Welcome to the bed. We'll go ahead and give you
the story. This is all going to happen super
fast. Welcome to the emergency room. Welcome
back to the deep dive. Today we are wading into
what I think it's fair to call the deep end of
the nursing home. Oh, absolutely the deep end.
We're standing at the bedside of a patient who
weighs maybe seven pounds, has a heart the size
of a walnut. And inside that walnut, the plumbing
is, well, it's trying to compromise their ability
to breathe and grow. We are talking about pediatric
cardiac nursing. It is the ultimate high -stakes
environment. I mean, I have seen seasoned nurses,
people who can handle a chaotic ER on a Saturday
night just... freeze up when they have to deal
with a congenital heart defect. And why is that?
What's the core of that fear? Because the margin
for error with a neonate is, it's effectively
zero. And unlike an adult who can grab their
chest and say, hey, I'm in pain, a baby tells
you nothing. Right. They just stop eating. or
they sweat, or they turn a color that human beings
simply are not supposed to be. Exactly. And I've
got to be honest, looking at the stack of materials
we have for this deep dive, I mean, textbook
chapters on congenital defects, specific clinical
guides for beta blockers, diagrams of fetal circulation
that look like subway maps drawn by someone in
a fever dream. It is intimidating. It really
is. It's a soup of acronyms. VSD, ASD, PDA, TGA,
HLHS. It feels like you need a degree in fluid
dynamics just to read the chart. It absolutely
feels that way. But that is exactly why we're
here. We're not just going to read the slides
to you. We're going to decode the logic behind
it all. A survival guide. We're calling this
the Pediatric Cardiac Power Hour. But yeah, it's
a survival guide. We are going to apply the Pareto
principle, the 80 -20 rule. I love the 80 -20
rule. So for the listener who's maybe staring
at a textbook right now and panicking, break
that down for us. It's simple, really. In pediatric
cardiac nursing, about 20 % of the concepts,
and specifically we're talking about the core
patterns of blood flow and pressure gradients,
that 20 % will answer 80 % of your exam questions.
OK, that's good for the test. But more importantly,
it will help you catch 80 % of the life -threatening
issues at the bedside. If you understand the
physics of why blood moves the way it does, you
don't have to memorize a list of 20 symptoms
for 20 different defects. You can figure it out.
You can derive them. You can predict them. That
is the promise we are making today. We are going
to give you that 20%. We're drawing heavily from
chapter 19 on alterations in perfusion and a
very specific clinical guide on propranol. Yes,
that one's crucial. We're going to map out the
transition from the womb to the room. the specific
defects that flood the lungs versus the ones
that starve them and the acquired diseases that
can strike later like Kawasaki. And we absolutely
cannot forget the pharmacology. That clinical
guide on propranolol is just full of red flags.
One wrong instruction to a parent about how to
handle that bottle. And what could happen? You
could crash a baby's blood sugar. You could cause
a seizure. It is that specific. So let's start
with that big picture. Before we get into the
weeds of, you know, ventricles and valves, what
is the fundamental shift we absolutely need to
understand. The fundamental shift is the transition
from fetal circulation to neonatal circulation.
Everything and I mean everything hinges on that
first breath. Okay. You have to remember in the
womb the fetus is well it's under water. The
lungs are effectively solid organ tissue because
they're filled with fluid. They are a high pressure
zone. You can't pump blood through them easily.
And you don't need to, right? Because the placenta
is doing all the breathing. Correct. The placenta
is the lung. It's the kidney. It's the gut. It
does everything. So the fetal heart is designed
with what I like to call bypass roads. Bypass
roads. I like that. It knows lungs are closed
for business. So it uses two specific shortcuts
to route blood around them. And let's name these
shortcuts because I'm guessing if they don't
close later, they become the defects we have
to treat. That's exactly it. The first is the
foreman oval. Foreman oval. This is a literal
hole, or well, more like a flap, between the
right atrium and the left atrium. Blood comes
into the right side, it hits that high resistance
from the fluid -filled lungs, and it basically
says, no thanks. About going that way. And it
just slips through this side door that form an
ovale directly into the left atrium to get pumped
out to the body. Efficient. Very efficient. And
the second one. The second one is the ductus
arteriosus. This connects a pulmonary artery
directly to the aorta. Another bypass. Exactly.
