accessory pathway, potentially producing ventricular fibrillation and sudden cardiac death (Figure 8). Therefore, atrial fibrillation + WPW must be suspected in any wide QRS rhythm with an irregularly irregular rhythm.
The use of digoxin and verapamil are contraindicated in WPW because they can promote conduction across the accessory pathway, increasing the risk of sudden death if the patient should develop AF (Figure 9).
What other disease/condition shares some of these symptoms?
Palpitations can be a common symptom in several conditions. Autonomic dysfunction, characterized by a decrease in blood pressure resulting in centrally-mediated catecholamine release, can produce palpitations in adolescents.
Symptoms of palpitations in autonomic dysfunction/vasovagal syndrome are often described as “heart pounding” or “hard heart beats”. The tachycardia usually develops and resolves gradually and is often accompanied by headache and lightheadedness or dizziness.
Typically, patients with tachydysrhythmias describe the heart beats as “rapid” or “fast” with sudden onset and offset. There is usually no prodrome, as seen with autonomic dysfunction.
What caused this disease to develop at this time?
The substrate for a tachyarrhythmia is preexisting. There are no clear predisposing factors. Possibly, illness with fever or exertion with sports may be a trigger for the tachycardia, but this is often not reproducible.
Supraventricular tachycardias initially present in early infancy, then resolve typically by one year of age, and then recur in a bimodal distribution later in early childhood or adolescence. Ventricular tachydysrhythmias are less predictable and may initially present at any age.
WPW syndrome and its variants arise from a developmental cardiac defect in the AV electrical insulation that insulates the ventricular myocardium from the atrial myocardium. These epicardial strands of tissue travel across this central fibrous body to connect the atria and ventricles, providing the substrate for reentry tachycardias.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Lab work: Electrolytes, including calcium and magnesium. In patients who present with a tachycardia-induced cardiomyopathy, high serum lactate levels and low blood pH may indicate a longer duration of tachycardia. It may be very difficult to treat a tachydysrhythmia acutely until these abnormalities are corrected.
Electrocardiogram: helpful to look for preexcitation or conduction delays
Treadmill stress test: sometimes used to evaluate the risk for sudden death in patients with WPW who might develop atrial fibrillation. Also, useful in patients with exercise- or exertion- related palpitations or syncope or seizures.
Signal averaged electrocardiograms: Mixed data on its usefulness in identifying postoperative congenital heart disease with ventricular scars, e.g., tetralogy of Fallot; these patients may be at increased risk for ventricular arrhythmias. Also, may be useful for identifying cardiomyopathy patients at risk for sudden death.
Microvolt T-wave alternans: there is evidence to suggest that it might be helpful as a negative predictor in patients with ischemic heart disease, who might be at risk for sudden death.
Event monitoring: used to detect episodic arrhythmias that last >5-15 minutes.
Loop recording: continuous 30-day ECG monitoring to detect fleeting arrhythmias or arrhythmias that result in syncope.
Implantable loop recorder: To identify arrhythmias that result in syncope that cannot be documented by conventional means.
Would imaging studies be helpful? If so, which ones?
Echocardiogram: look for congenital heart defects, e.g., Ebstein’s anomaly in WPW, that may be associated with a particular tachydysrhythmia.
Tissue Doppler imaging: scant evidence that it can be used to identify the location of accessory pathways.
Criteria to help determine if a wide QRS tachycardia is ventricular tachycardia vs. supraventricular tachycardia with aberrancy
AV dissociation- No discernible relationship between the p-waves or QRS complexes, especially if the QRS complexes are faster than the p-waves.
Sinus capture beats- During AV dissociation, a sinus beat may proceed down the normal conduction system to “capture” the ventricles, producing a normal narrow QRS complex.
Ventricular fusion- During AV dissociation, a sinus beat may proceed down the normal conduction system to activate the ventricles, producing a QRS complex morphology that is between the normal QRS and wide QRS morphologies.
