Characteristics of Chronic Bronchitis and Emphysema

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Characteristics of emphysema (a) and chronic bronchitis (b) 1. smoking hx 2. age of onset 3. barrel chest 4. wt. loss: 1. a. usual
b. usual
2. a. 40-50
b. 30-40; disability in middle age
3. a.often dramatic
b. may be present
4. a.may be severe in advanced disease.
b. Infrequent
characteristics of emphysema (a) and c.bronchitis (b) 1. SOB 2. Decreased breath sounds 3. Wheezing 4. Ronchi: 1. a. Characteristic
b. Predominant early symptom, insidious in onset, exertional.

2. a. characteristic
b. variable
3. a. usually absent
b. variable
4. a. usually absent or minimal
b. often prominent
characteristics of emphysema (a) and c. bronchitis (b): 1. sputum 2. cyanosis 3. blood gases 4. cor pulmonale: 1. a. may be absent or may develop late in the course.
b. frequent early manifestation, frequent infections, abundant purulent sputum.
3. a. often absent, even late in the disease when there is low PaO2.
b. Often dramatic
3. a. relatively normal until late in the disease process.
b. hypercapnia may be present, hypoxemia may be present
4. a. only in advanced cases
b. frequent, peripheral edema
characteristics of emphysema(a) and c. bronchitis (b): 1. polycythemia 2. prognosis: 1. a. only in advanced cases
b. frequent
2. a. slowly debilitating disease
b. numerous life-threatening episodes due to acute exacerbations.
1. how does asthma differ from other COPD diseases such as C.B. and emphysema? 2. COPD def.: 1. remission, normal PFT's and ABG's.

2. disease state characterized by presence of airflow obstruction.
1. COPD has airflow limitation that is ____. 2. May be accompanied by__. 3. Not fully __/may be partially __.: 1. progressive
2. airway hyperreactivity
3. reversible
Predisposing factors for COPD (5): 1. cigarette smoking #1 MAJOR risk factor
2. age
3. infection
4. heredity - alpha-1 antitrypsin (AAT) deficiency
5. environmental and occupational exposure (very sm. percentage)
1. __-__% COPD deaths in US r/t tobacco smoking 2. female smokers __X more likely than nonsmokers 3. male smokers __X more likely than nonsmokers 4. after only __yr(s) smoking, changes in __ __ __ can develop.: 1. 80-90%
2. 13
3. 12
4. 1
small airway function
Affects of cigarette smoking on the respiratory system (4): 1. hyperplasis of cells (increase in goblet cells =increased mucous prodn.;decreased airway diameter;increased difficulty in clearing secretions
2. reduces ciliary activity
3. abnormal dilation of distal air space w destruction of alveolar walls
4. decreased AAT (antitrypsin protects lung from injury)
Affects of aging on respiratory system (4): 1. Does not cause but contributes
2. loss of recoil of lungs (elasticity) means not fully exhaling
3. decrease in # of functional alveoli
4. some degree emphysema common in lungs of older persons, even nonsmoker, however, usually NOT clinically significant.
Affects of infection on COPD(3): 1. History of childhood respiratory infections can predispose
2. recurring respiratory tract infections are a major contributing factor to aggravation and progression of COPD
3. COPD patients more prone to respiratory infection (mucus is a medium for bacteria) which intensifies lung tissue destruction and progression of COPD.
Effects of heredity on COPD (3): 1. Alpha-1 antitrypsin (AAT) deficiency only known genetic abnormality that leads to COPD
2. Accounts for less than 1%
of COPD in US
3. Premature emphysema due to lysis of lung tissue by proteolytic enzymes that occur d/t AAT deficiency.
Def. of Emphysema: Pathological term that describes abnormal, permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls.
Pathology of emphysema: 1. Elastin and collagen destroyed by enzymes (proteases) that digest protein
2. air goes into lungs freely but unable to come out on its own and remains in lungs.
3. bronchioles collapse, esp. in expiration and air is trapped in distal alveoli resulting in hyperinflation and over distention of alveoli
4. trapped air gives pt. "barrel-chested" appearance
5. more alveoli destroyed and coalesce (grow together)
6. development of blebs and bullae
7. decreased surface area for diffusion of o2 in blood (dead space=no gas exchange)
Air trapping: Walls of alveoli are made of elastin and collagen; get damaged by protease; pt. can inhale but the air sacs fill up but don't squeeze to push air back out=air trapping. Increases with each inhalation. Plus bronchioles collapse.
