Supraventricular Tachycardia in Children - Case Study Example

SVT in 2 years old Introduction Supraventricular tachycardia (SVT) is a cardiac rhythm disorder where in the heart beats faster than normal. Theorigin of the heart rate is above the ventricles, either in the atria or in the AV node. But the rate affects both the ventricles and atria. It is the most common symptomatic arrhythmia in children (1). It is also known as paroxysmal supraventricular tachycardia or paroxysmal atrial tachycardia. It affects children of all ages and its prevalence is estimated at one in 500 children (1). However, the symptoms vary according to the age of presentation. Infact, SVT can manifest in the fetus and can lead to severe heart failure and hydrops fetalis. In the new born period, the babies present with signs of left ventricular failure. In the infants, SVT symptoms are inconspicuous and the infants may look irritable with poor feeding, tachypnoea, diaphoresis and poor color (1). These are all the more confusing when associated with fever or other illness. Preschool children may complain of tiredness, discomfort at throat or chest discomfort. Older children may complain of difficulty in breathing, light headedness, palpitations, chest discomfort and even headache (1). They make complain of sudden onset of increased heart rate which lasts for several minutes and does not subside even when they stop physical activity and take rest and then all of a sudden it stops (1). In some, there may be no symptoms at all. Severe complications such as fainting, atrial fibrillation, severe cardiac failure, myocardial dysfunction and cardiac arrest are rare except in newborns. In these babies, heart rates exceeding 200 per minute can cause life threatening myocardial dysfunction because of low cardiac reserve (1). In case of Wolff-Parkinson-White (WPW) syndrome, there is a small risk of sudden death and this risk is present whether there is SVT or not (2). SVT occurs when there is an extra pathway in the electrical circuit of the heart connecting the upper and lower chambers other than the AV node. In 80% of the cases, atrio-ventricular re-entry tachycardia including Wolff-Parkinson-White syndrome (WPW) as a consequence of accessory atrio-ventricular bypass tract is the cause (1). This is the most common cause of SVT in children. Other causes include atrio-ventricular nodal reentry (AVNRT), permanent junctional reciprocating tachycardia and automatic or ectopic atrial tachycardia (AET). AET is actually rare and is the most incessant form of SVT in children. It is due to increased automaticity of nonsinus atrial focus or foci (3). Atrio-ventricular nodal reentry type of SVT is more common in adolescents. SVT needs to be differentiated from sinus tachycardia which is seen in many conditions like febrile illness, anemia, heart failure, hyperthyroidism, hypoglycemia, dehydration, early stages of shock, emotions, anxiety, stress and medications like salbutamol, terbutaline, etc. Case history 2 year old baby girl Sarah was brought to the pediatrics out-patient department on a Thursday morning by her mother who complained that Sarah was becoming tired now and then for no reason. She said that during these episodes of tiredness Sarah would be seen having shortness of breath and in the previous episode she also noticed that Sarah’s heart beat was abnormally high. These symptoms, she said were noticed in Sarah on and off since about a month and each episode lasted for about 15 to 20 minutes. There was no history of any febrile illness or drug intake. There was no history suggestive of any cardiac problem in the past. There was no history of syncopal attacks or seizures during these episodes. Also, there was no family history of cardiac arrhythmias. Antenatal and postnatal histories were unremarkable. General and systemic examinations were normal and the pediatrician recorded normal heart rate and blood pressure in Sarah. The pediatrician advised the mother to bring the child to casualty in case of repetition of symptoms. The next day, Sarah was brought to the casualty at the onset of symptoms where an ECG was taken which revealed a heart rate of 180 per minute which was regular. There were p waves representing atrial activation and PR interval was longer than RP interval. A diagnosis of supraventricular tachycardia due to atrio-ventricular re-entry was made based on the ECG. ECHO revealed normal structure of the heart. The parents were explained about the diagnosis and treatment in detail. Since the symptoms in Sarah were not severe and were easily identifiable, conservative approach was advised. Parents were taught maneuvers to abort the SVT during an episode. They were advised to come back in case of worsening symptoms. They were also kept in light of the fact that worsening of symptoms may lead to introduction of pharmacotherapy. It is 6 months since the onset of symptoms in Sarah. Though she continues to have episodes of SVT, none of them were severe or life threatening. Parents could abort these episodes with the maneuvers explained to them. They got ECG tracings done on 2 more occasions to confirm the diagnosis. Discussion SVT may be defined as tachycardia resulting from an abnormal mechanism that requires structures in the proximal heart to the bifurcation of the bundle of His for