Nursing Care and Pathophysiology of COPD (Chronic Obstructive Pulmonary Disease)

Pathophysiology:
COPD stands for chronic obstructive pulmonary disease and includes emphysema, chronic bronchitis, and asthma. In a healthy individual air sacs are elastic and expand as the person inhales. When the healthy individual exhales the air sacs will then deflate. In COPD the air sacs are not as stretchy and are damaged with inflammation and thickness. The airways become obstructed with mucus. These factors make breathing and gas exchange a challenge.

Nursing Points

General

Emphysema
1. Destruction of alveoli due to chronic inflammation
2. Decreased surface area for gas exchange
Chronic Bronchitis
1. Chronic airway inflammation with productive cough
2. Excessive sputum production

Assessment

Barrel chest – expanded rib cage due to ↑ work of breathing and air trapping.
Accessory muscle use
Adventitious breath sounds
1. Diminished
2. Crackles
3. Wheezes
Congestion on Chest X-ray
ABG → ↓ pH, ↑ pCO2, ↓ PaO2

Therapeutic Management

Do NOT give O2 > 2 lpm
1. Stimulus to breathe = ↓ O2
Chest Physiotherapy (CPT)
1. Loosen secretions
Increase fluid intake (3 L / day)
1. Thin secretions
Medications
1. Bronchodilators
2. Corticosteroids

Nursing Concepts

Oxygenation
1. Listen to lungs
2. Monitor SpO2 (88-92%)
3. Caution with supplemental O2 – Do not give excessive supplemental O2 – aim for SpO2 88-92% only
Gas Exchange
1. Monitor ABG
2. Monitor for s/s CO2 toxicity
  1. ↓ LOC
  2. ↓ RR
Comfort
1. Encourage position of comfort

Patient Education

Smoking Cessation
Small, frequent meals
Identify and avoid triggers
Pursed lip breathing – helps complete expiration

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ADPIE Related Lessons

Related Nursing Process (ADPIE) Lessons for Nursing Care and Pathophysiology of COPD (Chronic Obstructive Pulmonary Disease)

Assess Lessons

Gas Exchange

Assess Lessons

Alveoli & Atelectasis

Assess Lessons

Lung Sounds

Assess Lessons

Thorax and Lungs Assessment

Assess Lessons

Adult Vital Signs (VS)

Assess Lessons

General Assessment (Physical assessment)

Assess Lessons

Head to Toe Nursing Assessment (Physical Exam)

Diagnose Lessons

Pulmonary Function Test

Diagnose Lessons

X-Ray (Xray)

Diagnose Lessons

COPD (Chronic Obstructive Pulmonary Disease) Labs

Diagnose Lessons

Red Blood Cell (RBC) Lab Values

Diagnose Lessons

Hemoglobin (Hbg) Lab Values

Diagnose Lessons

Hematocrit (Hct) Lab Values

Diagnose Lessons

White Blood Cell (WBC) Lab Values

Diagnose Lessons

Platelets (PLT) Lab Values

Diagnose Lessons

ABG (Arterial Blood Gas) Interpretation-The Basics

Diagnose Lessons

ABGs Nursing Normal Lab Values

Diagnose Lessons

Respiratory Acidosis (interpretation and nursing interventions)

Diagnose Lessons

ABG (Arterial Blood Gas) Oxygenation

Diagnose Lessons

Base Excess & Deficit

Diagnose Lessons

ABGs Tic-Tac-Toe interpretation Method

Diagnose Lessons

ROME – ABG (Arterial Blood Gas) Interpretation

Plan Lessons

Nursing Care Plan (NCP) for Chronic Obstructive Pulmonary Disease (COPD)

Implement Lessons

Hierarchy of O2 Delivery

Implement Lessons

Disease Specific Medications

Albuterol (Ventolin) Nursing Considerations

Implement Lessons

Salmeterol (Serevent) Nursing Considerations

Implement Lessons

Fluticasone (Flonase) Nursing Considerations

Implement Lessons

Sympathomimetics (Alpha (Clonodine) & Beta (Albuterol) Agonists)

Implement Lessons

Anti-Infective – Macrolides

Implement Lessons

Anti-Infective – Penicillins and Cephalosporins

Implement Lessons

Anti-Infective – Fluoroquinolones

Evaluate Lessons

Chronic Obstructive Pulmonary Disease (COPD) Case Study (60 min)

Supplemental Lessons

COPD Concept Map

Supplemental Lessons

COPD management Nursing Mnemonic (COPD)

Supplemental Lessons

Nursing Care Plan (NCP) for Impaired Gas Exchange

Supplemental Lessons

Steroids – Side Effects Nursing Mnemonic (6 S’s)

Transcript

Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, we’re going to be discussing chronic obstructive pulmonary disease. Also known as COPD. We’re going to dive a little bit into the patho, as well as some signs and symptoms and how we’re going to treat our patients. Without further ado, let’s dive in.

Now regarding some patho around COPD. It’s important to think about CIPD like being a tourniquet for the lungs, right? You have these bronchioles that come down and terminate in these alveoli, right? What is occurring in COPD is we have a chronic constriction, tightening, narrowing of these airways, of these bronchioles. Which as these tighten and narrow and clamp down, you’re having a decreased inside lumen, right? A more narrow pipe. What’s going to happen as a result of this, right? This is like a tourniquet on the lungs. I hope that makes sense. We’re tightening up these airways. So what’s going to happen as a result? In chronic obstructive pulmonary disease, we are chronically retaining CO2. We’re chronically having high CO2. Remember from our ABGs video, our CO2, in this instance, is going to be abnormal. It’s going to be chronically high. It’s going to be greater than 45, in patients with COPD. What’s happening here, basically, is as we have this tourniquet on our airways, we’re getting O2 in, but we’re having a lot of difficulty getting CO2 out, right? And as a result what’s going to occur is CO2 is going to build up. And we’re also going to have continual buildup of O2 in these alveoli. As we’re getting more pressure in, but we’re having difficulty getting that pressure out. So what ends up occurring as a result is you actually have destruction of the walls of the alveoli. Think about it as a hyperinflated balloon, right? More and more O2, more and more pressure increasing inside of these alveoli, pushing on the walls of the alveoli, eventually leading to the destruction of the alveolar wall. And this ends up leading to larger alveoli and fewer alveoli.

