SAMIR S. SHAH
HISTORY OF PRESENT ILLNESS
A 15-year-old boy felt the acute onset of his heart beating fast while he was on the phone with a friend. He became dizzy and lightheaded and fell backward onto his bed. He was not sure whether he lost consciousness, but remembered calling for his mother to help him. He was taken to the community emergency department for assistance. On arrival, he had some mild mid-sternal chest pain. He denied fever, nausea, vomiting, diarrhea, and cough. The remainder of his review of systems was negative.
He has been a healthy child with no significant illnesses. He was a good student at school and active in sports. His family history did not reveal any episodes of sudden unexplained death. Of note, his sister had coarctation of the aorta that required repair in infancy. He did not take any medications. He has received all of his childhood immunizations.
T 37.2°C; HR 230 bpm; RR 20/min; BP 105/68 mmHg
Weight 50th percentile and Height 90th percentile
On examination he was awake, but anxious appearing. His head and neck examination was normal. His lungs were clear to auscultation. His cardiac examination was significant for profound tachycardia with a rate that could not be counted manually. There was no jugular venous distention. His perfusion was adequate with a capillary refill of 1 second at the fingertip. His pulses were palpable throughout. His abdomen was soft without any enlargement of his spleen or liver. His extremities were well perfused. His neurologic examination was normal.
WBC count revealed 12 400 cells/mm3 (54% segmented neutrophils, 1% bands, 38% lymphocytes); hemoglobin, 13.2 g/dL; and platelets, 278 000/mm3. Measurement of serum chemistries revealed the following: sodium, 138 mEq/L; potassium, 4.3 mEq/L; chloride, 106 mEq/L; bicarbonate, 22 mEq/L; calcium, 9.2 mg/dL; and magnesium, 2.9 mg/dL.
COURSE OF ILLNESS
Chest roentogram (CXR) revealed a normal heart size and no pulmonary edema. The initial (Figure 18-2A) and subsequent (Figure 18-2B) electrocardiograms (ECG) revealed the acute and underlying diagnoses.
FIGURE 18-2. A. Initial ECG. B. Subsequent ECG.
DISCUSSION CASE 18-2
The initial ECG (Figure 18-2A) revealed a narrow complex tachycardia with a rate of almost 300 bpm. The patient had paroxysmal supraventricular tachycardia (SVT). Features consistent with the diagnosis of SVT included a compatible history, lack of heart rate variability, heart rate greater than 180 bpm, and absence of P waves on the ECG. Supraventricular tachycardia may be due to structural heart disease (e.g., Wolff-Parkinson-White syndrome), acute heart disease (e.g., myocarditis, pericarditis), hyperthyroidism, excessive caffeine consumption, pregnancy, illicit drug use (e.g., cocaine), and prescription medications (e.g., digitalis, beta-agonists).
Vagal maneuvers were unsuccessful so the patient received two doses of adenosine. When these failed to convert his rhythm, synchronized cardioversion using a dose of 0.5 J/kg and then 2 J/kg was performed and normal rhythm was restored. On subsequent ECGs he was found to have a short PR interval (<0.12 seconds) and a delta wave (slurring of the QRS complex) consistent with Wolff-Parkinson-White syndrome (WPW) (Figure 18-2B). The diagnosis is SVT due to WPW.
INCIDENCE AND EPIDEMIOLOGY
SVT encompasses three diagnostic etiologies, atrial tachycardia, nodal tachycardia, and AV reentrant tachycardia. Most episodes of SVT are caused by AV reentrant tachycardias. Ectopic tachycardias are rare in pediatrics. Nodal tachycardias originate from the AV node and tend to have slower rates (150-200 bpm) than the tachycardias that arise from above the node.
WPW is a form of preexcitation that results from an anomalous conduction pathway between the atrium and the ventricle and can result in a reentrant tachycardia. There is conduction down the accessory pathway that bypasses the normal conduction delay at the AV node. The premature depolarization of a ventricle produces a delta wave (i.e., an initial slurring of the QRS complex) and QRS prolongation. The diagnostic criteria for WPW include a short PR interval, delta wave, and wide QRS. Patients who have WPW are prone to getting SVT. About 20% of cases of SVT are due to WPW, about 20% are due to congenital heart defects such as Ebstein anomaly or corrected transposition of the great arteries, 20% are related to medication, and the remainder are considered idiopathic.
WPW presents with frequent episodes of SVT. It can be diagnosed by detection of a delta wave in asymptomatic patients when the ECG was obtained for another purpose other than the episode of SVT. SVT is the most common arrhythmia in childhood, with 40% presenting in the first 6 months of life and 30% presenting in the school age years. An infant who presents with SVT will typically be more fussy than usual, may have difficulty feeding, and may have episodes of grunting. Frequently, the infant will be in SVT for a longer period of time until there are behavioral changes that alert the caretaker that something is wrong with the infant. As the time spent in SVT continues, there is an increased chance the child will begin to show symptoms of heart failure. When the heart rate is actually measured, it will be in the range of 220-320 bpm. An older child who is verbal will be able to report the acute onset of a rapid heartbeat. Many children describe the feeling as having butterflies in their chest.
Electrocardiogram. An ECG obtained during an episode of SVT will reveal a tachycardia, narrow QRS complex, and P waves that are either partially obscured by the ST segment or not even visible at all. In infants, the typical rates are in the range of 220-320 bpm. In older children and adolescents, the rates are in the 150-250 bpm range. If the SVT is aberrantly conducted, the QRS complex will be wide and resemble ventricular tachycardia. If a wide complex tachycardia is detected, the patient should be treated as if they are in ventricular tachycardia until proven otherwise.
Treatment of SVT depends on the hemodynamic stability of the child. If the child has hypotension, decreased mentation, or decreased end organ perfusion, then the child is considered unstable and synchronized cardioversion is indicated. The energy used is 0.5-2 J/kg. Procedural sedation should be provided as long as administering the sedation does not delay the procedure significantly. If the patient is normotensive and there is no concern about shock, then administering adenosine (i.e., pharmacologic conversion) would be the next appropriate step. Adenosine blocks conduction through the AV node and hence provides pharmacologic cardioversion. Proper administration is critical to success since the half-life of the drug is short, less than a minute. Two syringes should be connected to a T-connector or stopcock; give adenosine rapidly with one syringe and immediately flush with 5 mL or more of normal saline with the other. Verapamil is used frequently in older children and adults with SVT, but should be avoided in young children because it can cause profound vasodilatation and cardiovascular collapse. If the patient has recalcitrant SVT, slow infusion of pro-cainamide or amiodorone should be considered.
Treatment of WPW typically involves radiofrequency catheter ablation. Patients at high risk for ablation-related complications may receive pharmacotherapy with class I (e.g., flecainide) or class III (e.g., amiodarone) antiarrhythmic medications to slow accessory pathway conduction.
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