Chapter 32: Concepts of Care for Patients With Cardiac Problems

Welcome to Last Minute Lecture.

This free chapter overview is designed to help students review and understand key concepts.

These summaries supplement not replaced the original textbook and may not be redistributed or resold.

For complete coverage, always consult the official text.

Welcome to the Deep Dive.

We're here to cut through the noise and focus on the critical concepts, pulling them straight from the source material for you.

That's right.

Today our mission is a pretty rapid but hopefully comprehensive look at cardiac care.

We're pulling from the latest medical surgical nursing insights.

And the core theme, the thing that ties it all together, really, is perfusion.

Simple as that.

If the heart structure is off, maybe failure, infection,

valve problems,

then it's function, pumping blood, well that fails too.

Makes sense.

So our main example today is heart failure, or HF.

And it's critical because, look, it's still the number one reason folks over 65 end up hospitalized in the U .S.

So our aim,

distill the key pathology, the management, make it quick to grasp.

Okay, let's dive in then.

Heart failure.

It seems straightforward.

The heart isn't bumping well.

But there's more to it.

Different ways it fails.

Exactly.

It's not just one thing.

We mostly talk about left -sided, right -sided, sometimes high output failure.

The last one's less common.

Happens when the body's metabolism just goes haywire, like in severe sepsis.

But usually it starts on the left side, in the left ventricle.

Yeah, that's where most HF begins.

And even within left -sided failure, there are two main types we need to unpack.

Right, systolic and diastolic.

What's the core difference there?

How is that ventricle actually failing?

So think of it like this.

One is a problem with squeezing.

The other is a problem with filling.

Systolic HF, or HFREF, the REF stands for reduced ejection fraction.

That's the people often think of first.

The heart muscle is weak, can't contract properly, maybe damaged, maybe too much volume.

And that ejection fraction, the EF, it drops.

Drops below 40%.

Normally it should be 50, 70%.

So we often call this forward failure.

Cardiac output goes down, blood backs up.

We're into the lung.

Okay, so that's systolic.

Then there's diastolic HF, HFPEF.

The P is for preserved EF.

How does that work if the EF is okay?

Yeah, this one's tricky.

The EF might look normal, over 40%.

But the problem is the ventricle itself is stiff.

It just can't relax properly to fill up with blood between beats.

So even though the squeeze seems okay, percentage -wise, the filling is poor, and the pressure inside skyrockets.

And that's more common in certain groups?

Very common in older adults, especially those with chronic hypertension that hasn't been well controlled.

That stiffness develops over time.

And then left -sided failure often leads to right -sided failure.

It's the most common cause, yeah.

Either LV failure backs everything up, or sometimes pulmonary hypertension is the culprit.

But the result is right -sided HF, where blood backs up systemically.

Not into the lungs this time, but into the body.

Think veins, organs,

systemic congestion.

Okay, now this part is fascinating.

The body tries to help, but actually makes things worse long -term, these compensatory mechanisms.

Oh, absolutely.

It's the body's short -term fix causing a long -term catastrophe.

First, the sympathetic nervous system, SNS, kicks in immediately when output drops.

Floods the body with adrenaline -like chemicals.

Which sounds good initially.

Increases heart rate, maybe swees.

Exactly.

Boosts heart rate, boosts incontracility, gets cardiac output up right now.

Yeah.

But the cost is huge.

It dramatically increases the oxygen demand on a heart that's already struggling.

It actually speeds up the death of heart muscle cells.

A vicious cycle.

And then there's the RAS system.

Right, the renin -angiotensin system.

When the kidneys sense low blood flow, they trigger this cascade.

What does it do?

Intense vasoconstriction narrows the blood vessels, increasing resistance, what we call afterload.

Making it harder for the heart to pump out blood.

Precisely.

And it also triggers aldosterone release, which makes the body hold on to salt and water.

That increases volume, or preload.

So you've got more resistance and more volume pushing back on a failing heart.

And this leads to physical changes in the heart muscle itself.

Yes.

This chronic stress, the increased volume and pressure, leads to what we call ventricular remodeling.

The heart muscle changes shape, gets thicker in the wrong ways, becomes less efficient.

It's permanent damage.

Wow.

Okay.

And where does BMP fit in?

We measure that a lot.