So if any blood does sneak past the first door
and gets into the pulmonary artery, instead of
fighting its way into the aorta, lungs it takes
this little off -ramp straight into the aorta.
Okay so just to get this straight in my head
in a fetus right to left flow bypassing the lungs
that's normal it's actually necessary. It's essential
for survival on the womb but then birth happens.
The big moment. The cord is clamped the placenta
is gone suddenly systemic resistance the pressure
of the body skyrockets and the baby takes that
first massive, life -changing breaths. And that
one breath changes all the physics. Completely.
The lungs inflate with air. The fluid is pushed
out. All of a sudden, the lungs go from being
a high -pressure brick to a low -pressure sponge.
Wow. Blood just rushes into the lungs. And that
massive rush of oxygenated blood returns to the
left atrium, which increases the pressure there.
And that pressure does what? It slams the foreman
ovals shut, like a trapdoor. And the ductus arteriosus.
that other bypass. The rise in oxygen levels
from breathing signals the smooth muscle in that
vessel to clamp down. It constricts and closes.
So within a few days, those bypass roads should
be gone. And you're left with a normal circuit.
You are now running on a series circuit, lungs
then body, lungs then body, over and over. But
when they don't close, or if, you know, the walls
weren't built right in the first place, that's
where we get congenital heart defects. Exactly.
Congenital means born with it. And this brings
us right to our master 80 -20 map. Instead of
memorizing 50 different defects, we look for
patterns. I love patterns. What's pattern number
one? Pattern number one is the hemodynamic shunt.
Blood going the wrong way. Just blood going the
wrong way. And this is all about pressure gradients,
right? High to low, always. Always. Blood flows
like water downhill from high pressure to low
pressure. The left side of the heart is the powerhouse.
It pumps to the whole body, so it's high pressure.
The right side is the low pressure pump, just
for the lungs. So pattern 1A, I'm guessing, is
when blood flows from left to right? Correct.
High pressure on the left leaks into the low
pressure on the right. And where does the right
side go? To the lungs. So this floods the lungs.
These are your pink kids with wet lungs. And
kids with wet lungs, okay. And 1B? That's the
reverse. If the right side is blocked for some
reason, the pressure builds up there and it forces
unoxygenated blue blood over to the left side
and out to the body. These are your blue kids.
Okay, so right there, that's a huge clue. If
I'm taking an exam and the question describes
a cyanotic or, you know, a blue baby, I immediately
know I'm looking for a defect that pushes blood
right to left. Precisely. You have just eliminated
half the possible answer choices. That is the
kind of shortcut we need. That's the 80 -20 in
action. What about pattern number two? Pattern
number two is the failing heart, or heart failure,
HF. But here is the critical can't miss takeaway.
Heart failure in a baby does not look like heart
failure in an adult. Okay, how so? An adult clutches
their chest. An adult says, I have an elephant
on my chest. A baby. A baby can't do that. So
what do they do instead? They stop growing. The
absolute classic assessment cue is sweating during
feeds. Sweating during feeds. That is such a
specific and kind of strange image. It is. But
imagine you had to run a marathon while trying
to drink a milkshake through a coffee stirrer.
Impossible. That is what breastfeeding feels
like for a baby in heart failure. Their metabolic
rate is just through the roof. So pattern two
is failure to thrive plus respiratory distress
plus that key feeding difficulty. You got it.
And pattern three, what's that one? Pattern three
is the inflammatory storm. This is the acquired
stuff. This isn't plumbing you're born with.
This is something that happens later. Think Kawasaki
and rheumatic fever. The danger here isn't usually
the initial plumbing. It's the immune system
attacking the heart structures like the valves
or the coronary arteries. And the final pattern.
Pattern four. Pharmacology safety. Specifically,
they can't miss rules for beta blockers, like
propranolol. Knowing when to hold the med is
just as important, if not more important, than
knowing when to give it. All right, let's go
deeper. Let's do the system -by -system breakdown.
