ARRITMIAS CARDÍACAS-DIAGNOSTICO DIFERENCIAL

Differential Diagnosis
Sinus tachycardia: The rhythm in this case is too fast (>220 bpm) and is regular; sinus tachycardia is often slower and fluctuates with the respiratory cycle.
Multifocal atrial tachycardia (MFAT): The rhythm in this case is regular; with MFAT it is usually slightly irregular.
Atrial tachycardia
Supraventricular tachycardia (SVT)
AV nodal reentrant tachycardia (AVNRT)
SVT with bypass tract
Sinus node reentrant tachycardia
Atrial fibrillation (A-fib) with rapid ventricular response: The rhythm in this case is regular; irregular rhythms are seen with A-fib.
Atrial flutter: No flutter waves are seen in this case.
Junctional ectopic tachycardia (JET): This arrhythmia can be seen after surgery in children with congenital heart disease.


Sinus Tachycardia
Tachycardia is common in pediatric patients. It is defined by patient age (Table 1). The differential diagnosis for a narrow complex tachycardia includes sinus tachycardia, SVT, atrial flutter, A-fib, JET, and atrial tachycardia.Table 1
Age
Upper Limit for Heart Rate
0-6 months
180
6-12 months
160
1-2 years
140
2-5 years
120
5-12 years
110
Older than 12 years
100
Sinus tachycardia has its origin in the sinoatrial (SA) node and is a normal physiologic response to increased circulating catecholamines or decreased vagal tone, as might be seen in the following scenarios:
Cardiac: Physiologic response to increased cardiac output in exercise, intravascular volume depletion (dehydration, hemorrhage), anemia, CHF, ACS, tamponade, peripheral vasodilation (ie, anaphylaxis)
Pulmonary: Hypoxia, hypercarbia, asthma, tension pneumothorax, pulmonary embolus
Endocrine/metabolic: Hypoglycemia, hyperthyroidism, acidosis
Infection/fever
Psychological: Fear, pain, anxiety
Neurologic: Seizure
Medication/drug: ß-agonist (albuterol), anticholinergic (ipratropium, antihistamines), stimulants (amphetamines, cocaine, ephedrine, epinephrine, caffeine), tobacco, antidepressants, theophylline
To be certain that a tachycardia is in fact sinus in origin, there must be P waves before each QRS complex and this P wave must have a normal morphology (ie, upright in leads I, II, aVf). Given the heart rates that these children and infants can have, it can be difficult to actually discern P waves on the monitor or ECG because they are obscured by the previous T wave. Adenosine blocks conduction through the AV node and thus removes the QRS complexes for a brief period of time, at which point the underlying P waves can be examined. These P waves should have a similar rate to the rate as measured based on the QRS complexes. Clues that a tachycardia is originating in the SA node include:
The rate can vary based on stressors, activity, or respiration.
The rate can vary based on respiratory patterns, where it increases during inspiration and decreases during exhalation (this is most pronounced when the heart rate is slow and usually resolves with faster heart rates, and as such, might not be as helpful in this setting).
There can be beat-to-beat variability (SVT has constant R-R intervals) as well. The heart responds to environmental stimuli, crying, and respirations with an increase in heart rate.
The rate will likely be less than 220 bpm for infants and less than 180 bpm for children.

Management - Sinus Tachycardia
The sinus tachycardia itself should not be treated; however, an underlying physiologic derangement (as discussed earlier) should be sought and when found, treated. In most settings the sinus tachycardia will resolve with appropriate treatment of the underlying disorder.


