Chapter 27: Concepts of Care for Patients With Noninfectious Lower Respiratory Problems

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Welcome back to The Deep Dive.

Today we're jumping into a really important area, non -infectious chronic lower respiratory problems.

It's a cornerstone of MedSurg nursing.

Absolutely.

We've got a lot of ground to cover, pulling from key nursing concepts and specific guidelines for managing these conditions.

And our goal here is to give you that essential framework.

Right, because fundamentally every single one of these disorders messes with the body's priority concept, gas exchange.

It's all about that.

When those lower airways, the bronchi, the alveoli get impaired, oxygen just can't get in effectively.

Exactly.

And that hits gas exchange right there in the lungs, but it also impacts perfusion all through the body.

And we'll keep coming back to related ideas too, won't we?

Like inflammation.

Definitely.

Inflammation is a huge driver.

And cellular regulation, especially when we talk about diseases that destroy tissue or cancer later on.

So the specific conditions we're focusing on are asthma, COPD, cystic fibrosis.

Pulmonary arterial hypertension, or PAH, adipatic pulmonary fibrosis, IPF, and lung cancer.

Quite a list.

Let's start with asthma.

It's probably the one folks encounter most often.

That's good.

Okay, so asthma.

How do we actually define it?

And, you know, what's happening inside the airways during an attack?

I know there are kind of two main things going on.

That's right.

Clinically, we define it as a chronic disease.

But the key is intermittent, reversible airway obstruction.

It's a dual mechanism.

Right.

First, you've got underlying inflammation.

The airway lining swells up, makes extra mucus, and that physically blocks the tubes.

Okay, inflammation.

And the second part?

That's airway hyperresponsiveness.

The smooth muscles around the airways basically spasm, that's bronchoconstriction, and squeeze the airways narrow from the outside.

So it's getting blocked from the inside and squeezed from the outside.

Exactly.

That double whammy is what causes the acute symptoms.

Now triggers.

We all know about allergens, smoke, maybe cold air.

But the sources mention a couple of less obvious ones.

First, NSAIDs, like ibuprofen.

Yeah, that's a really important one.

And the key is you don't have to be allergic to the NSAID.

Right.

How does that work, then?

It's about biochemistry.

NSAIDs can shift chemical pathways in the body, boosting the production of leukotrienes.

And leukotrienes are powerful bronchoconstrictors.

So no allergy needed, just that chemical shift.

Huh.

Interesting.

And the other one was GERD, acid reflux?

Yes, gastroesophageal reflux disease.

If stomach acid refluxes up and gets into the airway, especially when someone's lying down at night,

it can really irritate those already sensitive airways and trigger asthma symptoms.

That's often why people have worse asthma at night.

Makes sense.

So during an attack, we hear the wheezing, usually worse on breathing out, right?

See the fast breathing, using extra muscles.

Definitely.

Those accessory muscles kicking in, retractions.

You see that struggle.

But what about long term?

If someone has severe, poorly controlled asthma for years,

what visible change might we see in their chest structure?

That's where you might see the barrel chest.

It comes from chronic air trapping.

Because they struggle to get air out, the lungs stay overinflated.

So the chest kind of expands over time.

Exactly.

The front to back diameter, the AP diameter, starts to equal the side to side or lateral diameter.

Normally it's more like a 1 to 1 .5 ratio.

Seeing that 1 to 1 ratio is a big clue for long standing, severe air trapping.

Okay, got it.

So we see these signs.

What about lab tests like ABGs during a bad attack?

What do they show?

Arterial blood gases are crucial.

Initially, the patient might be breathing really fast, hyperventilating, trying to compensate.

So early on, their PECO2 might actually be low.

Oh, right.

Blowing off CO2.

Yeah.

But as the attack gets worse, they get tired, they can't keep up that work of breathing,

air gets trapped, they can't exhale effectively, and the PECO2 starts to rise.

So a really bad sign, CO2 retention.

And the oxygen level.

The PO2, oxygen will be low.

That's hypoxenia.