We've covered the transition. Now let's talk
vital signs. I feel like this is a massive trap
for students who are used to working with adults.
It is a huge trap. If you walk into a room and
you see a heart rate of 100 in an adult, you're
concerned. You're watching them. Sure. In a one
-month -old infant, a heart rate of 100 is, well,
it's actually on the low end of normal. Really?
100 is low? Yes. An infant's heart rate can range
from 90 all the way up to 160 beats per minute.
And if they're crying, it can go even higher.
A resting heart rate of 140 BPM is perfectly
totally normal. And blood pressure, I assume
it's the opposite, much lower, maybe around 80
over 55. As the child ages, the heart rate gradually
goes down, the blood pressure gradually goes
up. By the time they're an adolescent, they start
to reach those adult norms we're all used to.
OK, so exam tip right there. Do not apply adult
vital sign standards to a neonate. You will either
call a code on a perfectly healthy baby, or worse,
or ignore a crashing one. OK, let's dive into
that first category of defects, the pink defects,
the ones with increased pulmonary blood flow.
These are our left to right shunts. So the main
players you'll see are atrial septal defect,
or ASD, ventricular septal defect, VSD. Patent
ductus arteriosus, PDA, and then a more complex
one, atrioventricular canal defect. Let's group
them together. So ASD and VSD are basically holes
in the walls, right? ASD in the top chambers,
the atria, and VSD in the bottom, the ventricles.
Correct. You're just a hole in the septum. And
PDA, is that leftover fetal vessel staying open?
Why do we call them pink? What's the logic there?
It's because oxygenated blood is recirculating.
The blood has already been to the lungs. It's
red. It's full of oxygen. It went to the left
side of the heart. But instead of going out to
the toes where it's needed, it leaks back through
the hole to the right side and goes to the lungs
again. So the body is still getting oxygenated
blood. The baby isn't blue. They are pink. But
the lungs are getting double the volume, just
overwhelmed with blood. Exactly. It's a traffic
jam in the lungs. This leads directly to pulmonary
congestion. wet lungs. If you put a stethoscope
on their chest, you're gonna hear crackles. And
this brings us right back to that heart failure
pattern you mentioned. It's a direct line. The
heart has to pump so much harder to manage this
chaotic flow, so the right side of the heart
can enlarge, it gets overworked, and the baby's
metabolic demand just skyrockets. Let's talk
about the PDA specifically, the patent ductus
arteriosus. This one seems to have a very specific
treatment that exams just love to ask about.
They do. A PDA is that leftover connection between
the aorta and the pulmonary artery. Oh. And the
classic key word you need to listen for is a
murmur that sounds like a washing machine. A
continuous machine -like murmur. Washing machine
murmur. OK, got it. And how do we fix this one?
Well, surgically, you can ligate it. You can
tie it off. But before we do that, if it's supposed
to close and it hasn't, we can try to force it
close with medication. And we use indomethacin
or IV ibuprofen. Wait, ibuprofen? You mean like...
Like Advil? Essentially, yes. They are both NSAIDs
non -steroidal anti -inflammatory drugs and NSAIDs
inhibit prostaglandins. And what do prostaglandins
do? Prostaglandins are the chemical that keeps
the ductus open in the womb. That's their job.
So if you block the prostaglandins... You encourage
the hole to close. You take away the signal that's
keeping it open. So endomethacin closes the hole.
I'm repeating that out loud because I have a
feeling that later on things are going to get
confusing. Please do. Endomethacin equals a closed
PDA. Now, let's connect this to the developmental
impact. This is the need to know for nursing
care, right? We have a baby who is breathing
fast to chimney and they're burning calories
like crazy just to keep their heart beating.
What does that do to their growth? It stops it.
This is the definition of failure to thrive.
These babies, they just fall right off their
growth curve. So as the nurse, what's the priority
intervention? Do we just feed them more? You
can't. You have to completely rethink feeding.