B -type natriuretic peptide.

The ventricles release BMP when they get stretched too much by all that extra fluid.

It tries to counteract some of the bad stuff, cause a little vasodilation

But its real value for us clinically is as a diagnostic marker.

So if someone comes in short of breath.

An elevated BMP helps us say, okay, this shortness of breath is likely due to heart failure rather than say pneumonia or COPD acting up.

Especially useful for figuring out diastolic failure sometimes.

Got it.

So moving from the why to the what we see, how do we recognize left -sided failure at the bedside?

What are those pulmonary congestion cues?

You're looking for two main things.

Poor tissue perfusion signs and lung congestion signs.

Patients might just feel incredibly weak, unusually tired.

That's the poor perfusion.

And the breathing.

That's the classic stuff.

Exertional dyspnea, getting short of breath with activity.

Orthopnea, having to prop up on pillows to breathe, can't lie flat.

And PND, paroxysmal nocturnal dyspnea that's waking up suddenly hours after falling asleep, totally gasping for air.

That sounds terrifying.

And the cough.

It often starts as just irritating, maybe worse at night.

But if it progresses, gets really wet, and they start coughing up frothy, pink -tinted sputum, that's a critical sign.

That's pulmonary edema, a medical emergency.

What else do we listen for or feel?

On exam, you'll likely find tachycardia.

And a key finding, often one of the first reliable signs, is an S3 gallop.

That extra heart sound indicates rapid filling into a ventricle that's already volume overloaded.

You might feel a pulses alternans, the pulse strength alternates beat to beat.

And listening to the lungs.

You'll hear those late inspiratory crackles usually starting down at the bases and moving up as it worsens.

Okay, so that's left side, lungs filling up.

What about the right -sided failure cues, the systemic backup?

This is all about fluid overload in the body.

So dependent edema is key, swelling in the legs, the ankles, even the sacrum if they're bed bound.

Rings might feel tight, shoes won't fit.

And significant weight gain.

And this weight gain can sneak up on you, right?

It really can.

The textbooks say a patient might hold on to four to seven liters of extra fluid, that's like 10 to 15 pounds, before you even see pitting edema where you press in the indense stays.

10 to 15 pounds, that's staggering.

And that's exactly why daily weights are so critical, isn't it?

It's our safety net.

Our best early warning system?

Absolutely.

Daily weights are non -negotiable.

It's the most reliable way to track fluid gain or loss.

Has to be same time, usually first thing in the morning after avoiding, before breakfast, same scale, same clothes or gown.

And the conversion is simple.

Yep.

One kilogram gained or lost equals one liter of fluid retained or lost.

It's direct.

OK, so weights are key.

Besides B and P, what other tests really nailed down the HSA diagnosis?

The absolute best non -invasive tool is the echocardiogram, the ECHO.

It lets us see the heart working.

We can measure the ejection fraction accurately, see if the walls are too thick, hypertrophy, check the chamber sizes.

And imaging.

A simple chest X -ray can show if the heart is enlarged, what we call cardiomegaly.

And in really sick patients in the ICU, we might use invasive monitoring pulmonary artery catheters to directly measure pressures like the PAP and PAP.

If those are high, it confirms that backup from the left ventricle.

So once we've confirmed HF with the ECHO, the BMP, the assessment,

what are the immediate goals?

How do we manage this?

Two main goals.

Improve gas exchange and boost perfusion or cardiac output.

For gas exchange, simple things first.

Sit them up, high Fowler's position, get oxygen on them to keep their saturation ideally above 90%.

And then the medications, you mentioned three drug goals.

Right.

Non -surgical management really hinges on drugs that do three things.

Reduce the resistance the heart pumps against afterload, reduce the volume coming back to the heart preload, and sometimes improve the heart's actual squeeze contractility.

Think table 32 .3 in the text, it lays these out nicely.

Okay, reducing afterload, that takes us back to the RAS system, right?

Exactly.

That's why ACE inhibitors, the PROLs like Lysinopril or ARBs, the SARTENS like Losartan are the first line treatment for systolic heart failure, LV dysfunction.

They block that harmful RAS activation leading to vasodilation.

Less resistance means the heart can pump more effectively.

But there's a major warning with starting these.

Huge.

The drug alert is critical.

Start low, go slow.

