Chapter 19: Nursing Care of the Child With an Alteration in Perfusion/Cardiovascular Disorder

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Welcome back to The Deep Dive.

Today, we are tackling some really vital material, pulling out the core clinical knowledge on pediatric cardiovascular nursing.

We're drawing specifically from chapter 19 of Essentials of Pediatric Nursing.

Yeah, we're zeroing in on alterations in perfusion and cardiovascular disorders in kids.

And it's a huge topic because congenital heart disease or CHD is actually the biggest group of structural birth defects.

Right.

And then you also have acquired heart diseases, the ones that pop up after birth, adding to chronic illness and unfortunately, mortality too.

Exactly.

So our goal today really is to equip you with that essential knowledge base.

You need it for sharp assessments for the right interventions.

And let's be honest, a heart diagnosis for a child, it's incredibly overwhelming for families.

So being prepared with solid information for guidance and support,

that's, well, it's paramount right from the get -go.

Definitely.

And to really get the disorders, you have to start with the basics, that incredible switch over in circulation that happens the moment a baby is born.

Ah, the fetal to newborn transition.

It's pretty amazing.

In utero, the whole system's different relying on the placenta, right?

And you've got structures like the form and oval and the ductus arteriosus.

Ah, crucial shunts.

They basically let blood bypass the lungs, which aren't doing the oxygen exchange yet.

The ductus venus is part of that placental circuit too.

But then that first breath happens and everything changes.

It triggers this like cascade of pressure shifts.

It really does.

The lungs inflate and boom, pulmonary vascular resistance just plummets.

This means more blood flows to the left atrium.

Which ramps up the pressure there and slams the door shut on the form and oval.

Precisely.

And at the same time, the shifts in pressure plus the higher oxygen levels in the blood now encourage the ductus arteriosus and the ductus venusus to close up too.

So you go from this parallel system with bypasses to a series circuit basically, independent circulation.

Exactly.

But even after those structures change, the heart itself in an infant, well, it's still got some unique features and limitations.

Like how it sits in the chest.

I remember it's more horizontal at first.

The apex is higher up, like under the fourth intercostal space.

Right.

It gradually shifts down as the lungs grow and the heart size itself, it increases massively.

About 10 times its birth size by the time a child is maybe six to 12 years old.

Wow.

Okay.

But structurally isn't the most critical difference, right?

And it's about function, especially cardiac output.

Yes, absolutely.

This is probably the single most dangerous point of confusion for anyone moving from adult to pediatric care.

Infant heart muscle cells, the myocytes, they're just less compliant.

They don't stretch well.

Meaning the infant can't really increase their stroke volume much, the amount of blood pumped per beat.

So to increase cardiac output, they are incredibly dependent on heart rate.

Okay.

Let me try and rephrase that because it sounds critical.

If you see an infant you think needs more output and you just flood them with IV fluids thinking their heart will stretch and pump harder like in adults.

You could actually be making things much worse.

That stiff ventricle can't handle the extra volume.

You can easily push them into failure, cause pulmonary edema, basically cause a crash.

Got it.

So managing heart rate and being super careful with fluids is key, which is why knowing the normal vital signs is non -negotiable.

Totally.

An infant's normal heart rate is what?

Usually 90 to 160, which sounds incredibly fast if you're used to adults.

Compared to an adolescent where it settles down into that 60 to 100 range.

More like us.

And blood pressure is lower too, like an average of 80 over 55 in infants.

Right.

It gradually increases with age.

Okay.

So knowing that, let's shift to assessment.

When you're taking a health history, what are those immediate red flags that scream, think cardiac?

Good question.

You're looking for signs that the body's working too hard or not getting enough oxygenated blood.

Things like orthopnea, difficulty breathing, lying down, or just general dyspnea, frequent pneumonias can be assigned to.

And specifically in infants, the big ones are feeding issues.

Poor feeding that leads to failure to thrive, getting really tired during feeds,

or sweating profusely that diaphoresis while eating, sucking takes a lot of energy.

Okay.

That makes sense.

Now moving to the physical exam.

Inspection first.

What are we looking for?

Well, edema in infants is a bit sneaky.

It doesn't always show up in the feet first.

Like in adults, you might see it in the face or the presacral area, then maybe the extremity.

And cyanosis, a blue baby.

That's a major one.

If you have a newborn who is cyanotic and you give them oxygen, but their oxygen saturation doesn't improve, you have to suspect a structural heart defect.

Probably one that's shunting deoxygenated blood systemically.

What about clubbing of the fingers?