You can't just let them breastfeed for 45 minutes
straight. They will burn more calories eating
than they actually get from the milk. So what's
the strategy? Small frequent feeds. We use high
calorie formula. We'll even fortify breast milk.
bumping it up to 24 or even 30 calories per ounce
instead of the standard 20. And we might even
need to use a gavage feed. So putting down an
NG tube. An NG tube, yes. So they can get the
nutrition without the work of sucking. It lets
them rest. Rest becomes a medical intervention
here. Absolutely. Clustering your care is essential.
Don't go in every 10 minutes to poke and prod
them. Go in, do the vitals, change the diaper,
give them medication, and then let them sleep.
They need that energy to grow heart muscle. Okay,
let's flip the script. Let's talk about the blue
defects, the ones with decreased pulmonary blood
flow. This is our pattern 1b, the right to left
shunt. Something is blocking the blood from getting
to the lungs in the first place. An obstruction.
A major obstruction. So the unoxygenated blue
blood gets frustrated, it can't go forward, so
it pushes through a hole, usually a VSD, and
goes out to the body without ever picking up
oxygen. Hence, the baby is blue. Cyanotic. Right.
And the big bad wolf in this category is Tetralogy
of Fallot. Tetralogy. That means four. So we
need to memorize these four specific defects.
You absolutely do. Okay. Walk us through them.
What's number one? Number one is pulmonic stenosis.
The valve leading to the lungs is tight and narrow.
This is the main problem. It's the source of
the obstruction. Okay. A tight valve. What's
number two? Number two is a consequence of number
one. Right ventricular hypertrophy. The muscle
of the right ventricle gets really thick and
beefy from trying to push blood against that
tight stenotic valve. Makes sense. Number three.
Number three is a VSD, a ventricular septal defect,
a hole between the bottom two chambers. And the
last one, number four. Number four is the overriding
aorta. The aorta, instead of sitting neatly over
the left ventricle, is shifted over so it sits
right on top of that VSD. So it's sucking up
blood from both sides. Exactly. It's getting
a mix of red blood from the left and blue blood
from the right. That sounds like a recipe for
disaster. It is. And it leads to the single most
famous exam scenario in all of pediatric cardiac
nursing, the Tet spell. Also known as a hypercyanotic
spell. Correct. Paint the picture for us. You're
the nurse. What happens? Usually it's triggered
by something that increases oxygen demand. So
the infant is crying or feeding or even just
having a bowel movement. Suddenly that tight
pulmonary valve spasms and shuts down even more.
So even less blood gets to the lungs. Almost
no blood goes to the lungs. The baby turns profoundly
blue. They get limp. They might even lose consciousness.
It is absolutely terrifying for parents to witness.
And as the nurse, you walk into that room, what
is your immediate first line do it now action?
Knee to chest position. Okay, why? Why does shoving
a baby's knees into their chest help their heart?
It seems so counterintuitive. It's pure physics.
By kinking the femoral arteries in their legs,
which is essentially what you're doing, you dramatically
increase the systemic vascular resistance, or
SVR. So you're making it harder for blood to
go down to the legs. Right. And that back pressure,
that high pressure in the body, forces the blood
to choose the other path, the path of least resistance,
which is now back into the pulmonary artery into
the lungs. It reverses the shunt temporarily.
That is brilliant. It's like mechanical shunting
with your hands. It works. And what's amazing
is, for an older child with unrepaired tetralogy
of phallate, you'll see them do this instinctively.
What do you mean? They'll be running around on
the playground, they'll get winded, and they
will suddenly just squat down in the middle of
playing. They're giving themselves the knee -to
-chest position. They are self -treating a mild
tet spell. Wow. So squatting to breathe? That's
a major developmental red flag if you see it
in a toddler. It is a huge one. If a parent ever
tells you, oh, he always squats when he plays
tag, That kid needs an echocardiogram stat. Aside
from the squat, what else do we do for a tech
spell? OK, so after needed chest, you want to
apply 100 % oxygen, usually by blow by, so you
don't agitate them more. You want to calm the
child. Morphine can help relax that spasm and
reduce the agitation. And then IV fluids. But
needed chest is always step one. Okay, another
one of these blue defects is tricuspid atresia.
Yes, and the key word here is atresia. It means
missing or completely closed off. So the tricuspid
valve. The valve between the right atrium and
the right ventricle. It just isn't there. It's
a solid wall of tissue. So no blood can get from
the right atrium to the right ventricle. Nope.
