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 walking
into what is, I think, arguably the most intimidating
room in the pediatric hospital. Oh, absolutely.
We're tackling the beast. And when I say beast,
I mean the one unit that seems to strike absolute
fear into the hearts of nursing students, new
grads, and even seasoned nurses more than any
other system in the body. We are talking about
the heart. We are talking about the heart, specifically
chapter 19. the child with an alteration in cardiovascular
status. Now, I've got to be honest with you.
When I first looked at this stack of slides,
the textbooks, the ATI notes, all the stuff you
sent over, I felt my own blood pressure go up.
I believe it. You've got defects with names that
sound like, I don't know... complex spells from
Harry Potter to Trilogy of Fallot, Transposition
of the Great Arteries. You've got hemodynamics,
you've got physics, you've got medications with
therapeutic windows so narrow they're practically
invisible. It is intimidating. I think for a
lot of learners, the cardiovascular system, it
just feels like a maze. You turn one corner and
you're dealing with electrical conduction, you
turn another and it's plumbing and pressure gradients.
Right. And unlike, say, the skin or the bones,
you can't see what's happening. It's all hidden
inside. So if you don't have a map, you get lost
very, very quickly. And in pediatrics, getting
lost can have, well, catastrophic consequences.
Things happen fast. Oh, fast. Exactly. And the
stakes, they couldn't be higher. We're talking
about the engine of the body, keeping the blood
moving, keeping the brain oxygenated. So here
is our mission for today's deep dive. We are
not just going to read the textbook to you. We
are going to adopt a persona. Ah! Today, we are
the pediatric nursing exam coach. I like that
the exam coach. Yeah, right We are gonna cross
reference all these sources and we are going
to find the Pareto principle the 80 -20 rule
we want to identify the 20 % of the material
that is going to answer 80 % of the exam questions
and you know more importantly the 20 % of the
concepts that are actually gonna save a life
at the bedside that's the only way to do it because
you can't memorize everything if you try to memorize
every single anatomical variation you'll just
You'll drown. You will. That is the perfect way
to approach this, because if you try to memorize
every single anatomical variation of every single
defect, you will burn out before you even get
to the acquired heart diseases. You need a framework.
You need a map. A map. Yeah. If you understand
the why, the what becomes obvious. So lay out
the roadmap for us. How do we conquer this beast?
OK, so we're going to break this down into four
main... kill zones or priority areas. First,
we're going to build the master map. This is
the physics. If you understand pressure gradients
and the transition from fetal to newborn circulation,
that critical switch, you don't need to memorize
half the defects. You'll be able to predict the
symptoms just by, well... Just by logic. I love
that. Physics over memorization. Exactly. Second,
we're going to tackle the defects themselves.
But we aren't going alphabetically. That's a
huge mistake. OK. We are going to categorize
them by blood flow. Is the lungs getting too
much blood? Too little. Is the plumbing kinked?
That organizes the chaos. I like that. Grouping
them. Third, we have the acquired conditions,
things that happen after birth, like Kawasaki
disease and rheumatic fever. And finally, we
have the nursing safety kill zones. These are
the medications like digoxin and procedures like
cardiac cath, where if you don't know your stuff,
you can do serious harm. And throughout all of
this, because this is pediatrics, we have to
keep one question in the back of our minds, right?
Always. How does this heart problem stop a child
from being a child? Precisely. A heart defect
in a 40 -year -old is a medical problem. A heart
defect in a four -month -old, that's a developmental
crisis. It affects feeding, growth, play, I mean,
everything. We have to look at the patient, not
just the pump. OK, let's unpack this. Part one.
Yeah. The master 80 -20 map. You mentioned pressure
gradients. I feel like I need a refresher on
high school physics here. Why is this the absolute
need to know? Concept because blood is lazy.
That's the golden rule. You have to write down
blood is lazy Okay, if you write nothing else
down today write this blood will always always
flow from an area of high pressure to an area
of low pressure It follows the path of least
resistance. It doesn't want to work hard. It's
like water flowing downhill Simple as that. Okay.
Blood is lazy. I can relate to that. So let's
look at a normal healthy adult or child after
they're born. The heart has two sides. The left
side is the powerhouse. The left ventricle has
to pump blood all the way to your toes, your
brain, your fingertips against gravity. It has
to overcome the resistance of the whole body,
the systemic vascular resistance. So it's working
hard. It's working very hard. So the left side
is high pressure. Left is high. Got it. That's
the heavy lifter. The right side, well, it has
a much easier job. It only has to pump blood
next door to the lungs. The lungs are spongy.
They're low resistance organs. So the right side
is low pressure. So left is high, right is low.
That's our baseline. That's normal. Correct.
Now imagine someone punches a hole in the wall
between the left and right side, a septal defect.
