Читать книгу Protocols for High-Risk Pregnancies - Группа авторов - Страница 62

The largest group of fetal arrhythmias are intermittent and due to atrial, junctional or ventricular extrasystoles. They carry a small risk of co‐existent structural abnormality. A greater risk exists of an unrecognized tachyarrhythmia, or the development of a tachyarrhythmia later in gestation. Atrial extrasystoles predispose the fetus to development of reentrant atrial tachycardia, which can lead to fetal hydrops. We recommend weekly auscultation of the fetal heart, along with avoidance of caffeine or other sympathomimetics, until resolution of the arrhythmia.

Fetal tachycardias represent a management challenge, because determination of the precise electrophysiological cause of the arrhythmia is essential to any rational management strategy, but fetal electrocardiography is not yet clinically practical in the presence of intact membranes. The differential diagnoses of fetal tachycardias include reentrant atrial tachycardia, atrial flutter, and ventricular tachycardia. The treatment of these disorders differs significantly, and appropriate medications for one may be contraindicated for another. The correct diagnosis, which should be based on combinations of M‐mode, Doppler and color Doppler–M‐mode imaging, is essential to appropriate therapy.

If there is a fetal bradycardia, the first step is to determine if there is a regular or an irregular atrial rate. If the atrial rate is regular and slow, that is, below 100 beats per minute, there may be sinus bradycardia, which should prompt a complete evaluation of fetal well‐being. The most common clinically important fetal bradycardia results from complete heart block, which will demonstrate a normal regular atrial rate with a slower ventricular rate whose beats do not occur in conjunction with atrial beats. In structurally normal hearts this is usually caused by maternal antibodies associated with lupus erythematosus and Sjögren syndrome, termed SSA/Ro and SSB/La. A smaller group of patients, without maternal antibodies, may present with congenital complete heart block in a setting of complex congenital heart disease involving the central fibrous body of the heart (e.g., left atrial isomerism, corrected transposition of the great arteries). In these patients, the prognosis is directly related to the complexity of the heart disease and the association with congestive heart failure.

A more benign cause of fetal bradycardia, which may be mistaken for 2:1 heart block, is blocked atrial bigeminy. In such cases the atrial rate is not regular, but rather demonstrates paired beating in which a premature atrial beat follows closely after a normal atrial beat with no ventricular response to the premature beat. This arrhythmia has no significance beyond that of isolated atrial extrasystoles.