Nurse’s Guide to COPD: Patho, Assessments, Diagnosis, Interventions, & Medications

COPD

 

Chronic obstructive pulmonary disease (COPD) is the 8th leading cause of hospitalization in the United States and the 3rd leading cause of death. Nurses are involved with COPD care across the spectrum, from outpatient and home care education to intensive care and hospice management. COPD is a disease characterized by airflow limitation that is not fully reversible. COPD includes diseases that obstruct airflow, including emphysema and chronic bronchitis. Separate diseases like asthma, cystic fibrosis, and bronchiectasis were previously classified as types of chronic obstructive lung disease. Current guidelines place asthma in a separate category designated as an abnormal airway condition involving reversible inflammation.

Chronic bronchitis is defined as the presence of a chronic productive cough for a 3-month period during 2 consecutive years. Emphysema is defined as an abnormal, irreversible enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls. Airflow limitation in emphysema is due to loss of elastic recoil of the interstitial tissue that aids in exhalation. Chronic bronchitis is characterized by a narrowing of airways and an increase in airway resistance. Although these are 2 discrete diseases and some patients may display signs of both, most fall somewhere in the middle of the spectrum between the 2 conditions.

CAUSES

Risk factors for COPD include environmental exposures and host factors. Exposure to tobacco smoke accounts for an estimated 80 – 90% of all cases. Other risk factors include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution, and outdoor air pollution, which adds to the total burden of inhaled particles. The following are possible causative factors in COPD:

  • Cigarette Smoking: Induces macrophages to release neutrophil chemotactic factors and elastases, which destroy tissue integrity and elasticity. The lack of tissue elasticity compromises the patient’s ability to exhale sufficient volume at a necessary speed leading to air trapping.
  • Secondhand Smoke: Increases the risk of respiratory infections, increases asthma symptoms, and leads to appreciable reductions in pulmonary function.
  • Alpha 1 Antitrypsin Deficiency: Genetically susceptible patients become sensitive to environmental factors (smoking, pollution, allergens, etc.) and in time develop COPD symptoms. Carriers must be identified early to reduce exposure and delay symptoms. Alpha-protease inhibitor replacement therapy slows the progression.

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  • Environmental Exposure: Long-term exposure from living near highly-trafficked areas creates exposure to air pollution and may produce COPD symptoms, especially in patients with asthma.
  • Airway Hyperresponsiveness: Patients who have nonspecific airway hyperreactivity and also smoke are at a significantly higher risk of symptoms of COPD.
  • Intravenous Drug Abuse: Approximately 2 – 3% of people who abuse IV drugs will develop emphysema secondary to pulmonary vascular damage produced by impurities injected directly into the circulatory system and carried to the lungs.
  • Connective Tissue Disorders: Marfan syndrome and other connective tissue disorders can harm elastin, collagen, and other connective tissues responsible for the dynamics of passive breathing.

PATHOPHYSIOLOGY

In COPD, limited airflow is both progressive and associated with an abnormal inflammatory response to irritating particles and gases in the lungs. The inflammatory response occurs throughout the airways, parenchyma, and pulmonary vasculature. Narrowing of the airways occurs as the body attempts to repair the changes related to chronic inflammation. Eventually, scarring takes place due to this repeated process.

Airflow obstruction may also be due to parenchymal destruction from emphysema, most notably in the alveoli. Emphysema results in permanent enlargement of airspaces distal to the terminal bronchioles. This creates a decline in alveolar surface area as the walls between individual alveoli are destroyed. Elastic recoil is lost in this process as well as support structure. Airflow becomes limited when the lungs fail to deflate efficiently and surrounding tissue collapses, impeding movement of air.

Chronic bronchitis is characterized by deformed airways and narrow lumens. Airway structural changes include ciliary abnormalities, atrophy, smooth muscle hyperplasia, inflammation, and bronchial wall thickening. As damage accumulates to the mucociliary elevator, mobilization of secretions becomes difficult. Distortion of the airways from fibrosis warps their shape, creating a unique setting for the collection of mucous as well as mucous plugging.

Hyperinflation is the central mechanism that produces shortness of breath in this patient population. The ability for a patient with COPD to inhale is not altered. However, expelling air is hampered by damaged airways. During exercise or exertion the patient’s respiratory rate may rise creating less time to exhale before the next inhalation. The patient’s lungs begin to air-trap as a result of the unmet demand for additional time to exhale through poorly functioning airways. The oxygen is quickly extracted from this trapped air. The patient may become hypoxemic, especially if emphysema is present because the surface area needed to extract oxygen is significantly reduced in the alveoli.