It's a dead end. The only way this baby survives
is if there are other holes, an ASD or a VSD,
to let that blood escape and mix somewhere else.
And this brings us to a really important pharmacology
twist. Yes. In tricuspid atresia, or really any
severe obstruction to lung flow, the blood flow
to the lungs might be completely dependent on
that ductus arteriosus we talked about earlier.
The one that's supposed to close? The PDA. The
very same. But in this case, if it closes...
the baby dies, because that backflow from the
aorta through the PDA and into the pulmonary
artery might be the only blood the lungs are
getting. So we have to keep it open. We must
keep it open. So what do we give? The opposite
of what we gave before. Exactly. We give prostaglandins,
specifically a continuous high V drip of prostaglandin
E1. And this is the prostaglandin paradox. I
want to say this clearly. Go for it. For a simple
PDA where we want it closed, we give endomethacin,
which is an anti of prostaglandin. Correct. But
for something like tricuspid atresia, where we
need it to stay open for survival, we give prostaglandins
to keep it open. You have to know the defect
to know the drug. If you give endomethacin to
a baby with tricuspid atresia, you are effectively
cutting off their only source of oxygenated blood.
That is a massive can't miss safety item. Always,
always check the diagnosis before you even think
about touching the endomethacin. 100 percent.
OK, let's shift gears. Let's move to the obstructive
disorders. the pipes are pitched. Coarctation
of the aorta is the big one here. Coarctation
is just a fancy word for narrowing. It usually
happens in the aortic arch right after the arteries
branch off to the head and the arms, but before
the arteries go down to the legs and the rest
of the body. So if you imagine a kink in a garden
hose, it's the perfect analogy. Upstream of the
kink, so the head and the arms, the pressure
is super high. Downstream of the kink, the legs
and the kidneys, the pressure is just a trickle.
And this leads to a very, very specific assessment
finding, doesn't it? The Hallmark finding. The
disparity in pulses and blood pressure between
the upper and lower extremities. You check the
BP in the right arm and it's high. You feel the
brachial or radial pulses and they're bounding.
And then you check the legs. You check the BP
in the leg and it's low. and you try to feel
for femoral pulses, and they're weak or maybe
even absent. And normal physiology says that
leg BP should be a little bit higher than arm
BP, right? Correct. So if you find that the leg
pressure is lower than the arm pressure, you
have just diagnosed coarctation of the aorta.
And what's the long -term risk here? Well, you've
got two problems. Stroke for the brain because
of that severe hypertension in the upper body,
and poor perfusion to the gut and the kidneys
downstream. Developmentally, how might this present
in a slightly older child who's, you know, walking
and talking? These kids might complain of leg
pain or cramping with exercise, that's claudication.
Or they might have frequent headaches and nosebleeds
from the high blood pressure in their head. Nosebleeds
and leg pain, you know, taken separately, those
sound like typical growing pains. But if you
put them together... The smartiac red flag. Okay,
now for the really complex ones, the mixed defects.
Let's start with transhibition of the great arteries,
or TGA. This is a plumbing nightmare. The aorta
and the pulmonary artery are just swapped. They're
hooked up to the wrong ventricle. What does that
mean for blood flow? It means the right ventricle
pumps blue, unoxygenated blood into the aorta,
which goes out to the body and comes back blue.
And the left ventricle pumps red, oxygenated
blood into the pulmonary artery, which goes to
the lungs and comes back red. You've got two
completely separate parallel circles that never
touch. Exactly. The body gets zero oxygen. This
is incompatible with life unless... Unless there's
a hole. Right. There has to be a place for the
blood to mix. We need a PDA or an ASD or a VSD.
And again, this is a prostaglandin's end -now
emergency. Keep that ductus open at all costs
until surgery can switch the vessels back to
where they belong. And what about hypoplastic
left heart syndrome, HLHS? Hypoplastic just means
underdeveloped. So in HLHS, the entire left ventricle,
the main pump for the body, is tiny. non -functional
and undeveloped. It can't pump blood to the body.
