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Fetal distress is traditionally defined as a heart rate below 110 bpm or above 160 bpm during labor or between contractions. However, in this segment, we focus on a different scenario—fetal bradycardia detected during routine prenatal ultrasonography in nonlaboring patients. These findings often raise important clinical questions: is this a benign variant, or does it reflect an underlying conduction abnormality, such as congenital complete heart block (CCHB)? Recognizing how to evaluate, interpret, and monitor fetal bradycardia outside of labor is essential for timely diagnosis and optimal management.The video in this vignette demonstrates (Video 1 and Figure 1) a fetal heart rate of 83 bpm (Figure 2), which is consistent with fetal bradycardia. Fetal bradycardia (Video 1 and Video 2) is characterized by an abnormally low fetal heart rate, typically defined as less than 110 bpm for at least 10 minutes. However, recent studies suggest that a more precise threshold should be based on gestational age, with a heart rate below the third percentile being more indicative of underlying pathology.1 In the absence of other signs of fetal distress, persistent (ie, lasting more than 10 minutes) fetal bradycardia can result from various conditions, including sinus bradycardia, congenital complete atrioventricular (AV) block (also called third-degree [3°] AV block), 2 to 1 AV block, and blocked atrial bigeminy (BAB).2 Of note, a typical fetal heart rate at a given time does not exclude arrhythmia. A history of irregular or slow heart rate, regardless of duration, should prompt fetal echocardiography to evaluate for conduction abnormalities.Fetal echocardiography is the gold standard for assessing cardiac rhythm in utero because it evaluates mechanical events—such as valve movements and myocardial contractions—to infer the heart’s electrical activity and determine the fetal cardiac rhythm (Figure 3). M-mode imaging captures the sequential contraction of the atrial and ventricular myocardium by aligning the cursor from 1 ultrasonography beam across both atrial and ventricular walls. The fetal cardiologist can analyze the graphic representation of atrial and ventricular wall motion to assess the relationship between atrial and ventricular rates, determining whether the rates are comparable and whether a consistent timing (temporal relationship) exists between their contractions (Figure 3A).2 Pulsed-wave Doppler evaluates the AV conduction by assessing simultaneous blood flow patterns across the mitral and aortic valves or between the superior vena cava and aorta. This method provides an accurate measurement of the duration of the mechanical AV interval, which is prolonged in patients with first (1°) and sometimes second-degree (2°) AV block, and identifies AV dissociation, a hallmark of complete AV block (Figure 3B). Indeed, the AV contraction time interval (AVCTI) (Figure 4A) represents the mechanical equivalent of the electrical PR interval in postnatal electrocardiography.2CCHB is the most common form of fetal bradycardia, characterized by the loss of synchrony between atrial and ventricular contractions.3 It occurs in approximately 1 in 20 000 live births and can lead to a markedly reduced ventricular rate, fetal cardiac failure, and hydrops fetalis.3 CCHB is frequently associated with autoimmune conditions (immune-mediated) in the pregnant person and less commonly (nonimmune-mediated) with structural congenital cardiac anomaly, such as left atrial isomerism, congenitally corrected transposition of the great arteries, and AV septal defects.3 In some cases, a cause is not found.Heart block in structural heart disease is attributed to an anatomical disruption of the cardiac conduction system. This may result from a congenital failure of AV nodal tissue to fuse with the His bundle or from a secondary interruption of the AV conduction axis.4 When CCHB is associated with congenital heart disease, the fetal prognosis is generally worse given the combination of structural and electrical disease. One study reported a fetal mortality rate of 7%, particularly in cases complicated by hydrops and intrauterine demise, with an additional 10% to 15% mortality during infancy.5Immune-mediated CCHB occurs in fetuses with structurally typical hearts who have been exposed to SSA (Ro) antibodies from the pregnant person. There is ongoing debate regarding whether anti-SSB antibodies alone can lead to CCHB in the absence of anti-SSA. CCHB is believed to result from an inflammatory response triggered by the transplacental transfer of autoantibodies starting at 12 weeks’ gestation. Inflammation typically peaks between 18 and 25 weeks of gestation, leading to fibrosis of the fetal cardiac conduction system, especially of the AV node, but the sinus node can also be affected.2 This process often results in acute and irreversible fibrosis of the AV node, and it ultimately leads to 3° (complete) heart block.3 Infrequently, 1° or 2° AV blocks are observed prior to the onset of the 3° block.2 In CCHB, there is complete dissociation between the atrial and ventricular contractions. As the impulse from the atria is blocked, the ventricular contraction