Which way does the blood go? Well, if the left
is high pressure and the right is low and blood
is lazy, the blood is going to get pushed from
the left to the right. Boom. You just solved
50 % of the exam questions. I'm not kidding.
If there is a simple halt, like a ventricular
septal defect, a VSD or an atrial septal defect,
an ASD blood flows left to right. OK. And what
does that mean for the body? It means oxygenated
blood that should be going to the body is leaking
back into the right side and going to the lungs
again. It's doing an extra lap. An unnecessary
and damaging extra lap. The lungs get flooded.
They're overworked. And the body, well, it gets
less blood than it should. But the blood going
to the body is still pink, right? It's oxygenated.
Exactly. That's the key distinction. In a left
-to -right shunt, the blood that makes it out
to the body has plenty of oxygen. The kid is
pink. They aren't blue. OK. But their lungs are
wet. We call this pink but wet, or asianotic
but with signs of congestive heart failure. Pink
but wet. That's a great visual. Now flip the
script for me. What if something blocks the lungs.
OK, good question. Let's say the path to the
lungs is tight. We call that pulmonary stenosis.
The door to the lungs is narrowed. So the pressure
on the right side starts to build up because
the blood can't get out. It's a traffic jam.
It's a traffic jam. It's pushing against a closed
door. Eventually the right side pressure gets
higher than the left. Now which way does the
blood go through that hole? It would have to
reverse. It would go right to left. What kind
of blood is on the right side? Deoxygenated blue
blood. And now you're pumping that blue blood
across the hole and out to the body. That child
is cyanotic. that child is blue. That's the fundamental
trick. Left to right is wet, right to left is
blue. That simplifies it so much. I don't have
to just memorize a lift of symptoms for every
single defect if I can just stop and ask, where
is the pressure higher? That's the master map.
Now, before we apply this to the specific defects,
we have to talk about the switch because babies
don't just pop out with adult circulation. This
is where fetal circulation trips everybody up.
Right. In the womb. The fetus is basically underwater.
They aren't breathing air. Exactly. The lungs
are filled with fluid. They are clamped down,
high pressure. They are closed for business.
Mom is doing all the breathing work via the placenta.
So the body needs to work around. It has these
special shortcut shunts to bypass the lungs.
Because why send blood to the lungs if they aren't
doing anything? These are the famous Latin names.
Foramen, oval, and ductus arteriosus. Think of
them as escape hatches. The foramen oval is a
little flap, a hole between the atria. It lets
blood skip the right ventricle and go straight
to the left side. And the ductus arteriosus is
a little vessel connecting the pulmonary artery
directly to the aorta. It's like a highway bypass.
It says, hey, don't go to the lungs. It's a dead
end. Just go straight to the body. So in utero,
bypassing the lungs is good. It's necessary.
The right side pressure is high because the lungs
are clamped shut. So blood flows right to left
through these shunts. Correct. But then the baby
is born. The cord is cut. The baby takes that
first big breath. Wow. What happens in that moment?
I assume the lungs open up, like really open
up. That first breath is magic. It's an incredible
physiological event. The lungs expand with air.
The resistance in the pulmonary vessels drops
like a rock. Suddenly the right side becomes
the low pressure side. the left side. Well at
the same time the cord is clamped so the systemic
resistance goes way up. The left side becomes
high pressure. This dramatic pressure shift slams
those doors shut. The foramen ovale closes. The
ductus arteriosus starts to constrict and close
over the next few hours or days. It's like a
complete plumbing renovation that happens in
seconds. The walls go up, the doors lock. Ideally.
But this is the exam writer favorite section.
You need to know two medications regarding these
shunts. Because sometimes the door stays open
when we want it closed, or sometimes, and this
is critical, we need to force it open to save
a life. Okay, hit me. Let's start with closing
the door. When do we need to do that? Let's say
the ductus arteriosus stays open when it shouldn't.
We call that a PDA. A patent ductus arteriosus.
It's now acting like a left to right shunt flooding
the lungs. Because the pressure has switched.
Left is now high. Exactly. So we want to close
it. We give a drug called indomethacin. Indomethacin.
That's an NSAAD, right? Like a super strong ibuprofen.
It is. It works by blocking prostaglandins. Prostaglandins
are the chemical that keeps the ductus open in
the room. So if we block them with indomethacin,
the door closes. Indomethacin closes the door.
Got it. But, and here's where it gets really
interesting and really high stakes. Sometimes
a baby is born with a horrible defect where the
plumbing is totally messed up. Maybe the aorta
is connected to the wrong side. The only way
that baby survives is if some blood can mix through
that fetal shunt. So if the ductus closes? The
baby dies. because there is no other way for
oxygen to get to the body. So in that case, we
want to reverse nature. We want to keep that
fetal door propped open. Exactly. We need to
keep the fetal shunts open until the surgeon
can get there. For that, we give prostaglandins,
specifically a drug called alprazodadol. Prostaglandins
keep the ductus open. Okay, so I need a mnemonic
for this. Indomethacin sounds like, in comes
the door closing it, and prostaglandins... Well,
P for prostaglandin, P for propidopen. I usually
say prostaglandins provide a path, but propidopen
is great, whatever works. Just remember, NSAIDs
like endomethacin close, prostaglandins open.