Structural changes that occur in emphysema (5): 1. hyperinflation of alveoli
2. destruction of alveolar walls
3. destruction of alveolar capillary walls
4.narrowed tortuous, small airways
5. loss of lung elasticity
(air in but not out)
Clinical manifestations of emphysema(7): 1. dyspnea progressively more severe
2. hypoxemia with exercise (at rest later)- hypercapnia later
3. minimal coughing with little to no sputum
4. flattened diaphragm and increased A-P diameter of chest (barrel shaped chest)
5. chest breather w. sternal movement
6. underweight (more than with chronic bronchitis.
7. cacechtic
Chronic bronchitis is characterized by:: 1. excessive production mucous in bronchi
2. recurrent cough that persists for at least 3 months of the year during at least 2 successive years
Pathophys. of chronic bronchitis: 1. hyperplasia of mucous secreting glands (goblet cells) in trachea and bronchi
2. increase in goblet cells
3. disappearance of cilia
4. chronic inflammatory changes and narrowing of small airways
5. altered function of alveolar macrophages, leading to increased bronchial infections
1. major difference btwn. c.b. and emphysema is:: 1. in chronic bronchitis, the alveolar structure and capillaries remain normal! It's more in the airways.
Pathophysiology of the inflammation associated with chronic bronchitis: 1. chronic inflammation primary pathologic mechanism
2. inflammatory response causes vasodilation, congestion and mucous edema
3. mucous glands stimulated to become hyperplastic
More CB patho: 1. narrowing of __ 2. resistance to __=__ 3. bronchioles are __and__ 4. diminished ___ ___means pts. ___ and retain ___. 5. ___ and ___ develop more frequently in CB than emphysema.: 1. airway lumen
2. airflow; increased WOB
3. clogged and constricted
4. respiratory drive; hypoventilate; CO2
5. hypoxemia and hypercapnia
MORE CB patho: 1. cough stimulated by __ 2. Decreased __, and decreased ___activity 3. secretion removal 4. ___ may develop, due to airway hyperreactivity 5. effect of bronchospasms: 1. retained secretions
2. cilia; mucociliary activity (r/t smoking)
3. cough is ineffective in removing secretions
4. bronchospasms
5. bronchospasms increase airway resistance, further increasing the work of breathing and worsening impaired gas exchange. Worse in winter months.
Clinical Manifestations of Chronic Bronchitis: 1. frequent productive cough during most winter months
2. bronchospasms at end of paroxysms of coughing
3. frequent respiratory infections
4. later, dyspnea on exertion
5. Hx of cigarette smoking many years almost always present
6. normal weight or heavy
7. ruddy appearance r/t polycythemia and cyanosis
More clinical manifestations of Chronic Bronchitis: 1. Cor pulmonale
2. acute exacerbations of chronic bronchitis
3. acute respiratory failure
4. PUD and GERD
5. pneumonia
6. these pts. often sicker, w. earlier onset, more respiratory infections, less wt. loss than emphysema pts.
7. Blue bloaters (emphysema=pink puffers)
1. cigarette smoking will falsely elevate ___. 2. Cor pulmonale: 1. pulse ox readings.

2. Hypertrophy of rt. side of heart with or without heart failure from pulmonary hypertension...pressure on rt. side of heart must increase to push blood into lungs d/t constriction of pulmonary vessels in response to alveolar hypoxia with acidosis further potentiating vasoconstriction.
Signs and Symptoms of cor pulmonale (8): 1. EKG changes
2. heart sound changes (louder pulmonic phase)
3. JVD
4. Hepatomegaly with RUQ tenderness
5. Ascites
6. Epigastric distress (decreased appetite, GERD increased)
7. peripheral edema (pooling, dependent)
8. Weight gain (r/t fluid retention)
Management of Cor Pulmonale (3): 1. continuous low flow oxygen (biggest concern)
2. over CHF - salt restriction
3. diuretics cautiously
Signs and symptoms of acute exacerbation of chronic bronchitis (5): 1. worsened cough
2. hemoptysis
3. wheezing
4. increased SOB
5. Change in amount, color, consistence, or viscosity of sputum
Treatment of acute exacerbation of C.B. (5): 1. antibiotics
2. increase use of bronchodilator
3. possibly corticosteroids (IV for acute)
4. humidification of o2
5. postural drainage and chest pt
Emphysema vs. CB (3): 1. vast majority of patients have a mix of emphysema and c.b.