This sounds incredibly severe. It is one of the
most severe. These babies typically require a
series of three palliative surgeries. The Norwood,
the Glen, and the Fonten, starting in the very
first week of life, just to survive. The developmental
impact here must be absolutely massive. It is.
These children can spend months of their first
few years in the hospital. They have sternal
precautions after surgery. meaning you can't
lift them up under the arms. So their gross motor
milestones, like rolling over or crawling, are
often delayed because they're tethered to machines
or recovering from open heart surgery. And feeding
has to be a challenge. A huge challenge. Many
of these babies develop oral aversions. Think
about it. They've been intubated, suctioned constantly,
had NG tubes down their nose. They start to associate
anything near their mouth with pain or discomfort.
So even after the heart is fixed, you're left
with a major behavioral feeding issue. Exactly.
You might be dealing with a toddler who simply
refuses to eat by mouth. You know, that brings
us to the soft skills part of the outline, psychosocial
aspect. But honestly, calling it soft feels wrong.
It's hard. It's the hardest part. You, the surgeon,
you fix the hole. But you send home a family
that is completely terrified. So post -op teaching
is critical. What's one of the first things parents
ask? Can I pick them up? Can I hold my baby?
And the answer is yes, please do. But we have
to teach them how. You scoop them, support the
head and the bottom. You just don't lift them
under the arms because of the stress on that
fresh sternal incision. Why is that holding so
important? Because bonding is priority number
one. If the baby cries, their heart rate goes
up, their blood pressure goes up, the workload
on their heart goes up. A comforted baby is a
hemodynamically stable baby. I love that. A comforted
baby is a hemodynamically stable baby. Everyone
listening, write that down. Also, simple things.
Incision care. Keep it clean, keep it dry. No
lotions, no powders. And teaching them the signs
of infection redness, drainage fever. OK, let's
pivot. We've covered the born with it, the congenital
defects. Now let's talk about the acquired, that
inflammatory storm you mentioned, pattern number
three. Let's start with Kawasaki disease. This
is a weird one. We still don't know exactly what
causes it. It's idiopathic, but it's an acute
systemic vasculitis. So inflammation of all the
blood vessels. Exactly. All throughout the body.
And who gets it? What's the typical age group?
It's almost always toddlers and preschoolers.
Usually children under five years old. And what
does it look like? How does it present? It comes
in phases. The acute phase is the most dramatic.
The hallmark sign is a high fever, over 102,
that is unresponsive to Tylenol or Motrin and
it lasts for five or more days. That's the key.
A persistent high fever. Plus what else? Plus
the cream symptoms. It's a mnemonic. Okay, breakdown
cream for us. C is for conjunctivitis red eyes
but with no drainage or pus. R is for rash, usually
all over the trunk. E is for edema swelling of
the hands and feet and erythema bright red palms
and soles. A is for adenopathy swollen lymph
nodes, usually just one in the neck. And M is
for mucosal changes. And that's where we get
that classic exam description. The strawberry
tongue and cracked red bleeding lips. And I've
heard about peeling skin too. Yes, that comes
a little later in the subacute phase. The skin
on their fader tips and toes will start to peel
off in sheets. Why is this so dangerous? I mean,
it sounds miserable, like a really bad flu, but
why is it a cardiac emergency? The danger is
the heart. The inflammation has a special affinity
for the coronary arteries. It can cause aneurysms
weak, ballooning spots in the arteries, which
can then lead to blood clots and heart attacks
in a five -year -old. A heart attack in a child?
That's terrifying. So how do we treat it? This
brings us to a major pharmacology exception.
We treat it with two main things. First, a big
dose of IV intravenous immunoglobulin to calm
the whole immune system down and high dose aspirin.
And there should be a siren going off in your
head right now. Aspirin in kids. Normally, we
never give aspirin to children because of the
risk of Ray's syndrome, which causes massive
liver and brain swelling, especially after a
viral illness like the flu or chickenpox. But
this is the exception. Kalesaki is the one time
the benefit -preventing coronary artery clots
outweighs the risk. We need that antiplatelet
effect from the aspirin. So an exam writer's
favorite question would be, which of these children
requires a prescription for aspirin? And the
answer is always the child with Kawasaki disease.
