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• W2034200130 abstract "Fetal bradycardia can indicate fetal distress and an urgent need to deliver the baby to avoid fetal loss; in this case, its recognition, especially if it is intrapartum, is of paramount importance for pregnancy management and fetal wellbeing. Conversely, transient episodes of bradycardia often occur during routine obstetric scanning but are benign in nature and have no clinical implications. These brief episodes are considered to be a response to vagal stimulation1 due to partial cord occlusion, caused by pressing the transducer on the maternal abdomen1, 2, and invariably they resolve when this external pressure is lessened. Both of these situations can be considered as ‘secondary bradycardia’ and do not constitute the objective of this article. However, bradycardia that persists, whether or not intermittent, often being documented during routine ultrasound examination or at the time of routine antenatal visits, requires further investigation to clarify its mechanism. The focus of this Opinion is ‘primary bradycardia’: the occurrence of slow fetal heart rate (FHR) resulting from abnormalities related directly to the heart, i.e. related to the cardiac conduction system and/or myocardium itself. The main objectives are to provide an overview of normal cardiac rhythm, to understand the electrophysiological principles that underpin rhythm assessment by ultrasound in prenatal life and to highlight key features that allow correct diagnosis of different mechanisms of bradycardia. Listening to the fetal heart, usually with a Doppler device, and documenting FHR is common practice in the routine management of low- and high-risk pregnancies worldwide. Generally, rates between 120 and 160 bpm are considered normal and bradycardia is broadly defined as FHR < 100 bpm. There are, however, gestational-age-specific nomograms for baseline FHR. Serra and coworkers3 obtained data from a large population of normal fetuses at 25–42 weeks of gestation and showed a decrease in baseline FHR as pregnancy advances. Briefly, the 5th centile is around 135 bpm at 25 weeks, 125 bpm at 30 weeks and 120 bpm at 40 weeks. The definition of bradycardia has also been refined based on computerized cardiotocography. In 2009, the American College of Obstetricians and Gynecologists defined intrapartum bradycardia as FHR < 110 bpm, but this cut-off can also be used for antepartum observations4. Applying this slightly higher value of 110 bpm, as opposed to 100 bpm, to diagnose bradycardia (i.e. having a lower threshold) has the potential to help identify fetuses with incomplete forms of atrioventricular (AV) block that may present with rhythm irregularity, such as those with 3:2 AV conduction. Similarly, having gestational-age-specific centile charts may help in monitoring fetuses known to be at risk of developing bradycardia, such as those with a family history of long QT syndrome. In the following sections a methodical approach is presented to the differential diagnosis of bradycardia that should facilitate reaching the correct diagnosis, ultimately leading to appropriate management of the rhythm abnormality and, consequently, pregnancy management. The normal cardiac rhythm starts at the sinus node, which is located in the right atrium. As a natural pacemaker, the sinus node dictates the frequency of overall cardiac contraction. The impulse generated triggers an atrial contraction and travels towards the atrioventricular node (AV node), reaching the ventricles via specialized conduction cells, namely the ‘bundle of His’, the right and left bundle branches and the Purkinje fibers; this eventually leads to myocardial depolarization and ventricular contraction. Thus, the electrical equivalent of one cardiac cycle consists of one atrial contraction followed sequentially by one ventricular contraction, with only a slight time delay (the AV delay) between them. This normal sequence of electrical and mechanical activities means there is a ‘1:1 AV relationship’ (or 1:1 AV conduction) between atrial and ventricular contractions. Understanding this simple but essential sequence of events constitutes fundamental knowledge on which basis various arrhythmia patterns can be analyzed. At the cellular level, cardiac-chamber contraction results from electrical stimulation of the heart and is followed by chamber relaxation. Both stimulation and propagation of the electrical impulse occur in the specialized cells which form part of the conduction system. Whilst most cardiac cells maintain a resting transmembrane gradient due to equilibrium generated by ion transfer, and are unable to start an electrical stimulation, these specialized cells behave differently. Their intrinsic properties relate to ion transfer across the cell membrane that allow them to depolarize spontaneously once a transmembrane gradient threshold is reached, triggering an action potential. Thus, the specialized cells of the conduction system can trigger and conduct the electrical impulse that will ultimately lead to muscle contraction followed by relaxation. Elucidating the underlying electrophysiological mechanism leading to fetal bradycardia is of the utmost importance, as management strategies vary and