Supraventricular Tachycardia
In pediatrics, SVT is the most common tachydysrhythmia (excludes sinus tachycardia). SVT has many different definitions; the most strict refers to any abnormal tachycardia that originates above the ventricles. According to this definition, all of the following would be classified as SVTs: atrial fibrillation, atrial flutter, atrial tachycardia, multifocal atrial tachycardia (MFAT), AV nodal reentrant tachycardia (AVNRT), sinus node reentrant tachycardia, and SVT with bypass tract. There seems to be somewhat of a consensus that this definition of SVT is too broad and should be narrowed to include narrow complex tachycardias involving a reentrant mechanism. This is the definition we shall use in this case; atrial fibrillation, atrial flutter, atrial tachycardia, and MFAT will not therefore be classified as SVTs. This leaves AVNRT, SVT with bypass tract, and sinus node reentrant tachycardias.
These three are similar in that they contain two separate conduction pathways with different speeds of conduction and different refractory periods. These two pathways become dissociated when one side of the pathway cannot conduct an arriving impulse (following a premature atrial contracture [PAC]) because it is still in its refractory period. The impulse then travels down the slow conducting pathway, which is not in its refractory period, and finally reaches the base of the other pathway (this pathway was in its refractory period before; however, it is now ready to conduct), which rapidly conducts back to the region of impulse origin. Thus begins the reentrant tachycardia. A reentrant circuit requires both antegrade and retrograde conduction. Antegrade conduction refers to normal downward conduction, usually from the atria toward the ventricles. Retrograde conduction is abnormally conducted backward or upward, usually from the ventricular to the atrial region. The SVTs are divided into categories based on where the reentrant circuits are located (SA node, AV node, bypass tract outside of the SA or AV node).
Approximately 70% of pediatric SVTs utilize a bypass tract that is located outside the AV node but between the atria and ventricle; AV reentrant tachycardia (AVRT). If this extranodal pathway can also conduct antegrade during sinus rhythm, ventricular preexcitation will occur — the classic delta wave seen in Wolfe-Parkinson-White (WPW) syndrome. If the extranodal pathway cannot conduct antegrade, and therefore is not seen on ECG, it is considered a concealed bypass tract. This SVT begins in a similar manner as AVNRT; however, there are P waves on the ECG (retrograde following the QRS complex) because it requires atrial depolarization to maintain the rhythm.
The relative frequency of AVRT and AVNRT is age dependent. In infancy, AVRT is seen almost exclusively. At approximately 2 years, the AV nodal tissue matures. As the patient ages, AVNRTs gradually begin to be seen and by adulthood account for 70% of SVTs. In childhood, 70% of SVTs are AVRTs.
20% of pediatric SVTs have the reentrant pathway within the AV node — AV node reentrant tachycardia (AVNRT). This SVT begins when a PAC occurs right after a normal sinus contracture. At this point, one half of the reentrant loop (AV node) is in its refractory period, so one half conducts down a slow pathway and then the other half conducts retrograde up the fast pathway leading back to the top and then retrograde into the atria. Given that this returning atrial impulse is arriving from an abnormal location (not from the SA node), atrial depolarization will proceed abnormally. This can be seen on the ECG by inverted P waves (the signal of atrial contracture) in leads II, III, and aVF following the QRS complex (retrograde). This pattern is seen in only 30% of patients with AVNRT. The remaining AVNRTs have the P wave buried in the QRS complex where it will not be seen.
10% of SVTs have the reentrant pathway within the SA node. These occur when there is a very early PAC that cannot be conducted through one portion of the SA node secondary to its refractory period. The PAC is conducted through the other SA tissue into the atria, depolarizes the atria, and then reenters the SA node through the portion that was refractory. This sets up the reentrant circuit in the SA node similar to the AV node in AVNRT. Since the SA node is the impulse origin, the P waves are normal in morphology and appear regularly before each QRS complex (which explains why it is often misdiagnosed as atrial tachycardia or sinus tachycardia).
After the SVT has resolved, it is crucial to obtain an ECG in sinus rhythm looking for WPW syndrome or any other underlying conduction disturbance that might have predisposed the patient to SVT. Most patients with WPW who present with tachydysrhythmias will have a narrow complex SVT. During normal sinus rhythm, these patients will have the classic delta wave with a shortened PR interval (WPW and Lown-Ganong-Levine syndrome are the only conditions that cause a shortened PR interval). The delta wave is an upsloping of the initial QRS complex. This upsloping is caused by rapid antegrade conduction from the atrium to the ventricles through the accessory pathway, thus causing ventricular preexcitation. AVNRT has an accessory pathway that is only capable of conducting retrograde and therefore does not have ventricular preexcitation and thus no delta wave.
For unclear reasons, SVT usually begins at rest but can rarely begin during exercise. No cardiac abnormalities are found in approximately half of the cases. Cardiac abnormalities associated with SVT include but are not limited to WPW (found in 10% to 20% of the cases), Ebstein anomaly, and transposition of the great vessels. Heart rates usually range from 160 to 300 bpm, with younger patients usually having a more rapid SVT rate than their older counterparts, including adults. Episodes of SVT usually end as they begin — abruptly. Lasting from minutes to days, an episode can spontaneously resolve without treatment or resolve only with intervention.
Presenting signs and symptoms depend on the age of the child. Infants might not present until their prolonged SVT has produced symptoms of congestive heart failure (tachypnea, fussiness, poor feeding, lethargy, shock, vomiting). It is rare for older children to present in heart failure because they usually complain of palpitations, rapid heart beat, shortness of breath, vague chest discomfort, presyncope, or syncope soon after the onset of the SVT and thus seek medical care.