relies on an escape rhythm originating from a junctional or ventricular focus, which is slower and less reliable with decreased cardiac output and increased risk of fetal heart failure and hydrops.Pregnant persons with SSA (Ro) antibodies have a 1% to 2% risk of their fetus developing CCHB, which increases to 3% if both SSA (Ro) and SSB (La) antibodies are present.3 The risk is even higher in pregnant individuals with active disease and/or elevated antibody titers. Moreover, those with a history of a previous fetal CCHB are at even greater risk. In fact, if a person previously had a child with CCHB, the risk increases to a range of 16% to 40% in subsequent pregnancies.3 Genetic factors, age of the pregnant person, and concomitant thyroid disease also increase the risk.3 Notably, autoantibodies are found in 95% of pregnant persons of fetuses with isolated CCHB, yet only 20% to 30% of affected infants have birth parents with a diagnosed autoimmune disorder such as lupus or Sjögren syndrome.3 Close monitoring during pregnancy and after delivery is essential, given the significant risks of fetal and neonatal morbidity and mortality associated with these conditions.Fetuses with immune-mediated CCHB are also at risk of myocardial and vascular inflammation, which can lead to adverse remodeling and fibrosis. Prognostic markers include endocardial fibroelastosis and AV valve dysfunction.6,7 Endocardial fibroelastosis reflects ongoing fibrotic changes in the myocardial wall and may result in ventricular dysfunction, end-stage heart failure, and death.8 The intense inflammatory response affecting the myocardial wall can also trigger additional arrhythmias, including junctional and ventricular tachycardia, long QT syndrome, and ventricular fibrillation.9 AV valve insufficiency, caused by inflammation or tensor apparatus dysfunction or rupture, may cause severe ventricular volume overload, which further increases the risk of fetal heart failure and hydrops fetalis.9 Additionally, these fetuses are prone to aortic and pulmonary artery dilatation, which may result from increased ventricular stroke volume or primary inflammation of the vascular wall.9,10 Rarely, severe bradycardia and akinesis of portions of the ventricular walls could potentially create conditions conducive to intracardiac thrombus formation, increasing the risk of thromboembolic events.11The 2020 American College of Rheumatology guidelines on reproductive health management in rheumatic and musculoskeletal diseases recommend serial fetal echocardiography for pregnant persons with anti-Ro/SSA and/or anti-La/SSB antibodies to monitor for fetal conduction abnormalities.12 For women without a prior child affected by CCHB or neonatal lupus, echocardiographic surveillance is suggested at less frequent than weekly intervals, beginning between 16 and 18 weeks of gestation and continuing until 26 weeks’ gestation; however, the optimal frequency remains unspecified.12 For those with a history of a previous infant with CCHB or neonatal lupus, weekly fetal echocardiography is advised, starting at 16 to 18 weeks’ gestation and continuing through week 26, given the significantly increased recurrence risk.12 The daily use of fetal heart rate monitors by expectant persons at home is currently being studied. Although promising, this approach has not been evaluated to determine whether it can prevent progression to CCHB, but trials are ongoing (Clinical Trials: NCT04474223).13In neonates exposed to autoantibodies during gestation with no significant conduction anomalies or endocardial fibroelastosis during the pregnancy, an electrocardiogram (ECG) should be performed within the first 24 hours after birth. If the postnatal ECG result is normal, there is no indication for further cardiac surveillance.14 If there is a history of transient 1° AV block in utero, follow-up with a postnatal ECG and echocardiogram before hospital discharge and at 1 year of age is recommended.14 For infants who had a transient 2° AV block that resolved to typical sinus rhythm at birth, a repeat cardiac evaluation should take place within the first 3 months of age to assess for any residual or evolving conduction abnormalities because they are still at risk of developing complete AV block. These patients will possibly require follow-up indefinitely.14CCHB is associated with a non-negligible mortality rate, approximately 7% in the absence of a concomitant congenital cardiac anomaly, primarily owing to ventricular dysfunction and the development of postnatal cardiomyopathy.3 Fetal monitoring should be conducted vigilantly to assess for worsening bradycardia, cardiac dysfunction, and signs of hydrops. Comprehensive ongoing fetal cardiac evaluations should include quantification of the AVCTI, ventricular rate, assessment of fetal cardiac performance, endocardial fibroelastosis, AV valve insufficiency, and Doppler studies of the aortic, umbilical, ductus venosus, and cerebral blood flow patterns, all of which contribute to prognostication.15In patients with 1°, 2°, or 3° heart block related to an immune-mediated process, dexamethasone administration may help reduce inflammation in the cardiac conduction system and myocardium, with observational data