Chapter 38: Heart Failure Nursing Care

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Welcome to the Deep Dive.

Today we're tackling a really central topic in medsurg nursing, heart failure.

We'll be drawing from resources like Lewis's to pull out the absolute essentials for you.

Our goal here is pretty clear.

Make the why behind heart failure click.

Connect the symptoms to what you'll actually see and really nail down those key nursing actions.

It's foundational stuff, you know, for exams, sure, but really for taking care of patients.

Absolutely.

Heart failure, HF, it's a complex clinical picture.

It's basically the heart not being able to pump enough oxygenated blood for what the body needs and that kicks off a whole cascade, lower cardiac output, tissues not getting enough perfusion, major fluid balance issues.

It's a huge health problem and yeah, the number one reason older adults end up hospitalized.

So understanding it inside and out is crucial for nurses.

Okay, so when we say heart failure, sometimes people think the heart just stops working entirely.

That's not quite it, is it?

Can you break down what we really mean and maybe touch on that key measure, the LVEF?

Yeah, that's a common misconception.

It hasn't stopped.

It's just failing to pump effectively.

It's not meeting the demand and the left ventricular ejection fraction, LVEF, that's our main metric here.

It tells us, you know, what percentage of blood the left ventricle pushes out with each beat.

Normally that's somewhere between say 55 % and 65%.

That's our baseline.

From there, we mostly talk about two main types of left -sided heart failure because that's usually where it starts.

First is heart failure with reduced ejection fraction, HFREF.

You might know it as systolic HF.

Here, the heart muscle itself is weak it just can't squeeze hard enough.

So the LVEF drops usually below 40%.

I think causes like a previous heart attack, maybe uncontrolled high blood pressure making the heart pump against resistance or different cardiomyopathies and clinically blood backs up usually into the lungs.

Okay, a weak pump.

Exactly.

Then there's the second type, heart failure with preserved ejection fraction, HFPEF or diastolic HF.

Now this one's interesting.

The squeeze, the pump strength might actually be normal.

The problem here is filling.

The ventricles are stiff.

They can't relax properly during diastole to fill up with blood.

So less blood in means less blood out even if the squeeze is okay.

So it can't fill up right.

Precisely.

And the main driver for this one, hypertension but also older age, being female, diabetes, obesity,

they all play a role.

So it's either that weak squeeze with HFREF or the stiff fill with HFPEF.

That distinction really helps clarify things.

Now what about right -sided heart failure?

How does that fit in?

Does it usually follow the left side?

Great question.

And yes, most commonly right -sided HF happens because of left -sided HF.

It's the most common cause by far.

See, when the left ventricle fails, blood backs up into the lungs.

That increases the pressure in the pulmonary arteries.

So the right ventricle is suddenly pushing against much higher resistance trying to get blood into those congested lungs.

Oh, okay.

So it gets overworked.

Exactly.

Over time, that constant strain just weakens the right ventricle and eventually it starts to fail too.

And when the right side fails, the backup is different.

Now the fluid backs up into the body's venous system.

So you start seeing those classic signs, peripheral edema, swelling in the legs, ankles, maybe the sacrum or even scrotum.

You might see a sites, which is fluid in the abdomen, an enlarged liver, hepatomegaly, and a really key sign, jugular venous distension, JVD, those bulging neck veins.

Right, the systemic backup sign.

Yeah.

Though sometimes you can get isolated right -sided HF from other things like a right ventricular heart attack or a big pulmonary embolism, but the left -sided failure causing it is much more common.

And if both sides are failing, that's biventricular failure.

This is clearly a massive issue.

You mentioned over 6 million adults in the U .S.

and rising.

Leading cause of hospital admission over 65 linked to one in eight deaths.

Those are serious numbers.

What are the main risk factors we really need to be focusing on?

The scale is huge.

And the two big ones, the primary risk factors are hypertension, high blood pressure, and coronary artery disease or CAD.

