Transcript Egan Ch 23 Obstructive Lung Disease

Chapter 23
Obstructive Lung Disease:
Chronic Obstructive Pulmonary
Disease (COPD), Asthma, and
Related Diseases
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Learning Objectives
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State definitions of chronic obstructive
pulmonary disease (COPD), asthma, and
bronchiectasis.
Identify how many Americans are diagnosed
with COPD and how many deaths from
COPD occur each year.
Understand the major risk factors associated
with the onset of COPD.
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Learning Objectives (cont.)
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Identify the common signs and symptoms
associated with COPD.
Describe a treatment plan for the patient with
stable COPD and for the patient with an acute
exacerbation.
State the factors associated with the onset of
asthma.
Describe the clinical presentation typical for
the patient with asthma.
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Learning Objectives (cont.)
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Identify the treatment currently available for
the patient with acute asthma.
Describe the treatment currently available for
patients with bronchiectasis.
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COPD: Overview & Definitions
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COPD - inflammatory disorder characterized
by not fully reversible, typically progressive,
airflow obstruction
Composed of 2 major disease entities:
1.
2.
Emphysema
Chronic bronchitis
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COPD: Overview & Definitions
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The COPD condition characterized by permanent
enlargement of distal airspaces and destruction of
the wall of the airspaces, without fibrosis is called:
A.
B.
C.
D.
Asthma
Cystic Fibrosis
Emphysema
Bronchiectasis
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COPD: Epidemiology
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Incidence: ~24 million Americans have COPD
COPD is 3rd leading cause of death in U.S.
Number of deaths-per-year has continued to
rise over years paralleling (with lag time) prior
smoking trends
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Risk Factors for COPD
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Lung Decline Tied to Smoking
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COPD Risk Factors &
Pathophysiology
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Cigarette smoking’s impact on COPD
mortality & morbidity far outweighs all other
factors combined
2nd most common cause - AAT deficiency

Genetic deficiency in AAT results in early onset
emphysema
 Preventive measures may avoid early onset
COPD
• Smoking cessation key to managing disorder
• Treatment with IV augmentation therapy may prevent
neutrophil elastase damage to lung tissue
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Cigarette Smoking & Emphysema
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COPD Risk Factors &
Pathophysiology (cont.)
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COPD may occur in absence of smoking or
AAT deficiency
Other risk factors:
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Passive smoking (second hand)
Air pollution
Occupational exposure
AW hyperresponsiveness
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The risk of developing emphysema for individuals
with AAT deficiency increases as the level in the
serum of AAT falls below:
A.
B.
C.
D.
11 µmol/L
8 µmol/L
13 µmol/L
20 µmol/L
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COPD Risk Factors &
Pathophysiology (cont.)
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Mechanisms of airflow limitation in COPD
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Inflammation & obstruction of small airways
• Occurs in airways <2 mm in diameter
Loss of elasticity
• Destruction of elastin resulting in destruction of alveolar
walls

Active bronchospasm
• Some element of reversibility is noted in 2/3rds of COPD
patients
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COPD: Signs & Symptoms
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Common symptoms
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Productive cough
Wheezing or diminished breath sounds
Shortness of breath (SOB); particularly on exertion
Progressive dyspnea; usually manifesting in 6th or 7th
decade of life (AAT deficiency ~45 years of age)
Late signs include
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Barrel chest with flattened diaphragms
Accessory muscle usage
Edema from cor pulmonale
Changes in mental status due to ⇓O2 or ⇑CO2
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Management of COPD

Establishing diagnosis with airflow obstruction
 Separating COPD from asthma is major challenge
 Features favoring COPD are
• Chronic productive cough, ⇓diffusing capacity
• Diminished vascularity on chest radiograph
 Asthma favored if diminished FEV1 is normalized
after use of an inhaled bronchodilator
 Once COPD established, check for AAT deficiency
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During pulmonary rehab a COPD patient is told
that in two months he should be able to go up to
the second floor of his house without any
shortness of breath. This goal is categorized as:
A.
B.
C.
D.
prolong survival
simplify medical treatment
maximize functional status
control airway flow obstruction
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Optimizing Lung Function:
Stable COPD
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PRN bronchodilator for all COPD patients
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Systemic corticosteroid trial (6–29% respond)
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Sympathomimetic &/or anticholinergic
Reversibility if postbronchodilator FEV1 ⇑12%
No survival benefit, but often improves symptoms
If patient responds (⇑FEV1), use inhaled steroids
Lung decline continues, but decreases exacerbations
May lead to higher rate of pneumonia in COPD users
Methylxanthines decrease feeling of dyspnea

Try to avoid toxicity serum levels of 8–10 µg/mL
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Optimizing Lung Function:
Stable COPD (cont.)
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Optimizing Lung Function:
Acute Exacerbations
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Inhaled bronchodilators, especially 2-agonists
Oral antibiotics if purulent sputum is present (7–
10 days)
Short course of systemic corticosteroids
Supplemental oxygen to keep SaO2 >90%
With hypercapnia (pH <7.3), NIV is attractive
option

