“Clinical Presentation of Congenital Heart Disease:  Arrhythmias” by Michael Freed, MD

“Clinical Presentation of Congenital Heart Disease: Arrhythmias” by Michael Freed, MD

Clinical Presentation of Congenital Heart
Disease in the First Week of Life: Arrhythmias, by Dr. Michael Freed. Introduction. My name is Michael Freed and I’m a Pediatric
Cardiologist at Boston Children’s Hospital and at Harvard Medical School. So we finished murmurs. Let’s go to arrhythmias. In the newborn period, the heart can beat
too fast, too slow, or irregular. Irregular Heart Rate. Let’s start with irregular. I think this is by far the most common. I used to get a lot of calls from primary
care doctors around that they were in the nursery, they listened to a child they were
going to discharge, the heart rate that was irregular, they got an electrocardiogram,
and the baby was having atrial or ventricular premature beats, what should they do? I always told them the same thing. That if the baby otherwise looks okay, and
doesn’t have a murmur or heart failure or cyanosis, if it’s still there in a month,
just give me a call and we’ll figure out what to do. I think it’s probably benign. I think that babies have very high catechol
levels and one of the auxiliary pacemakers just fires off and gives you frequent extra
heartbeats– even sometimes bigeminy or trigeminy. As long as they’re not having runs of ventricular
tachycardia or have symptoms from it, I think it’s benign. Over the next few days or weeks, as the catechol
levels, these things usually calm down and are not a problem in the future. And we’ve not seen any long term problems
from this. Bradycardia. When I’m talking about too slow, I mean rates
in the 60s and 70s. These are almost all from congenital complete
heart block. And kids with congenital complete heart block
come in two different flavors: one with heart disease– and these are usually L-transpositions
or some other form of complicated congenital heart disease– or without heart disease,
or without structural heart disease. And these are almost all maternal lupus or
anti-nuclear antibodies that somehow attack the conduction system. But these kids raise a question: why do these
kids with heart rates that are so slow do okay? In utero, the stress response is to increase
heart rate. And these kids can’t really do that. There are not very many catecholamine receptors,
so they don’t have much of an ability to deal with stress. Why do kids with heart rate do so well? Well, we don’t really care much about heart
rate. What we’re really interested in is cardiac
output. And cardiac output is a function of heart
rate and stroke volume. And what happens is these kids are just able
to increase their stroke volume significantly so they can make up for the deficit in heart
rate. When you’re born, the work of the heart doesn’t
change very much. OK, the work of the heart is generating a
pressure and pumping a volume of blood. The old pressure volume loop that you probably
learned about in medical school– the work of the heart is the area inside this curve. And when you’re born, the pressure doesn’t
change very much. The fetus is generating a pressure of 70 or
80 millimeters above amniotic fluid as you are when you’re born. And the volume doesn’t change very much. So the work of the heart doesn’t change very
much. So these children who did OK in utero with
congenital heart block usually do okay after they’re born as well. They only get into trouble when they really
have to increase their cardiac output significantly, which interestingly can usually deal with
feeding and toddling around. In our area, they tend to get into trouble
in Kindergarten or first grade with town soccer. The kids with congenital heart disease, however,
they can get into difficulty much sooner. Because remember, they’ve really maximized
their stroke volume. So even a relatively simple disease like ventricular
septal defect, when the pulmonary resistance drops, they start developing a significant
left-to-right shunt. And these kids have already maximized their
stroke volume. So they have great difficulty if they do have
structural heart disease. So our job, as a cardiologists or as primary
care doctors, is to figure out, of these kids with congenital heart block, which have structural
heart disease. If they have structural heart disease, then
you have to watch them very carefully because they don’t tolerate it very well. The ones without structural heart disease,
as I mentioned, usually don’t get into difficulties in the perinatal period and frequently go
long periods of time before actually needing any help, usually a pacemaker. Tachycardia. Too fast– when I’m talking about too fast,
usually talking about greater than 200 beats per minute. These are usually supraventricular tachycardias. Can be atrial flutter, and very infrequently
atrial fibrillation. I would say this is probably 90%, 9%, and
1%. Atrial fibrillation’s quite uncommon because
usually you don’t have large enough– you need a large atrium to support the electrical
fibrillatory waves. So we don’t really see that very often in
the newborn. These newborn it can be quite sick, with a
very, rapid heart rate that shortens diastolic filling of the coronary arteries. And in addition to the very fast heart rate,
they can get an ischemic congestive heart failure component. This may occur in utero with intrauterine
supraventricular tachycardia, probably the number one cause of fetal hydrops in developed
countries, where Rh incompatibility has been virtually eliminated. The number one issue is to get them out of
SVT. Some children will break spontaneously, others
require vagal maneuvers, or an intravenous injection of adenosine at a dose of 0.1 milligrams
per kilogram, with an increase to 0.2 milligrams per kilogram for subsequent doses if the initial
medication is not sufficient. For a few where the adenosine is not effective,
external cardioversion may be required. Some children, with a relatively short re-entry
window may not develop supraventricular tachycardia again. These children are usually followed with medications
such as beta blockers, for a year or so, and if no further episodes occur, the medicine
is discontinued. For some children with the larger re-entry
window, the supraventricular tachycardia can be terminated, but within moments they go
back into the abnormal rhythm. This group may be particularly difficult to
treat. Medications, usually beta blockers such as
sotalol, a beta blocker with class three antiarrhythmic effects, or Flecanide, a class one C antiarrhythmic,
or both drugs in combination may be necessary to change the refractory period sufficiently,
so they don’t go back into the abnormal rhythm. These children may be problematic, and a consultation
with a pediatric cardiac electrophysiologist is probably the best approach. This concludes our video on Clinical Presentation
of Congenital Heart Disease in the First Week of Life: Arrhythimias. Please continue with the next video in this
series, Clinical Presentation of Congenital Heart Disease in the First Week of Life: Cyanosis. Thank you. Please help us improve the content by providing
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