Clubbing, that softening of the nail beds, the rounding of the fingernails.

It's definitely a sign of chronic long -term hypoxia from severe CHD.

But the key word is chronic.

It doesn't happen overnight.

It takes at least maybe six months, often closer to a year to develop.

Okay.

So not an acute sign.

Now palpation, feeling the pulses.

This can give you some really specific clues, right?

Huge clues.

You always, always compare femoral pulses down in the groin to brachial pulses in the arm.

If those femoral pulses feel weak or even absent compared to the brachials, that's the classic sign pointing towards coarctation of the aorta.

A narrowing of the aorta, restricting blood flow downwards.

Okay.

And what about the opposite?

Really strong pulses.

Yeah, bounding pulses.

That makes you think of patent ductus arteriosus or PDA.

We'll talk more about that defect later.

Got it.

And auscultation, listening with the stethoscope.

Obviously we're listening for murmurs.

Right.

And you need to describe them properly where you hear it best, when it happens in the cardiac cycle, the quality, the pitch, and the intensity graded from grade the first, which is super faint.

You can barely hear it.

All the way up to grade the sixth, which the book says you can hear even with the stethoscope lifted off the chest.

Wow.

It's rare, but yeah, signifies massive turbulence.

Okay.

One more physical exam piece.

Yeah?

Blood pressure comparison.

Crucial.

You need to take BP in all four extremities.

Normally there shouldn't be a big difference between the arms and legs, but if the pressure in the arms is significantly higher, like more than 20 millimeters of mercury higher than in the legs.

Coarctation again.

Strongly suggests coarctation.

And related to PDA, sometimes you'll find a widened pulse pressure.

That's the difference between the systolic and diastolic numbers.

That's often seen with PDA too.

Makes sense.

Okay.

So exam uses clues.

What about definitive tests?

Well, the echocardiogram, the heart ultrasound is fantastic.

It gives you detailed pictures of the structure, pinpoints, defects, and ECG gives you baseline rhythm and can show if ventricles are hypertrophied or enlarged.

And labs, like at CBC.

Yeah.

You check hemoglobin and hematocrit.

In chronic synotic conditions, you might see polycythemia.

That's an increased number of red blood cells as the body tries to compensate for

But the gold standard often is still cardiac catheterization.

It often is.

Yeah.

It gives you the most detailed pressures and oxygen saturation inside the heart chambers and vessels.

Plus sometimes they can actually do interventions during the cath procedure itself.

Okay.

Perfect lead in.

Let's connect these findings to action the nursing process.

High priority nursing diagnoses.

Let's start with decreased cardiac output.

What are the key interventions?

The big theme here is conserving energy.

So clustering your care, doing multiple things at once so the child can rest in between.

Anticipating their needs so they don't have to cry or exert themselves to get attention.

Basically minimizing oxygen demand.

And there's one really specific critical intervention for kids with tetralogy of phallate having a hyper cyanotic spell, right?

The tet spell.

Yes.

Absolutely life saving.

You immediately put the child in a knee to chest position.

If they're older, they might instinctively squat down.

Let's break down why that works because it's so important.

It increases systemic pressure, doesn't it?

Exactly.

Squatting or pulling the knees to the chest kinks the femoral arteries, dramatically increasing the resistance in the systemic circulation of the SVR.

Which makes it harder for blood to flow out the aorta.

Right.

So it forces more of that deoxygenated blood from the right ventricle to go through the narrowed pulmonary artery to the lungs instead of shunting across the VSD into the aorta.

It temporarily improves pulmonary blood flow and oxygenation.

Fast action is key.

Brilliant.

Okay.

Next diagnosis.

Excess fluid volume.

Usually from heart failure.

How do we monitor that best?

There's one thing that's absolutely the best indicator of fluid status changes.

Better than anything else.

Daily weights.

Daily weight.

Same scale, same time, similar clothes or naked.

Every single day.

That plus strict INO and maybe fluid or sodium restriction helps manage the volume overload.

Diuretics are often used too, of course.

Makes sense.

What about activity intolerance, especially in infants?

The big thing here is that crying and prolonged feeding use up a ton of calories and energy.

So a key intervention is trying to avoid long crying spells or really extended nipple feeding sessions.

Keep feeds efficient.

Which ties right into imbalanced nutrition.

These kids often struggle to take in enough calories because they tire so easily and their metabolic rate is high.

Right.

So the strategy is small, frequent feedings.

And really importantly, try to offer the highest calorie options or fortified feeds when the child is most rested and likely to have the best appetite.