Some causes of COPD, the biggest one, the biggie is smoking, right? This is the one that you need to be most concerned with. Smoking actually accounts for more than 75% of all COPD cases, of all patients who have COPD, greater than 75%, were caused from smoking. That is the big one. Also long-term exposure to lung irritants, right? An irritant, a foreign body, in the lungs, right, that you’re inhaling. A long-term exposure to these lung irritants leads to that chronic constriction of the airways, leads to COPD. Genetics as well as asthma. There’s a predisposition to possibly developing COPD if you have asthma, although a low, low proportion of people who have asthma actually develop COPD. And then also age. Patients, people who are greater than 40 years old are at a higher probability of developing COPD as well.

So what are some common assessment findings in patients with COPD? Well, some clinically significant things that we may end up seeing with patients are these top two, right? Barrel chest, clubbing of the fingers. Patients develop what looks like a more rounded thorax, right? As they basically use their accessory muscles over a long period of time, over a long period of time, they’re having difficulty getting oxygen in, they’re having difficulty getting CO2 out a tourniquet is on those lungs. And as a result, they’re using all of these accessory thoracic muscles that ends up leading to the development of barrel chest. Also clubbing of the fingers. As we have chronic hypoperfusion of these distal phalanges of the fingers, this is going to lead to the actual structural change in the shape of the fingers, looking like finger clubbing. Some adventitious lung sounds that we’re going to hear, what patients are going to have a cough, but we’re going to hear wheezing, right? Whenever we actually listen to those lung sounds, we may hear wheezing as we have air trying to pass through an incredibly narrow pipe, right? Also, we could also hear diminished lung sounds in general. This is also classic for patients with COPD. Less ventilation, less movement of air, less air movement to actually be auscultated diminished lungs. We could also see abnormalities on chest x-rays, CTs of the chest, as well as something that we’re going to be certainly mindful of, our arterial blood gases. Remember in patients who have COPD, they are chronically retaining CO2. Their CO2 is chronically high, greater than 45. And as a result, we’re going to usually be checking frequent ABGs on them. Make sure that you check out our video on ABGs if you’re not sure what I’m talking about, but this is actually a cellular look through the lens of how well a patient is oxygenating as well as how well they’re getting rid of CO2.

So how are we going to treat patients with COPD? Well, one could be through the use of something such as bronchodilators, right? This could be like medication such as theophylline, any bronchodilators that you may have researched in pharm. Remember that we have these narrow airways that are feeding into these alveoli. We have this tourniquet on the lungs, right? Well, we need to loosen up that constriction, right? We need to loosen that up. So what we do is we end up administering these bronchodilators, which dilate these airways. They dilate these bronchi and these bronchioles to allow more air to move in and out of those alveoli. We can see things such as steroids being given, right, steroids. Remember, what do steroids do? They reduce inflammation, and in patients who have COPD, whether that chronic constriction, we’re going to see inflammation in these airways. We want to reduce that inflammation. Overall, dilate the airway, reduce inflammation so air can more easily flow in and out. Of course, patients who have COPD, they have low O2, but we want to make sure that we’re supplementing them with oxygen. But it’s also a caveat with COPD to know that patients who have COPD are now CO2 dependent. They’re no longer dependent on oxygen in their body. So if we actually give too much oxygen, this can kill your respiratory drive and lead to apnea. It’s a caveat, but something important to remember. You may also see chest physiotherapy, actual mechanical physiotherapy of the chest to try and break up any secretions that may be forming in those lungs. And we also want to increase fluid intake to maybe thin any secretions that may be forming in the lungs as a result of this chronic obstruction.

How are we going to educate our patients? Of course, smoking cessation is the biggest one, right? Remember greater than 75% of all patients with COPD, it’s from smoking. So we want to make sure that we educate patients on smoking cessation. Proper use of inhalers, those bronchodilators. We want to make sure that we’re educating our patients on the proper use of inhalers, as well as increasing those fluids to try and break up those pulmonary secretions, as well as ensuring that they go to any follow-up appointments that they may have with their pulmonologists.

And so summarizing some key points from COPD. Remember in COPD, what we have is a tourniquet on those lungs, right? A chronic constriction of the airways, making it difficult to get O2 into the alveoli, but making it especially difficult to get rid of CO2. Remembering that there are several different causes, but that smoking is our culprit cause of COPD. Knowing our assessment findings, right, barrel chest from chronic use of those accessory muscles when breathing, clubbed fingers from chronically low O2 to those fingers, all of these are a constellation of symptoms caused by that chronic obstruction. Knowing that our therapeutic management is geared at relieving the obstruction, relieving this constriction, right, through the use of bronchodilators, reducing inflammation through the use of steroids, also O2 delivery and the patient education, which we just discussed.

Guys, that was COPD. I hope that it helped make more sense of it. And I hope that you use this information as you carry forward in nursing school. Guys, go out there and be your best selves today. And as always, happy nursing.