If you mix those up on a test or in real life,
you've killed the patient. It's that serious.
All right, we have the physics, we have the fetal
switch. Now, let's walk into the patient's room,
part two. Assessment red flags. You're looking
at a six -week -old baby. What is the number
one absolute Can't miss sign of cardiac disease.
Sweating during feeds. Sweating. Not chest pain.
Not clutching the arm. Infants don't clutch their
chest. And they don't run on treadmills. Their
stress test is eating. That's a great way to
put it. Feeding takes a huge amount of energy
for a baby. They have to suck, swallow, breathe,
coordinate, all of that. If a baby has heart
failure, their heart just can't keep up with
that demand. So the sympathetic nervous system
kicks in fight or flight. They start sweating,
usually on the salp and forehead, while they
nurse or take a bottle. That is such a vivid
image. We have a case study in the source material,
Logan, six weeks old. His parent says he falls
asleep while feeding. but he never finishes the
bottle and his little head is always wet with
sweat. That is a classic textbook clinical one
-liner. Diaphoresis plus fatigue during feeding
equals early heart failure. If you see that on
an exam or in triage, alarm bells, flashing red
lights, everything should be going off in your
head. And why is that so bad? Because that child
is not gaining weight. They are burning all their
calories just trying to breathe and circulate
blood. We call it failure to thrive, but really
it's the heart failing to support growth. So
developmentally, this child is just completely
stalling out. Exactly. The calories are going
to survival, not to growing the brain or the
bones or hitting milestones. What about vital
signs? I know kids aren't just small adults.
The numbers are totally different. They are drastically
different. And you have to know the ranges. The
younger the child, the faster the heart rate
and the lower the blood pressure. A newborn might
have a heart rate of 140 or 150, even 160. That's
perfectly normal. And if you saw 150 in an adult.
You're grabbing the crash cart. Yeah. But in
a newborn, you document it as normal. An adolescent,
on the other hand, might have a heart rate of
70, just like an adult. And blood pressure. This
is the trap. In an infant, a normal BP is something
like 80 over 55. If you see 80, 55 in an adult,
they are hypotensive and you're worried. In a
baby, you're happy. You have to know the age
-specific norms. They're not intuitive. And the
source material mentions a specific trap about
when to assess these vitals. Yes, this is huge.
If a baby is crying, screaming, or fighting you,
their heart rate and BP will be sky high. You
cannot interpret that data. It's useless. A crying
baby might have a heart rate of 200 just from
rage. It doesn't mean they have SVT. It means
they're mad. You have to measure vitals when
the infant is calm or, ideally, sleeping. Quiet
exam. It is a skill. You have to learn to be
a ninja. You enter the room. You listen to the
heart and lungs before you stick the thermometer
in or put the cold cuff on. Do the least invasive
things first. Once they cry, your good data is
gone. One last assessment piece before we move
on. Clubbing and polycythemia. These sound like
old timey pirate terms. They kind of do and they
go together. If a child has a defect where they
are chronically hypoxic, low oxygen for months
or years, the body tries to compensate. Two things
happen. One, the tips of the fingers and toes
get wide and round. The nail bed gets spongy.
That's clubbing. It's a sign of chronic long
-term oxygen deprivation. You will not see this
in a newborn. It takes time to develop. OK, so
clubbing tells me this has been going on for
a while. It's a history lesson on their fingertips.
What about polysthythemia? Poly means many, cythemia
means cells in the blood. The kidneys sense low
oxygen and they scream at the bone marrow, send
more red blood cells. We need more oxygen carriers.
So the body produces a ton of RBCs. That's polycythemia.
More red blood cells sounds good though, right?
More oxygen carriers. It's a double -edged sword.
It's a good intention with a bad outcome. Yes,
you have more carriers, but your blood becomes
thick. like a milkshake instead of water. Oh,
I see. And thick blood moves slowly. It can clot.
So these kids are at a huge risk for strokes.
That's why hydration is so critical for them
to keep that thick blood moving. If a polycythemic
kid gets dehydrated from, say, vomiting or diarrhea,
their blood can turn to sludge. It's a medical
emergency. Fascinating. OK. OK. Let's move to
the meat of the episode, part three, the defects.