Make every feeding count.

Okay.

Let's move into the specific congenital heart defects now.

Grouping them by how they affect blood flow.

First up,

decreased pulmonary blood flow defects.

These are your classic blue baby or cyanotic defects.

The core problem is some kind of obstruction that prevents blood from getting to the lungs easily.

This causes pressure on the right side of the heart to be higher than the left.

Leading to a right to left shunt.

Deoxygenated blood mixes with oxygenated blood and goes out to the body.

Exactly.

Which causes the cyanosis.

And over time, that chronic hypoxia leads to the body making extra red blood cells polycythemia trying to compensate.

The classic example here is of phallate or TOF.

Right.

The one with the four parts.

Pulmonary stenosis.

That's the obstruction.

A ventricular septal defect.

VSD.

A hole between the ventricles.

And overriding aorta.

The aorta sits over the VSD.

And right ventricular hypertrophy.

The right ventricle gets muscular from pumping against the obstruction.

That's the one.

Now the next category is increased pulmonary blood flow defects.

Okay.

So these are initially a cyanotic, not blue.

Examples like atrial septal defect, ASD, VSD, and the PDA we mentioned earlier.

Correct.

Here, the pressure on the left side of the heart is normally higher than the right.

So if there's a hole connecting the two sides, blood shunts from left to right.

So oxygenated blood is going back to the lungs where it just came from.

Precisely.

It overloads the pulmonary circulation.

This leads to pulmonary congestion, makes the lungs wet, increases the workload on the heart, and can eventually cause pulmonary hypertension and heart failure if it's not corrected.

Now here's a really counterintuitive point we need to stress for these defects.

Oxygen therapy.

Yeah, this is critical.

For these increased pulmonary blood flow defects, giving supplemental oxygen is often not helpful and can actually be harmful.

Why is that?

It seems backwards not to give O2 if they're heading towards heart failure.

Because oxygen is a potent pulmonary vasodilator.

It makes the blood vessels in the lungs relax and open up.

If you decrease the resistance in the lungs, you actually increase the amount of blood shunting from the high pressure left side back into the lungs.

So you make the pulmonary overload worse.

Exactly.

You can worsen the congestion and exacerbate the heart failure.

It's a crucial distinction.

Okay, good point.

Let's take PDA patent ductus arteriosus as an example here.

That's the fetal vessel between the aorta and pulmonary artery that failed to close.

Right.

And the classic signs are that harsh, continuous machine -like murmur that you can often hear throughout the cardiac cycle.

Plus the bounding pulses and the widened pulse pressure we talked about earlier.

Okay, third category, obstructive disorders.

These involve some kind of narrowing or blockage that obstructs blood flow out of the heart or through a major vessel.

Coarctation of the aorta is the prime example.

And we already covered the key sign, that difference in blood pressure and pulse quality between the upper and lower body.

Higher in the arms, lower in the legs.

Yep, because the narrowing restricts flow beyond the point of the coarctation, typically after the arteries branching to the arms.

Finally, the mixed defects category.

These are complex ones where oxygenated and deoxygenated blood mix,

often because survival depends on keeping fetal pathways open, like hypoplastic left heart syndrome, HLHS.

HLHS is one of the most severe and complex defects.

Basically, the entire left side of the heart mitral valve, left ventricle, aortic valve, ascending aorta is severely underdeveloped, hypoplastic.

It can't support systemic circulation.

So the right ventricle has to do all the work.

Pump blood to both the lungs and the body.

Correct.

And the only way blood can get to the body is if the ductus arteriosus stays open, allowing blood from the pulmonary artery, pumped by the right ventricle, to flow into the aorta.

So if that PDA closes.

It's catastrophic.

Systemic perfusion is lost very quickly.

That's why starting a prostaglandin E1 infusion immediately is absolutely life -saving for these babies.

It keeps the ductus open, buying time until surgery.

Wow.

Okay, a lot to absorb with CHD.

Let's quickly touch on some key acquired cardiovascular disorders.

Heart failure comes up a lot, right?

It does.

It's actually the most common reason kids with CHD end up hospitalized.

The heart just can't pump effectively enough to meet the body's demands.

Compensatory mechanisms kick in, like the rennan -angiotensin system, leading to fluid retention.

What are the earliest signs we might see in kids?

Often subtle at first.

Tachycardia, a fast heart rate, and tachypnea fast breathing are usually the very first signs as the body tries to compensate.

And if medications like digoxin are needed, big safety point.

Huge safety point.