Especially the first dose can cause a sudden significant drop in blood pressure.

If their systolic BP falls below 90, you need to hold the dose and notify the provider immediately.

It could be dangerous.

And there's that newer combination drug too, the ARNI.

It's a cubitrol, Vulsartan.

Yes, on Dresto.

It's very effective, works on both the RAS system and enhances beneficial natriuretic peptides.

But the crucial point is the timing.

You absolutely cannot give it within 36 hours of an ACE inhibitor.

The risk of angioedema, that severe swelling is too high.

That 36 hour washout period is a key safety fact.

Got it.

36 hours.

OK, so that's afterload.

What about reducing preload the volume?

Here we're talking diet and diuretics.

Sodium restriction is fundamental, usually down to two or three grams a day.

Sometimes fluid restriction too, maybe 1 .5 to two liters a day, especially if they have issues with excessive thirst or severe fluid overload.

And the drugs for volume?

Diuretics.

The heavy hitters are the loop diuretics, like furosemide, LASIX, or bumetanide, BMX.

They work fast and effectively to pull off fluid.

But the big watch out?

Potassium.

Hypokalemia.

And dehydration, especially in older adults who might already have decreased their sensation.

So monitor electrolytes, monitor kidney function, monitor for orthostatic hypotension.

For patients in later stages, stages three or four, we often add spironolactone.

It's potassium sparing, so it helps counteract the potassium loss from loops.

And it also has some benefit in blocking aldosterone's negative effects.

OK.

And the third goal, enhancing contractility, the squeeze.

Where does digoxin fit in now?

Digoxin.

Its role has changed.

It used to be first line.

Now it's more of a second line agent.

It does increase contractility and it slows the heart rate, which can be beneficial.

But toxicity risk.

Exactly.

It is a very narrow therapeutic window.

And hypokalemia, low potassium, which those loop diuretics can cause, makes the heart much more sensitive to digoxin, increasing the risk of toxicity.

And the signs of toxicity are subtle.

Very subtle and easily missed, especially in older adults.

Things like anorexia, fatigue, confusion, vision changes, blurry or yellow green halos.

But the real danger is it can cause serious, even fatal heart rhythm problems like PVCs or worse.

So monitoring levels, potassium and patient symptoms is key.

So if digoxin is tricky, what else helps with the long term picture, reversing that SNS damage?

That's where beta blockers come in.

Drugs like Carverdalol or Metoprolol succinate, really the long axing form.

They're crucial because they actually reverse some of that harmful remodeling caused by chronic sympathetic overstimulation.

But you have to be careful starting them too.

Extremely careful.

You start with incredibly low doses and increase very, very slowly over weeks or months.

The goal is to gradually lower the resting heart rate down to maybe 55 or 60 beats per minute.

Too much too soon can actually worsen HF symptoms initially.

Patience is key.

Beyond drugs, what other non -surgical options are there?

Well, CPAP is important for patients who also have sleep apnea, which often goes hand in hand with HF.

Then there's cardiac resynchronization therapy, CRT, or biventricular pacing.

This involves a special pacemaker that coordinates the pumping of both ventricles, which can significantly improve EF and symptoms in select patients, usually those with more severe HF class 3, and evidence of dyssynchrony on ECG.

And that implantable monitor?

Cardiomems.

Right, the cardiomem system.

It's a tiny sensor implanted in the pulmonary artery that wirelessly transmits daily pressure readings.

This is pretty cool because it allows us to detect rising pulmonary pressures that fluid buildup before the patient even feels symptoms like shortness of breath or gains weight.

So you can adjust meds earlier.

Yeah.

Prevent hospitalizations.

That's the idea.

Proactive management based on pressures, not just symptoms.

And for people with truly end -stage heart failure, when medications aren't enough, we have ventricular assist devices or VADs.

These are mechanical pumps that take over the work of the failing ventricle.

As a bridge to transplant, or sometimes long -term.

Exactly.

Either a bridge to transplant while waiting for donor heart, or increasingly as destination therapy for patients who aren't transplant candidates but need long -term support.

Okay, we need to pause here and address the absolute emergency.

Pulmonary edema.

You mentioned the pink frothy sputum.

This is life -threatening.

It is.

A true critical rescue situation.

The left ventricle just fails catastrophically.