That's pretty much always there in the significant attack.

And for diagnosis, pulmonary function tests, PFTs, are key because they show that reversibility we talked about.

What's the number we need to remember?

The magic number is 12%.

So during an assessment, their FEV1 or peak expiratory flow might be down say 15 or 20 % from their baseline.

But the diagnosis of asthma is confirmed when you give them a rescue inhaler, a bronchodilator, and those numbers improve by 12 % or more.

That quick bounce back shows the obstruction is reversible.

That reversibility is so fundamental.

And it leads straight into management, focusing on that personal asthma action plan.

Patients have to know the difference between their meds.

Absolutely critical.

They need to understand control therapy drugs versus reliever drugs.

Explain that difference.

Control drugs, like inhaled corticosteroids, are taken every day, even when feeling fine.

They work long -term to reduce that underlying inflammation and hyperresponsiveness, basically preventing attacks.

Okay, the preventers.

Right.

Then you have the reliever or rescue drugs.

These are usually the short -acting beta -2 agonists, SEBAs like albuterol.

They work fast to relax those smooth muscles and open the airways during an attack.

Only use when needed.

Got it.

Preventers daily, rescuers for attacks.

Now, there's a really important safety warning about one class of preventer drugs, the long -acting ones.

Yes, the drug alert for labas, the long -acting beta -2 agonists is super important.

What's the alert?

ABIAs should never be used alone for asthma therapy.

They must always be paired with an inhaled corticosteroid.

And crucially, they are not rescue drugs.

They don't work quickly enough for an acute attack.

So using a LABA during an attack is dangerous.

Extremely dangerous.

It gives a false sense of security while not actually relieving the acute bronchospasm effectively.

They're purely for long -term control, taken on schedule.

Misusing them can have dire consequences.

Wow.

Okay.

And even with the right drug, how they take it matters immensely, right?

Inhaler technique.

Oh, hugely.

The sources really emphasize this.

Studies show error rates with inhalers, MDIs, DPIs, the soft -missed ones are incredibly high.

Critical errors are common.

So what's the nursing role there?

We have to teach and then reteach and use that teach -back method.

Watch the patient use their inhaler.

The sources mentioned that videos like the ones drug companies provide can be really effective tools for showing correct technique.

Good tip.

Okay.

One last thing on asthma.

The absolute emergency status asthmaticus.

Right.

This is basically an asthma attack that just won't quit.

It doesn't respond to the usual rescue inhalers.

It's life -threatening.

What's the immediate plan?

Aggressive treatment.

IV fluids, potent IV bronchodilators, systemic steroids, high flow oxygen.

It's all hands on deck.

And is there one really ominous sign we need to watch for?

Yes.

If a patient was wheezing loudly and then suddenly the wheezing stops,

that's terrifying.

It often means the airways are now completely obstructed, no air moving at all.

That's a precursor to respiratory arrest.

Wow.

Sudden silence is deadly.

Okay.

Let's shift gears to COPD.

All right.

COPD.

Our main gas exchange exemplar, it's really an umbrella term, isn't it?

Covering chronic bronchitis and emphysema.

Exactly.

They often occur together, but they damage the lungs in slightly different ways, both leading to airflow limitation that's not fully reversible, unlike asthma.

So let's break them down.

What's the primary issue in chronic bronchitis?

Chronic bronchitis is all about the airways themselves, the bronchi and bronchioles.

It's caused by irritants, mostly smoking, leading to chronic inflammation.

Like asthma, but chronic.

Sort of, but the result is different.

The bronchial walls thicken, glands produce way too much thick mucus, and those smaller airways get plugged up.

This creates a huge mismatch between air getting in and blood flow, leading to low oxygen hypoxemia and high carbon dioxide hypercapnia.

Plus all that mucus is a breeding ground for infection.

Okay.

So inflammation, mucus, blockage.

How does emphysema differ?

Emphysema is more about destruction of the lung tissue itself,

specifically the elastic tissue in the walls of the alveoli, the tiny air sacs.