outlining a potential role in reducing the risk for postnatal cardiomyopathy.15 Despite steroid therapy, more than half of fetuses with CCHB require pacemaker implantation by 18 months of age.2 The use of intravenous immunoglobulin is more controversial and typically reserved for worsening conduction disease or evidence of myocardial inflammation. β-receptor agonists can support fetal cardiac output by increasing ventricular heart rate. However, they may promote the occurrence of other arrhythmias and cause adverse effects in the pregnant person. For fetuses with ventricular rates below 55 bpm, β-sympathomimetics such as terbutaline, salbutamol, or isoprenaline, may increase the ventricular rate, particularly in the setting of structural heart disease or signs of heart failure. Fetal pacing remains experimental and has not demonstrated improved survival or prolonged gestation. Poor outcomes, including fetal or neonatal death, have been strongly linked to the presence of structural heart defects, hydrops fetalis, and severe bradycardia, particularly when the atrial rate is below 120 bpm or the ventricular rate falls below 55 bpm.2Pregnant individuals with circulating SSA/SSB antibodies should be cotreated by rheumatology and maternal-fetal medicine, with consideration for antibody titer assessment if available, to evaluate fetal risk. Postnatally, dexamethasone therapy in the birth parent should be tapered, in collaboration with pharmacy, obstetric medicine, and maternal-fetal medicine specialists to ensure appropriate steroid weaning.The time of delivery will depend on the well-being of the fetus and pregnant person, balancing the risks of prematurity with those of an intrauterine fetal demise. Delivery planning should prioritize a scheduled cesarean delivery during daytime hours on a weekday, given the inability to monitor fetal well-being during labor with persistent fetal bradycardia. Neonatal and cardiologic teams should be notified well in advance soon after the pregnant person is admitted to the hospital, and neonatal personnel should be present at delivery. The feasibility of delayed cord clamping should be evaluated on a case-by-case basis, with immediate cord clamping recommended if the newborn lacks vigorous respiratory efforts. Given the likelihood of neonatal bradycardia, the team should be prepared for respiratory support, line placement, and potential resuscitation maneuvers if the newborn shows signs of hemodynamic instability. When there are signs of fetal cardiac compromise, hydrops fetalis, or other concerning features, delivery should be arranged at a tertiary center with neonatal cardiac care, pacing, and potentially extracorporeal membrane oxygenation capabilities.16In many instances, the fetal ventricular rate, often around 55 bpm to 60 bpm, may increase during the postnatal transition due to adrenergic stimulation, but some infants may require support if myocardial inflammation or valvular dysfunction limits adaptation.16 When the ventricular rate is sufficient and cardiac function is stable, standard Neonatal Resuscitation Program (NRP) guidelines may be applied, keeping in mind that the baseline heart rate may be lower than typical.16 However, current neonatal resuscitation guidelines, such as the NRP, are not fully adapted to the unique needs of infants with critical congenital cardiac anomalies, including those with CCHB because they do not incorporate specific algorithm modifications or tailored educational content.17,18In cases of significant hypoperfusion (eg, prolonged capillary refill, pallor, weak pulses) or lack of respiratory effort, respiratory stabilization, intubation, and umbilical venous line placement should be prioritized before considering chest compressions. Isoproterenol infusion should be readily available in the delivery room, initiated at 0.01 μg/kg/min and titrated to effect and increase ventricular rate in neonates with a low perfusion. Higher doses (>0.1 μg/kg/min) should be used cautiously due to their proarrhythmic and vasodilatory effects. Indeed, for neonates showing signs of compromise, initial treatment should include endotracheal intubation, sedation, and neuromuscular blockade to minimize metabolic demands.16 Pharmacologic agents such as epinephrine or isoproterenol are used to increase ventricular rate, and temporary pacing may be considered based on institutional protocols.16Transcutaneous pacing should be reserved as a last resort to avoid the risk of serious skin burns. Ideally, it should only be initiated after consultation with cardiology, except in critical emergencies when cardiologic support is not immediately available in the delivery room or at the bedside. The skin must be thoroughly dried beforehand, and care should be taken to ensure the pads do not touch each other, placing one on the chest and the other on the back. Output is typically initiated at 20 mA with a rate of 90 bpm. Output may be increased by increments of 5 mA until there is QRS capture and a mechanical pulse response confirmed by palpation and with a readable blood pressure. The pacer machine is set on “fixed” mode in the delivery room and transitioned to “demand” mode only when the ECG leads are connected to the pacer machine