2. emphysema pts. known as "pink puffers"
3. CB pt. are known as "blue bloaters"
COPD - Diagnostic Tests(6): 1. ABGs
2. CXR
3. EKG
4. Chest examination
5. PFTs/spirometry
6. Hgb and Hct
Expected results in COPD pts: 1. ABGs 2. CXR 3. EKG 4. Chest exam: 1. Can be variable. Hypoxemia; PaSO2 decreased; PaCO2 increased (hypercapnia) late; CO2 more with bronchitis;
2. Emphysema - hyperinflated=flat diaphragm in x-ray; C.G.: atelectasis, enlarged R. heart, fluid
3. changes in both emphysema and C.B.
4. Emphysema - breath sounds are quiet; percussion elicits hyperresonance; C.B - loud breath sounds; percussion elicits dull sound.
Spirometry (3): 1. used to evaluate airflow obstruction
2. determined by ration of FEV1 to FVC
3. COPD defined as FEV1/FVC ratio of less than 70%
COPD Treatment Goals (5): 1. Improve ventilation
2. promote secreton removal
3. prevent complications and progression of symptoms
4. promote pat. comfort and participation in care
5. improve quality of life (most important)
Treatment-smoking cessation (3): 1. most significant factor in slowing progression in early stages
2. pulmonary function generally improves or decline slows
3. decreases cough and sputum production
Treatment of COPD involves: (6): 1. broncholdilator drugs
2. corticosteroids
3. oxygen
4. breathing retraining/pulmonary rehabilitation
5. chest physiotherapy
6. nutritiional therapy
1. Which medication for COPD has been shown to modify the long-term decline in lung function? 2. What is the goal of pharmacotherapy in COPD?: 1. none
2. to provide relief of symptoms and prevent complications &/or progression with minimum of side effects
1. bronchodilators are used to __ 2. They are given when? 3. Rt. of administration? (2) Acute will use which?: 1. relieve bronchospasm and reduce airway obstruction
2. routinely and prn
3. Inhaler (MDI) or nebulization
Oral route
acute=nebulizer
1. Corticosteroids may be used for __ 2. Benefit of corticosteroids 3. Routes 4. long term side effects (7): 1. short term use for exacerbation or long-term
2. inhaler/po/IV bolus with tapered doses
3. no systemic effects
4. Increased BP
osteoporosis
cataracts
muscle weakness
easier bruising
slow wound healing
hyperglycemia
1. Corticosteroids and hyperglycemia: 1. watch labs
may be on sliding scale and sugar tests
education pt. that they don't have diabetes
1. While on corticosteroids patients may have: 2. teach pts. about:: 1. increased appetite, acne, mood swings, fluid retention, peripheral edema, thin, fragile skin.
2. rinsing mouth after inhaled treatment of corticosteroid to avoid thrush.
1. What does guaifensin do? 2. what forms does it come in? common in... 3. Name of a mucolytic and what do they do? 4. Mucolytic above also used for:: 1. increases fluid in lungs and airways to liquify and thin secretions.
2. pills, liquid. Common ingredient in OTC cough expectorants.
3. Mucomyst - breaks down mucous to make it easier to clear the airways.
4. pt.having contrast dye tests to protect the kidneys, or for pt.with tylenol overdose.
1. Immunizations important for COPD pts. 2. respiratory teaching for COPD pts. (4) 3. what does pursed-lip breathing do?: 1. yearly influenza vaccine
pheumococcal vaccine every 5-7 years.
2. pursed lip breathing
diaphragmatic breathing
huff cough
chest percussion, vibration and postural drainage.
3. creates positive pressure in airways; helps keep airways open; prolongs expiratory phase
1. Chest PT for cystic fibrosis pts.: 1. should be done 1 hour before meals or 2 hours after a meal, and last 20-30 minutes. Time with RT to be done after nebulizer treatments.
Pulmonary Rehab (4) Who can do pulmonary rehab?: 1. develop exercise program in a monitored setting
2. educates pt. on breathing techniques
3. provides support; help pt. cope physically, psychologically and socially
4. tips to decrease oxygen demands
Can be done by nurse, PT, exercise physiologists.
1. LVRS for COPD: 1. Lung volume reduction surgery (LVRS)
2. relieves symptoms in advanced emphysema
3. portion of most diseased lung tissue removed
4. limited to patients with disease focused in one area and not widespread throughout lungs
5. may improve lung elasticity, oxygenation, activity tolerance, and O2 dependency
1. Lung Transplantation (7): 1. prolongs life
2. enhances QOL
3. improves lung functional capacity
4. rejection and immunosuppression for life
5. limited by supply of organs
6. criteria=no smoking
7. adults receive cadaver lungs
1. Oxygen therapy in COPD pts. improves: 2. Therapeutic goal of O2 therapy:: 1. survival, exercise, sleep and cognitive performance.
2. keep SpO2 greater than 90% at rest, sleep and exertion.
