![]() ![]() FHR is gestational age dependent, it normally gets slower as the pregnancy advances. The established range of fetal heart rate is 110–160 bpm. PVCs are not uncommon and appear in patients without structural heart disease and in those with cardiac disease, independent of severity. Premature ventricular complexes (PVCs also referred to as premature ventricular beats, premature ventricular depolarizations, or ventricular extrasystoles) are triggered from the ventricular myocardium. ![]() PACs are triggered from the atrial myocardium in a variety of situations and are almost ubiquitous in the general population. The interval between the last sinus beat and the ectopic beat is shorter than the interval between two normal sinus beats. Premature atrial complexes (PACs also referred to as premature atrial beats, atrial ectopic beats, or atrial extrasystoles) are caused by early activation of the atrial myocardium because of an impulse generated by an ectopic focus within the atrial myocardium rather than the sinus node. Premature beats (extrasystoles or ectopic beats) can be atrial, ventricular, or rarely junctional in origin. Some of the specific terminology used in the article is explained in Appendix A ( Table A1). There are three main categories of fetal arrhythmias: (1) an irregular rhythm with a normal fetal heart rate (FHR), as a consequence to premature beats or to conduction anomalies (2) tachyarrhythmias (defined as FHR > 180 beats per minute-bpm), and (3) bradyarrhythmias (defined as FHR < 110 bpm). Persistent fetal arrhythmia can cause low cardiac output, heart failure, hydrops, and fetal demise. Most fetal arrhythmias are benign and transient however, in some cases, the irregularity of the fetal heart rhythm can indicate a serious condition-either of fetal or maternal origin. Our review aims to provide a practical guide for the diagnosis and management of common fetal arrythmias, from the joint perspective of the fetal medicine specialist and the cardiologist.įetal arrhythmias are detected in 1–2% of pregnancies. The efficacy of prenatal treatment for fetal AV block is limited. Approximately half of fetal heart blocks are in cases with structural heart defects, and AV block in cases with structurally normal heart is often caused by maternal anti-Ro/SSA antibodies. Persistent bradycardia outside labor or in the absence of placental pathology is mostly due to atrioventricular (AV) block. ![]() Fetal bradycardia is diagnosed when the fetal heart rate is slower than 110 bpm. Most fetal tachycardias can be terminated or controlled by transplacental or direct administration of anti-arrhythmic drugs. The most common fetal tachyarrhythmias are paroxysmal supraventricular tachycardia and atrial flutter. Tachyarrhythmias are diagnosed when the fetal heart rate is persistently above 180 beats per minute (bpm). Irregular rhythm due to atrial ectopic beats is the most common type of fetal arrhythmia and is generally benign. The analysis of fetal heart rhythm is based on ultrasound (M-mode and Doppler echocardiography). However, some of them are associated with structural defects or can cause heart failure, fetal hydrops, and can lead to intrauterine death. Fetal arrhythmias are mostly benign and transient. ![]()
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