Hypertension is particularly key because it's modifiable.

We know that really getting blood pressure under control can slash the incidence of heart failure by about 50%.

That's massive.

50%.

Yeah.

Then you add in other things, diabetes, metabolic syndrome, getting older, smoking.

They all contribute significantly.

And sometimes there's genetic component, especially with certain cardiomyopathies.

Okay.

So the heart's struggling,

but the body doesn't just sit there, right?

It tries to compensate.

Can you walk us through those compensatory mechanisms?

Because I understand they can actually end up making things worse long -term.

That's exactly right.

This is where it gets really fascinating physiologically.

The body has these immediate responses, these survival mechanisms that are initially helpful, but when they stay activated chronically, yeah, they become part of the problem.

It's that double sword.

So the first big one is the neurohormonal response.

When cardiac output dips, the kidneys sense they're not getting enough blood flow.

That triggers the renin angiotensin aldosterone system,

RAAS.

You remember the system?

Right.

It releases angiotensin the second, which is a powerful vasoconstrictor, tightens up blood vessels.

It also triggers aldosterone and ADH release.

The goal, hold on to sodium and water, increase blood volume, increase preload, trying to boost that cardiac output short -term.

It may be helpful, but chronically, you've got constant vasoconstriction, chronic fluid overload, and angiotensin the second even has direct toxic effects on heart muscle, promoting that harmful remodeling and fibrosis.

Okay.

So RAAS is one major player.

What else?

Then there's the sympathetic nervous system, the SNS, fight or flight.

Low blood pressure signals the SNS to release catecholamines epinephrine nor pinephrine.

This speeds up the heart rate, increases contractility.

Again, a quick fix to try and maintain output.

Like flooring the gas pedal.

Exactly.

Like flooring the gas on an engine that's already sputtering.

The sustained SNS activation dramatically increases the heart's oxygen demand.

It puts tremendous strain on an already weakened muscle.

Makes sense.

Then the heart itself tries to adapt.

We see ventricular adaptations.

One is dilation.

The chambers literally enlarge.

The muscle fibers stretch to hold more blood.

Think of the Frank Starling law up to a point.

More stretch means a stronger contraction.

But only up to a point.

Right.

Stretch it too far and it just gets baggy and ineffective like an old rubber band.

Yeah.

The other adaptation is hypertrophy.

The heart muscle actually thickens, gets bigger, trying to generate more force.

Initially, that might help the contraction,

but hypertrophied muscle becomes stiff.

It doesn't contract well long -term.

It needs more oxygen and it's much more prone to developing dangerous arrhythmias.

So bigger isn't necessarily better here.

Not in the long run.

And all of this, the chronic RAS, the chronic SNS, the dilation, the hypertrophy leads to ventricular remodeling.

This isn't just getting bigger.

It's a pathological change in the heart's actual shape and structure.

It tends to become less elliptical, more rounded, more like a sphere.

Which is a terrible shape for pumping efficiently.

Exactly.

It becomes a much less effective pump.

LVEF often drops further and the patient's prognosis gets worse.

So the very mechanisms designed to help the heart survive acutely are actually driving the chronic progression of the disease.

That's kind of ironic.

And it really highlights why so many of our drugs aim to block these systems, right?

Like ACE inhibitors blocking RAS, beta blockers blocking the SNS.

Precisely.

That's the core of our neurohormonal blockade strategy in chronic HF management.

But the body does have some counter -regulatory mechanisms trying to fight back against the bad stuff.

Oh, okay.

What are those?

The main heroes here are the natriuretic peptides.

Specifically ANP, atrial natriuretic peptide, and BNP, brain natriuretic peptide.

The heart muscle cells release these when the walls get stretched by too much blood volume.

Their job is essentially the opposite of RAAS.

They promote diuresis getting rid of fluid and natriuresis getting rid of sodium.

They cause vasodilation, relax blood vessels, and they actually inhibit RAAS and ADH release.