EPIDEMIOLOGY & PROGNOSIS

In 2011, an estimated 12.5 million adults in the U.S. had COPD. However, under-diagnosis leads experts to believe that the number may be closer to 24 million based on documented impaired lung function. That same year, 10.1 million Americans had a diagnosis of chronic bronchitis. The highest rate of chronic bronchitis was in older adults age 65 years or greater. Emphysema affects a total of 4.7 million people. The prevalence of COPD varies considerably by state, from < 4% in Washington to > 9% in Alabama. Based on spirometry results, studies have determined that approximately 1 in 5 patients older than 30 years with at least a 10-year history of smoking are likely to have COPD.

A clinical scoring system was developed called the BODE index. This system was developed to approximate a patient’s risk of death or hospitalization. The point system is as follows:

  • BMI
    • > 21 = 0
    • < 21 = 1

 

  • FEV 1(post-bronchodilator % predicted)
    • > 65% = 0
    • 50-64% = 1
    • 36-49% = 2
    • < 35% = 3

 

 

  • Modified Medical Research Council (MMRC) dyspnea scale
    • MMRC 0: Dyspneic on strenuous exercise
      • 0 points
    • MMRC 1: Dyspneic on walking a slight hill
      • 0 points
    • MMRC 2: Dyspneic on walking level ground, must stop occasionally due to breathlessness
      • 1 point
    • MMRC 3: Dyspneic after walking 100 yards or a few minutes
      • 2 points
    • MMRC 4: Cannot leave house; dyspneic doing activities of daily living
      • 3 points

 

  • Six-minute walking distance
    • > 350 meters = 0
    • 250-349 meters = 1
    • 150-249 meters = 2
    • < 149 meters = 3

 

The predicted 4-year survival based on the BODE index:

  • 0-2 points = 80%
  • 3-4 points = 67%
  • 5-6 points = 57%
  • 7-10 points = 18%

 

SIGNS & SYMPTOMS

A mixture of symptoms of reactive airway disease, emphysema, and chronic bronchitis are usually present in patients diagnosed with COPD. The following symptoms are typically found in this patient population:

  • Wheezing
  • Productive cough
  • Dyspnea
  • Respiratory infection

 

The following physical signs are present in more advanced stages of COPD:

  • JVD
  • Cyanosis
  • Dyspnea and tachypnea on exertion
  • Accessory muscle use
  • Peripheral edema

 

Chest exam:

 

  • Wheezes, crackles, & decreased breath sounds
  • Prolonged expiratory period
  • Hyperinflation
  • Percussive hyper-resonance

 

Chronic bronchitis:

  • Productive cough
  • Obesity & Cyanosis (“blue bloater”)
  • Accessory muscle use
  • Right-sided heart failure with edema
  • Wheezes & Rhonchi

 

Emphysema:

  • Non-productive cough
  • Cachexia
  • Barrel chest with significant air-trapping
  • Pursed-lip breathing (“pink puffer”)
  • Hyper-resonance in chest

 

NURSE ASSESSMENT

 

  • History: An accurate history, which will assist with the differential diagnosis, should include:

 

  • Family history of heart and lung disease
  • Childhood diseases
  • Environmental exposures to gas and dust
  • Occupational exposure
  • Tobacco use:
    • 1 pack-year = 20 cigarettes/day for 1 year
    • 10 pack-year = 1 pack/day for 10 years
  • Oxygen saturation: Goal pulse oximeter > 92%
  • ABG:
    • pH < 7.2 consider invasive or non-invasive positive pressure ventilation strategies
    • PaCO2 > 55 mmHg assess baseline and pH for correlation
    • PaO2 < 60 mmHg consider supplemental oxygen, be mindful of O2-induced hypoventilation
  • Infection:
    • temperature
    • sputum volume, color, tenacity, and smell
    • mucous membranes for hydration
    • palpate tactile fremitus
  • Skin:
    • cyanosis
    • clubbing
    • edema
  • Breathing:
    • dyspnea
    • pursed lip breathing
    • symmetrical chest expansion
    • intercostal retractions
    • tracheal deviation
    • respiratory rate > 20 bpm
    • ability to speak
    • tripod position: use of arms to press down and raise rib cage to produce greater diaphragmatic downward excursion
  • Breath Sounds:
    • rhonchi
    • wheezing
    • crackles
    • diminished/absent
  • Chest X-ray:
    • pulmonary congestion: heart failure
    • pneumothorax
    • secretions consolidation: infection
    • blunted costophrenic angle: hyperinflation
  • LOC: somnolence can be a byproduct of hypercapnia, exhaustion, or both. Patient may be in danger of impending respiratory failure
  • Level of Activity: exercise tolerance
  • Sleep Patterns: orthopnea may indicate right-sided heart failure and pulmonary congestion when recumbent
  • Nutrition:
    • obesity with chronic bronchitis
    • cachexia with emphysema
    • bowel sounds diminished from shunting of blood to more vital organs during periods of hypoxia
    • oral hygiene may lead to lowered appetite
  • Knowledge:
    • breathing exercises
    • coughing & deep breathing
    • oral care
    • risk for infection
    • triggers
      • cold air
      • pollen
      • smoke
    • smoking cessation
    • alternating rest & activity
    • pursed lip breathing
    • follow-up care
    • oxygen safety
    • inhaler technique