Concordant QRS axis during tachycardia- There is usually a progressive change in QRS axis in the precordial leads during normal sinus rhythm and SVT. However, when all of the QRS complexes precordial leads are either positive or negative, VT is more likely.
Hemodynamics- Generally, rapid SVT is much better tolerated than rapid ventricular tachycardia, probably due to the loss of AV synchrony during VT and the underlying substrate that may have caused the VT.
QRS duration: typically, SVT with aberrancy will have a QRS duration < 0.14 secs, although preexcited or antidromic SVT QRS duration may be longer.
Polymorphic QRS complexes generally favor ventricular tachycardia. Although SVT may initiate with varying degrees of aberrancy, the QRS complexes usually become stable during sustained tachycardia.
If you are able to confirm that the patient has SVT, what treatment should be initiated?
Acute management of SVT
Hemodynamically unstable (hypotension/poor perfusion/mental status changes)
Synchronized DC cardioversion (0.5-2.0 joules/kg)
If IV present, adenosine 0.1 – 0.3 mg/kg IV push
Adenosine terminates SVT by producing block at the level of the AV node. Because adenosine is metabolized by the red blood cells, it must be given by rapid IV push and its effect is usually transient (half-life 2-3 seconds). Adenosine is effective in most SVTs that use the AV node as an obligatory part of the circuit (AV reciprocating tachycardias and AV node reentry tachycardia). Because it also has effects on the myocardium, it may also cause termination of atrial ectopic tachycardia, as well as some VTs
IV amiodarone 5 mg/kg over 15-30 minutes
IV procainamide 15 mg/kg over 15 minutes
Total digitalizing dose is age- and weight-dependent
Contraindicated if suspect atrial fibrillation with WPW
5 mg/kg IV over 15-30 minutes
IV calcium if hypotension in neonates
15 mg/kg IV over 15 minutes
Initiate chronic oral therapy
Chronic oral management of SVT
3-4 mg/kg divided q 6-8 hours
50-200 mg/m2/day divided bid, may be given tid in infants
Check electrolytes and liver function tests
Trough level just prior to 6th dose in infants.
Absorption is hindered by milk products, so must adjust dose in infants who are made NPO
Sotalol (Betapace) or dofetilide (Tikosyn)
Sotalol: 75-200 mg/m2/day
Dofetilide 250-500 mg po twice daily (not approved for children)
Check electrolytes and renal function
May prolong QTc interval; may produce Torsades de pointes
Must be initiated during inpatient monitoring
10 mg/kg/day daily – load for 2-4 weeks, maintenance 5 mg/kg daily
Needs baseline LFTs, thyroid function, CBC, pulmonary function test (older patients)
3 mg/kg/day divided three times daily in infants
1-3 mg/kg daily sustained release in older patients
>95% cure rate
Low complication risk in experienced hands
Low recurrence risk
Pearl: Adenosine and DC cardioversion produce acute termination of SVT. Because there has been no change in the substrate that caused the SVT/VT originally, it may recur. This is an indication for longer-acting medications to maintain normal sinus rhythm (NSR).
Pearl: Pharmacologic or electrical cardioversion of SVT may produce a hemodynamically unstable dysrhythmia, e.g., ventricular fibrillation or severe bradycardia (Figure 10). Don’t be caught unaware!! With electrical cardioversion, use electrode patches if possible so that you can concentrate on the post-cardioversion rhythm. With pharmacologic cardioversion, always have a defibrillator nearby… just in case.
What are the adverse effects associated with each treatment option?
Medical therapy may lead to toxicity. The ability to metabolize an antiarrhythmic may change as an infant matures. This may be particularly important in a premature infant who is delivered due to hydrops from a sustained tachydysrhythmia. As the infant matures, the dose of medication may need to be adjusted to account for the changing pharmacodynamics.
Also, if there is worsening renal or hepatic function, the levels of medication must be followed or toxicity monitored by serial electrocardiograms to evaluate conduction intervals, e.g., QTc interval or QRS duration.
