Management of fetal arrhythmias (Table IV):

Fetal electrocardiographic tracings and a complete fetal echocardiography with M- mode analysis and a Color Doppler flow pattern at the mitral and aortic valve helps to distinguish atrial and ventricular components of the cardiac cycle and thus determine the nature and type of arrhythmia. Additionally, cardiac dimensions, presence of hydrops and ventricular functions should be assessed to determine the haemodynamic consequences of these arrhythmias on the fetus. Most cases of fetal arrhythmias are benign and are premature atrial or ventricular contractions. Routine antenatal follow-up for noting the fetal heart rate is advised at 2-4 weekly interval . If fetal tachycardia is noted repeat scan is advocated. The mother should also be advised to avoid caffeine and sympathomimetic drugs. Fetal tachycardia is defined as sustained heart rate of more than 200 beats per minute.

Fetal echocardiography assessment is done and if any three of the seven criteria are present : fetal HR (> 200 bpm), hydrops, cardiomegaly (heart area / chest area - HA/CA>0.42), atrio-ventricular valve regurgitation, fractional shortening (FS) < 25% suggestive of ventricular dysfunction, ventricular dysfunction reversal of flow in the IVC and distended hepatic and umbilical veins > 6 mm , then fetal therapy is warranted. If the fetus is near term with good lung maturity and in absence of hydrops, an early delivery with anti-arrhythmic treatment of the neonate is advised. Fetus if premature with poor lung maturity and hydrops, fetal anti-arrhythmic treatment is advised which is delivered either by maternal administration or intra-amniotic or direct instillation in umbilical vessels, though the former is preferred. The mother is admitted and a base line assessment of serum electrolytes, serum calcium, serum magnesium, renal profile , thyroid functions and electrocardiogram is done. The anti-arrhythmic drugs are started in a stepwise manner as shown in table (IV), monitoring for side-effects. If the fetus responds and tachycardia reverts these medications are continued till term.

Fetal bradycardia is defined as sustained heart rate of less than 100 beats per minute. A structurally normal heart by fetal echocardiography determines the prognosis, with complex heart lesions carrying a poor outcome. If the heart is structurally normal, maternal Systemic Lupus has to be ruled out. Maternal therapy with steroids and immunoglobulins have been tried with success and arrest the destruction of fetal conduction pathways by the maternal antibodies. In fetus with ventricular rate less than 55 bpm in a structurally normal heart and 45 bpm in abnormal heart and an atrial rates less than 80 bpm with or without hydrops, maternal administration of sympathomimetics like isoproterenol, terbutaline or salbutamol is advocated. An early delivery with neonatal management of the arrhythmias is generally advocated.

Fetal echocardiography has indeed revolutionized the present day management of fetus with structural and functional heart diseases. Early diagnosis, frequent monitoring of fetus for cardiac functions and haemodynamics have greatly improved the outcome and helped in better understanding of the Congenital Heart Disease

1. Hoffman JIE, Christianson R. Congenital heart disease in a cohort of 19,502 births with long term follow- up.Am J Cardiol 1978;42:641.

2. Achiron R, Rostein Z, Lipitz S, Et al. First trimester diagnosis of fetal congenital heart diseases by transvaginal ultrasonography.Obstet Gynecol 1994;84:69-72.

3. Mitchell SC, Korones SB, Berendes HW. Congenital heart diseases in 56,109 live births: Incidence and natural history. Circulation 1971;43:323-332.

4. Benacerraf BR, Pober BR, Snaders SP. Accuracy of fetal echocardiography. Radiology 1987;165:847-49.

5. Smythe JF, Copel JA, Kleinmann CS: Outcome of prenatally detected cardiac malformtions.Am J Cardiol ,1992; 69:1471-74.

6. Tworetzky W, Mc Elhinney DB, Reddy VM et al :Does prenatal diagnosis of hypoplastic left heart lead to improved surgical outcome J Am Coll Cardiol , 1998 ; 13(suppl A):71-75

Last created on 26-02-2004
Last updated on 01-07-2006