Management – Unstable Supraventricular Tachycardia
Cardioversion: For the unstable (hypotensive/poor peripheral perfusion, altered mental status, shock) patient, synchronized cardioversion is the treatment of choice. Cardioversion is electrically resetting the cardiac conduction system. It is important to ensure that the “synchronized” option is selected on the defibrillator/cardiovertor. When this option is selected, you will see a dot or hash mark on each QRS complex. This ensures that during cardioversion the shock is not delivered on the T wave, thus preventing an R on T phenomenon and possibly resulting in ventricular fibrillation. The first attempt at cardioversion is with 0.5 J/kg and subsequent attempts with 1 J/kg. If the patient is in extremis no sedation is needed; however, if the patient is still alert, then sedation prior to cardioversion is recommended. The ideal agent for sedation would have rapid onset and offset, no hemodynamic effects, no respiratory depression, and adequate sedative effect along with some analgesic component. Unfortunately no such agent exists, and all agents have advantages and disadvantages. The clinician must select an agent based on its profile and the clinical scenario.
Etomidate (0.1-0.3 mg/kg/dose IV) is the likely agent of choice in this setting because it does not produce cardiovascular depression and only rarely causes respiratory depression. The dose can be repeated as needed for additional sedation. It is thought to produce some adrenal suppression, so it should be used with caution in those thought to be suppressed.
Benzodiazepines: The most commonly used agent is midazolam. It is given IV 0.05 to 0.2 mg/kg/dose to maximum of 2 mg/dose. The dose may be repeated every 2 to 3 minutes to a maximum of 10 mg. It has a fast onset and short duration; however, it is known to produce respiratory and cardiovascular depression.
Medications to be used with caution in this setting include:
Fentanyl (1 to 5 mcg/kg/dose IV) (max single dose 0.05 mg): Dose should be reduced in infants, typically 1 to 2 mcg/kg/dose. Caution is called for when using this agent, as fentanyl is known to produce respiratory and, to a lesser extent, cardiovascular depression.
Ketamine (1 to 2 mg/kg/dose IV) is a dissociative amnestic agent (similar to the street drug phencyclidine). It is given over 1 to 2 minutes with the ability to repeat the dose as needed. It generally causes little to no cardiovascular or respiratory depression; however, it does increase sympathetic tone (might be undesirable in this setting) and can produce emergence reactions. Although rare, it can also produce cardiovascular compromise.
Barbiturates are rarely used because they cause significant cardiovascular and respiratory depression.
Adenosine: In the unstable patient in whom vascular access is immediately available, a trial of adenosine is acceptable as long as it does not delay cardioversion. Adenosine blocks the AV node and will successfully convert greater than 90% of SVTs. It will convert SVT (or produce no change in the heart rate) in those with AVNRT and SVT with a bypass tract. Adenosine will not terminate SVTs in patients with SA node reentrant tachycardias; however, it might increase AV node blockade and thus decrease the heart rate slightly.
Adenosine dosage is 0.1 mg/kg, with a maximum first dose of 6 mg. The half-life of adenosine is approximately 10 to 20 seconds; therefore, it should be given intravascularly, as proximal as possible, and IV slam (as rapid as possible with at least 5 to 10 mL of saline flush to follow immediately either via 3-way stopcock or simultaneous needles in the same IV hub). If the first dose is ineffective, then double the dose (to a maximum of 12 mg) and administer in a similar manner. The side effects of adenosine are rare but include flushing, hypotension, bronchospasm, and asystole. Continuous ECG monitoring and external pacing equipment should be present at all times throughout administration.
Pharmacologic: Both amiodarone and procainamide may be considered in stable SVT refractory to vagal maneuvers and adenosine and in those with shock-refractory SVT.
Amiodarone (5 mg/kg IV over 20-60 minutes) is a class III antiarrhythmic because it prolongs the QT interval, but it has many other cardiac effects. It slows both the heart rate and AV nodal conduction via calcium channels and ß-blockade. It prolongs refractoriness via potassium and sodium channel blockade and slows intracardiac conduction via sodium channel blockade. Its side effects include bradycardia, hypotension (expect after administration), and polymorphic ventricular tachycardia.
Procainamide (15 mg/kg IV over 20-60 minutes) increases the effective refractory period, slows conduction, and decreases myocardial excitability of the atria, bundle of His-Purkinje system, and ventricles. It is the drug of choice in wide complex atrial fibrillation at very high ventricular response rates given the increased likelihood of WPW in this setting.
Other modes of acute treatment for unstable patients include calcium channel blockers, ß-blockers, digoxin, and transesophageal or transvenous pacing. All of these should be done only in the refractory setting and strictly under the supervision of a cardiologist.