We're going to use your method grouping them
by hemodynamics, by blood flow. Let's start with
group A. Increased pulmonary blood flow. The
wet lungs group. Right. Remember our map. This
is a left to right shunt. Blood is leaking from
the high pressure left side back to the low pressure
right side and going to the lungs again. The
lungs are over -circulated. They're boggy. They're
wet. The usual suspects here are ASD, VSD, and
PDA. So let's break down the VSD first. The source
says this is the most common congenital anomaly.
It is. Ventricular septal defect. hole between
the ventricles. Because the left ventricle is
the big pumper, it pushes blood forcefully through
that hole into the right ventricle. This creates
a lot of turbulence. Which you can hear. Which
you can hear. So on the exam you are listening
for a loud harsh murmur at the left sternal border.
Loud and harsh. Left sternal border and What
happens to the kid? How do they present? They
usually aren't blue, so they're asianotic because
plenty of oxygenated blood is still getting to
the body. But they are tired. They have pulmonary
congestion. You'll hear crackles, wet lungs.
They get respiratory infections constantly. Why
the constant infections? Wet lungs are a petri
dish for bacteria. Fluid stasis just breeds infection.
So, developmentally, this kid is the one who's
always missing school or daycare because they
have pneumonia. Again. And they're probably not
growing well. They're falling off the growth
chart because they're too tired to eat and they're
burning all their calories just trying to breathe
against those wet lungs. The good news is many
of these close on their own. That's right. Spontaneous
closure happens in about half of small VSDs by
age two. So often we just watch and wait. But
if it's large and causing significant heart failure,
we have to go in and patch it. Kate, what about
an ASD, atrial septal defect? a hole between
the atria. How is that different from a VSD?
It's still a left to right shunt, so the lungs
are still getting extra blood, but the pressure
difference between the atria is much lower than
between the ventricles. So the murmur is much
softer. It's not that loud, harsh sound. It's
often described as a systolic ejection murmur
with a wide fixed splitting of the second heart
sound. That sounds very specific. It's an audiophile's
term. But basically, these kids are often asymptomatic
for years. They might get diagnosed as a teenager
when they get tired playing sports. are less
likely to have that profound heart failure in
infancy that you see with a big VST. So it's
a quieter, more subtle version of the same problem.
In a way, yes. Still wet lungs, but less dramatically
so in many cases. OK. Next in this group is the
PDA patent, ductus arteriosus. Yeah. We talked
about the drugs. Indomithicin closes it. But
what does it sound like? This is a classic board
question. PDA has a machine -like murmur. A machine?
Yeah, it sounds like a washing machine. A continuous,
churning, hum -like sound right under the left
clavicle. You'll also feel bounding pulses. Why
bounding? What causes that? It's because during
diastole, when the heart is relaxing, blood is
constantly running off from the aorta through
the PDA and into the pulmonary artery. This makes
the diastolic pressure drop. So there's a wide
gap between the top number, the systolic, and
the bottom number, the diastolic. A wide pulse
pressure. Exactly. And that wide pulse pressure
makes the pulse feel really strong and snappy,
bounding. Yeah. Machine murmur, bounding pulses
give endomethacin to close it. Got it. Now, what
happens if we ignore these defects, if we let
the lungs stay wet for years and years? That's
the nightmare scenario. We call it Eisenmenger
syndrome. Eisenmenger. Eventually, the lungs
get sick of being flooded. The delicate blood
vessels in the lungs start to harden and thicken
to protect themselves. This is called pulmonary
hypertension. And that increases the pressure
on the right side of the heart. Exactly. The
right side now has to pump against this super
high resistance in the lungs. And if the right
side pressure gets high enough, it actually exceeds
the left side pressure. So the shunt. The shunt
reverses. It goes right to left. The kid turns
blue. And once that happens, the damage is permanent
and you're reversible. You can't just fix the
hole anymore. The lungs are shot. That's why
we fix these defects early before that permanent
damage sets in. OK, that makes sense. Let's move
to group B. The obstructive defects. The kinked
hose group. Right. So here, the problem isn't
a hole, it's a blockage. The king of this group,
the one you'll see on exams the most, is coarctation
of the aorta. Coarctation just means narrowing,
right? Exactly. Imagine you have a garden hose
and you pinch it in the middle. pressure builds
up behind the pinch and the flow is weak after
the pinch. And in the aorta, the pinch is usually
right after the arch after the arteries branch
off to the head and arms. Exactly. So blood flows
easily under high pressure to the head and arms.
That's the high pressure zone. But it can't squeeze
past that pinch to get to the legs, the gut,
the kidneys. That's the low pressure zone. This
leads to the famous four extremity blood pressure
test. This is the absolute need to know for coarctation.