 

DIAGNOSIS

  • Arterial Blood Gas
    • May have mild to moderate hypoxemia
    • Hypercapnia develops with progression of disease
    • Renal compensation occurs with chronically elevated PaCO2 as evidenced by increased HCO3 & normalized pH
    • pH < 7.2 signals acute distress
  • Hematocrit
    • Polycythemia may develop due to chronic moderate hypoxemia
    • Hct > 52% for males, and 47% for females
  • Serum Chemistry
    • May retain Na
    • Diuretics & Beta-adrenergics may decrease K
    • Beta-adrenergics decrease Ca & Mg
    • Monitor increased HCO3 as a sign of compensated respiratory acidosis
  • B-Type Natriuretic Peptide
    • Elevation can differentiate CHF exacerbation from COPD
  • Alpha-1 Antitrypsin
    • AAT < 11 mmol/L can explain COPD symptoms in patients < 40 yrs
  • Cytologic Exam
    • Rule out malignancy
  • Sputum Sample
    • Chronic bronchitis = mucoid
    • Purulent = presence of neutrophils
    • Increased production = exacerbation
    • Streptococcus pneumoniae & Haemophilus influenza are common
  • Chest X-ray
    • Emphysema = hyperinflation, flattening of diaphragm, diminished heart shadow (pictured below)
    • Chronic bronchitis = bronchovascular markings & cardiomegaly

Emphysema2008

  • Bronchogram
    • Shows cylindrical dilation of bronchi on inspiration
    • Shows bronchial collapse on forced expiration (emphysema)
    • Show enlarged mucous ducts (chronic bronchitis)
  • Six-Minute Walking Distance
    • Part of BODE index described above
    • Desaturations predict mortality rates
  • Exercise ECG/Stress Test
    • Evaluate effectiveness of bronchodilator therapy
    • Plan & evaluate exercise regimen
    • Assess degree of pulmonary dysfunction
  • Pulmonary Function Test (PFT)
    • Total lung capacity = increased
    • Functional residual capacity = increased
    • Residual volume = increased
    • Vital capacity = decreased
    • FEV1 = no increased response to bronchodilator therapy
    • Carbon monoxide diffusing capacity (DLCO) = decreased with emphysema
    • FEV1/FVC = < 80%

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NURSE MANAGEMENT

The ultimate aim of care is to increase or maintain the patient’s functional status. Management focuses on optimizing lung function, avoiding infection, adhering to treatment schedules, and avoiding exacerbations. Education is essential for patient investment and ownership of treatment.

  • Ineffective Airway Clearance
    • Assist patient to comfortable position
    • Remove environmental gas, dust, smoke, micro-fibers
    • PO fluids 3000 mL/day between meals
    • Mucolytics: N-acetylcysteine

 

  • Impaired Gas Exchange
    • Elevate HOB
    • Provide rest
    • Encourage pursed-lip breathing
    • Encourage cough and suction PRN
    • Provide O2 if SpO2 < 92%
    • Home O2 for sustained PaO2 < 55 mmHg, educate on fire safety
    • Non-invasive positive pressure ventilation (NIPPV) = CPAP or BiPAP

 

  • Imbalanced Nutrition
    • Frequent oral care
    • Drink before or after meals
    • No carbonated beverages (bloating)
    • Supplemental O2 during meals

 

  • Risk for Infection
    • Encourage coughing & deep breathing
    • Document temp. & sputum character
    • Use spacer & rinse/spit after corticosteroid inhaler
    • Administer antibiotics as ordered

 

  • Smoking Cessation
    • Personalize the message
    • Choose quit date
    • Educate on expected effects: increased mucous production, lethargy, anxiety
    • Inquire about social support
    • Follow-up support from health care team or support group
    • Pharmacological support: chantix, wellbutrin, nicotine patch, etc.