What does losing that elastic tissue do?

It means the lungs lose their natural ability to spring back or recoil during exhalation.

Air gets trapped deep inside.

This leads to hyperinflation, that over -expanded lung state.

The diaphragm gets flattened, making breathing even harder work.

And critically, those alveolar walls break down, meaning less surface area for gas exchange.

So less space for oxygen and CO2 to swap.

Got it.

Now, COPDB puts a huge strain on the heart, right?

Tell us about cor pulmonel.

Yes, that's a major complication.

Cor pulmonel is right -sided heart failure caused by lung disease.

How does that happen?

Well, the chronic low oxygen and damage in the lungs cause the blood vessels in the lungs to constrict and narrow.

This increases the pressure in the pulmonary artery.

The right ventricle of the heart has to pump harder and harder to push blood through those high -pressure vessels.

Eventually just wears out and fails.

That makes sense.

The biggest risk factor for COPD is obviously smoking.

Overwhelmingly, yes.

Cigarette smoking is number one.

But there's a genetic condition that can cause severe COPD, even in young nonsmokers.

Right, and it's often missed.

That's alpha -1 -antitrypsin, AAT deficiency.

AAT is a protein that normally protects the lungs from damage by enzymes called proteases.

If you inherit faulty genes and don't make enough functional AAT, these proteases basically chew up the lung tissue, especially that elastic tissue, leading to early and severe emphysema.

So important to consider, even if the patient says they never smoked, clinically, how might these patients look when they come in?

They're often quite thin, maybe lost muscle mass because breathing takes so much energy.

You'll frequently see them sitting leaning forward in that tripod or orthopnaic position.

Trying to make breathing easier.

Exactly, using gravity to help expand the chest.

You might also see that barrel chest we discussed, the 1 .1 AP to lateral diameter from the chronic hyperinflation.

And later signs of chronic low oxygen could include cyanosis, maybe sluggish capillary refill, and definitely finger clubbing.

Okay.

Management -wise, improving gas exchange is priority one.

Breathing techniques are key.

You mentioned pursed lip breathing earlier.

Why is that one so helpful for CRPD?

It's incredibly effective.

By breathing out slowly through pursed lips, like whistling, the patient creates a little bit of back pressure inside their airways.

Okay, a positive pressure.

Yes, and that positive pressure helps keep the smaller airways from collapsing prematurely during exhalation.

This allows them to push out more of that trapped stale air and reduces that feeling of breathlessness.

It prolongs exhalation.

Simple but powerful.

Now let's tackle the oxygen issue.

There used to be this big fear about giving oxygen to COPD patients who retained CO2, thinking it would knock out their drive to breathe.

What's the rule now?

That's largely outdated thinking, thankfully.

The clinical consensus now is clear.

Hypoxia kills.

You must treat the low oxygen.

Okay.

So all hypoxic patients, including those with COPD and known hypercarbia, should receive oxygen.

The key is careful titration.

The goal is generally to maintain their oxygen saturations, PO2, between 88 % and 92%.

Not necessarily aiming for 100%, but ensuring adequate oxygenation.

88 % to 92%.

That's the target range.

Good.

What about medications similar to asthma?

The classes of drugs are similar bronchodilators, sometimes corticosteroids, but the emphasis in COPD is really on long -acting maintenance therapy.

Lab Bs, long -acting muscarinic antagonists, or LAMAs, often combination inhalers, are the mainstays to keep airways open day to day.

Makes sense.

And for very specific cases of emphysema, there's even surgery.

Yes, lung volume reduction surgery, or LVRS.

It's for a select group of patients with severe emphysema, predominantly in the upper lobes.

They remove the most diseased hyperinflated parts of the lung.

What's the goal there?

By removing that non -functional overinflated tissue, it allows the remaining healthier lung tissue and the diaphragm to work more effectively.

But the criteria are, strict patients need to be ambulatory, have stopped smoking for at least six months, and meet specific PFT criteria.

Right.