Management – Stable Supraventricular Tachycardia
Vagal maneuvers stimulate the vagus nerve. They are nonpharmacologic interventions that increase parasympathetic tone and thus slow conduction through the AV node. This slowed conduction can just be enough to interrupt the reentrant loop and reset normal cardiac conduction. Vagal maneuvers may also assist with the identification of tachydysrhythmias. They can cause sudden termination of an AVNRT or SVT via bypass tract and gradual slowing of the rate in sinus tachycardia, atrial flutter, atrial fibrillation, and increased AV block (and thus decrease heart rate) in those with sinus node reentrant tachycardias. In the field or while establishing vascular access, vagal maneuvers are definitely worth a try, as follows:
Induce the diving reflex: Placing ice on an infant’s face or submersing a child’s face in ice water causes peripheral vasoconstriction and subsequently increased vagal tone.
Valsalva: Instruct the patient to inhale, hold his or her breath, and bear down as if to have a bowel movement and hold this position for 20 to 30 seconds. This is often slightly advanced for younger children, so an alternative is to have the child blow forcefully through a straw (or IV catheter) for as long as possible (at least 20 seconds).
Carotid sinus pressure is not generally used as a vagal maneuver for children.
Adenosine is the mainstay of treatment in the stable patient in whom vascular access is available. If after two ineffective doses of adenosine or if intravenous access is unavailable, move to synchronized cardioversion or some other pharmacotherapy.
Pharmacotherapy:
Calcium channel blockers (diltiazem 0.25 mg/kg or verapamil 0.1 mg/kg slow IV bolus) prolong the conduction time in the AV node and thus disrupt AVNRTs and SVTs with bypass tracts. Calcium channel blockers will convert 90% of SVTs to sinus rhythm and will do so within 10 minutes of administration. Do not use these medications in patients who have hypotension or known left ventricle dysfunction or who are already taking ß-blockers. Expect a transient period of hypotension after administration due to vasodilation. Use caution in infants, as verapamil has been shown to cause refractory hypotension and cardiac arrest in young children. It is not recommended in children younger than 2 years.
ß-blockers (metoprolol, esmolol, atenolol) are similar to calcium channel blockers in that they increase AV nodal conduction time. Do not use in patients with asthma or left ventricle dysfunction.
Digoxin generally should not be used in the acute setting.
Amiodarone: See the unstable management discussion.
Procainamide: See the unstable management discussion.
Cardioversion: See the discussion of cardioversion under management of unstable SVT.
Consult cardiology: Patients discharged to home should be followed by a cardiologist. Inpatient cardiology consultations should be obtained in all patients with unstable SVT or those in whom WPW is diagnosed.
Long-term management: Long-term management must always include input from a cardiologist. Most infants who present with SVT will have no recurrences after they are 1 year old and thus will require no ongoing therapy. Older children who present with SVT are more likely to have recurrences and thus require ongoing management. Long-term management depends on the severity and frequency of episodes. For those with infrequent, mild episodes that easily convert, with no ventricular preexcitation, no ongoing treatment is needed. Those with more frequent episodes, severe symptoms such as syncope, or ventricular preexcitation should probably be started on a ß-blocker, calcium channel blocker, or digoxin. Digoxin should be given only to children who do not have ventricular preexcitation. With preexcitation, digoxin can increase antegrade conduction down the accessory pathway. If these patients, who are already more prone to atrial flutter or fibrillation, develop them, there is a risk of 1:1 conduction from the atria through the accessory pathway to the ventricles. This will produce a very rapid ventricular response, possibly leading to ventricular tachycardia or fibrillation. Radiofrequency ablation is another treatment option: an interventional electrophysiologist (cardiologist) maps out the accessory conduction pathways that contribute to the SVT and then thermally ablates it with radiofrequency energy. The prognosis for patients with SVT is very good with a normal life expectancy and little to no morbidity.


Atrial Fibrillation and Atrial Flutter
Atrial flutter and fibrillation are rare in children. When present, they are usually associated with an underlying organic heart disease, postoperative cardiac surgery, or digoxin toxicity.
In atrial flutter, the atria beat at a rate greater than 240 bpm and often actually greater than 300 bpm. The ventricular rate depends on the rate of AV nodal conduction. In other words, the AV node is the gatekeeper that controls at what interval the atrial impulses will reach the ventricle — 1:1, 1:2, 1:3, or 1:4. Atrial flutter can mimic SVT, and the diagnosis is often made only when adenosine is given and the underlying P waves seen on the ECG have the classic sawtooth appearance (flutter waves).
Atrial fibrillation can be differentiated from SVT by its irregularity. This irregular rhythm is never seen in SVT.

Management – Atrial Fibrillation and Atrial Flutter
In the unstable patient with atrial fibrillation or flutter with rapid ventricular response (as for any tachydysrhythmia that is unstable), cardioversion is the treatment of choice. If this is ineffective, then overdrive pacing is usually the answer. For those with stable atrial flutter or fibrillation, medications such as ß-blockers, calcium channel blockers (avoid in infants), or digoxin are going to be the agents of choice. Before converting either of these two rhythms in the stable patient, consultation with cardiology and consideration for anticoagulation are needed.

Case Development
The child’s heart rate decreased to 90 bpm. She continued to be in no apparent distress. She was discharged home from the emergency department with cardiology follow up and had no recurrence.