 

  • Airway Inflammation
    • Inhaled corticosteroids
    • Azithromycin

 

  • Vaccination
    • Pneumococcal vaccine for all patients > 65 years
    • Influenza annually for all COPD patients

 

MEDICATIONS

– Albuterol

  • Trade Name: Proventil, Ventolin, Proair
  • Indication: Acute bronchospasm
  • Action: Relaxes bronchial smooth muscle by activating beta-2 receptors with slight effect on beta-1 and heart rate, dilate bronchial airways
  • Class: Beta-2 agonist
  • Considerations:
    • 1 – 2 inhalations q4 – 6h
    • Duration 3 – 6h
    • May cause tremor or tachycardia
    • Take last dose several hours before bedtime
    • Review proper inhaler technique with patient

– Salmeterol

  • Trade Name: Serevent Diskus
  • Indication: Prevention of COPD or asthma related bronchospasms
  • Action: Long-acting beta-2 agonist stimulates receptors and relaxes bronchial smooth muscle with little effect on heart rate
  • Class: Beta-2 agonist
  • Considerations:
    • 2 inhalations aerosol (42 mcg) or 1 powder diskus (50 mcg) b.i.d. 12h apart
    • Duration 12h, do not use for acute asthma
    • Withhold and notify physician if bronchospasms occur after use
    • May cause tachycardia
    • Monitor LFT’s
    • Take 30 – 60 min prior to exercise

– Ipratropium

  • Trade Name: Atrovent
  • Indication: COPD
  • Action: Parasympatholytic agent that inhibits vagally mediated reflexes by antagonizing acetylcholine leading to bronchodilation
  • Class: Anticholinergic, Respiratory
  • Considerations:
    • 2 inhalations of MDI q.i.d. at no less than 4h intervals
    • Not intended for PRN use due to delayed onset
    • Anticholinergic effect may lead to blurred vision, nausea, dry mouth, and constipation
    • May change urinary pattern in older adults
    • Review proper inhaler technique with patient

– Fluticasone

  • Trade Name: Flovent
  • Indication: COPD, Asthma
  • Action: Exhibits anti-inflammatory effects on neutrophils, eosinophils, macrophages, mast cells, and histamine
  • Class: Corticosteroid
  • Considerations:
    • Inhaled powder 100 – 250 mcg q12h
    • Rinse mouth after use to prevent oral candidiasis
    • May increase intraocular pressure with cataracts and glaucoma
    • Adrenal insufficiency may occur after abrupt withdrawal
    • May suppress growth in children
    • Immune-suppression possible with long term use

– Prednisone

  • Trade Name: Rayos
  • Indication: Acute exacerbation of COPD
  • Action: Elicits mild mineralocorticoid activity and moderate anti-inflammatory effects by suppressing migration of PMN’s and fibroblasts, reversing capillary permeability, and stabilizing lysosomes
  • Class: Corticosteroid
  • Considerations:
    • PO 40 mg q12h X 3 – 5 days
    • Can lead to immune-suppression with prolonged use, monitor for poor wound healing
    • Give at mealtime to avoid gastric irritation
    • Do not abruptly stop, reduce dose gradually
    • Monitor BG, weight, sleep patterns, and blood pressure closely
    • Monitor for adrenal suppression
    • Monitor bone density

– Albuterol/ipratropium

  • Trade Name: Combivent
  • Indication: COPD patients who require second bronchodilator
  • Action: Bronchodilation through beta-2 adrenergic and anticholinergic mediated antagonization of vagal reflexes
  • Class: Respiratory inhalant combo
  • Considerations:
    • Aerosol 100 mcg/20 mcg 1 puff q6h, not to exceed 6 per day
    • Anticholinergic effect may lead to blurred vision, nausea, dry mouth, and constipation
    • May change urinary pattern in older adults
    • May cause tremor or tachycardia
    • Take last dose several hours before bedtime
    • Review proper inhaler technique with patient

– Budesonide/formoterol

  • Trade Name: Symbicort
  • Indication: COPD uncontrolled with mono-therapy
  • Action: Decreased inflammation of airways through inhibition of inflammatory cells and long-acting beta-2 adrenergic agonism with rapid onset leading to bronchodilation
  • Class: Respiratory inhalant combo
  • Considerations:
    • 160 mcg/9 mcg (2 puffs of 80 mcg/4.5 mcg) q12h
    • Implement step-down therapy as soon as possible to prevent long-term issues with corticosteroids like immune-suppression, adrenal suppression, and decreased bone density
    • Not for relief of acute asthma symptoms
    • Monitor blood pressure and heart rate
    • Rinse mouth after using to avoid oral candidiasis
1 reply
  1. GatorNation
    GatorNation says:

    I hadn’t hear of the bode index before, thanks.
    also wasn’t sure what pack year history meant. Nice free resource, ty.

    Reply

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