Treatment of Supraventricular Tachyarrhythmias



Treatment of Supraventricular Tachyarrhythmias


Stacy Ann Stratemann Killen

Frank A. Fish



INTRODUCTION

The goal of fetal arrhythmia treatment is the vaginal delivery of a full-term, nonhydropic infant in sinus rhythm. Fetuses with supraventricular tachyarrhythmias (SVT) are at risk for preterm cesarean delivery with its associated morbidities and mortalities for baby and mother.1,2 In the modern era, successful in utero treatment of SVT is the rule rather than the exception; nonetheless, management of fetal SVT can be challenging for several reasons. First, the provider is caring for two (and with twins, three) patients, only one of whom can be monitored directly for “well-being” and antiarrhythmic medication side effects. Second, successful management depends on a team of obstetricians, nurses, and fetal cardiologists who may view the management of the pregnancy differently (delivery vs treatment). Third, conversion to sinus rhythm can take many days, require several medications and necessitate different routes of medication delivery. However, understanding the tachycardia mechanisms, the pharmacology of the antiarrhythmic medications, and facilitating effective communication between family and care team can lead to excellent outcomes.

This chapter will describe the management, including treatment, of fetal SVT, which includes atrial flutter, atrioventricular reentrant tachycardia (AVRT), permanent junctional reciprocating tachycardia (PJRT), and atrial ectopic tachycardia as defined in Part 3, Chapter 2. The general approach to the fetus with tachycardia has been described in Part 1, Chapter 1.


WHEN TO TREAT FETAL SVT

The decision to treat fetal SVT depends on several factors, including tachycardia duration, the fetal hemodynamics and well-being, and, to some extent, the gestational age. Treatment is recommended if tachycardia is sustained or incessant, defined as ≥12 hours of uninterrupted tachycardia or tachycardia present ≥50% of the echocardiographic monitoring time (typically ˜30 minutes).1,3,4 Intermittent tachycardia is diagnosed if present <50% of the echocardiographic monitoring time or in <12 hours of a 24-hour fetal monitoring period.1,3 If there is uncertainty regarding the duration of
tachycardia, the mother can undergo continuous electronic fetal heart rate monitoring for several hours or overnight, with the caveat that in tachycardia, electronic fetal heart rate monitors often halve the true heart rate. Thus, a monitor rate of 130 beats per minute (bpm) without variability may represent a true fetal heart rate of 260 bpm (see Part 2, Chapter 1, for more discussion of fetal monitoring). Intermittent tachycardia without hydrops or other signs of hemodynamic compromise may not require treatment but close fetal monitoring is essential.1 Home monitoring by mothers using a handheld Doppler device can successfully detect tachycardia recurrence.4

Regardless of tachycardia rate or duration, any fetus with evidence of hemodynamic compromise (cardiomegaly plus cardiac dysfunction, more than mild atrioventricular [AV] valve insufficiency, or hydrops) should be treated, because in these settings mortality can be 30% to 50%.5,6 Forty percent of fetuses with SVT, especially AVRT, are hydropic at presentation.

The cardiovascular profile, a 10-point score assessing the degree of cardiac compromise based on Doppler flow patterns in the ductus venosus, umbilical vein and artery, AV valve function, hydrops, and shortening fraction,7 is not accurate in the presence of sustained SVT. This is because flow in the ductus venosus will be abnormal (to-and-fro flow) based on heart rate alone.

The decision to treat is also influenced by the gestational age at presentation. In the presence of a fetal arrhythmia, many obstetricians will perform a cesarean delivery since fetal well-being, as determined by fetal heart rate variability and absence of decelerations, cannot be assessed unless the rhythm is normal. With agreement of the parents, obstetricians, and fetal cardiologists, pharmacological conversion can be successful after 37 weeks with the goal of a spontaneous vaginal delivery shortly thereafter. One may set a time limit for successful conversion such as “if the fetus has not converted in 3, 5, or 7 days, he will be delivered.” On the other hand, if a >37-week fetus is severely hydropic and has a nonreassuring biophysical profile score, Cesarean delivery and tachycardia conversion in the operating room with ECMO on standby may be the best option.

