Abstract

Cardiac arrhythmias are among the most common cardiac complications encountered during pregnancy.1 In some, pregnancy may trigger exacerbations of pre-existing arrhythmias, whereas in others arrhythmias may manifest for the first time.2 Fortunately, severe arrhythmias requiring aggressive or invasive therapies are rare. There are unfortunately few randomized studies, little data on the efficacy or safety of antiarrhythmic drugs (AADs), or even explicit guidelines to support decision making on pregnant women with arrhythmias. Thus, much of the clinical care is guided by knowledge of the physiology of pregnancy and educated risk/benefit decisions made in collaboration with high-risk obstetric colleagues in Maternal-Fetal Medicine, as well as with the patient. The precise mechanism of increased arrhythmia burden during pregnancy is unclear, but it is likely because of a combination of hemodynamic, hormonal, and autonomic changes. Increases in effective circulating blood volume of 30% to 50% are seen beginning at 8 weeks of gestation and peaking at ≈34 weeks. Cardiac output is increased as well, with an average of 6.7 L/min in the first trimester and ≤8.7 L/min in the third trimester. This is the result of a 35% increase in stroke volume and a 15% increase in heart rate. The increase in plasma volume causes stretching of atrial and ventricular myocytes, and this may result in early after depolarizations, shortened refractoriness, slowed conduction, and spatial dispersion through activation of stretch-activated ion channels.3,4 A larger heart can also potentially sustain re-entry more easily because of an increase in path length of potential reentrant circuits. The increase in heart rate during pregnancy, seen predominantly in the third trimester, may also predispose to arrhythmia, as a high resting heart rate has been associated with markers of arrhythmogenesis.5 Hormonal and autonomic changes may also contribute to arrhythmogenesis. Estradiol and progesterone have been …

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