One last crucial nursing point for COPD,

preventing weight loss.

Why is that such a challenge?

It's tough.

They burn a huge number of calories just breathing.

That increased work of breathing is exhausting.

But at the same time, feeling short of breath makes eating difficult, and they often feel full quickly.

So what's the advice?

High calorie, high protein foods are essential.

But instead of big meals, recommend small, frequent meals and snacks throughout the day.

And here's a key tip.

Advise them to use their bronchodilator inhaler about 30 minutes before eating.

Ah, to open things up before they eat.

Exactly.

It can reduce breathlessness during the meal, making it easier to take in enough nutrition.

And don't forget,

vaccinations, annual flu shots, and pneumococcal vaccines are vital for preventing exacerbations.

Okay.

Let's move into some of the more specialized conditions now, starting with cystic fibrosis, CF, that this is genetic, right?

Yes.

Autosomal recessive.

The basic problem is a faulty gene that leads to blocked chloride transport in cells.

And what does that faulty chloride transport cause?

It results in the production of incredibly thick, sticky mucus.

While it affects multiple organs, like the pancreas, the biggest impact is usually on the lungs.

How so?

That thick mucus plugs up the airways, making it really hard to clear secretions.

This leads to chronic inflammation and critically recurrent and persistent bacterial infections.

The most common bug is Pseudomonas aeruginosa.

Eventually, this progressive lung damage leads to respiratory failure, which is still the main cause of death in CF.

That sounds relentless.

What does daily management involve?

It's intense.

Daily therapy is non -negotiable.

It typically includes inhaled bronchodilators to open airways, mucolytics to help thin the mucus, and then rigorous chest physiotherapy, CPT.

Is that the vest thing?

Often, yes.

Many patients use a high -frequency chest wall oscillation vest, which vibrates at high speed to help shake that thick mucus loose so it can be coughed out.

It's a cornerstone of care.

Now, there's been exciting progress with new drugs for CF, right?

The source mentioned gene therapies.

They're not quite gene therapy, but they are CFTR modulators, drugs like ivacaftor, lumicaftor, or combinations.

They work on the faulty protein that the gene creates.

How do they help?

For patients with specific CF mutations, these drugs can actually help the faulty CFTR protein work better, improving that chloride transport.

This makes the mucus less thick and sticky.

They've been game changers for eligible patients, but they are incredibly expensive.

The source mentioned around $250 ,000 a year.

Wow.

A huge cost, but potentially life -altering.

Next condition,

pulmonary arterial hypertension, PAH.

Right.

Primary PAH is high blood pressure, specifically in the pulmonary arteries.

The vessels going from the heart to the lungs.

Often, the cause is unknown idiopathic.

And the consequence.

That high pressure puts an enormous strain on the right side of the heart, leading to that cor pulmonale we talked about, which is often fatal in PAH.

The treatment involves some pretty serious drugs and a major safety warning.

Absolutely.

Drug therapy is complex, often involving anticoagulants like warfarin and potent vasodilators like endophilin receptor antagonists or prostacyclin agonists.

Many patients require continuous 5E infusion of prostacyclin agents.

And the critical safety alert.

This is a critical nursing safety priority.

For patients on continuous 5E prostacyclin infusions like traprosynol, any interruption of that infusion, even for a few minutes, can be fatal.

Fatal in minutes.

Yes.

These drugs have incredibly short half -lives.

Stopping the infusion causes rebound pulmonary hypertension,

right heart failure, and potentially death very quickly.

So what does that mean for nursing care and patient teaching?

Meticulous attention to detail.

The patient and family must understand this risk.

They need to know how to manage the pump, always have backup drug cassettes ready, keep battery packs charged, and know exactly what to do with the pump alarms.

And the IV line itself.

Because it's a central line, often running 2047 for years,

strict aseptic technique is paramount to prevent bloodstream infections, sepsis, which these patients are very vulnerable to.

Okay.

Incredibly high stakes there.

Let's touch on idiopathic pulmonary fibrosis, IPF.