But you still have to teach the parents to be
vigilant, to watch for signs of raise, and to
avoid other viral illnesses because the risk,
while small, is still there. Next up in the acquired
category, rheumatic fever. This is another autoimmune
reaction, but this time we know the trigger.
It's group A strep. So an untreated case of strep
throat. Exactly. About two to four weeks after
a sore throat that wasn't fully treated, the
child's body develops antibodies that are supposed
to fight the strep, but they mistakenly attack
their own heart valves. And which valve is most
commonly affected? Usually the metral valve.
But the antibodies can also attack the joints
in the brain. How do we diagnose it? It sounds
like it could be vague. We use something called
the modified Jones criteria. You need evidence
of a recent strep infection. like a positive
titer, plus either two major symptoms or one
major and two minor symptoms. What are the major
symptoms? The big ones are carditis, which is
inflammation of the heart, polyarthritis, which
is a migrating joint pain, it'll be in the knee
one day, the elbow the next, subcutaneous nodules,
a specific rash called erythema marginatum, Korea.
The Korea, that's St. Vitus dance, right? The
jerky movement. Yes. Sudden, aimless, jerky movements
of the arms and legs. It can be really scary
for parents to see. Does it go away? It does
resolve, but it's very distressing while it's
happening. But the real priority here is prevention.
Treat the strep throat. Just treat the strep
throat. Right. If a kid has a sore throat and
a fever, get a culture. If it's positive, make
sure they finish the entire course of antibiotics.
And if they do get rheumatic fever, what's the
long -term management? Long -term antibiotics,
sometimes for years or even into adulthood, to
prevent a recurrence and to prevent further damage
to the heart valves. Okay, one more required
condition, infective endocarditis. This is basically
bacteria growing on the valves or the lining
of the heart. It often happens in kids who already
have a congenital heart defect or who have prosthetic
valves or central lines. What are some of the
weird classic signs for this one? The classic
ones are Osler nodules, which are painful, tender
bumps on the finger pads. I remember it as oh
for ouch. Oh for ouch. Good one. And then there
are Janeway lesions, which are flat, painless
red spots on the palms of the hands or the soles
of the feet. And you might also see splinter
hemorrhages under the fingernails. And what's
the key to prevention here? Prophylactic antibiotics
before dental procedures. If you have a high
-risk kid, one with a prosthetic valve or a history
of endocarditis, they need a dose of amoxicillin
before the dentist even cleans their teeth. Because
the bacteria from the mouth. Love to travel to
the heart and set up shop on damaged tissue.
Okay, we are heading into the final stretch.
Section C, the pharmacology deep dive. We've
talked aspirin, endomethacin, prostaglandins.
Now let's talk about a daily driver, propranolol.
Propranolol. It's a beta blocker, a class 2 antiarrhythmic.
And the key descriptor here is non -selective.
What does that mean for us clinically? It means
it blocks more than one type of beta receptor.
It blocks beta 1 receptors, which are primarily
in the heart, and it also blocks beta 2 receptors,
which are primarily in the lungs. So what's the
effect? Blocking beta 1 is what we want. It slows
the heart rate and lowers the blood pressure.
Good. Blocking beta 2, however, causes bronchoconstriction.
Bad. So... High caution in any child with a history
of asthma. Extremely high caution. It can trigger
a full -blown asthma attack. Now, looking at
our clinical guide here, propranolol is used
for arrhythmias, sure, but also for something
pretty surprising, infantile hemangiomas. Yes,
those bright red raised strawberry burst marks.
But Cranwall works wonders to shrink them. The
brand name for this formulation is often hemangiol.
And there are some very, very specific administration
rules for hemangiol in infants. Let's run through
the need -to -know safety check. Okay, rule number
one, feedings. You absolutely must give it during
or immediately after a feeding, never on an empty
stomach. Okay, why is that so critical? Because
beta blockers can mask the signs and symptoms
of hypoglycemia low blood sugar. Normally when
your blood sugar drops, your body releases adrenaline.
You get shaky, jittery, your heart races, tachycardia.
