Fetal Heart FAQs: Arrhythmia

Transcription:

Prakash Chandran (Host): You are listening to Pediatric Insights, Advances and Innovations with Children's Health, where we explore the latest in pediatric care and research. Today, we're going to learn about the Fetal Heart Program and answer some frequently asked questions about fetal heart arrhythmias with Dr. Penn Laird and Dr. Michael Day. They're both Cardiologists at Pediatric Heart Specialists, a Children's Healthcare Network Provider. My name is Prakash Chandran. And Dr. Laird and Dr. Day, really appreciate you both being here today. Dr. Laird, can you start by giving an overview of the Fetal Heart Program and why it's important to address common arrhythmia questions?

Penn Laird, MD (Guest): Yes. The Fetal Heart Program is a group of cardiologists, cardiac surgeons, anesthesiologists, and associated staff that we're based out of Children's Medical Center of Dallas. But we cover pediatric heart-related issues, basically all over the state of Texas and really all over the south, and sometimes even the entire United States. And we deal with everything pediatric heart related, children with congenital heart disease, kids with any type of acquired heart issue or problem. And then we also deal with fetuses with arrhythmias, which I know is the topic that we're talking about today.

Host: So I guess, expanding on that a little bit, what are the common fetal arrhythmias that a pediatric cardiologist actually sees?

So the most common arrhythmias that we see are isolated, extra beats. What we call extra systoles or prematature contractions. And by that, we simply refer to extra electrical impulses that are generated either in the atrium or the ventricle. Fortunately, those are generally benign and they don't cause any issues or problems. The, the next most common issue that we run into would be what we call fetal tachycardia. That being an elevated heartrate. And that can be anything from sinus tachycardia to supraventricular tachycardia or atrial flutter. Much less common would be something like ventricular tachycardia. And then the final group of fetal arrhythmias that we see would be fetal bradycardia. So a low heart rate. And that can include anything from fetal sinus bradycardia to blocked premature contractions, and finally fetal atrial ventricular block. So that's typically what we deal with when we talk about fetal arrhythmias.

Michael Day, MD: I think Dr. Laird hit the nail on the head exactly about the scope of what we deal with. And by and large, most of the questions that we get in the consults are related to those premature extra beats. And then the concern for super ventricular tachycardia, that tends to be the questions that we get the most commonly.

Host: So Dr. Laird, could you describe your approach to isolated, fetal cardiac ectopy?

Dr. Laird: Yeah. So this is the most common thing that we see referrals for, and, one point to make up front, which I think most medical professionals are very well aware of, but we can't do an ECG on a fetus. So, as opposed to an infant or a child where we can place stickers directly on their chest and measure the electrical impulses that the heart is creating, we can't do that on a fetus, so we have to use different ways to evaluate them. And the most common thing that we use is going to be sonography or fetal echocardiography, where we're using ultrasound to look at the fetal heart. But when we get a patient referred in for extra beats, usually the question from the referring doctor is, hey, is this anything dangerous?

Is this anything worrisome? Is there any associated congenital heart defect or birth defect along with this? So, our approach is, we usually do a thorough fetal echocardiogram. So, we look at the fetal anatomy and function from top to bottom. And then we do a thorough assessment of the fetal heart rhythm, and there's a lot of different ways to do that.

But the most common approaches would be to use either the modality of M-mode or a pulse wave Doppler. And basically since we can't do an ECG on the fetus, we're trying to figure out what is the atrium? What is the ventricles doing? Are they beating in conjunction or are they not? And the typical way we would do that, the way I like to do it would be to use the fetal pulse wave Doppler sample. I like to put it right, at the junction of the left ventricular outflow track and mitral inflow. At that location, you can measure atrial inflow and atrial contractility and compare it with ventricular outflow.

And that'll give you an idea of, what is the atrium doing? What is the ventricle doing? Do we think these are isolated premature beats? Do we think that there's something else? Do we think they're coming from the atrium or the, or the ventricles. As I mentioned, PACs or extra beats, which originate in the atrium, PVCs are those that come from the ventricle. PACs are a lot more common, probably by about 10 to one.

Sometimes it can be difficult to distinguish the two. Usually a PVC would, will not be proceeded by an atrial contraction. In other words, you won't see any A wave when you look at the pulse wave Doppler flow and then PACs on the other hand, they may or may not be followed by a ventricular contraction. In other words, a V-wave. It just depends on whether that extra beat is conducted down to the ventricle. Whatever the case is, once we've confirmed that they're isolated PACs or PVCs, in the vast majority of cases, these don't require any kind of treatment. We just recommend continued observation. Very commonly, they resolve during the remainder of pregnancy or early on in infancy. So usually it's a very benign type of thing.