and the pacemaker is recording reliable underlying QRS-waves readings. Once stabilized, the infant should be given analgesia if transcutaneous pacing is ongoing. Notably, transesophageal pacing is not an option in these infants because it stimulates the atrium, not the ventricles. Cardiac surgery also needs to be aware of these deliveries in advance because of the potential for urgent pacemaker implantation. In cases involving hydrops, additional procedures like draining pleural or pericardial effusions may be necessary to support hemodynamic stability.16 Extracorporeal life support may be considered if, despite all interventions, the newborn is unable to maintain adequate ventricular output.In instances where the infant has been chronically exposed to dexamethasone for more than 1 to 2 weeks during pregnancy, there is a risk of adrenal suppression, necessitating coverage.19–22 Eventually, a corticotropin stimulation test should be performed to assess adrenal function. The role of ongoing postnatal steroid therapy for modulating cardiac inflammation and cardiomyopathy remains controversial. Potential adverse effects in the neonatal period must be weighed against the uncertain benefits.23,24 Postnatal intravenous immunoglobulin should be reserved for cases with significant concern for carditis and cardiac dysfunction. Inotropic support may also be necessary with use of epinephrine or dobutamine infusions based on hemodynamic status and cardiac function. However, it is important to note that these medications have proarrhythmogenic effects.Of note, there is evidence that treatment of pregnant persons with hydroxychloroquine reduces the recurrence of CCHB by more than 50% and therefore should be prescribed for secondary prevention in anti-SSA/Ro-exposed pregnancies (PATCH trial, ClinicalTrials: NCT0137957).19 Hydroxychloroquine’s protective effect is believed to stem from its immunomodulatory action, specifically through inhibition of Toll-like receptors, which play a key role in the inflammatory cascade associated with autoimmune-mediated fetal cardiac injury.19Fetal sinus bradycardia is typically defined by a persistent fetal heart rate between 90 bpm and 130 bpm, with a regular atrial rhythm and 1 to 1 AV conduction. This condition can arise from various causes, including factors in pregnant individuals such as hypothyroidism or the use of certain medications like β-blockers, antithyroid drugs, and methadone.25 Autoimmune-mediated sinus node dysfunction, particularly due to anti-Ro/SSA antibodies, has also been implicated. Other potential causes include myocarditis, metabolic diseases like Pompe disease, and genetic syndromes such as Holt-Oram syndrome caused by TBX5 mutations.25 Additional genetic abnormalities, including NKX2.5 mutations, certain types of long QT syndrome, and other inherited or bradycardia may contribute to the and factors such as fetal system abnormalities, severe fetal or distress, and umbilical cord which is often transient and linked to ultrasonography can also play a Although treatment cardiac conduction is generally not for isolated fetal sinus or low atrial bradycardia, primary management of the underlying and monitoring are essential to assess for fetal or underlying is a of atrial contractions (Figure in which other atrial is and to to the ventricles. It is characterized by an irregular atrial and long intervals, and a regular and slower ventricular rate with sinus Although typically increases the risk of developing by In affected a postnatal ECG is and for instances where until or monitoring should be performed to assess the risk of atrial It is to this because a slower fetal heart rate in the of may be as fetal bradycardia owing to fetal distress and lead to interventions, including delivery by urgent cesarean and 3° AV block can be from by the presence of a regular atrial and in the of 3° block, by AV dissociation and slower ventricular rates A key is the interval, which is in with in 2° AV block (Figure Additionally, may be prolonged in 2° AV block, a that is not observed in 2° AV block can be observed in the of fetal long QT bradycardia during routine prenatal ultrasonography in nonlaboring patients particularly when Although some cases reflect benign rhythm may serious conduction abnormalities such as Fetal echocardiography a role in rhythm and CCHB, most commonly associated with antibodies in the pregnant person, significant risks for fetal and cardiac serial and timely steroid therapy, consideration of and of delivery essential for Postnatal care surveillance for residual conduction disease and potential As signs and a approach can significantly prognosis in these a routine prenatal ultrasonography at weeks of gestation, fetal heart rate and rhythm findings The is fetal movements are and there are no signs of fetal distress or A fetal echocardiogram is (Video 1 and Figure 1 and is the most cause of the heart rate in this atrioventricular (AV) atrial bigeminy complete heart block This condition is diagnosed as CCHB by Doppler is the most common cause of conditions in the pregnant of the great septal complete heart conditions in the pregnant of assessment of fetal and medications affecting the fetus and newborn to cardiac