Certain antiarrhythmics may also produce direct toxicity to end-organs, e.g., liver, eyes, bone marrow, etc. The patient must be monitored for these toxicities specific to the antiarrhythmic that has been prescribed.
Certain antiarrhythmics, e.g., sotalol, affect the sinus node. This can cause symptomatic bradycardia in certain post-operative congenital heart defects that are predisposed to sinus node dysfunction, e.g., Mustard procedure.
Intravenous verapamil use in children <1 year of age is contraindicated due to the low calcium stores in the sarcoplasmic reticulum.
What are the possible outcomes of supraventricular tachyarrhythmias?
The prognosis of supraventricular tachyarrhythmias is good. Supraventricular tachycardias that present in infancy usually are amenable to antiarrhythmic therapy. For complex arrhythmias, multiple antiarrhythmic agents may be required; however, even the most complex supraventricular arrhythmias resolve by one year of age and antiarrhythmic agents may be discontinued.
There may be recurrence of tachycardia later in childhood, but it is much better tolerated by earlier diagnosis due to symptoms. If tachycardia recurs in later childhood, the patient may be treated with antiarrhythmics or undergo a curative ablation procedure.
The risk of antiarrhythmic therapy is toxicity, as described above. The benefit of antiarrhythmic therapy is that it allows the patient to achieve adequate size so that he/she may safely undergo an ablation.
The benefit of transcatheter ablation is that it is a curative procedure, with low complication rates and low recurrence rates.
The rate of recurrence with the use of cryoenergy is greater than that of radiofrequency energy. Cryoenergy, however, is felt to have a better safety profile and, in select cases, is preferable to the use of radiofrequency energy.
What causes this disease and how frequent is it?
In all pediatric age groups, SVT using an accessory pathway is more common than SVT due to AV node reentry or a primary atrial tachycardia. There appears to be a bimodal distribution. Most patients are diagnosed before the age of 1 year following an initial bout of SVT. The recurrence rate is variable in the first year, but sustained tachycardia usually resolves by 1 year of age, even in the presence of preexcitation on the electrocardiogram. Recurrence of tachycardia will typically occur in mid adolescence.
Accessory pathways are due to specialized conduction tissues that exist on the epicardial surfaces of the atrium and the ventricles along the AV groove. When there is antegrade conduction from the atrium to the ventricles, it produces “preexcitation” on the surface electrocardiogram. Manifested WPW occurs in 0.15% to 0.25% of the general population, with a higher prevalence of 0.55% in first-degree relatives.
In general, there is no clear inheritance pattern for the majority of patients with WPW, and there are no known predisposing factors to this disease. Certain congenital heart defects, e.g., Ebstein’s anomaly or congenitally corrected transposition of the great vessels, have been associated with an increased incidence of WPW and reentrant tachycardias, usually due to accessory pathways associated with an Ebsteinoid tricuspid valve. Familial WPW is a rare syndrome, with an autosomal dominant inheritance pattern that may be associated with other diseases. Patients with mutations in the PRKAG2, TNNI3 and MYBPC3 genes may have WPW associated with hypertrophic cardiomyopathy (HCM). Patients with Pompe disease and WPW may have mutations in alpha-1,4-glucosidase.
Variants in the sodium-channel SCN5A gene have been associated with atrial fibrillation and long QT syndrome. Familial atrial fibrillation has been associated with cardiac potassium-channel defects in the KCNQ1, KCNE2 and KCNE3 genes.
How do these pathogens/genes/exposures cause the disease?
Other clinical manifestations that might help with diagnosis and management
In infants, incessant tachycardias may present with a tachycardia-induced cardiomyopathy. In the case of PJRT, the tachycardia rate may be in the 160-180 bpm range and be misinterpreted as a sinus tachycardia in the presence of a primary cardiomyopathy, resulting in a referral for transplantation due to recalcitrant heart failure. Medical treatment of the tachydysrhythmia could result in return to normal sinus rhythm and resolution of the tachycardia.
What complications might you expect from the disease or treatment of the disease?