A current approach to fetal SVT therapy based on tachycardia duration, associated fetal compromise, and gestational age is presented in TABLE 4.1.1. In addition to these parameters, tachycardia mechanism and duration, the biophysical profile score, and maternal risk factors for tolerating therapy are important to consider when choosing whether to initiate fetal antiarrhythmic therapy, selecting the type of therapy or electing to proceed with premature, Cesarean delivery.1








TABLE 4.1.1 CURRENT APPROACH TO FETAL SUPRAVENTRICULAR TACHYARRHYTHMIAS (SVT)












Tachycardia Duration


Treatment Strategy


Intermittent SVT without hydrops




  • Ambulatory monitoring or twice-weekly fetal heart rate auscultation and frequent fetal echoes


Sustained SVT with/without hydrops


OR


Intermittent SVT with hemodynamic compromise




  • <37 wk of gestation → drug therapy



  • >37 wk of gestation → delivery or drug therapy




PHARMACOLOGY OF ANTIARRHYTHMIC THERAPIES (TABLE 4.1.2)

Most types of fetal SVT respond to treatment with survival rates of 80% to 100%,5,8 but it is important to remember that both mother and fetus are affected by the therapy. Current pharmaceutical agents are administered “off-label” via the maternal circulation (“transplacental therapy”) or directly into the fetus (intracordal or intramuscular injection) to treat fetal SVT. The primary antiarrhythmic agents used for treating fetal SVT include digoxin, sotalol, and flecainide.5 Amiodarone is typically reserved for refractory tachycardia with hydrops given its significant side effect profile.5,8 Standard doses of the antiarrhythmics and side effects are shown in TABLE 4.1.2.

Digoxin inhibits the Na+/K+ ATPase to prolong refractoriness of the AV node and slow the sinus node. Digoxin is usually well absorbed in the absence of hydrops and reaches steady state in 3 to 5 days after loading. Fetal levels are 20% to 40% lower than maternal levels.9 Because flecainide and amiodarone can increase digoxin levels, digoxin doses should be decreased when used in combination with these drugs. Digoxin is generally safe for mothers and fetuses but is commonly associated with significant the following side effects: maternal nausea, vomiting, anorexia, and extreme fatigue.10 Other possible side effects include blurred vision, headache, dizziness, and nocturnal Wenckebach (Mobitz type 1°, 2° AV block).5,10,11,12 Signs of digoxin effect must be separated from signs of toxicity, the former including PR interval prolongation, sinus bradycardia and ST-T wave changes. Signs of digoxin toxicity include symptomatic bradycardia or AV block, ventricular tachycardia or fibrillation, hypotension, altered mental status, weakness, abdominal pain, and visual changes. No serious adverse events related to digoxin have occurred in healthy women, but digoxin is contraindicated in mothers with hypertrophic cardiomyopathy, AV block, and Wolff-Parkinson-White syndrome. A recent study demonstrated that transplacental digoxin given orally to the mother was just as effective as IV digoxin at reaching therapeutic serum concentrations.13,14

Sotalol is a K+ channel blocker and β-adrenergic receptor-blocker with the combined effect of prolonging action potential duration and cardiac tissue refractoriness, slowing AV node conduction, and decreasing heart rate. It is well transferred across the placenta, even with hydrops. Fetal levels are similar to maternal levels within 2 to 4 hours after oral administration.15 After prolonged treatment, fetal levels can be even higher than maternal levels. Common maternal side effects of sotalol include nausea, dizziness, fatigue, hypotension, depression, insomnia, worsening asthma, bradycardia, QTc prolongation, and 1° AV block/PR prolongation.1 Acquired long QT syndrome with torsades de pointes is the most important risk of sotalol administration. Therefore, serial ECG monitoring or telemetry; withholding other QT prolonging medications; maximizing vitamin D, potassium, and magnesium levels; and keeping QTc duration <500 ms are essential if sotalol treatment is given. In the setting of prolonged treatment, fetal magnetocardiography (fMCG) can be considered to assess the fetal QTc interval.