So they're trying to balance things out.

Trying to restore balance, exactly.

And clinically, BNP levels are really useful.

High BNP tells us there's significant ventricular stretch and failure.

It even correlates with mortality risk.

We also have things like nitric oxide and prostaglandins helping out with vasodilation too.

Okay, that helps paint the picture of this internal battle.

And I guess whether the detrimental compensatory mechanisms or these counter regulatory ones are winning determines if someone is compensated versus decompensated, which leads us right into how they actually present clinically.

You got it.

When compensation fails, decompensation happens.

And that's when symptoms flare up, often acutely.

All right, let's talk about what that looks like.

What are the signs when someone tips over into acute decompensated heart failure or ADHF?

What does a nurse need a spot right away?

ADHF is often sudden or really traumatic worsening.

Frequently, it presents as pulmonary edema that's fluid flooding the air sacs in the lungs.

A true medical emergency.

Okay, so breathing problems.

Major breathing problems.

You'll see severe dyspnea, shortness of breath, orthopnea.

They can't breathe lying flat.

They need pillows.

Yeah.

And paroxysmal nocturnal dyspnea, PND.

They wake up suddenly at night gasping for air.

Their respiratory rate will be high.

You'll auscultate, listen to their lungs and hear crackles.

Often throughout the fields, they'll likely be very anxious.

Skin might be pale, maybe even cyanotic, bluish.

And in severe cases, they might cough up that classic pink frothy sputum.

Also, look for JVD, that jugular venous distension.

It's a pretty sensitive indicator of high filling pressures in the left ventricle.

Pink frothy sputum.

That's a classic sign.

It is.

Now, we often categorize ADHF presentation using clinical profiles.

The most common one is described as wet and warm.

Wet and warm, meaning?

Meaning they are congested.

They have fluid overload.

That's the wet part.

But their peripheral perfusion is still adequate.

Their skin is warm, pulses are good.

That's the warm part.

Okay.

Let's use a quick scenario.

Say you're assigned a patient with ADHF.

They've got crackles bilaterally in the mid to lower lung fields.

They get short of breath, just moving from the bed to the commode.

But their skin feels warm, pulses are strong.

How would you categorize that?

What does it tell you?

Okay.

Yeah, perfect example for thinking clinically.

Based on that description, crackles, dyspnea mean congestion, wet.

But warm skin and good pulses mean adequate perfusion, warm.

So that patient fits squarely into the wet -warm profile.

Functionally, this suggests they're likely NYHA class 2 or maybe 3 symptoms with mild or ordinary exertion.

And ACC -FAHA stage C structural heart disease with current symptoms.

Knowing that profile helps guide our immediate interventions.

That makes it really practical.

Okay.

So that's the acute flare -up.

What about chronic heart failure, the ongoing progressive condition?

What are the common things we see day in, day out?

Chronic HF is more of a slow burn, a progressive syndrome.

Fatigue is huge, often one of the earliest and most limiting symptoms.

Dyspnea is usually the most common symptom overall.

It gets worse with exertion or even at rest as the HF progresses.

And you'll

know that.

Right.

And the fluid signs.

Definitely.

The edema, we talked about peripheral swelling in ankles, feet, maybe pitting edema where you press and leave an indent.

Also,

potentially sacral or scrotal edema, ascites, hepatomegaly from that systemic backup.

Changes in urine output too, like nocturia having to pee frequently at night as fluid shifts when they lie down.

You might notice skin changes, dusky, cool, clammy skin due to poor perfusion.

And don't forget neurologic changes.

Dizziness, confusion, forgetfulness can happen from reduced blood flow and oxygen to the brain.

Also really important, there's a very high rate of depression in HF patients and that significantly impacts their self -care and overall outcomes.

It's helpful to keep those clusters of symptoms in mind.

So broadly, for chronic left -sided HF,

pulmonary crackles, a shortness of breath.