This is how you find it. If you take a BP in
the arm, it's high, maybe 30, 30, 80 in a child,
which is hypertensive. Then you take it in the
leg and it's low, maybe 80, 50. And the pulses,
they're bounding in the neck and arms, but they're
weak or even absent in the feet. Upper body hypertension,
lower body hypertension. What does the patient
complain of? If they're older, they might complain
of leg pain with exercise claudication because
the muscles just aren't getting enough blood
flow. And they might get frequent headaches,
nosebleeds, or dizziness because of the high
pressure in the head. And the risk here if it's
not fixed? Stroke from the high pressure upstairs?
Or, even worse, rupture of the aorta. It's a
mechanical problem that needs a mechanical fixed
surgery to cut out the narrowed section or a
balloon angioplasty to stretch it open. If you
see a test question about BP disparity between
upper and lower extremities, you click coarctation
immediately. Okay. Group C. The scary ones. Decreased
pulmonary blood flow. The blue group. This is
the right -to -left shunt. Yes. And the poster
child for this group is Tetralogy of Fallot.
Tetralogy means four. You have four distinct
defects occurring at the same time. I always
use the mnemonic RAPS to remember them. RAPS.
That's a good one. R for right ventricular hypertrophy.
A for aorta overriding, P for pulmonary stenosis,
and S for septal defect, VSD. That's a great
mnemonic. Let's break it down so it makes sense.
The real villain here, the one that causes all
the other problems, is the pulmonary stenosis.
The exit to the lungs is extremely tight and
narrow. So blood can't get out of the right ventricle
easily. It can't. So the right ventricle has
to push against this tight door and the muscle
gets huge. That's your right ventricular hypertrophy.
So the blood is stuck in the right ventricle.
Where does it go? It takes the path of least
resistance. It looks at the tight pulmonary valve
and says, no thanks. And then it sees this big
VSD, the hole, and it shoots right through it.
To the left side. And because the aorta is overriding
or sitting right on top of that hole, the blue
blood shoots straight from the right ventricle
through the VSD and into the aorta and out to
the body. Bypassing the lungs entirely. The result
is instant cyanosis. Right. And this leads to
the most dramatic, terrifying event in pediatric
cardiology. The Tet spell or hypercyanotic spell.
Okay, paint the picture for me. You're the nurse.
You walk into the room. A toddler with known
tetralogy of fallot is crying because they dropped
a toy or maybe they're straining to poop. Suddenly
they turn a deep dark blue. They start gasping.
They go limp. What is happening physiologically?
The crying or straining increase their oxygen
demand. At the same time, the muscle right below
the pulmonary valve, the infundibulum, goes into
spasm and clamps down completely. It slams the
door shut. It slams the door to lungs completely
shut. Zero blood is going to the lungs. It's
all shunting right to left and out to the body.
They are profoundly hypoxic. This is a medical
emergency. This is a kill zone. What is the number
one priority nursing action? You have seconds.
Knee to chest position. Immediately. Explain
that. Why does shoving their knees up to their
chest help? It seems so simple. It's physics
again. When you scrunch the legs up like that,
you are kinking the femoral arteries. You are
dramatically increasing the resistance in the
systemic circulation in the body. You're making
it harder to pump to the body. Exactly. Remember,
blood is lazy. If the pressure in the body suddenly
gets really, really high, the blood in the heart
says, whoa, it's too hard to go out the aorta
now. It forces the blood to try the other path
back into the pulmonary artery and to the lungs,
even if it's tight. You essentially force the
blood back to the lungs by making the body a
harder place to go. You reverse the shunt temporarily.
It's an incredible, life -saving maneuver. So
set one, knee to chest, or if they're older,
have them squat. Step two, 100 % oxygen. Step
three, morphine. Yes. The oxygen helps with what
little blood is getting to the lungs. And morphine
is key. It calms the child, which reduces their
oxygen demand. But it also has a sedative effect
that can help relax that cardiac spasm. And developmentally,
you'll see toddlers doing this on their own,
right? It's amazing to watch. A tet kid will
be running on the playground. They'll get tired
and short of breath. And they will instinctively
drop into a squat for a few seconds. They're
self -treating. They are. The teacher might yell,
get up. Stop being lazy. But the school nurse
should know to say, let them squat. They are
increasing their systemic vascular resistance
and improving their own oxygen saturations. Incredible.
Nature finds a way. OK, group D mix defects.
The source material calls this the survival depends
on mixing group. Right, and the big one here,
the classic example, is transposition of the
great arteries, or TGA. The plumbing is crossed.
Completely swapped. The pulmonary artery leaves
the left ventricle. The aorta leaves the right
ventricle. So, wait, let me trace that. The right
side pumps blue blood out the aorta to the body,
which comes back blue to the right side and gets
pumped to the body again. A closed loop of no
oxygen. Correct. A completely futile deoxygenated
loop. And the left side pumps red oxygenated
blood to the lungs, which comes back red to the
left side and goes right back to the lungs again.