If NIV fails, then make decision on intubation & MV
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Which of the following are criteria for a NIV trial on a
patient suffering from a COPD exacerbation?
1. respiratory acidosis (pH <7.30)
2. hemodynamic stability
3. SpO2 <92%
4. Ability to protect the airway
A. 1, 2and 3only
B. 2 and 3only
C. 1, 2, and 4 only
D. 1 only
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COPD: Maximizing Functional Status
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Primary goal is to maximize ability to perform
daily tasks
In addition to therapies mentioned previously:
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Comprehensive pulmonary rehabilitation is
indicated for all Class II, III, & IV COPD patients
• Improves exercise capacity
• Upper body strength and ventilatory function
Transcutaneous neuromuscular electrical
stimulation
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Preventing Progression & Enhancing
Survival
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Smoking cessation is first-line intervention
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Long-term oxygen therapy (LTOT)
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Slows rate of FEV1 decline to same-age nonsmokers
Enhanced survival rates
Survival benefit noted with minimum 15 hours/day
Closer to 24 hours/day is better
Annual influenza & pneumococcal vaccinations
Some end-stage COPD patients may benefit
from lung transplant or lung volume reduction
surgery
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A pulmonologist orders pulmonary rehabilitation
sessions for a 66 y/o COPD patient. Which of the
following outcome should be expected from this
intervention?
A. Improve lung function
B. Improve survival
C. Decreased airway obstruction
D. Decreased dyspnea perception
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Preventing Progression of COPD &
Enhancing Survival (cont.)
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Asthma
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Definition
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Iinflammatory airway disease characterized by
reversible airway obstruction
Incidence
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Increasing prevalence in U.S. since 1980
Affects people of all ages
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Asthma (cont.)
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Etiology & pathogenesis
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Genetic susceptibility to allergens, RTI,
occupational and environmental stimuli, etc.
Whatever trigger, it can produce “asthma”
• Airway inflammation & bronchial hyperreactivity, resulting
in airway obstruction
• Once above are present, asthma can be triggered by:

Exercise, cold dry air, hyperventilation, stress, cigarette
smoke, etc….
• Once triggered, asthma causes mast cell degranulation,
releasing proinflammatory substances

Starts cycle of asthma
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Asthma (cont.)
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Early & Late Asthmatic Response
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Late response is usually more severe and
longer lasting.
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Clinical Presentation & Diagnosis
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Diagnosis by clinical & laboratory evaluation
History plays key role, as patients can be
entirely normal between episodes
Classic symptoms are episodic wheezing,
SOB, cough
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If present, send for PFTs to demonstrate
reversible airways obstruction
PFTs may be normal between exacerbations
or show some degree of airway obstruction

⇓FEV1 & FEV1/FVC ratio
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Clinical Presentation & Diagnosis
(cont.)
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Airway reversibility in asthma is noted just like in
COPD
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If PFTs are normal, bronchoprovocation is
undertaken
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Post-bronchodilator FEV1 ⇑12% & 200 ml
Most common agent used: methacholine
Arterial blood gases taken during an acute attack.
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Most often show hypoxemia with hyperventilation
Normal PaCO2 level is indicative of severe attack &
impending ventilatory failure
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Asthma Management
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Goals of asthma management
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Maintain high-quality, asymptomatic life
No limitations on the job or during exercise
No medication side effects
Stepwise approach to long-term management of
asthma:
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Medication therapy is based on disease severity
Control is attained when (there are)
• Minimal to no daily symptoms or limitations
• Infrequent exacerbations, with little or no use of 2-agonists
• PFTs = normal or near normal
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Asthma Management (cont.)
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An asthmatic patient complains of nocturnal
asthma attacks four times/wk. His current PFT
exam shows and FEV1 of 82% predicted. The
patient tells you that he takes levalbuterol TID and
Advair 100/50 BID. The severity of his asthma
should be classified as:
A. Intermittent
B. Mild persistent
C. Moderate persistent
D. Severe persistent
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Pharmacotherapy
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Corticosteroids
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Most effective medication in treatment of asthma
• Reduces symptoms & mortality
Use of inhaled steroids for long-term treatment
preferred
• Use spacer & rinse mouth to eliminate or minimize side
effects
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Long-term use of oral steroids should be restricted
to patients with asthma refractory to other
treatment
Short-term oral steroid use during exacerbation
reduces severity, duration, & mortality
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Pharmacotherapy (cont.)
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Cromolyn (NSAID)
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Protective against allergens, cold air, exercise
Administered prophylactically, CANNOT be used
during an acute asthma attack
Of limited use in adults
Drug of choice for atopic children with asthma
Nedocromil (NSAID)

Similar to cromolyn, it is 4–10 times more potent in
preventing acute allergic bronchospasm
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Pharmacotherapy (cont.)
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Leukotriene inhibitors
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Leukotrienes mediate inflammation &
bronchospasm
Modestly effective to control mild to moderate
asthma
Inhaled steroids remain antiinflammatory drug
of choice
Methyxanthines (use is controversial)