Digoxin has a very narrow therapeutic range, meaning toxicity is a real risk.

You must check the apical pulse for a full minute before giving it.

And the rule is hold the dose if an infant's heart rate is less than 90 beats per minute.

Different cutoffs for older kids, but 90 for infants.

Got it.

What about Kawasaki disease?

That's an acute systemic vasculitis inflammation of blood vessels throughout the body.

We don't fully know what causes it, maybe an infectious trigger.

The biggest danger is inflammation of the coronary arteries, which can lead to aneurysms.

And the signs to look for.

It's a pattern.

High fever, usually for five days or more, that doesn't respond to antibiotics.

Plus things like bilateral conjunctivitis, red eyes without pus, changes in the mouth like cracked lips or a strawberry tongue, rash, swollen hands and feet.

Treatment.

High dose aspirin, surprisingly, for its anti -inflammatory effect, and intravenous immunoglobulin, IVE.

Okay.

Two quick infection -related ones.

Infective endocarditis.

That's an infection of the inner lining of the heart or the valves.

Kids with existing heart defects or prosthetic valves are at higher risk.

Prevention is key.

Meaning?

Good hygiene is really important as bacteria from the mouth can enter the bloodstream.

And for high -risk kids,

antibiotic prophylaxis, taking antibiotics before certain procedures, especially dental work, is crucial.

And acute rheumatic fever, ARF.

That's a delayed reaction that can happen weeks after a group A strep infection, like strep throat, that wasn't fully treated.

It's an autoimmune response where the body mistakenly attacks tissues, particularly the heart valves, joints and brain.

Diagnosis is based on the modified Jones criteria, right?

Yes.

You need evidence of a recent strep infection plus a combination of major and minor criteria.

Major ones include carditis, heart inflammation,

migratory polyarthritis, joint pain that moves around,

subcutaneous nodules, a specific rash called erythema marginatum, and sydenum correa in voluntary movements.

Okay, last big section.

Nursing management for procedures, especially cardiac cath and surgery.

Cardiac cath first, pre -procedure.

Usual stuff like NTO status, checking for allergies, especially iodine or shellfish since contrast dye is used.

But the absolute critical nursing action beforehand.

Marking the pedal pulses.

Marking the location of the pedal pulses the ones on top of the feet with an indelible marker.

You need that baseline to compare against after the procedure.

Makes sense.

And post -procedure priorities.

Bed rest is vital.

Keeping the leg the catheter went into straight for usually four to eight hours to prevent bleeding and then constant monitoring of that extremity.

Checking what specifically?

The pulse distal to the site comparing its quality and presence to the baseline you marked.

Also color, temperature, capillary refill, full neurovascular checks.

And if bleeding does happen at the site, what's the immediate action?

Apply firm, direct pressure, but critically apply it about one inch above the insertion site.

You want to compress the artery itself, not just the hole in the skin.

Good tip.

And monitor urine output too because of the contrast dye.

Yes, the dye acts like a diuretic so they can get dehydrated.

Strict INO is important.

Okay.

Finally, post -cardiac surgery, lots of monitoring, obviously vitals, hemodynamics,

but what about chest tubes?

Is there a major warning sign there?

Absolutely.

Chest tubes drain blood and fluid after surgery.

If you suddenly see the chest tube output abruptly stop, especially if the child's heart rate goes up and maybe their filling pressures increase.

You worry about cardiac tamponade.

Exactly.

Cardiac tamponade.

It means blood might be accumulating around the heart, compressing it and preventing it from filling properly.

It's a surgical emergency.

That sudden stop in drainage when you expect drainage is a huge red flag.

Wow.

Okay.

That is a ton of critical information we've unpacked from those huge circulatory shifts at birth.

To understanding that infant hearts just can't compensate with volume, they rely on rate.

Knowing what a weak femoral pulse means versus a bounding one.

The importance of daily weights for fluid status.

And those key interventions like needed chest for tet spills and being conscious with oxygen in those increased pulmonary blood flow defects.

Yeah, it's a lot.

And while we focused a lot on the acute stuff, the surgeries, the immediate post -op, the reality for many of these now is survival into adulthood.

That's a great point.

So the focus shifts, right?

It becomes about managing the long -term picture, the potential neurodevelopmental challenges some face, the psychosocial impact, navigating things like insurance, employment.

It's a whole lifelong journey.

A really important reminder that the knowledge we build helps support patients, not just through a crisis, but potentially over decades.

Thank you so much for walking us through all that.

And thank you for joining us for this deep dive.