After establishing a diagnosis of ventricular tachycardia (VT), a major decision is to determine if the VT is torsades de pointes, the polymorphic VT of long QT syndrome (LQTS) or the VT is unrelated to LQTS. This is important because many antiarrhythmic medications used in treating VT prolong the QT interval and may exacerbate TdP leading to fetal demise. The decision to treat VT depends on numerous factors including etiology, gestational age, cardiac function, the presence of hydrops fetalis, duration and frequency of VT, and ventricular rate.

In general, a diagnosis of fetal VT requires hospital admission for continuous fetal heart rate monitoring and at least daily biophysical profile score testing and fetal echocardiograms regardless of the etiology. There is little consensus regarding the best treatment of fetal VT due to its rarity. Restoring sinus rhythm is often difficult, drug efficacy is variable, and multiple antiarrhythmic medications are frequently necessary.¹ Treatment should aim at maintaining the fetus in a stable condition with adequate cardiac output to allow for fetal maturation, restoration of sinus rhythm if possible, regression of hydrops, and the achievement of a normal vaginal delivery at term.

Antiarrhythmic drugs are classified into five main classes depending on their mechanism of action (FIG. 4.2.1).² Class I agents interfere with the sodium channel. They depress the maximum rise of the cardiac action potential and slow conduction through the His-Purkinje system and myocardium. They are divided into three groups depending on their onset of depression, effect on the action potential duration, and effective recovery period. Class Ia drugs have an intermediate onset of depression and include quinidine, procainamide, and disopyramide. They also have potassium channel blocking effects. Class Ib agents have a fast onset of depression
and include lidocaine and mexiletine. Flecainide and propafenone are Class Ic drugs and have a slow onset of depression. Class II agents are antisympathetic nervous system agents and are predominantly beta-blockers, that is, propranolol and metoprolol. Propranolol also shows some class I effects. Class III agents affect potassium efflux and lengthen the action potential duration. Examples are amiodarone and sotalol. Sotalol has additional class II effects and amiodarone also has class I, II, and IV activity. Class IV agents such as verapamil and diltiazem affect calcium channels and the AV node. Usage of verapamil for fetal VT has not been described and it has been associated with sudden death when used in infants with supraventricular arrhythmias.³ Class V agents, including digoxin and magnesium, work by other or unknown mechanisms.

All class I drugs have a negative inotropic effect and should be avoided during cardiac failure.³ Quinidine⁴ and procainamide⁵ have been used for an intermittent fetal VT without a positive effect. Monomorphic VT unrelated to LQTS associated with a mild pericardial effusion responded to flecainide (SAB Clur, personal communication).

The first report describing successful intrapartum treatment of persistent fetal ventricular ectopy associated with fetal hemodynamic compromise was described in 1975. The fetus was treated with transplacental intravenous propranolol (5 mg × 2). Postnatally a short run of VT was recorded. Since then the positive effect of propranolol usage has been described in idiopathic VT and accelerated ventricular rhythm.¹,⁶ A potential problem associated with its use is the transplacental passage of only 25% to 35%.⁷

Improvement in fetal VT with sotalol has been described in one case.⁸ Sotalol, alone or in combination with digoxin or propranolol, given in the treatment of VT in five fetuses that subsequently were diagnosed with LQTS resulted in either no improvement or worsening of the hydrops.⁹,¹⁰ This is not surprising as sotalol prolongs the QTc interval and is thus contraindicated in LQTS.

Digoxin is contraindicated in treatment of VT. Digoxin use has been reported in two patients with LQTS, both with deleterious effects. In a patient with 2:1 AV block, VT, digoxin treatment exacerbated the hydrops and resulted in an emergency cesarean delivery at 28 weeks gestation.¹¹ In another case with VT and hydrops associated with ungenotyped LQTS, no improvement was seen with digoxin treatment, and a cesarean delivery followed at 36 weeks gestation.¹²

From 1999 onward, reports of transplacental therapy of fetal VT with amiodarone appeared.¹³,¹⁴,¹⁵ In the absence of LQTS, the effect of amiodarone was favorable with a reduction of hydrops and the restoration of sinus rhythm.¹³,¹⁴ The use of amiodarone in cases that subsequently were diagnosed with LQTS led to worsening hydrops.¹⁰,¹⁴,¹⁶ Amiodarone has a very long half-life (6 weeks),³,¹³ and a transient elevation of the thyroid-stimulating hormone in the fetus and mother postnatally, suggesting thyroid suppression, has been reported in some cases.¹³,¹⁵

Although the optimal prenatal therapy for the fetus with LQTS presenting with TdP has not yet been established, there are 16 such cases reported in the literature that were treated with maternal administrations of various antiarrhythmic drugs (TABLE 4.2.1). The findings in TABLE 4.2.1 underscore the importance of differentiating TdP from other fetal VT. Fetuses with TdP treated with amiodarone and/or sotalol had exacerbation of tachycardia (case #2) resulting in premature emergency delivery (cases #3 and 11) or stillbirth (case #4). TABLE 4.2.1 also suggests that the prenatal rhythms predict postnatal rhythm; thus, if a fetus has TdP, the postnatal care team should be prepared to treat TdP. However, if only 2° AV block is seen in utero, TdP may still occur after birth, as seen in case #5.

First-line treatment with IV magnesium sulfate (class V antiarrhythmic) is extremely successful in terminating or reducing salvos of TdP. Infusion of magnesium in tocolytic doses has a rapid onset of action, and most obstetricians are familiar with its usage in the management of maternal preeclampsia.⁷,¹⁴ The mechanism of action of magnesium sulfate is only partially known. It is a cofactor of the sodium-potassium pump. By stimulating the efflux of sodium and influx of
potassium, it has effects opposite to digoxin and results in a decrease in intracellular calcium. It has been used with complete or partial success in the management of VT runs and TdP in fetal LQTS, either alone or in combination with intravenous lidocaine¹⁶,¹⁷,¹⁸,¹⁹ or propranolol or mexiletine.⁷,¹⁷,¹⁸,²⁰,²¹,²²,²³ Propranolol decreases the transmural dispersion of repolarization and the induction of TdP and has been a successful adjunct therapy for TdP. However, because the transplacental transfer of propranolol is extremely low (25%-30%), higher doses may be necessary. See TABLE 4.2.2 for recommended doses of antiarrhythmic drugs used in the treatment of TdP.