its perpetuation (4). Of course, the heart rate that is considered as tachycardia depends upon the age of the patient and the site of origin of the heart beat. In a 2 year old child, a heart rate above 160 per minute can be considered as tachycardia. Symptoms at this age are vague and a high degree of suspicion is required to make the diagnosis because, most of the times examination is normal by the time the child reaches the hospital. Then how is it possible to diagnose SVT? The diagnosis of SVT is made based on clinical history and ECG recorded at the time of tachycardia, preferably a complete 12 lead ECG (1). The ECG will show p waves representing atrial activation during tachycardia (1). The PR interval may be shorter than or longer than the RP interval depending on the origin of tachycardia. Often QRS is narrow. When SVT arises due to ectopic atrial tachycardia or due to permanent junctional reciprocating tachycardia, the PR interval is shorter. On the other hand in SVT arising due to atrio-ventricular re-entry tachycardia, the PR interval is longer. Diagnosis using ECG can be made only if it is recorded at the time of the episode. After the SVT episode has subsided, the ECG recording will be normal. Hence clinicians must instruct the parents to get the ECG done during episodes. A study by Vos and others (5) revealed that the mean interval between first clinical presentation suggestive of SVT and ECG proof of SVT was 138 days. Though most cases of SVT are benign, it is important to obtain the diagnosis because; firstly, SVT needs to be differentiated from sinus tachycardia and life threatening ventricular tachycardia and other arrhythmias and secondly, the type of SVT is important to decide on therapy. In those with recurrences of paroxysmal SVT, ambulatory Holter monitoring may be useful (1). Diagnosis of SVT may also be established by cardiac event recorder and by determining the response to vagal maneuvers (1). The next question is whether it is necessary to get an ECHO done in children with SVT? Most of the children with SVT have normal hearts structurally. Also, only in 15% of the cases association with heart disease, pulmonary hypertension, febrile illness or drug administration (1) can be noted. In those with structural heart disease, impairment of ventricular function and disturbance in the coronary circulation may be the cause for paroxysmal SVT (1). In neonates, ECHO must be done to rule out structural heart disease and assess ventricular function (1). Are any other investigations required? Usually ECGs and ECHO are enough to arrive at a diagnosis. Further investigations are warranted only if EHO is abnormal. However, one might consider checking electrolyte levels, hematocrit, thyroid function and tests to rule out pheochromocytoma (3). In case of WPW syndrome, electrophysiological studies may be necessary to identify high risk patients (2). Once the diagnosis is made, how is SVT treated? Treatment is usually chosen based on the specific form of SVT, age and clinical status of the patient (4). The most common form of SVT is AV nodal reentry. In this condition, SVT can be aborted by simple maneuvers like carotid sinus pressure, Valsalva maneuver, and application of ice water bag directly over the center of the child’s face (4). Rarely, children with SVT may become sick, hypotensive, acidotic and land up in cardiac failure. Such children require quick means of aborting SVT. Those with mild to moderate cardiac failure may be treated with adenosine initially and then be supported with digoxin, amiodarone, verapamil or procainamide (4). Adenosine must be given intravenous as a quick push. It has a short half life of 10 seconds. The recommended dosage is 50 to 200 microgram per kg (1). The SVT aborts quickly but may reappear very soon. It is important to monitor this aspect using ECG. If SVT reverts back, then longer acting intravenous medication must be considered which include propranolol, digoxin, procainamide, verapamil or amidarone (1). IV verapamil is contraindicated in young children. For those who are severely tachycardic and sick with unstable vital signs, cardioversion with 1-2J/kg of direct current is recommended (4). Once the emergency phase is over, the next question that arises is whether it is required to provide long-term treatment, if so, who should be given and what form of treatment is to be given? The aim of long term treatment is to prevent recurrence of the tachycardia (4). Again, the treatment depends on the specific form of SVT, age of the child, symptoms produced by SVT and the effect of SVT on the quality of life (1). In other words, the long term treatment should be individualized (1). In infants who are less than one year of age, the clinical symptoms are vague and complications due to SVT are more common. In such children, prophylactic treatment with anti-arrhythmic drugs is recommended (1). The most commonly used drugs in these patients are beta-blockers. In those with no ventricular preexcitation, digoxin also can be used (1). Sotalol, flecainide and amidarone also may be used if there is intolerance to digoxin. Once the treatment is started, it can be discontinued at the age of one year to see if SVT rebounces. If there is no recurrence of SVT, then a wait and watch policy may be used. Usually about 50% of these