Pressure skyrockets in the pulmonary vessels and fluid floods the air sacs, the alveoli.

What are the absolute key signs we need to recognize instantly?

Rapid onset of severe dyspnea.

Feeling like they're suffocating, often very anxious.

Ociclation reveals crackles spreading rapidly up the lung fields.

They might become confused or disoriented.

That can be an early sign in older adults due to hypoxia.

Tachycardia is common.

And that classic sign.

Coughing up large amounts of frothy pink tinged sputum.

Their BP might be high initially, but can crash later.

Commediate actions.

What do we do first?

And this is important.

If their blood pressure is stable, not hypotensive, the absolute first move is positioning.

Get them sitting upright, high -fowers position, with their legs dangling down over the side of the bed, if possible.

Why the legs down?

Gravity.

It helps pool blood in the legs, decreases venous return to the overloaded heart, produces preload.

Then high flow oxygen immediately, aiming for high saturation.

Then comes the rapid medication push.

IV diuretics.

Nitroglycerin.

Exactly.

Fast acting IV loop diuretics like ferosemide or bimetinide to pull off fluid quickly.

And IV nitroglycerin, if their systolic BP is over 100, to vasodilate and reduce both preload and afterload.

Maybe morphine too, cautiously for anxiety and vasodilation.

It's an all hands on deck situation.

Shifting gears slightly, but still related to heart function valvular heart disease.

What causes these valve problems typically?

Historically, rheumatic fever was a big cause, leading to rheumatic carditis that damages valves.

Now, especially in developed countries, it's often more related to degenerative changes, just wear and tear over time, calcification, particularly with aortic stenosis, or sometimes congenital defects.

Let's focus on aortic stenosis, since the text highlights it as most common in the US.

What's the core issue there?

The aortic valve opening narrows, becomes stiff.

This obstructs blood flow out of the left ventricle.

The key concept here is it creates a fixed cardiac output.

The heart literally cannot pump more blood out, even when the body demands it, like during exercise.

And that leads to specific symptoms.

The classic triad, usually brought on by exertion, dyspnea, shortness of breath, angina, chest pain because the thick heart muscle isn't getting enough oxygen, and syncope, fainting because the brain isn't getting enough blood flow.

Once symptoms appear, especially syncope, the prognosis worsens dramatically without intervention.

And there's a critical point where surgery becomes urgent.

Yes, when that valve opening shrinks down to one square centimeter or less, that's severely stenotic,

and surgery, usually valve replacement, is needed promptly.

Regardless of the specific valve issue, what's a universal precaution for anyone with valve disease or a repaired valve?

This is absolutely crucial.

Antibiotic prophylaxis.

They must get prophylactic antibiotics before certain procedures, most notably invasive dental work or any significant oral procedures.

Why?

To prevent infective endocarditis.

Bacteria from the mouth can easily travel to the damaged or artificial valve and set up a dangerous infection.

That's a huge patient teaching point.

What about blood clots?

Big risk, especially with mitral valve disease.

Michael's stenosis or regurgitation often leads to atrial fibrillation, AFib.

When the atrium quivers, instead of beating properly, blood can pool and form clots, which can then travel anywhere, causing a stroke if they go to the brain.

So patients with valve disease and chronic AFib need long -term anticoagulation, usually with warfarin.

And surgery isn't always open heart anymore, right?

No, the options have really expanded.

For aortic stenosis, especially in older or higher risk patients, transcatheter aortic valve replacement, TAVR, is becoming much more common.

The valve is replaced via catheter, usually through the groin, no need to crack the chest.

And for severe mitral regurgitation, there's the metroclip, another catheter -based procedure to help the valve close better.

But if they do have traditional surgery and get a replacement valve, the type of valve makes a huge difference long term.

Absolutely fundamental difference.

If they get a mechanical valve made of durable materials like carbon,

it can last a lifetime.

But it requires lifelong anticoagulation with warfarin.

And not just any anticoagulation.

The target INR range is usually higher, often 3 .0 to 4 .0, increasing bleeding risk.

Versus a tissue valve.

A biologic valve, made from animal tissue like cow or pig, or sometimes human tissue, don't typically require long -term anticoagulation beyond the initial post -op period.

That's a big advantage.

But the trade -off is durability.