Sustained untreated tachycardia: Tachycardia-induced cardiomyopathy
Atrial fibrillation with WPW: sudden death
Treatment of atrial fibrillation/WPW with digoxin or verapamil: rapid conduction of atrial fibrillation, resulting in ventricular fibrillation and death
Involvement in potentially hazardous activities (e.g., swimming, climbing heights, etc.) during a tachyarrhythmia: traumatic injury and possibly death
Transcatheter ablation: AV node injury, cardiac perforation during transseptal puncture, injury to blood vessels
Are additional laboratory studies available; even some that are not widely available?
Fetal echocardiography to evaluate a fetal tachyarrhythmia for congenital defects, heart failure, or hydrops.
Fetal magnetocardiography to obtain an electrocardiographic tracing of a fetal tachycardia.
Tissue Doppler imaging has been used to localize accessory pathway location prior to an ablation procedure.
Three dimensional mapping at the time of the transcatheter ablation procedure.
How can tachyarrythmias be prevented?
There are no known preventative measures.
What is the evidence?
Kugler, JD, Danford, DA, Houston, K. “Radiofrequency catheter ablation for paroxysmal supraventricular tachycardia in children and adolescents without structural heart disease. Pediatric EP Society, Radiofrequency Catheter Ablation Registry”. Am J Cardiol. vol. 80. 1997. pp. 1438-43.
Strasberg, B, Ashley, WW, Wyndham, CR. “Treadmill exercise testing in the Wolff-Parkinson-White syndrome”. Am J Cardiol. vol. 45. 1980. pp. 742-48.
Garson, A, Kanter, RJ. “Management of the child with Wolff-Parkinson-White syndrome and supraventricular tachycardia: model for cost effectiveness”. J Cardiovasc Electrophysiol. vol. 8. 1997. pp. 1320-6.
Ongoing controversies regarding etiology, diagnosis, treatment
There is controversy on the role of stress testing in identifying those patients with WPW who may be at risk for sudden death. Evidence suggests that there may be considerable false negative results. Most pediatric electrophysiologists feel that patients with WPW manifested on an electrocardiogram should undergo an electrophysiology study during early school age years. There is evidence that a transesophageal electrophysiology study is a less-invasive means of assessing accessory pathway conduction properties.
There is also controversy on the use of digoxin to treat supraventricular arrhythmias in infants with WPW. Generally, digoxin is avoided in older patients with WPW because of its ability to increase conduction over the accessory pathway in the presence of atrial fibrillation. Because infants with and without structural heart disease have a much lower incidence of atrial fibrillation, probably due to the small size of their atria, it is common practice to use digoxin in these patients. There are, however, rare reports of sudden death in infants with WPW while taking digoxin. For that reason, some physicians choose to use an oral beta-blocker as their first-line therapy. However, in preterm infants, beta-blockers have been associated with hypoglycemia, apnea, and bradycardia. Also, in preterm infants, enteral therapy may not be an option due to GI concerns. in these patients, the use of intravenous digoxin as the first-line therapy may be the most prudent choice.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has a supraventricular tachyarrhythmia? What are the typical findings for this disease?
- Normal conduction and heart rates
- Supraventricular tachycardias
- Focal supraventricular tachycardias
- Atrial ectopic tachycardia
- Junctional ectopic tachycardia
- Reentrant tachycardias
- Orthodromic (AV) reciprocating tachycardia
- Wolff-Parkinson-White syndrome (WPW)
- Permanent Junctional Reciprocating tachycardia (PJRT)
- Atrioventricular nodal reentrant tachycardia
- Antidromic (VA) reciprocating tachycardia
- Atriofascicular ("Mahaim") tachycardia
- Intra-atrial reentrant tachycardias
- Atrial flutter (AFL)/ Atrial fibrillation (AF)
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has SVT, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of supraventricular tachyarrhythmias?
- What causes this disease and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- Other clinical manifestations that might help with diagnosis and management
- What complications might you expect from the disease or treatment of the disease?
- Are additional laboratory studies available; even some that are not widely available?
- How can tachyarrythmias be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment