Case
Hi, thanks for taking my call. I have a 6-year old female who presents today for what appears to be an otitis media on her right ear. Mom says she has had a day of fever and has been complaining of ear pain. The reason I am calling is that when she came into the office, her heart rate was 150 bpm. She had a temperature of 39.5°C at the time, so I thought maybe it was related to the fever. I had the mom give her a dose of acetaminophen and a few hours later had them come back for a heart rate check and it remains at 150 bpm with a normal temperature. I’m honestly not sure what to make of this heart rate. She appears asymptomatic except for her ear but the heart rate worries me. Anything I should do about it?
What am I thinking?
I am impressed by the pediatrician’s efforts to investigate an anomaly rather than excuse it. While a fever can certainly increase heart rate, a heart rate of 150 bpm for a 6-year old female is higher than would be expected. Rather than excuse the heart rate as a normal variant, the pediatrician appropriately treats the fever and asks that the patient return for follow-up demonstrating that the heart rate remains elevated. From this point, I begin to consider arrhythmia in the differential as to why this patient is tachycardic. Sinus tachycardia may have occurred for other reasons outside of fever, but my first thoughts are to help identify the rhythm using an electrocardiogram and long-term monitoring for determianation of the persistence of the rate. From there, an assessment of cardiac function may be performed to rule-out a tachycardia-induced cardiomyopathy.
| Differential diagnosis |
|---|
| Likely |
| Ectopic atrial tachycardia, multifocal atrial tachycardia Persistent junctional reciprocating tachycardia |
| Possible |
| Ventricular tachycardia |
| Rare |
| Myocarditis leading to arrhythmia Sinus tachycardia due to thyrotoxicosis Sinus tachycardia due to pheochromocytoma |
History and physical
Assessment of the patient with a persistent arrhythmia should focus on identification of the rhythm and hemodynamic consequences of said rhythm. In most cases, the patient is young and cannot identify the timing of the arrhythmia initiation or cessation. In cases where patients may be able to better communicate, using colloquial language to discuss arrhythmias may be helpful. Pediatric patients can use creative language to describe the feeling of palpitations including “heart beeping” or “heart flashing.” Sometimes children will describe a sensation of palpitations as “pain” (i.e., “my heart hurts”). It should be noted that chest pain in pediatrics is relatively common and may not necessarily reflect arrhythmia but should be considered in the differential.
Additional symptoms should be elicited from family members and caretakers. Those patients who begin to have tachycardia-induced cardiomyopathy symptoms may describe a decrease in physical activity or an inability to keep up with other children. An increased propensity for taking naps compared to prior habits may be a sign of fatigue. In severe cases, patients may have more telling features of congestive heart failure such as respiratory distress due to pulmonary edema, nausea and/or vomiting, and poor growth. Recent ill contacts or recent respiratory illnesses may provide clues to a developing myocarditis. Review any new medications or supplements that may be in use.
Assessment of vital signs for elevated respiratory rate, decreased pulse oximetry, elevated heart rate, or reduced blood pressure would be concerning for cardiomyopathy. Fever may be suggestive of an infectious etiology as in myocarditis. On examination, cardiac auscultation should reveal an elevated heart rate and possibly an irregular rhythm due to ectopic beats. In severe cardiomyopathy, an S3 or S4 gallop may be present though an S3 gallop may be a normal finding in children. A murmur could be present as a result of valvular regurgitation (i.e., mitral valve regurgitation). Evidence of hepatosplenomegaly and peripheral edema are also signs of congestive heart failure. Assessment of the child’s breathing pattern and listening for crackles suggestive of pulmonary edema help complete the clinical picture.
Diagnostic testing
The first test for assessment of the rhythm is an electrocardiogram. If the rhythm is persistent or frequent, it is possible that an ECG and rhythm strip may be able to capture the necessary information. In those cases where the rhythm occurs intermittently, a Holter (or other ambulatory) monitor may be necessary but such rhythms are unlikely to result in a cardiomyopathy. An echocardiogram should be considered to assess cardiac function. If an arrhythmia is noted, other lab work may be indicated such as evaluation for electrolyte abnormalities or thyroid testing. Other lab testing may be beneficial if ruling out rare diseases such as a pheochromocytoma where urine catecholamines may be diagnostic.
Action plan
Patient stability is the primary action. This usually involves hospitalization for the management of any heart failure symptoms for those who have decompensated due to the arrhythmia. Appropriate treatment for electrolyte abnormalities or the use of diuretics may be helpful in the immediate term. Inotropic (improved systolic function) and lusitropic (improves diastolic function) medications may be utilized for those with severely depressed function but deserve a word of caution as these agents may also be proarrhythmic. In the significantly compromised patient, other supportive measures may be required including the use of ventricular assistance utilizing extracorporeal membrane oxygenation. With hemodynamic stability, attention is turned immediately to rhythm control.
Depending on the suspected etiology and age of the patient, electrophysiology study and potential ablation can be diagnostic and therapeutic. This is particularly true for persistent junctional reciprocating tachycardia (see Fig. 10.1 ), which is a reentrant form of arrhythmia secondary to an accessory pathway most often located in the posterior septal region of the tricuspid valve annulus. This form of the accessory pathway has decremental conduction properties resulting in an easily sustainable arrhythmia (see Fig. 10.2 ). Ablation of the pathway eliminates the substrate for arrhythmia and cures the patient of further arrhythmia allowing for recovery of ventricular function. This has become the gold standard of treatment in most patients unless there are significant concerns for harm by ablation such as in very small children. Medications are considered less optimal, and patients often need treatment with strong antiarrhythmics from the sodium channel blocker or potassium channel blocker groups.