They usually only last about 7 to 10 years, sometimes longer now, but eventually they degenerate and need replacing again.

Okay, let's quickly cover cardiac infections.

Infective endocarditis, i .e.

you mentioned the risk with valve disease.

What else causes it?

It's a microbial infection, usually bacterial, of the heart's inner lining, the endocardium, often involving the valves.

While valve disease is a risk factor, a major driver of rising incidents currently is injection drug use.

Sharing contaminated needles introduces bacteria directly into the bloodstream.

And the biggest danger with IE?

The vegetations.

These are clumps of bacteria, platelets, fibrin, that form on the infected valve.

They're fragile and pieces can easily break off and travel through the bloodstream they embolize.

And these emboli cause problems wherever they land.

What signs should we look for?

Exactly.

Beyond the typical infection signs like recurrent fever, chills, fatigue, and maybe a new or changed heart murmur, you have to look for evidence of emboli.

Tiny ones can cause pedicure, those little pinpoint purplish spots on the skin, mucous membranes, or conjunctiva,

or splinter hemorrhages, reddish -brown lines under the fingernails.

And larger emboli.

Larger emboli cause organ damage, depending on where they go.

Sudden flank pain and blood in the urine could mean a renal infarction, kidney.

Sudden neurologic changes weakness, slurred speech, confusion could indicate a cerebral embolus, basically a stroke or TIA.

Sharp abdominal pain could be a splenic infarct.

You have to think systemically.

Okay, what about pericarditis?

Inflammation of the sac around the heart?

How does that pain differ from, say, angina?

The pain description is key.

It's usually a substantial sharp grating.

But the classic feature is that it's worse when taking a deep breath or coughing.

And importantly, it's often relieved by sitting up and leaning forward.

That postural change is a big clue.

And we listen for something specific.

You listen for a pericardial friction rub.

It's a scratchy sound, heard best with the diaphragm of the scathoscope, often with a patient leaning forward.

It's caused by the inflamed layers of the pericardium rubbing against each other.

But pericarditis can lead to a serious complication if fluid builds up.

Yes, if fluid accumulates rapidly in that pericardial sac, called a pericardial effusion, it can lead to cardiac tamponade.

This is an emergency.

The fluid pressure squeezes the heart, preventing it from filling properly, and cardiac output plummets.

What are the key signs of tamponade?

Vextriode.

Vextriode is the classic description.

Jugular venous distension, JVD, because blood can't get into the right heart.

Muffled or distant heart sounds because the fluid dampens them.

And hypertension because the cardiac output is so low.

And there's that pulse finding.

Pulse is paradoxes.

Right.

Pulse is paradoxes.

This is an exaggerated drop in systolic blood pressure more than 10 mmHg during inspiration.

Normally, systolic BP drops slightly when you breathe in, but in tamponade, it's a much bigger drop because the filling of the right heart during inspiration further compresses the already squeezed left ventricle.

And the treatment is immediate drainage.

Yes, pericardiosynthesis.

A needle is inserted into the pericardial sac to withdraw the fluid and relieve the pressure.

It's life -saving.

All right.

Let's round out the pathologies with cardiomyopathies.

These are diseases of the heart muscle itself.

Exactly.

Chronic conditions affecting the myocardium.

The main types are dilated, hypertrophic, and restrictive.

Dilated cardiomyopathy, TCM, is the most common.

The ventricles enlarge, become thin -walled and weak like an overstretched balloon.

The heart can't pump effectively.

And management for DCM is similar to heart failure.

Generally, yes.

The goals and medications, ACE inhibitors, beta blockers, diuretics, maybe digoxin, are largely the same as for systolic heart failure, aiming to reduce symptoms and improve function.

But hypertrophic cardiomyopathy, HCM, is different, and there's a really important drug warning.

Very different.

HCM is often genetic, characterized by thickening of the heart muscle, particularly the septum between the ventricles.

This thickening can actually obstruct blood flow out of the left ventricle, especially during exertion.

And it carries a high risk.

Yes.

Tragically, HCM is a leading cause of sudden cardiac death in young athletes.

Many people are asymptomatic until a catastrophic event.

So what's the critical medication difference?

What can we not give?

This is vital.

Drugs that are standard for regular heart failure vasodilators, like nitrates, diuretics, and positive inotropes, like digoxin, are generally contraindicated in obstructive HCM.