Flecainide inhibits Na+ channels and has weak β-adrenergic receptor-blocker properties, thus prolonging conduction and refractoriness of all cardiac tissues, including accessory pathways and, to a lesser extent, the AV node. This drug usually reaches therapeutic concentrations within 3 days.16 Common maternal side effects of flecainide include headache, dizziness, visual disturbances/blurred vision, nausea, constipation,
QRS widening (intraventricular conduction delay or bundle branch block), QTc prolongation, and 1° AV block/PR prolongation.1 Proarrhythmia risk can be minimized by keeping maternal serum concentrations <1 µg/mL and by avoiding excessive QRS prolongation (>50% change from baseline or >100 ms). Mothers with coronary artery disease, ventricular arrhythmias, Brugada syndrome, and congestive heart failure should not be treated with flecainide.17








TABLE 4.1.2 PHARMACOLOGIC TREATMENT OF FETAL SUPRAVENTRICULAR TACHYARRHYTHMIAS






























Drug


Standard Transplacental Dosages


Common Side Effects


ECG Effects


Digoxin


Load: 375-500 micrograms (µg) every 8 h × 3 doses or 500 µg every 12 h × 4 doses


Maintenance: 250-500 µg every 12 h (goal drug levels 1.5-2.5 ng/mL)


Intramuscular digoxin = 88 µg/kg estimated fetal weight


Nausea, vomiting, fatigue, blurred vision, sinus bradycardia


1° and 2° AV block, including nocturnal Wenckebach (Mobitz type 1 2° AV block)


Flecainide


300 mg daily (100 mg every 8 h or 150 mg every 12 h)


Goal drug levels 0.2-1 µg/mL


If using a combination of digoxin and flecainide, decrease digoxin dose by 50%


Headache, dizziness, visual disturbances


QRS widening (intraventricular conduction delay/bundle branch block), QTc prolongation, 1° AV block


Sotalol


240-480 mg daily (120-160 mg every 12 or 8 h); 160 mg every 12 h (starting dose with hydrops)


Nausea, dizziness, fatigue, hypotension, bradycardia


QRS widening (QTc prolongation, 1° AV block


Amiodarone


Load: 600 mg every 6-8 h (1800-2400 mg/d) × 2-5 d


Maintenance: 200-600 mg/d


Goal drug levels 0.7-2.8 µg/mL


Must decrease doses of digoxin (by 50%) and flecainide if these are being used in combination with amiodarone


Intraperitoneal amiodarone


Nausea, thrombocytopenia, photosensitivity, rash, maternal/fetal thyroid dysfunction, liver dysfunction, visual disturbance, gait/coordination/movement problems, peripheral neuropathy/paresthesia


QRS widening (intraventricular conduction delay), QTc prolongation; wide P-waves, QTc ˜0.48, bradycardia, 1° AV block


Adapted from Donofrio MT, Moon-Grady AJ, Hornberger LK, et al. Diagnosis and treatment of fetal cardiac disease: a scientific statement from the American Heart Association. Circulation. 2014;129(21):2183-2242.


Amiodarone inhibits K+ channels, Na+ channels, Ca++ channels, and β-adrenergic receptors and thus prolongs cardiac tissue refractoriness and slows conduction throughout atrial and ventricular myocardia. High doses are needed to treat fetal tachycardia, because amiodarone and its active metabolite incompletely cross the placenta.18 This drug is a pregnancy class D therapy, because it is associated with known fetal risk. Common maternal side effects of amiodarone include nausea, thrombocytopenia, photosensitivity, rash, thyroid dysfunction, liver dysfunction, visual disturbance, gait/coordination/movement problems, peripheral neuropathy/paresthesia, intraventricular conduction
delay or bundle branch block, QTc prolongation (rarely, torsades de pointes), and bradycardia. Pulmonary toxicity and hepatotoxicity are rare but serious complications usually associated with chronic use. Fetal thyroid dysfunction, growth restriction, and neurodevelopmental abnormalities can also occur.9,12,19,20,21 Because amiodarone elimination is slow (via shedding of epithelial cells of the skin and gastrointestinal tract), drug effects may persist for weeks after amiodarone is discontinued.

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Dec 30, 2020 | Posted by in CARDIOLOGY | Comments Off on Treatment of Supraventricular Tachyarrhythmias
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