Dr. Day: One of the other important items to identify are the causality of those. And sometimes they just occur and they're just isolated, premature contractions. Sometimes they could be directed by things that the mom might not even recognize is a risk factor. Double-check on caffeine intake. That can sometimes cause isolated premature contractions to be a little bit more common. And then oddly enough the use of cocoa butter, which is common sometimes for people to put on the skin to relieve or reduce stretch marks can actually be metabolized into a caffeine, an analog that can sometimes precipitate these factors. Heard that at a number of fetal conferences. And it's interesting to see how often, if caffeine intake may be the culprit behind some of these, particularly the benign PACs or premature atrial contractions.

Host: So Dr. Laird, you started to touch on this briefly, but how exactly do you differentiate fetal atrial flutter from other forms of fetal tachycardia?

Dr. Laird: Yeah. So when we talk about fetal tachycardia, we're generally talking about an elevated fetal heart rate. Usually it's going to boil down to a couple of different possibilities. Those would include what we call sinus tachycardia. So, an increase in the heart rate, that's directed by the sinus node. The second thing would be what we call accessory pathway mediated supraventricular tachycardia, the third thing being atrial flutter, and then the fourth thing being ventricular tachycardia. Usually most clinicians are pretty experienced in differentiating sinus tachycardia from the others.

Ventricular tachycardia is very rare. So, usually when we get a fetus referred in with a fast heart rate, it boils down to, hey, is this run of the mill fetal SVT? Or is this atrial flutter? So, it's always good to know how to differentiate the two. And really the best way is to look at what the atrium is doing in comparison to the ventricle. With what I call run of the mill fetal SVT or accessory pathway mediated fetal SVT, you're always going to see a one-to-one relationship between the atrium and the ventricle. Whereas with fetal atrial flutter, it's a problem where you have an abnormal circuit in the atrium that's causing the atrium to go very fast, much faster than the ventricle. Due to block in the AV node, the ventricle ends up only going half or a third as fast as the atrium. So, what I like to do is to drop in M-Mode through the atrial wall and the ventricular wall, and you can see contraction of the atrial wall and compare that to the ventricular wall. If you get something on the order of two to one, two atrial contractions for every one ventricular contraction or three atrial contractions for every one ventricular contraction, that would highly suggest that you're dealing with atrial flutter.

And that's important only because the treatment modality is going to differ for atrial flutter in a lot of cases than how you would treat run the mill fetal SVT.

Dr. Day: think Dr. Laird, again, pointed out the most important mechanism that we all use when we're trying to differentiate the atrial flutter from just garden variety, reentrant type SVT. Sometimes it can be difficult to obtain the M-Mode that includes both the atrial wall and ventricular wall. That can be frustrating because again, with the fetus, you can't do an EKG. You also can't control the position of the fetus. And so sometimes we struggle with that. I've found in those circumstances, it really zoom in and take an isolated sort of long look at the atrial wall in and of itself to get, appreciate the contraction rate and then an isolated picture of the ventricular wall, in close juxtaposition, it can supplant the M-Mode if you're not able to look at those simultaneously. Obviously that's the gold standard and the best way to approach it. But I've found that trick works well in circumstances where you can't obtain that particular image.

Host: So, talking about different treatment modalities, what's the current approach to treatment of fetal atrial flutter and other forms of fetal SVT?

Dr. Laird: So for the longest time digoxin was the drug of choice for most fetal arrhythmias. But recently it's been found and shown through studies that sotalol is probably more effective for terminating fetal atrial flutter. So, that's what we use now as our first line therapy for fetal atrial flutter. And sotalol, as most people know, it's a class three anti-arrhythmic agent, which simply means it's got effects in lots of different areas. But it is a beta adrenergic blocker and it prolongs repolarization, and that is the mechanism by which it often can terminate atrial flutter. So I usually start with a dose.

And one word about dosing medications, obviously we can't dose the fetus directly. So anytime we're talking about dosing for fetal arrhythmias, we're talking about maternal doses. So, mom's going to take the medicine. It's going to get metabolized in her and then transferred through the placenta to the fetus. So, typically with fetal atrial flutter, I'll start with sotalol 80 milligrams, every 12 hours.

If the infant looks in distress, if there's any hydrops, then definitely start with a higher dose, probably closer to 160 milligrams twice a day. Because the sotalol can affect mom's heart as well, it's always important to check her out thoroughly before administering the medication, take a good history, get an ECG on the mom and then follow ECGs closely on the mom, just to make sure that there's no significant changes in her electrical conduction properties. But generally speaking, our approach to fetal atrial flutter is once we have an accurate diagnosis, get the mom started on sotalol and then follow them very closely. Always like to hospitalize these patients just because of the effects of the sotalol and the potential risk to both mom and fetus. And so particularly we'll have the mom on a telemetry unit just to watch her heart rhythm carefully.