depend on achieving a correct diagnosis. During normal sinus rhythm, each atrial contraction is followed by one ventricular contraction, which happens after a constant and short time interval. Thus, it is essential that atrial and ventricular activities be registered simultaneously when analyzing any form of rhythm disturbance. The most frequently used ultrasound techniques in clinical practice are M-mode echocardiography and pulsed wave Doppler5-8. Each allows recording and analysis of atrial and ventricular wall motion or Doppler flow waveform across valves and vascular structures which are used as markers of atrial and ventricular contraction and, ultimately, of electrical stimulation. Other diagnostic modalities, such as tissue Doppler imaging, fetal electrocardiography (ECG) and fetal electromagnetocardiography9-12, may also help but are less commonly used. Bradycardia can be regular or irregular. Regularity can be ascertained by simply listening to the fetal heart or by visual inspection of M-mode or Doppler recordings, which should show equal time intervals between ventricular contractions (regular V-V interval). However, a meticulous assessment of the pattern of atrial activity (to determine if it is regular or irregular) and the temporal relationship between each atrial and ventricular activity (AV interval) is needed. This analysis constitutes the cornerstone that allows correct diagnosis of the underlying electrophysiological mechanism of any form of arrhythmia. A simple visual observation of atrial waveforms on M-mode or pulsed-wave Doppler may suffice, but only if the atrial rhythm is clearly irregular. A cautious approach is needed when the distance between two atrial contractions (A-A interval) appears to be either similar or slightly dissimilar. In such cases, it is important that the A-A intervals (expressed in ms) be measured accurately over a period of time, as inspection alone can lead to errors in diagnosis. It is also important that the AV interval for each cardiac cycle (also expressed in ms) be measured meticulously. Recordings should be long enough to allow such analysis, often possible by using the cine-loop facilities of ultrasound equipment. Five to 10 cardiac cycles are usually sufficient to determine the mechanism but repeated assessments to confirm measurements or a longer recording may be necessary. Persistent bradycardia with a regular pattern of ventricular contraction (Figures 1-3) is often observed with ventricular rates around 70–80 bpm. However, rates of 50–60 bpm are not uncommon and, occasionally, rates can be as high as 90–100 bpm. The initial approach to diagnosis requires ascertaining if: (1) atrial and ventricular activities are at the same rate, i.e. if there is a 1:1 AV ratio or (2) the atrial rate is faster than the ventricular rate, implying that some atrial activity is not followed by ventricular activity (A-V ratio is greater than 1:1). In this form of bradycardia, for every atrial contraction there is a corresponding ventricular contraction. This pattern is uncommon. If present, it often indicates sinus bradycardia (Figure 1) but it may also represent a low atrial rhythm in fetuses with left atrial isomerism. Primary bradycardia with 1:1 conduction is often well-tolerated by the fetus and is not usually associated with hemodynamic disturbance. Its significance lies in the possibility of there being underlying diagnoses: sinus bradycardia can be a manifestation of sinus node dysfunction or long QT syndrome13-15, or it can be associated with circulating maternal antibodies16, 17. It is therefore important to check maternal blood for anti-Ro and anti-La antibodies, to perform parental ECG and to obtain a detailed family history, with emphasis on potential symptoms that may be related to arrhythmic events such as syncope. Measurement of the QT interval by fetal ECG and magnetocardiography may be of value, but these techniques are not widely available. An AV relationship > 1:1 implies atrial rate is faster than ventricular rate. The latter can vary but is often < 100 bpm. The main differential diagnosis is between: (1) pathological AV block and (2) blocked ectopic beats. 1. Pathological block, regular atrial activity (A-A interval). If the pattern of atrial contractions is regular i.e. the sinus node sends impulses at regular time intervals, and some or all of these are not transmitted to the ventricles, this indicates pathological heart block. The AV block can be partial or complete. The differential diagnosis is made by determining if there is any regular pattern of AV relationship (e.g. 2:1 partial AV block, often associated with FHR ∼70 bpm) (Figures 2a and 3a) or if atrial contractions are completely independent of ventricular contractions (i.e. complete AV block, often associated with FHR around 50–90 bpm) (Figures 2b and 3b). The occurrence of AV block is often related to transplacental transfer of circulating maternal antibodies (anti-Ro and anti-La) but it can also be associated with congenital heart disease18, 19. The latter carries a worse prognosis. 