Treatment of tachyarrhythmias during pregnancy and lactation

The incidence and severity of tachyarrhythmias, both supraventricular tachycardia and ventricular tachycardia may increase during pregnancy. Although the reasons for this observation are unclear, some explanations have been proposed: increased awareness, haemodynamic, hormonal, autonomic, and emotional changes related to pregnancy, which may include: increases in plasma catecholamine concentrations and adrenergic receptor sensitivity, atrial stretch and increased end-diastolic volumes due to intravascular volume expansion. Treatment of tachyarrhythmias during pregnancy and lactation is complicated by concerns regarding safety and tolerability for the fetus or infant. All commonly used antiarrhythmic drugs cross the placenta and are excreted in breast milk. Their plasma concentration in the fetus and infant are partly determined by differences in pH between their serum and that of the mother (most antiarrhythmic drugs are alkalic compounds and accumulate in acidic environments). Teratogenic risk is greatest during the period of organogenesis, i.e. during the first 8 weeks. However, other adverse effects may still occur during the latter periods of pregnancy, e.g. uterine perfusion and contractility may be affected by antiarrhythmic drugs, influencing fetal growth and labour. However, quinidine, procainamide, lidocaine, flecainide, propranolol, amiodarone, verapamil, and digoxin do not reduce human placental blood flow (but adenosine does). Physiological changes in the mother may alter the effective plasma concentration of antiarrhythmic drugs. The increased intravascular