Dr. Day: Like Dr. Laird had mentioned, sotalol is the primary choice currently in the modern state the art treatment of atrial flutter. Important to also note that sotalol all is renally cleared. And so we all know that there's enhanced renal clearance for pregnant mothers. And so the doses that we have to use of these medications at times, give adult providers pause, because they're higher than you would use to just treat the mother for a particular arrhythmia, because we're actually trying to treat the fetus.

So that's why it's important to work together and collaborate with the team of physicians that are going to be caring for the mother, watching the telemetry, making sure that you're monitoring the ECG and providing reassurance and guidance that the doses, which may seem at first blush, to be a little bit high are actually the appropriate doses in the setting of pregnancy.

Host: So, just as we start to close, I was hoping we could talk a little bit more, or you could explain the natural history of the different fetal arrhythmias, both during pregnancy and following birth.

Dr. Laird: Yeah. So, we didn't really get a chance to touch much on more common accessory pathway mediated fetal SVT. And that's what we see the most of. We usually start with digoxin in that setting. We like to load the mom initially, and then if there's any evidence of hydrops or it's a more emergent situation, I'll usually start right off the bat with flecainide and that usually does a very good job of converting the arrhythmia very quickly. And I've had a lot of good luck with that in the past. But when we talk about the natural history of different fetal arrhythmias, it depends a little bit on what you're dealing with. Fetal and infantile atrial flutter, in many cases is a one-time event. And once the infant is converted there, there can be a relatively low chance of recurrence. So, if we have to treat a fetus with atrial flutter, then we will definitely leave the mom on medication for the remainder of the pregnancy.

But more often than not, we don't see a recurrence. The baby's born. We won't treat the baby after birth. We'll just observe them carefully. If there's no issues then DC them home with just careful monitoring and observation at home. Accessory pathway mediated SVT, on the other hand, it can be a little more malignant in the sense that recurrences are more common. In that setting, if we're close to delivery, then we'll certainly continue to treat the newborn after birth. On the other hand, if it's a fetal SVT that shows up relatively early in the second trimester, and it's well-controlled throughout the remainder of the pregnancy, we don't have any recurrences; then I think it's perfectly reasonable to simply observe the baby after birth. If there's not a recurrence, then again, discharge them home off of medication, just with close observation. Whatever the case is, the natural history of fetal SVT in most infants, once they're born is that probably 60 to 70% spontaneously resolves by a year of age.

So, the majority of kids won't require medication past a year of age, which is nice. Those that do, they tend to have the more persistent pathways that probably are going to persist throughout childhood. Most of those kids end up getting an ablation by the time they're big enough to have it done safely, which is usually in the range of four to seven years of age.

Dr. Day: Few words to add to what Dr. Laird was saying that are important to consider. The natural history of fetal arrhythmias, I always think about kind of in two big buckets. Number one, a fetus presents to you in that arryhthmia, but it's otherwise not in distress. There's no hydrops, there's good cardiac performance. And those patients, by and large tend to do very well. Dr. Laird walked us through that quite well. Those patients, and it's rare, that present with fetal arrhythmia and hydrops need special mention. Because those fetuses are at a higher risk because they can number one, be difficult to treat and get to convert. And it already shows evidence that the heart is suffering to some degree and the heart performance is impaired. I agree with Dr. Laird as well, that if you encounter one of those patients that has hydrops and a fetal arrhythmia, flecainide is overwhelmingly more successful in those circumstances at stopping the arrhythmia and converting it in the setting of fetal hydrops.

Fortunately, a lot of times, the majority of these cases that we see that end up do needing treatment are able to be treated with digoxin, which is a little bit less of a powerful antirrhythmic. And doesn't have quite as many side effects as some of those other medications and it can be controlled quite well and quite easily in conjunction with maternal fetal medicine specialists and OB specialists. And those kids tend to have a really good outcome.

Host: Well, Dr. Laird and Dr. Day, this has been a fascinating conversation. I really appreciate your time. Just before we close, is there anything else that you'd like to share with our audience?

Dr. Laird: The only other thing that I might share is just a quick mention about fetal bradycardia. We didn't really get into it and it's can be a really big topic. Fetal bradycardia is something that we do see on occasion. It can include things like sinus bradycardia, blocked premature beats, both of which are usually benign. And then the most significant cause of fetal bradycardia would be complete heart block. And that can be seen in the setting of congenital heart defects or maternal lupus and antibodies from the mother that they cross the placenta and damage the fetal conduction system. But that's probably a topic for another podcast.

Host: Okay. Wonderful. Well, thank you both again so much for being here today. I truly appreciate it.

Dr. Day: Thanks so much.

Dr. Laird: We appreciate it.

Host: That was Dr. Penn Laird and Dr. Michael Day, both Cardiologists at Pediatric Heart Specialists, a Children's Healthcare Network provider. Thank you for listening to Pediatric Insights. You can head to children's.com/fetalheart for more information. My name is Prakash Chandran. Stay well.