For chronic right -sided, think systemic venous congestion, the JVD, the swelling, the liver enlargement, weight gain.

That distinction is key for assessment.

Absolutely.

Your assessment needs to capture both sides.

And we use tools like the NYHA functional classification, Classes 1 IV based on how much symptoms limit activity, and the ACCFHA staging system, stages A through D, which emphasizes the progression from risk factors to end stage disease.

These aren't just labels.

They help us track progress and guide therapy.

Okay.

Let's pivot to management.

How do we diagnose HF definitively and what's the nursing process look like, starting with diagnostics and acute care?

Diagnosis always aims to find the underlying cause.

The echocardiogram or echo is really the workhorse here.

It's non -invasive, uses ultrasound.

Gives us that LVEF number.

Exactly.

It shows heart chamber size, wall motion, valve function, and critically gives us that LVEF to help differentiate HFREF from HFPEF.

We also rely heavily on BNP and NT -pro -BMT levels.

These blood tests measure those natriuretic peptides we discussed.

Generally, the higher the level, the more severe the LV failure, but you always interpret them in context.

Other things can affect the levels too.

Right.

Okay.

So someone comes in with ADHD.

What are the immediate nursing priorities?

In ADHD, the goals are rapid symptom relief, getting fluid balance under control, and supporting oxygenation and perfusion.

Priority nursing interventions start immediately.

Get the patient upright, high Fowler's position, often with their feet dangling over the side of the bed.

This helps decrease venous return to the heart, reducing preload.

Take some load off the heart.

Exactly.

Provide supplemental oxygen.

If they're really struggling, they might need non -invasive positive pressure ventilation, like BiPAP, to help keep the airways open and improve gas exchange.

And continuous monitoring is critical.

Vital signs, oxygen saturation, strict intake and output, and daily weight, same time, same scale.

If they're really unstable, we might need invasive hemodynamic monitoring, like a pulmonary artery catheter to measure POPLVP to really fine tune therapy.

Makes sense.

What about the meds in ADHD?

Pharmacologic management is key.

Diuretics are first line for volume overload.

4V loop diuretics like furosemide -lasix are common.

Our job as nurses is huge here.

Monitor urine output closely to see if it's working, assess for symptom relief like easier breathing, and watch electrolytes like a hawk, especially potassium and magnesium, which can drop quickly.

Right.

Got to watch that potassium.

Always.

If the patient isn't hypotensive, vasodilators like IV nitroglycerin or sodium nitroproside can be used.

They reduce both preload and afterload, decreasing the heart's workload, and improving function.

But you have to monitor blood pressure very frequently during infusion.

Okay.

And if the pump is really weak?

If they have really low cardiac output, cardiogenic shock signs, we might use positive inotropes.

Drugs like dobutamine or milrinone, they increase the heart's contractility, make it squeeze harder.

But these are usually short -term fixes for ADHD because they increase myocardial oxygen demand and carry a significant risk of dysrhythmias.

So continuous cardiac monitoring is absolutely essential.

Got it.

Any non -drug therapies in ADHD?

Yeah.

Sometimes if patients are really resistant to diuretics, ultrafiltration or aquiferesis can be used to mechanically remove excess fluid.

And for very unstable patients needing more support, temporary mechanical devices like the intraortic balloon pump, IABP, can reduce afterload and improve coronary blood flow.

Or even short -term ventricular assist devices, VADs, might be used to support the failing ventricle.

That's a lot for the acute phase.

So shifting gears now.

What about managing chronic heart failure day to day?

What's the nursing focus outside of that crisis situation?

Right.

For chronic HF, the focus broadens.

We want to manage their ongoing symptoms, prevent hospitalizations, slow disease progression, improve their quality of life, and ultimately reduce mortality.

The absolute cornerstone of drug therapy here is that neurohormonal blockade we talked about earlier hitting those bad

the RAAS and SNS blockers.

Exactly.