patients will not have recurrence of symptoms until they are of school age (1). In others in whom SVR has recurred, prophylactic treatment may be continued until preschool age (1). Also, one more thing to take care of is to upgrade the dosage of medication at every follow up. In children who are of school age and who can recognize and complain symptoms of SVT, treatment is advocated only if quality of life is affected or the symptoms are severe. Infrequent SVT, accompanied by mild symptoms, especially if the child is able to abort the symptoms with appropriate maneuvers, does not require any pharmacological treatment (1). Such children must be advised to avoid substances like caffeine and drugs like salbutamol, certain antihistaminics, amphetamine, and pseudephidrine (1). It is important to note that drug therapy only attempts to suppress the arrhythmia rather than cure it and the benefits of pharmacotherapy must be outweighed with its potential side effects (2). In those with AV nodal reentry, drugs which primarily affect the AV node are used. These include digoxin, propranolol and verapamil. However, calcium channel blockers are avoided in children who are less than 2 years in view of possibility of cardiac arrest. In case of WPW syndrome, betablockers are preferred. The rule in all patients with WPW syndrome, who have suffered syncopal attacks is that they must be treated appropriately (1). In these patients, non-response to pharmacological treatment usually means that there is a need to go in for ablation procedures where in the bypass tract that is causing electrical signals for SVT is ablated with the help of radiofrequency current or cryoablation. Catheter ablation has a high success rate and low complication rate in patients with common forms of SVT like WPW syndrome and AVNRT and in fact, it is the first choice of therapy in children beyond 6 to 7 years (2). Those who fail to respond to this treatment also will need anti-tachycardia pacemakers (1). The pacemaker will recognize occurrence of paroxysmal tachycardia and interrupt it with overdrive atrial pacing. Conclusion SVT is a common arrhythmia in children. It can be identified even in the fetus. It occurs due to an extra pathway in the electrical circuit of the heart connecting the upper and lower chambers other than the AV node. Conventionally, atrial fibrillation and atrial flutter are not included in this condition. The most common causes of SVT in children are atrio-ventricular nodal reentry tachycardia and atrio-ventricular reentry tachycardia. Most of the times SVT is not life threatening and it does not affect life style. Presentation depends upon the age and type of SVT. In the new born and infancy, symptoms are vague and often high degree of suspicion is necessary to arrive at a diagnosis. Complications like heart failure and cardiac arrest are more common in this age group because of low cardiac reserves. Older children complain of palpitations and chest discomfort and complications are few in this age group. Diagnosis is established by non-invasive methods like ECG and Holter monitoring. Most of the times, no structural heart abnormality is detected in the patients. Treatment again, depends upon the age of the patient, the specific form of SVT and the symptoms of SVT. Acute attacks are aborted by specific vagal stimulation maneuvers and IV anti-arrhythmics like adenosine and digoxin. Long term treatment includes conservative management in most of the children. This includes vagal stimulation maneuvers and avoiding SVT precipitating drugs and foods. Younger children, in view of their vague symptoms and increased complications may need long term pharmacotherapy for 6 months to one year after which they are observed. If pharmacotherapy does not help, other options include ablasive treatment and pacemaker. References 1. Kantoch MJ. Supraventricular tachycardia in children. Indian Journal of Pediatrics 2005; 72 (7): 609-619. 2. Balaji S. Supraventricular tachycardia in children. Current Treatment Options in Cardiovascular Medicine 2000; 2(6): 521-528. 3. Sanatani S, Hamilton R. Supraventricular tachycardia, Atrial Ectopic Tachycardia. [Online] 2007 eMedicine from WebMD. [Cited 2007 Sep22]; Available from URL: http://www.emedicine.com/ped/topic2534.htm 4. Toganel R, Gozar L, Tunde N. Supraventricular tachycardia in children. Cardiologia Hungarica 2002; 32(1): 29-33 5. Vos P, Pulles-Heintzberger CFM, Delhaas T. Supraventricular tachycardia: an incidental diagnosis in infants and difficult to prove in children. Acta Paediatrica 2003; 92 (9): 1058–1061. Bibliography Balaji S. Supraventricular tachycardia in children. Current Treatment Options in Cardiovascular Medicine 2000; 2(6): 521-528. Kantoch MJ. Supraventricular tachycardia in children. Indian Journal of Pediatrics 2005; 72 (7): 609-619. Sanatani S, Hamilton R. Supraventricular tachycardia, Atrial Ectopic Tachycardia. [Online] eMedicine from WebMD 2007. [Cited 2007 Sep 22]; Available from URL http://www.emedicine.com/ped/topic2534.htm Toganel R, Gozar L, Tunde N. Supraventricular tachycardia in children. Cardiologia Hungarica 2002; 32(1): 29-33 Vos P, Pulles-Heintzberger CFM, Delhaas T. Supraventricular tachycardia: an incidental diagnosis in infants and difficult to prove in children. Acta Paediatrica 2003; 92 (9): 1058–1061. Read More