Why?

Because decreasing preload with diuretics or nitrates or increasing contractility with digoxin can actually make the outflow obstruction worse.

So what do we use for HCM?

We use drugs that relax the heart and slow the heart rate to improve filling and reduce the obstruction.

So beta blockers are first line.

Calcium channel blockers, like verapamil, can also be used.

We want negative inotropic effects here, the opposite of what we usually want in HF.

Fascinating difference.

And for end -stage cardiomyopathy, both dilated and restrictive types, what's the ultimate treatment?

Heart transplantation.

It remains the definitive therapy for eligible patients with end -stage heart failure from DCM or restrictive cardiomyopathy when medical management fails.

So transplanted heart has unique physiology nurses need to know.

Absolutely.

The key thing is the transplanted heart is denervated.

The nerve connections are severed during surgery.

This means it won't respond to normal autonomic signals or certain drugs the way a native heart does.

Like atropine.

Exactly.

Atropine won't increase the heart rate.

Digoxin's effects are altered.

The resting heart rate is usually higher because there's no vagal tone.

If bradycardia occurs post -op, they might need isoproterenol or even pacing.

It also means patients might not experience typical angina pain with ischemia.

And of course, the lifelong risks are infection due to immunosuppression and rejection.

Okay, we've covered a massive amount the mechanics of failure, valves, infections, muscle diseases.

Let's bring it back to the bedside and discharge planning.

What are the absolute must -knows for patients managing HF at home?

This is where nursing makes a huge difference in preventing readmissions.

Consistent, clear self -management teaching is key.

We often use the acronym M .I .W .D .S.

to structure this teaching.

It covers the five essential pillars.

Okay, walk us through M .I .W .D .S.

again, hitting that critical symptom alert.

Sure, M is for medications.

Take them exactly as prescribed.

Don't skip doses.

Know the side effects.

And crucially, avoid NSAIDs like ibuprofen or naproxen.

They cause sodium and water retention and can worsen HF.

Got it.

A.

A is for activity.

Stay active.

Encourage regular exercise like walking, but teach them to know their limits.

Rest when needed.

Don't push through symptoms.

W.

We know this one.

W is for weight.

Daily weights.

First thing in the morning, same scale.

After voiding before eating.

This is non -negotiable for tracking cluit status.

D is for diet.

Follow the prescribed sodium restriction, usually 2 -3 grams per day.

Read labels.

And adhere to any fluid restrictions if ordered.

And finally, S.

The critical part.

S is for symptoms.

They need to know exactly what symptoms to report immediately to their provider.

The big one is rapid weight gain.

Typically 3 pounds in a week or 1 -2 pounds overnight.

That signifies fluid retention.

Also, any sudden increase in shortness of breath, new chest pain, increased swelling, or waking up breathless, PND.

They need to call right away, not wait.

A.

That rapid weight gain 3 pounds a week, 1 -2 overnight, that's the trigger.

D.

That's the key action trigger for seeking help.

A.

And just telling them isn't enough.

Right.

How do we make sure they actually understand MADWDS before they leave the hospital?

D.

We have to use the teach -back method.

It's not just asking, do you understand?

It's asking them to explain it back to you in their own words.

Okay, can you tell me when you need to call the doctor about your weight?

Or how will you track your sodium intake?

So you confirm comprehension.

A.

Exactly.

It identifies any gaps in understanding before they go home during that really vulnerable transition period.

Doing teach -back well is probably one of the most effective things we can do to reduce those bounce -back hospital readmissions for HF.

D.

It really brings it all together.

We've journeyed deep into the heart's struggles.

Failure, valvular issues, infections,

cardiomyopathies, that central theme of perfusion.

It's woven through everything.

A.

It absolutely is.

And at the end of the day, whether you're titrating an ACE inhibitor based on blood pressure, listening for that subtle S3 gallop, recognizing the postural relief of pericarditis pain or teaching MADWDS using teach -back,

it all comes down to understanding that fundamental link.

How the heart structure affects its function and how that impacts perfusion to the entire body.

D.

Couldn't have said it better.

Well, thank you for joining us on this deep dive into these vital cardiac concepts.

Hopefully you feel well -informed and ready to apply this knowledge.

Go forth.