Sinus tachycardia is defined as a rate of sinus node discharge higher than normal for the patient's age. In early versions of the PALS resuscitation guidelines, sinus tachycardia was considered a dysrhythmia. However, sinus tachycardia is a common, normal presentation and is often caused by such benign conditions as fever, dehydration, pain, and anxiety. Sinus tachycardia may also be associated with pathologic conditions such as anemia, sepsis, hypoxia, hyperthyroidism, and drug ingestions. More serious but less common causes include cardiac tamponade, tension pneumothorax, and thromboembolism. The treatment of sinus tachycardia is directed toward treating the underlying condition.6
The most common dysrhythmia in the child is supraventricular tachycardia (SVT). SVT is a narrow complex tachycardia (QRS ≤0.09 seconds), and is differentiated from sinus tachycardia by its abrupt onset, rates >220 bpm, the absence of normal P waves (Fig. 42-1), or by little rate variation during stressful activities, such as phlebotomy. SVT occurs with an estimated incidence of 1/250 to 1/1000 children. The prognosis for most pediatric patients is excellent. Previously, the fatality rate was poorly defined for SVT. A recent study of 1755 patients with SVT reported a total of 4% fatalities. Only 1% of those deaths occurred without associated structural heart disease. Case fatality rate was higher in infants <1 month of age, in patients with structural heart disease, and in those with associated cardiomyopathy.7
SVT, with concomitant right ventricular hypertrophy. This 4-year-old male was postoperative from repair of congenital heart disease (Fontan repair). He was eventually converted to normal sinus rhythm after multiple doses of adenosine.
Symptoms of SVT in infants include poor feeding, tachypnea, and irritability. They may appear ill or septic. Approximately 50% present within the first year of life, and likely present in congestive heart failure. Infants usually present within the first 24 hours. There are two mechanisms to consider: AV reciprocating tachycardia or AV nodal reentry. Younger children are more likely to have accessory pathway tachycardia, which is very important in choosing treatment.
AV reciprocating tachycardia or accessory pathway tachycardia is most common in children. Conduction during SVT is usually orthodromic, with antegrade AV conduction and retrograde accessory pathway conduction (Fig. 42-2). Conduction during sinus rhythm can be via the accessory pathway, resulting in a short PR interval and appearance of a delta wave. This characterizes the Wolff–Parkinson–White (WPW) syndrome. Some accessory pathways only conduct retrograde during bouts of SVT and are termed “concealed” because they are not apparent on surface ECG.
Diagrammatic representation of accessory pathway disease during sinus rhythm and SVT. Sinus—short PR, delta wave, characteristic of WPW; Orthodromic—fast retrograde conduction through accessory pathway leads to reentry. His–Purkinje conduction is normal, complexes are narrow. Retrograde P waves are abnormally directed and buried in T wave; Antidromic (rare)—fast antegrade conduction through accessory pathway leads to abnormal His–Purkinje conduction and wide complexes. Retrograde P waves are abnormally directed and buried in T waves.
The other mechanism, AV nodal reentry, is more common in adults, but may be responsible for one-third of cases of SVT in adolescents. Within the AV node, fast pathways with long refractory periods are blocked during a PAC, allowing for antegrade conduction down the slow tract. The impulse then propagates up the fast tract, initiating reentry. Distinguishing nodal from accessory pathway SVT is difficult during episodes of SVT. Negative P waves in II, III, and avF may indicate retrograde conduction through the accessory pathway but they are usually buried in the QRS complex. Pointed or peaked T waves suggest retrograde P waves. P waves are almost never seen in AV nodal reentry. Lack of delta wave during sinus rhythm does not rule out concealed accessory tracts. Information from parents may be helpful, but first episodes of SVT or unstudied children make diagnosis difficult in the ED.
Unstable SVT is treated with synchronized cardioversion, 0.5 to 1 J/kg, increasing to 2 J/kg as needed. Vagal maneuvers may convert stable patients. A bag containing ice and water is placed over the nose and forehead for intervals of 15 to 20 seconds. Another technique is to have the child blow into an occluded straw. Ocular pressure and nasogastric stimulation are discouraged. If vagal maneuvers fail, adenosine, 0.1 mg/kg followed by 0.2 mg/kg, is recommended. Given its short half-life, it should be administered through an IV closest to the heart. Recent case reports have suggested that the intraosseous route is an unreliable method of delivery.8 Adenosine terminates nodal and accessory pathway tachycardia by blocking adenosine receptors in the AV node and slowing conduction. Adenosine has a fairly wide safety margin because of its short half-life. Transient side effects include headache, flushing, and chest pain. Rhythm disturbances, such as atrial fibrillation, accelerated ventricular rhythm, and wide-complex tachycardia, may require resuscitation. Other side effects include bronchospasm, apnea, and asystole. Adenosine can be used in hypotension but should be avoided in the patient on theophylline.
Digitalis is commonly used to prolong AV nodal conduction and refractoriness of fast and slow tracts. A pediatric cardiologist should be consulted prior to administration as it can promote accessory pathway conduction and ventricular tachycardia (VT); therefore, it is best used in the well-known, stable patient with AV nodal reentry. It may take hours to work and if cardioversion is necessary, there is a risk of ventricular fibrillation.
Verapamil is not routinely used and is reserved for children >2 to 3 years of age. Hypotension, cardiovascular collapse, and death have occurred with its use in infants since it can cause myocardial depression, hypotension, and even cardiac arrest. Older children with stable but recalcitrant SVT may respond to IV verapamil, 0.1 to 0.3 mg/kg slowly. Calcium chloride, 10 mg/kg and IV saline should be available to treat hypotension.
β-Blockers such as propranolol or esmolol may be used with caution, as propranolol may cause hypotension, tachycardia, or ventricular fibrillation. If the above measures fail or SVT resumes, procainamide may be useful. Procainamide is preferred in narrow complex tachycardia thought to be ventricular. In the 2009 PALS guidelines, it was introduced as a possible therapy for refractory SVT.9 A 15 mg/kg bolus is given over 20 to 30 minutes, watching for hypotension or prolongation of the QRS complex. Propranolol, 0.1 mg/kg IV, is useful in WPW or other accessory pathway diseases. Esmolol dosage is 0.1 to 0.5 mg/kg IV over 1 minute, and then 0.05 mg/kg/min, titrated as noted in PALS protocols. Amiodarone, 5 mg/kg administered over 20 to 60 minutes, is another option. However, it should not be given in conjunction with procainamide because of the risk of refractory hypotension or increased prolongation of the QRS interval. β-Blockers, calcium-channel blockers, and digoxin should be avoided in SVT or atrial fibrillation/flutter with a wide complex (i.e., WPW) as these agents can increase the transmission through the bypass tract and induce ventricular fibrillation.
Any infant with new onset SVT should be hospitalized and have structural heart disease ruled out. Infants are likely to have accessory pathway disease and require further therapy. A child with immediate recurrence is at higher risk for repeat episodes or recalcitrant SVT and may require surgical ablation.