Beta blockers stop all of that. They stop the
jitters and they stop the tachycardia. So the
baby could be dangerously hypoglycemic and you
would have no idea until they have a seizure.
That is a critical life -saving teaching point
for parents. No food equals monolally. Absolutely.
Which leads to rule number two, the vomiting
rule. If the child is vomiting or just not eating
well, hold of the dose. Call the provider. Got
it. What's rule number three? Rule number three
is the shake rule. Do not shake the hemangel
bottle. But why not? Almost every liquid suspension
tells you to shake well. Because this specific
one creates a lot of bubbles and foam. If you
draw up a syringe full of foam, you're not getting
an accurate amount of medication. You're almost
certainly going to underdose the child, so you
just invert the bottle gently a few times. And
what about the black box warning? Abrupt discontinuation.
You cannot just stop propranolol cold turkey.
It can cause a severe rebound effect, rebound
hypertension, tachycardia, or in adults, even
a heart attack. You must taper it slowly, usually
over about two weeks. So if a parent calls the
clinic and says, oh, we ran out three days ago,
that is an urgent situation. That is an emergency.
They need to get a refill immediately. Wow. We've
covered a massive amount of ground. Let's try
to synthesize some of this. I want to do a rapid
fire compare and contrast. Ready? Let's do it.
Congenital versus acquired. Congenital is structural
plumbing issues. You're born with it. The main
problem is hemodynamics, so flow. Acquired is
inflammatory or infectious, like Kawasaki or
strep. It happens later. The main problem is
damage to the vessels or the valves. OK. The
prostaglandin paradox. A simple PDA. We want
to close it. We use endomethacin. Complex blue
baby defects like TGA or trichespid atresia.
We might need to keep the PDA open for survival.
We use prostaglandins. Perfect. Fluid overload
versus cyanosis. Left to right shunt. like a
VSD or ASD, gives you wet lungs and a pink baby.
Your priority is monitoring for heart failure.
Right to left shunt, like Tetralogy of Fallot,
gives you a blue baby. Your priority is monitoring
for Tet spells. This really brings us to the
so -what for the listener. We've given them the
80 -20. We've given them the patterns. What does
it all mean at the bedside? The so -what is that
pediatric cardiac nursing isn't just about the
heart. It's about the whole child. A heart defect
affects feeding, which affects growth, which
affects brain development. It affects the parent's
ability to bond with their sick infant. So it's
not just about the monitors. When you walk into
that room, don't just look at the monitor. Look
at the baby. Are they sweating when they eat?
Are they squatting when they play? Are the parents
terrified to touch them? Your interventions,
knowing to put their knees to their chest, clustering
their care to let them rest, teaching parents
how to do high calorie feeds, those are the things
that save lives and save brains. And just realizing
that a normal heart rate for a two -month -old
is 130 helps you not panic and helps you focus
on what actually matters. Exactly. Know your
norms so you can spot the real outliers. We always
like to end with a provocative thought, something
for our listeners to chew on after we're done.
Okay, here's one. We've gotten really, really
good at saving these kids. The survival rates
for even the most complex congenital heart disease
are higher than they have ever been. But that
means we are creating a brand new patient population
the adult with congenital heart disease ACHD
right and a heart that was fixed with a patch
or a conduit at age 2 isn't a normal heart at
age 40 They have scar tissue, they have a higher
risk of rhythm issues, they have different hemodynamic
pressures. So what's the question? The question
is, how does lifelong acquired heart disease
management, things like cholesterol, stress,
diet, exercise, how does that change for someone
who was born with a fundamental structural defect?
We're entering an era where our pediatric cardiac
patients are outliving their initial repairs.
What does that long -term nursing care look like?
That is a fascinating frontier. The pediatric
patient who is now 45 years old. A whole new
world of nursing. All right, friends. Take a
deep breath. Your heart rate should be returning
to normal. Unless you're an infant, in which
case, you know, try to stay around 140. Check
the show notes for our 80 -20 cheat sheet on
all this. Keep those pressure gradients flowing.
And remember, never, ever shake the soprano off.
I'll see you in the next e -talk.