Fetal and neonatal arrhythmias are diverse in type and severity. They include both tachycardias and bradycardias.1 The innate physiological properties of the fetal and neonatal myocardiums make them more vulnerable to these high or low ventricular rates. Irregularities of fetal and neonatal cardiac rhythm commonly occur, and rarely have serious consequences; however, it is important to realize that sustained tachycardias and bradycardias can lead to heart failure and hydrops fetalis.2,3
Fetal arrhythmias are noted in only 1% of all pregnancies and can be categorized by rate and regularity. Almost all arrhythmias fall into one of three categories: irregular, tachycardic, or bradycardic.4 Normal fetal heart rates range from 120 to 160bpm at 30 weeks of gestation, and from 110 to 150bpm at term.5,6 Heart rates below 100bpm are classified as bradycardia, and rates greater than 180bpm as tachycardia.1,7
Fetal arrhythmias are often first noted on auscultation during routine maternal pre-natal examinations once heart tones are appreciated, at around 10th weeks. Generally, the mother is asymptomatic and does not notice any decreased fetal activity.1,4 If a fetal tachycardia is heard, the referring practitioner should attempt to determine its rate and characteristics. Gradual onset and cessation are associated with normal fetal accelerations, especially with a rate below 200bpm. Abrupt changes, especially if the rate is over 200bpm, are more often associated with pathological tachycardias.8 Transient slowing of the fetal heart rate with immediate return to normal rates is common mid-trimester when patients lie supine, caused by normal variable-type fetal heart rate decelerations, and does not need further cardiac evaluation. This isolated physiological slowing of the heart must be differentiated from persistent bradycardia, which requires expedited evaluation.8,9
Approximately 50% of fetuses referred for evaluation of fetal arrhythmias are in normal sinus rhythm, with the vast majority having isolated supraventricular systoles. Fewer than 10% of fetuses are found to have sustained tachyarrhythmias or bradyarrhythmias.2
Once an arrhythmia is detected by auscultation, an additional evaluation is indicated. Currently, external acquisition of fetal electrocardiography is not available.8 Other non-invasive approaches include 2D fetal echocardiography, to exclude structural cardiac defects, and M-mode ultrasonography, which depicts cardiac motion as a function of time. A cursor placed through both the fetal atrium and ventricle allows the timing of atrial and ventricular contractions to be determined and premature beats to be identified.8,10,11 Similarly, pulsed Doppler can be used to identify fetal rhythms by assessing intracardiac flow patterns.10,12 Fetal magnetocardiography uses the magnetic field generated by electrical activity of the fetal heart for a more precise delineation of fetal rhythms.13,14
Fetal tachycardias may have several causes. It is important to exclude fetal distress (with loss of beat-to-beat variability) and chorioamnionitis (with maternal fever), which may cause fetal heart rates of up to 200bpm.8 The three most common fetal tachyarrhythmias, aside from premature atrial contractions (PACs), are supraventricular (re-entrant) tachycardia (SVT), atrial flutter (AF), and ventricular tachycardia (VT). PACs are fetal extra-systoles, and are associated with good outcomes.8 In 0.4% of cases, PACs may progress to fetal tachycardia. Therefore, it is recommended that these patients be monitored weekly to exclude the development of tachyarrhythmias.8,15
AF accounts for approximately 21% of fetal tachycardia, and may be associated with structural abnormalities. Fetal hydrops is associated with 7% of AF cases.16,17 AF is defined as an atrial rate ranging from 250 to 500bpm with either fixed or variable atrioventricular (AV) block,18and diagnosis can be confirmed by fetal echocardiography, which documents the atrium beating at a faster rate than the ventricle.1 Medical management in cases without hydrops may consist simply of digoxin therapy, whereas in other cases adding a second agent such as flecainide, procainamide, or amiodarone may be needed.8 Drug therapy is successful in 82% of patients. Hydropic fetuses may require more medication and a longer treatment period to control the condition.19
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- Kleinman CS, Neghme R, Copel JA, et al., Fetal cardiac arrhythmias: diagnosis and therapy. In: Creasy RK, Resnik R (eds), Maternal├óÔé¼ÔÇ£fetal Medicine, Philadelphia, PA: Saunders, 1998;301├óÔé¼ÔÇ£18.
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- Cameron A, Nicholson S, Nimrod C, et al., Evaluation of fetal cardiac dysrhythmias with two-dimensional, M-mode, and pulsed Doppler ultrasonography, Am J Obstet Gynecol, 1988;158:286├óÔé¼ÔÇ£90.
- Silverman NH, Enderlein MA, Stanger P, et al., Recognition of fetal arrhythmias by echocardiography, J Clin Ultrasound, 1985;13(4): 255├óÔé¼ÔÇ£63.
- Kleinman CS, Copel JA, Hobbins JC, Combined echocardiographic and Doppler assessment of fetal congenital atrioventricular block, Br J Obstet Gynaecol, 1987;94(10):967├óÔé¼ÔÇ£74.
- Quartero HW, Stinstra JG, Golbach EG, et al., Clinical implications of fetal magnetocardiography, Ultrasound Obstet Gynecol, 2002;20(2):142├óÔé¼ÔÇ£53.
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