A closed loop of oxygen that never reaches the
brain. Right. Two separate serpents that never
cross. That sounds completely incompatible with
life. It is, unless, unless there is a connection
somewhere. This is where we go back to our fetal
shunts. If that baby is lucky enough to have
a PDA or a hole in the heart like an ASD or VSD,
the blood can mix and they can stay alive for
a few days. So this is a scenario where you are
literally running to the poxies to grab the prostaglandins.
You are not walking. You are starting a prostaglandin
drip immediately. Keep that ductus open. It is
the only lifeline, the only bridge between those
two circuits, until the surgeons can go in and
physically switch the vessels back to where they
belong. We call it the arterial switch operation.
And then there's the really tough one. hypoplastic
left heart syndrome or HLHS. This is one of the
most severe and complex defects. The entire left
side of the heart, the main pump, is tiny and
underdeveloped. It barely exists. How do you
fix half a heart? You can't fix it in the traditional
sense. You have to completely rewire the entire
circulation so the single working right ventricle
does all the work of pumping to both the lungs
and the bottom. That sounds incredibly complex.
It is. It takes a series of three major staged
open heart surgeries over the first few years
of life, or the only other option is a heart
transplant. These are the most fragile babies
in the entire cardiac ICU. That wraps up the
congenital defects, the ones they're born with.
Let's shift gears to part four. acquired heart
disease, the afterbirth group. These are kids
who were born with healthy hearts, but then get
sick. And the scariest one for parents, I think,
is often Kawasaki disease. Kawasaki, it's an
acute systemic vasculitis. So inflammation of
all the blood vessels, what does this kid look
like? They look miserable. We are talking a high...
persistent fever 103, 104 that lasts for more
than five days. And the scary part for parents
is Tylenol or Motrin doesn't touch it. The fever
just will not break. They're beside themselves.
So fever for more than five days, that doesn't
respond to antipyretics. What else? The diagnostic
criteria are very visual. The mnemonic is CRH
and burn. C is for conjunctivitis, red eyes,
but no goop, no drainage. R is for rash. A is
for adenopathy, swollen lymph nodes in the neck.
S is for strawberry tongue, a bright red bumpy
tongue with red cracked lips. And H is for hands
and feet, which get red, swollen, and then start
peeling. The burn is the fever. Serration burn.
That's a good one. And the real danger here isn't
the fever itself. It's what the inflammation
does to the heart. Specifically, the coronary
arteries. The vessels that feed the heart muscle
itself can get inflamed and balloon out, forming
coronary artery aneurysms. And if those burst.
Or if a clot forms in them, a five -year -old
can have a massive heart attack. So the treatment
protocol has a huge exam exception. Yes. This
is the one time you will see this. We give aspirin.
Whoa. We are taught in Pediatrics 101, never
give aspirin to children because of the risk
of Reye's syndrome, which is liver failure and
brain swelling. This is the one and only major
exception. In this case, the risk of the heart
clotting off and these aneurysms forming far
outweighs the risk of Reye's syndrome. We give
high dose aspirin for its anti -inflammatory
and anti -platelet effects. And what else? Along
with aspirin, the main treatment is IVH intravenous
immunoglobulin. It's a blood product that helps
to calm the whole immune system down and reduce
the inflammation in the arteries. So if you see
a test question asking which child gets aspirin,
you look for the kid with the strawberry tongue
and the five -day fever. Absolutely. And long
term, these kids need echocardiograms for years
to make sure those aneurysms don't develop or
worsen later in life. Next up, rheumatic fever.
I feel like this is something out of a Charles
Dickens novel, but it's still around. It is.
And it's tragic because it is entirely preventable.
Rheumatic fever is a delayed autoimmune reaction
to a group A strip infection's strep throat.
So a kid gets strep throat, maybe it's untreated,
or maybe they stop the antibiotics too soon because
they feel better. Then what happens? Two to four
weeks later, the immune system gets confused.
The antibodies that it created to fight the strep
bacteria start attacking the body's own tissues,
specifically the heart valves, the joints, and
the brain. This brings us to the Jones criteria
for diagnosis. Right, the major criteria. One
is carditis, inflammation of the heart. Another
is polyarthritis, swollen, painful joints that
migrate. One day it's the knee, the next day
it's the elbow. And then there's the really strange
one. Korea. Seidenham's Korea. It's involuntary,
jerky movements of the face and limbs. It looks
terrifying for parents. The kid starts twitching,
dropping things, making funny faces. They can't
control it. And erythema marginatum. the rash
with red rings on the trunk. Right. The career
resolves, the rash fades, but the real permanent
damage is from the carditis. It scars the heart
valves, especially the mitral valve. That damage
is for life. So the exam tip here is prevention.
It's all about prevention. Treat strep throat.
Take all your penicillin for the full 10 days.