What's the core issue here?

IPF is a restrictive lung disease, meaning the lungs can't expand properly.

It's thought to be a problem of cellular regulation, basically.

Excessive wound healing or scarring runs amok in the lungs.

So the lung tissue gets scarred and thick.

Exactly.

That fibrosis thickens the alveolar walls, making them stiff and severely impairing gas exchange.

Sadly, the prognosis is generally poor, maybe only two, three years on average after diagnosis.

What can be done?

Treatment focuses on trying to slow down the scarring process with newer anti -fibrotic drugs like ninted nibib or profanidone.

Otherwise, it's mainly supportive care, oxygen therapy, pulmonary rehab to maximize function, energy conservation techniques, and sometimes morphine for severe breathlessness or dyspnea.

A tough diagnosis.

Finally, let's cover lung cancer.

Still the leading cause of cancer deaths, largely because it's often diagnosed late.

And the biggest risk factor, overwhelmingly.

Smoking.

Cigarette smoking is linked to something like 80 % of lung cancer deaths.

But secondhand smoke and chronic exposure to inhaled irritants like asbestos or radon are also major risks.

When surgery is an option like removing a lobe, lobectomy, or a whole lung pneumonectomy, what's the critical post -operative management piece?

Closed chest drainage.

Almost always.

Chest tubes.

Okay, tell us about managing chest tubes.

What are we looking for?

After lung surgery, you need the chest tube system to drain fluid or air from the pleural space and help the remaining lung re -expand.

The standard system has three chambers.

One collects drainage, one provides the water seal, and one connects to suction.

What does the water seal do?

It acts like a one -way valve, allowing air to bubble out of the chest, but preventing air from being sucked back in.

You need at least two centimeters of water in that chamber for it to work.

And what are the key things a nurse needs to monitor with that system?

Three main things.

First, titling.

You should see the water level in the water seal chamber gently rise and fall, with the patient's breathing.

That tells you the tube is patent and pressure changes are being transmitted.

What if titling stops?

It could mean the lung has fully re -expanded, which is good.

Or it could mean the tube is blocked or kinked, which is bad.

Needs investigation.

Okay.

Second thing.

Look for air leaks.

Occasional bubbling in the water seal when the patient coughs might be okay initially.

But continuous, vigorous bubbling suggests a persistent air leak, either from the lung or the system itself.

That needs to be addressed.

Got it.

And the third.

Monitor the drainage.

Note the amount, color, consistency.

A sudden cessation of drainage, especially in the first 24 hours when you expect some, could signal a clot blocking the tube.

Also ensure the drainage collection chamber doesn't get so full that fluid backs up into the tubing.

So titling, air leaks, and drainage.

Crucial post -op care.

Hashtag, tag, outro.

Absolutely.

So looking back across all these conditions, asthma, COPD, CF, PAH, IPF, lung cancer,

the common thread is that constant struggle to maintain gas exchange.

It really comes back to that core concept every time.

And effective nursing care relies on understanding those specific nuances we talked about.

Hitting that 88 to 92 % spio 2 target in COPD, mastering inhaler technique in asthma, the absolute vigilance needed for PAH infusions.

It's all tailored.

It really is.

So maybe the final thought to leave listeners with.

Think about the person living with these diseases day to day.

It's not just about the pathophysiology or the drugs.

Consider the sheer mental load and constant planning involved.

Timing your inhaler 30 minutes before you try to eat.

Making sure you always have your rescue inhaler within reach,

247.

Or managing a complex life -sustaining pump and knowing a mistake could be fatal in minutes.

It's an immense burden.

It really is.

These chronic, often progressive conditions take a huge toll physically and emotionally.

So our role as nurses goes way beyond just the tasks.

It's about supporting coping, helping manage the anxiety that inevitably comes with breathlessness, and really integrating that self -management education so it becomes part of their life, not just instructions on a page.

Well said.

Always remember that holistic impact when you're caring for these complex pulmonary patients.

Thank you so much for walking us through all of that today.

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