2. Blocked ectopic beats, irregular atrial activity (A-A interval). If the pattern of atrial contractions is irregular, this indicates the presence of blocked ectopic beats. Atrial ectopics are the most common cause of irregular heart rhythm but are often associated with FHR within the normal range20. They can be conducted to the ventricles but may also be blocked. The lack of AV conduction in cases of atrial ectopics is due to a physiological rather than a pathological block. The premature electrical impulse cannot be transmitted downstream to the ventricles as the specialized conduction cells and ordinary myocardial cells are in a refractory period. This means they cannot depolarize and therefore the ectopic beat is blocked. Following an ectopic beat there is a pause before the sinus node can initiate another stimulus. If blocked atrial ectopic beats occur at regular intervals and persist over a relatively long period of time, they can lead to persistent fetal bradycardia. The typical pattern of regular bradycardia due to ectopic beats corresponds to blocked atrial bigeminy (Figures 2c, 2d, 3c and 3d). It is often associated with FHR around 70–80 bpm and it was a common cause of regular bradycardia in one series, accounting for 45% of all cases21. Whilst accurate diagnosis of blocked bigeminy can be ascertained by visual inspection of the A-A intervals (Figures 2c and 3c), blocked bigeminy can also mimic pathological 2:1 AV block (Figures 2d and 3d). These have opposing management implications. Blocked bigeminy has no hemodynamic significance, but 2:1 block has long-term consequences. Making the distinction between these two possibilities can be difficult. Carvalho and Jaeggi22 highlighted the importance of accurate measurement of A-A intervals (as they may ‘appear’ constant, Figures 2d and 3d) and suggested that such ectopics are likely to be of junctional rather than of atrial origin. Sonesson and colleagues23 studied isovolumetric time intervals in fetuses with blocked bigeminy and fetuses with 2:1 AV block and report their results in this issue of the Journal. Isovolumetric contraction time was systematically shorter and below 2 SD in fetuses with blocked ectopics compared with fetuses with autoimmune-mediated block, all of whom showed values above 2 SD. Persistent, irregular bradycardia occurs less frequently than does regular bradycardia, and is associated with an AV relationship > 1:1 (Figure 4). Average ventricular rates are often around 110 bpm and, not infrequently, the irregularity can be regular. Similar to regular bradycardia with atrial rate greater than ventricular rate, the main differential diagnosis is also between pathological AV block and presence of blocked ectopic beats. However, as the FHR is often closer to the lower limits of the normal range, it is essential to be aware that this type of bradycardia can potentially represent second-degree AV block and be the first manifestation of antibody-mediated block. Thus, making this distinction is paramount. The approach to diagnosis of the underlying mechanism is similar to that described for regular bradycardia with AV relationship > 1:1. 1. Pathological block, regular atrial activity (A-A interval). This is an uncommon form of bradycardia and usually corresponds to second-degree AV block with variable AV conduction. The pattern often represents a 3:2 AV relationship, with two of three sinus beats being conducted to the ventricles and one being blocked (Figure 4b). The regular atrial activity indicates that lack of conduction is due to a pathological AV block. For the conducted beats, the AV interval is constant. Heart rates are often around 110 bpm. 2. Blocked ectopic beats, irregular atrial activity (A-A interval). Infrequent blocked ectopic beats cause an irregular rhythm but do not reduce FHR significantly. However, if they are frequent, bradycardia may develop. Sustained blocked atrial trigeminy is the most common pattern leading to irregular bradycardia with FHR around 110 bpm. This means that of every three atrial contractions, two consecutive sinus beats are conducted to the ventricles and the atrial ectopic is blocked. This leads to an irregular heart rhythm, with FHR similar to that produced by the occurrence of pathological AV block with 3:2 AV conduction. However, as the blocked atrial activity is related to a premature atrial contraction, the atrial rhythm is irregular (Figure 4c). Fetal bradycardia of primary cardiac origin can be a benign finding if it is due to blocked ectopic beats. These have no hemodynamic consequence, are well-tolerated by the fetus and have no long-term consequences. The slow FHR can cause anxiety but requires no treatment as almost invariably it resolves spontaneously. At times, bradycardia can alternate with episodes of tachycardia. If these occur and persist, treatment for the tachycardia may be indicated. Conversely, fetal bradycardia that is linked to pathological AV block is often an autoimmune process. It can affect myocardial function as well as the conduction tissue. Both require monitoring and life-long follow-up. Differential diagnosis is crucial as management strategies differ considerably. Figure 5 shows a flowchart that may facilitate this diagnostic process." @default.
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• W2034200130 title "Primary bradycardia: keys and pitfalls in diagnosis" @default.
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