It's not just about a sore throat. It's about
saving the heart valve from being destroyed by
your own immune system 20 years down the road.
One more in this category. This is an infection
of the inner lining of the heart. It usually
affects kids with existing heart defects, artificial
valves, or central lines. Bacteria usually from
the mouth gets into the blood and sets up camp,
colonizing the heart valves. This leads to a
surprising nursing intervention focus. Dental
hygiene. It's huge. The dentist is a high -risk
zone for these kids. Every time you clean teeth,
you can release bacteria into the blood. So high
-risk kids, those with artificial valves or certain
unrepaired defects, need prophylactic antibiotics
about an hour before any dental procedure. So
good brushing is actually a cardiac intervention
for these kids. It really, really is. OK. Let's
move to part five. Nursing management and safety
kill zones. We've diagnosed the problem. Now
we have to treat it. and the drugs we use in
cardio are not to be messed with. Let's talk
about digoxin. Digoxin or linoxin. It's an old
drug derived from the foxglove plant, but we
still use it a lot. It does two main things.
It increases contractility, which means it makes
the heart squeeze harder. A positive inotrope.
Right. And it decreases the heart rate, a negative
chronotrope. It gives the heart more time to
fill between beats. So it makes the pump stronger
and more efficient, squeeze harder, beat slower.
but the therapeutic window is tiny. The difference
between a helping dose and a killing dose is
microscopic. Which is why the need to know assessment
is the apical pulse. You cannot just feel the
wrist. You must put your stethoscope on the apex
of the heart and listen for one full minute,
not 15 seconds times four, one full uninterrupted
minute. And what are the cutoff rules? When do
we hold the drug? This has to be tattooed on
your brain. For an infant, if the apical heart
rate is below 90, you hold the drug and you call
the provider. For an older child, the cutoff
is below 70. Less than 90 for a baby. Less than
70 for a child. Write that down. Now, how do
I know if the kid is toxic? What's the first
sign? Just vomiting. Kids vomit all the time.
This sounds tricky. That's why it's so dangerous.
But if a cardiac kid on digoxin starts vomiting,
especially more than once, or they lose their
appetite completely, do not assume it's the flu.
Your first thought must be dig toxicity until
proven otherwise. Other signs are profound bradycardia,
a very slow heart rate, and dysrhythmias. And
there's a critical electrolyte connection here,
right? Potassium. Hypokalemia, or low potassium,
potentiates digoxin toxicity. It makes the heart
muscle much more sensitive to the drug. So a
normal dose of DIG can become a toxic dose if
your potassium level is low. And what's a common
drug we give that lowers potassium? Lasix, furosemide,
the diuretic we give to treat the very heart
failure we're using the digoxin for. It's a vicious
cycle. We give Lasix to get the fluid off the
wet lungs. Lasix makes them pee out potassium.
Low potassium then makes the digoxin toxic. Which
is why the nurse has to be a hawk. You are monitoring
potassium levels daily. You're encouraging potassium
-rich foods like bananas, spinach, potatoes,
if they're old enough. If your patient is on
both DIG and Lasix, you are watching that potassium
like your license depends on it because it does.
Okay, let's talk about the big procedure. Cardiac
catheterization. We thread a long thin catheter
up the femoral vein or artery into the heart
to measure pressures, fix a valve or patch a
hole. The kid comes back to the floor. What is
the number one kill zone? Post procedure. Hemorrhage.
We just poked a hole in a major artery or vein
in the groin. If that clot blows, the kid can
bleed out into their thigh very, very quickly.
So how do we assess for that? You check the dressing,
obviously, for any visible bleeding. But blood
follows gravity. If the kid is lying on their
back, the blood might not come out the front.
It might pool under their leg and buttocks. So
you have to physically slide your hand under
them. If you feel wetness, check your glove.
Is it blood? And you have to check the pulses
below the site. Absolutely. Check the pedal pulses
in the foot on the affected side. If that leg
is cool, pale, and the pulse is weak or gone,
you may have thrown a clot that's blocking the
femoral artery. That is a medical emergency.
The leg could die. What's the main nursing intervention
to prevent bleeding? Keep the affected leg completely
straight. No bending at the hip. For four to
eight hours, depending on the protocol. Have
you ever tried to keep a two -year -old's leg
straight for six hours? It is a special kind
of nursing nightmare. This is where pediatric
nursing becomes an art form. You use soft knee
immobilizers, you use iPads, you read books,
you have parents literally hold the leg, but
they cannot sit up because sitting up flexes
the hip, puts pressure on that groin site, and
can pop the clot. And if you see active bleeding,
if the dressing suddenly becomes soaked with
blood. Direct, firm pressure, but not just on
the little bandaid. You apply pressure with your
gloved hand about one inch above the insertion
site. You're trying to compress the artery proximally
to stop the flow coming from the heart. And you
hold it, and you yell for help. You do not leave
that room. OK. We've covered the drugs, the procedures.