Control of respiratory drive (3): 1. Chemoreceptors (pH, CO2 and O2) control respiratory drive with pH/CO2 primary stimulus to breath.
2. In patients with chronically elevated PaCO2 pt. becomes insensitive to further increases as stimulus to breath
3. theoretically "O2 drive" to breath becomes hypoxemia.
Concerns with CO2 narcosis: 1. when hypercapnia present/risk titrate oxygen using serial ABG assessment rather than relying solely on oximetry. Check blood gases periodically but do what it takes to get patient up to 90% American Thoracic Society says "reversal of hypoxia supersedes concerns about carbon dioxide retention."
Nutritional Therapy for COPD pts.: 1. Wt. loss and muscle wasting observed irrespective of degree of airflow limitation
2. wt. loss and being underweight contribute significantly to morbidity, disability and handicap in COPD pts.
3. muscle wasting may be preseent with normal weight.
4. nutritional intervention focus on prevention and early treatment of wt. loss ot preserve energy balance.
Offer 6 small meals a day
Breathing treatments and oral care before eating to get rid of taste of treatment.
avoid gassy foods
cold foods easier to digest and pt. will feel less full than with warmed food so will eat more.
Pt. should drink between meals instead of with meals.
Use supplements to give oral meds.
Nursing Dx. for COPD pts. (5): ineffective airway clearance
impaired gas exchange
imbalanced nutrition: less than body requirements
ineffective breathing patter
activity intolerance
1. ABGs are a reflection of: 2. ABGs provide essential data about:: 1. the interaction of states occurring in the cardiovascular, pulmonary and renal systems

2. Acid-base state
ventilatory status
(alveolar ventilation)
oxygen delivery
ABG Normals: 1. pH 2. pO2 3. pCO2 4. HCO3 5. SaO2: 1. 7.35-7.45
2. 80-100
3. 35-45
4. 22-26
5. 95-100%
1. respiratory acidosis 2. respiratory alkalosis occurs when: 3. metabolic acidosis occurs when: 4. metabolic alkalosis occurs when there is an:: 1. occurs when alveolar hypoventilationis present
2. hyperventilation is present
3. there is a loss of base or accumultation of acid in the body
4. increase in the amount of base or a loss of acid in the body.
1. normal pH pH in acidosis/emia pH in alkalosis/emia 2. normal PaCO2 PaCO2 in acidosis/emia PaCO2 in alkalosis/emia 3. normal HCO3 HCO3 in acidosis/emia HCO3 in alkalosis/emia: 1. 7.35-7.45
<7.35
>7.45
2. 35-45
>45
<35
3. 22-26
<22
>26
A. Primary Cause, B.pH up/dn 1. Resp. acidosis 2. resp alkalosis 3. met. acidosis 4. met. alkalosis: 1. Increased PaCO2
pH down
2. Decreased PaCO2
pH up
3. decreased HCO3
pH down
4. increased HCO3
pH is up
Systematic approach to figuring out acid/base problems: 1. Look at pH: reflects acid-base status and tells you the PRIMARY problem. Then determine if primary problem is respiratory or metabolic:
2. Look at CO2 - reflects respiratory
3. Look at HCO3 - reflects metabolic.
Compensation: 1. Any value NOT in the expected acid-base status represents the compensatory system's attempt to reverse the underlying problem (acid-base balance.)
2. Compensation may be absent, partial, or complete.
1. Absent compensation 2. partial 3. Complete: 1. Look at the value (CO2 or HCO3) that does not match pH. If it is within normal range, then no compensation has taken place.
2. If the value that doesn't match the acid-base status of the pH is above or below normal AND the pH is also outside normal range, then partial compensation exists.
3. When the value that doesn't match the pH status is above or below normal and the pH is within normal range. Complete compensation takes some time to develop.
1. Age considerations in PaO2: 1. "normal" PaO2 is related to age.
--expected PaO2=105-(1/2age)
Or, for every yr. above age 60 a patient's "normal" Pa(2 drops by 1mmHg.
Clinical indications of Hypoxia (6): 1.Restless>confusion>lethargy->coma.
2. Tachycardia->dysrythmias
3. Tachypnea
4. Use of accessory muscles
5. Mild hypertension (early)->hypotension(late)
6. Cyanosis may be present (depending on hemoglobin level)
Clinical Indicators of Hypercapnia (8): 1. Tachycardia then dysryghmias
2. Hypotension
3. Bradypnea (decreased resp rate)
4. Headache
5. Facial rubor
6. Irritability
7. Confusion
8. Inability to concentrate, then somnolence, then coma.

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