ACE inhibitors like Lisinopril or ARBs like Wasarten are usually first line for HFREF.

They reduce afterload, help prevent that harmful remodeling, and have proving mortality benefits.

Nursing role.

Monitor blood pressure for hypotension, watch for that ACE inhibitor cough, and keep a close eye on potassium levels as they can cause hyperkalemia.

Okay.

What else is in the cocktail?

A major player now is the combination drug secubitrolvulcidin, brand name Entresto.

It's an ARNI angiotensin receptor nipolysin inhibitor.

It offers dual blockade and has shown really significant benefits over ACE SARBS alone for reducing mortality and hospitalizations in symptomatic HFREF.

Then we have aldosterone antagonists like spironolactone or epilarnone.

These are potassium sparing diuretics that also block aldosterone's harmful effects and improve survival in HFREF.

Again, careful potassium monitoring is essential.

So more potassium checks.

Definitely.

And then beta blockers.

Specific ones like metoprolosuccinate, the long -acting form, carvetolol, or bisoprolol.

These block the harmful effects that SNS, decrease mortality, and can actually improve LVEF over time.

The key with the beta blockers is starting low and titrating up slowly, as they can initially worsen symptoms if started too quickly or too high a dose.

Patients need education on that.

Good point.

Any other key drug classes?

Yeah, depending on the patient, we might use iveberdine to specifically lower heart rate if it remains high despite beta blockers.

And more recently, SGLT2 inhibitors, originally diabetes drugs like dapagliflozin, have shown remarkable benefits in HF patients, even those without diabetes.

Interesting how drugs find new uses.

What about devices for chronic HF?

Device therapy is huge too.

For certain HFREF patients whose ventricles aren't beating in sync, cardiac resynchronization therapy, CRT, which is a special kind of pacemaker,

can help coordinate contractions and improve symptoms and LVEF.

And for patients at high risk of life -threatening ventricular arrhythmias, which is common in HF, an implantable cardioverter defibrillator, ICD, is often recommended to prevent sudden cardiac death.

So CRT helps the pump, ICD prevents sudden death.

You got it.

And what's really cool now is that many of these devices allow for remote monitoring.

They can transmit data about the patient's heart rate, rhythm, activity level, sometimes even indicators of fluid status directly to the clinical team.

That sounds like a game changer for catching problems early.

It really is.

It allows for potentially intervening before a patient fully decompensates and needs hospitalization.

It's shifting care towards being more proactive.

That proactive approach seems vital.

Thinking about patient education, which is such a core nursing role, if you had to pick the absolute most critical piece of teaching for chronic HF patients, what would it be?

The thing that really moves the needle.

Oh, that's tough because it's all important.

But if I had to pick one actionable piece, it's probably daily weights and knowing when to call.

Daily weights.

Yes.

Teaching them how to do it consistently, same time, morning, after voiding, before breakfast, same scale, similar clothing.

And then crucially teaching them the specific parameters for calling their provider.

Usually it's a weight game of three pounds in two days or three to five pounds in a week.

Catching that rapid weight gain, which usually signifies fluid retention and intervening can prevent a full blown ADHD episode and hospitalization.

It empowers the patient to be part of their own surveillance system.

And that makes so much sense, giving them a concrete action tied to a number.

What are the other key education points?

Well, diatherapy is huge, especially sodium restriction, typically aiming for around two grams per day.

That means teaching label reading, identifying hidden sodium, finding alternative flavorings.

It's challenging.

Also guiding them on an appropriate activity program,

balancing activity with rest, listening to their body, maybe cardiac rehab, reinforcing the signs and symptoms of worsening HF.

They need to report increased shortness of breath, more swelling, worsening cough, fatigue, and of course, drug therapy, ensuring they understand why they're taking each med, the importance of adherence, how to monitor their pulse and blood pressure if needed, and recognizing signs of potential side effects like hypo or hyperkalemia.

It's a lot to cover.

Let's circle back to that clinical scenario thinking.