Let's touch on the day -to -day management of
congestive heart failure, or CHF. The goal is
to decrease the workload on the heart. How do
we feed these babies? Right. We mentioned the
sweating. Feeding is work. It's a marathon for
them. So we need to make it as easy as possible.
How do we do that? A few key ways. One. Small,
frequent feeds. Don't overfill their stomach
because a full stomach pushes up on the diaphragm
and makes it even harder to breathe. Every three
hours is standard. Two, high calorie formula.
Standard formula is 20 kilocalories per ounce.
We might fortify it with extra powder to make
it 24 or even 30 kilocal per ounce. The goal
is more energy and less volume. And what about
the mechanics of eating? Three. Use a soft nipple
with a slightly larger hole. We don't want them
working hard to suck. The milk should almost
drip into their mouth with minimal effort. And
if they take longer than, say, 20 or 30 minutes
to finish a bottle? You stop. If they are still
trying to eat after 30 minutes, they are burning
more calories than they are taking in. It's a
net loss. At that point, you have to prioritize
growth over the skill of eating. You drop an
NG tube and you gavage feed the rest of the formula.
It's about conserving every last calorie. And
what about positioning? Keep them in a semi -fowler's
position, even in the car seat. Keep their head
up. It allows for maximal chest expansion and
makes the work of breathing a little bit easier.
Part 6. Psychosocial and family. We can't forget
the parents. They are terrified. They are grieving.
They expected a perfect healthy baby and now
they are in the ICU surrounded by tubes and wires
and beeping machines. They often feel intense
guilt like they did something wrong. And they
live with the constant fear that the child will
die. So what's our role? Our role is to be a
calm, clear educator. You need to explain things
simply. Get a whiteboard. Draw pictures of the
heart. Here is the hole. Here's the patch the
surgeon will put in. Empower them with knowledge.
Let them participate in care bathing, changing
diapers, to restore some sense of normalcy and
control. And what about activity restrictions
for older kids? The kid with a big scar on their
chest who wants to go play soccer. What do we
tell them? For most repaired defects, we generally
tell them to self -limit. The child knows their
body better than anyone. If they get tired, they
will stop and rest. We don't usually have to
bench them from sports unless it's a specific
arrhythmia condition or they're on anticoagulants.
But there is a very specific safety rule for
kids who have had recent open -heart surgery,
the sternotomy care. Yes, this is a big one.
After open -heart surgery, their sternum is wired
shut. It takes about six to eight weeks to heal.
You absolutely cannot lift that child up under
the arms. Why not? If you pick them up by the
armpits, you can pull on that healing bone, pop
the wires, and destabilize their entire chest.
It's incredibly painful and dangerous. So you
have to teach parents to scoop the butt, not
pull the arms. Good tip. Okay, we have covered
a massive amount of ground, from pressure gradients
to strawberry tongues to keeping legs straight.
Let's wrap this up with our big three takeaways.
If our listener is walking into an exam tomorrow,
what are the three things they absolutely must
have locked in? Okay, number one, hemodynamics
is king. Don't just memorize defects. Understand
the flow. Left to right is wet and pink. Right
to lad is blue and cyanotic. If you know the
pressure, you know the symptoms. Okay, number
two. Number two, safety first. Know the Dagoxin
hold parameters, less than 90 for infants, and
always watch the potassium. And know the tech
spell drill. Knee chest position immediately.
Those are life or death concepts that will be
on the test. And number three. Number three.
Assessment nuance. A sweating baby is a failing
heart. A crying infant gives you bad data, so
get your vitals when they're quiet. Trust your
eyes and your hands, not just the monitor. Brilliant.
And as we close, I want to leave our listeners
with a provocative thought. We spend so much
time and energy fixing the pump, the plumbing,
the valves, the pressure. But what about the
computer that the pump serves? That is the new
frontier of research in this field right now.
We are saving these kids' hearts with amazing
surgeries. Mortality is way down. But we are
now finding that children with significant congenital
heart disease have much higher rates of neurodevelopmental
delays, ADHD, and learning disabilities later
in life. Is it the time on the heart -long bypass
machine during surgery? the periods of low oxygen
before they get fixed? It's likely a mix of all
of the above. The brain is incredibly sensitive
to perfusion and oxygenation, especially in those
first few years. So as nurses, our job doesn't
end when the incision heals. We need to be screening
these kids for developmental delays. We need
to be pushing for early intervention. We fix
the hardware, now we have to protect the software.
We fix the hardware, now we have to protect the
software. That is a powerful place to end. to
all the nursing students and nurses out there
tackling this unit. You can do this. Blood is
lazy. Follow the flow. You've got this. We've
got this. Thanks for diving deep with us. See
you next time.