Consider NC, our 82 year old with recurrent ADHD and some cognitive impairment.

Her daughter's involved and wants to help.

How do we tailor our teaching here to actually make it stick and reduce those readmissions?

This feels like a real world challenge.

Absolutely.

And it requires adapting our approach.

For NC, relying solely on her memory might not work.

Caregiver engagement is paramount.

The daughter needs to be central to all teaching.

We need to simplify instructions, use clear, simple language, maybe visual aids like a chart for daily weights or a marked pill box, provide written materials, large print if needed, focus on the absolute must do's, daily weights, key symptoms to report, taking medications correctly, maybe involve the daughter in setting up the pill box weekly.

We should also assess the daughter's understanding and ability to help and provide her with support too.

Connecting them with resources like home health nursing or telehealth monitoring could provide an extra layer of safety and reinforcement.

So really empowering the caregiver as a partner.

Exactly.

It's collaborative care in action, especially with cognitive impairment.

That partnership is often the key to preventing decompensation and keeping the patient safe at home.

That's a really practical patient centered approach.

Okay, let's briefly touch on the end of the road for some patients advanced therapies for stage D and the really important, sometimes difficult end of life conversations.

Right.

For patients with end stage or stage D -HF who remain symptomatic despite optimal medical and device therapy, we consider more advanced options.

Mechanical circulatory support, MCS devices, particularly durable ventricular assist devices, VADs, can be long term, sometimes called destination therapy, or as a bridge to get someone strong enough for transplant.

These devices basically take over the pumping function of the weakened ventricle.

Like an artificial heart pump.

Essentially, yes.

The ultimate treatment, though, for eligible patients with end stage HF is heart transplantation, replacing the failing heart with a healthy donor heart.

But this involves really strict selection criteria, finding a suitable donor match, the major surgery itself, and then critical lifelong immunosuppressive therapy afterwards to prevent the body from rejecting the new heart.

Managing infection and rejection, especially in the first year, are major challenges.

A huge undertaking.

And what about when those options aren't feasible or desired?

That brings us to palliative and end of life care, which honestly should be part of the conversation much earlier for many HF patients, given the prognosis can be quite poor in advanced stages.

Palliative care focuses on symptom management, quality of life, and supporting patients and families, regardless of whether they're pursuing curative treatments.

Hospice becomes an option when life expectancy is estimated at six months or less, and the focus shifts entirely to comfort care.

There are specific criteria, like being NYHA class four refractory symptoms, but referring HF patients to hospice can sometimes be tricky.

The disease trajectory isn't always a clear decline.

There can be ups and downs, and patients or families might be reluctant, especially if they have devices like ICDs or have had previous resuscitations.

Those are difficult conversations.

They are.

And the nurse's role in providing compassionate support, facilitating communication about goals of care and ensuring patient comfort and dignity is absolutely invaluable during this time.

So just to kind of wrap up the main takeaways from our dive today, heart failure is incredibly multifaceted.

You need to understand the underlying pump problem, yes, but also those complex compensatory and counter regulatory responses.

As nurses, early recognition of symptoms, whether it's acute decompensation or subtle chronic changes, along with vigilant monitoring, a really robust tailored patient and caregiver education are absolutely key to managing this condition effectively across all settings.

Absolutely well summarized.

This really brings together the core concepts from texts like Lewis's into a clinical context.

I hope everyone listening feels more equipped to think critically about their heart failure patients.

Here's something to ponder as we finish.

Given how much cognitive impairment seemed to affect heart failure outcomes and readmissions, how could we as nurses build proactive cognitive screening and tailored support strategies into all our HF patient education plans right from the start instead of just reacting when problems become obvious?

Something to think about for improving care.

Thank you so much for joining us for this deep dive into heart failure.

Every patient situation is different and your knowledgeable, compassionate care truly makes a difference.

For the deep dive and from all of us at the Last Minute lecture team, thanks for tuning in.