Oral or IV use if admitted for acute asthma attack
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Pharmacotherapy (cont.)
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2-Adrenergic agonists
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Most rapid & effective bronchodilator
Drug of choice for exercise-induced asthma &
emergency relief of bronchospasm
• Should be used PRN
Improves symptoms not underlying inflammation
• Regular use may worsen asthma control & increase risk
of death
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Pharmacotherapy (cont.)
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Anticholinergics
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Can be used as adjunct to first-line
bronchodilators if there is inadequate response
Has additive affect to 2-agonists
Tiotropium when added to corticosteroid enhances
asthma control & improve symptoms
Anti-IgE therapy:



IgE plays role in asthma pathogenesis
Omalizumab (Xolair) blocks IgE biologic effects
Indicated in patients with allergic asthma, poorly
controlled with corticosteroids
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Emergency Management of Asthma
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Early & frequent use of aerosolized 2-agonists
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Consider continuous therapy for severe attack
High-dose parenteral corticosteroids
Oxygen therapy for hypoxemia
Antibiotics if evidence of infection
In severe ventilatory failure, use MV with
permissive hypercapnia: small VT, low rate, PIP
<50 cm H2O to avoid air-trapping & barotrauma
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Bronchial Thermoplasty
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Promising new treatment for asthma patients
Indicated for uncontrolled asthma despite use
of corticosteroids & LABAs
Uses heat (by ways of radiofrequency waves)
to decrease airway smooth muscle mass
Reduces ability of airways to constrict
Long-term side effects have not been studied
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Asthma & Environmental Control
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Recognized relationship between asthma &
allergy
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
75–85% asthma patients react to inhaled
allergens
Environmental control is aimed at reducing
exposure to allergens


Avoid outdoor allergens by remaining inside,
windows closed, AC on
Indoor allergens are combated by:
• Air purifiers & no pets
• Dust mites: airtight covers on bed & pillow, no carpets in
bedroom, chemical agents to kill mites
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Special Considerations in Asthma
Management
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Exercise-induced asthma (EIA)
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Occupational asthma
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Common particularly in cold weather
• Heat loss from airways may precipitate attack
Prophylactic inhalation of 2-agonists or cromolyn
Most common form of occupational lung disease
Early identification & cessation of exposure are
key
Cough-variant asthma

Cough is sole complaint, amenable to 2-agonists
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Special Considerations in Asthma
Management (cont.)
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Nocturnal asthma
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

Present in 2/3rds of poorly controlled asthmatics
May be due to diurnal decrease in airway tone or
gastric reflux
Treatment should include:
• Steroid treatment targeted to relieve night symptoms
• Sustained release theophylline
• New long-acting 2-agonists
• Antacids for reflux
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Special Considerations in Asthma
Management (cont.)
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Aspirin sensitivity
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5% of adult asthmatics will have severe, lifethreatening asthma attacks after taking NSAIDs
All asthmatics should avoid; suggest Tylenol use
Asthma during pregnancy
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1/3rd of asthmatics have worse control at this time
Much higher fetal risk associated with uncontrolled
asthma than that of asthma medications
Theophyllines, 2-agonists, & steroids can be used
without significant risk of fetal abnormalities
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Special Considerations in Asthma
Management (cont.)
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Sinusitis may cause asthma exacerbation
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

CT of sinuses will diagnosis problem
Treatment: 2–3 weeks antibiotics, nasal
decongestants, & nasal inhaled steroids
Surgery

Asthmatics at higher risk for respiratory
complications:
• Arrest during induction
• Hypoxemia with/without hypercarbia
• Impaired cough, atelectasis, pneumonia
 Optimize lung function preoperatively
 Use steroids during procedure.
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Asthma caused by rapid inhalation associated with
physical exertion can be classified as:
A. Occupational asthma
B. Cough-variant asthma
C. Exercise-induced asthma
D. Nocturnal asthma
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Bronchiectasis
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
Abnormal, irreversible dilation of bronchi
caused by chronic airway inflammation &
destruction
Presents in 3 major anatomical patterns
Cylindrical: airway is uniformly dilated
2. Varicose: irregular constrictions & dilations
3. Cystic: progressive distal, sac-like dilations
1.
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Bronchiectasis (cont.)
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Bronchiectasis (cont.)
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Clinical presentation & evaluation
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
Hallmark: chronic production of copious amounts
of purulent sputum
Dyspnea variable; depends on extent of disease
Hemoptysis frequent, though rarely severe
Chest radiograph shows tram lines (airway
dilation)
Definitive diagnosis made with fine-cut CT
• Reversible airway changes consistent with
bronchiectasis may follow pneumonia
• Wait 6–8 weeks following pneumonia resolution
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Bronchiectasis (cont.)
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Mainstays of Management
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
Antibiotics
• As needed or regularly scheduled
• Sputum cultures should guide therapy
Bronchopulmonary hygiene
• Postural drainage & cough maneuvers
• Humidification & hyperosmolar substances
• Dry powder inhaled mannitol may be helpful
Massive hemoptysis may embolize artery or
surgically repair
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RT Role in COPD
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Diagnostic role:
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
Performing PFTs
Physical assessment
Management:



Medication delivery, bronchial hygiene, oxygen
delivery
Invasive/Non-invasive ventilatory support
Invasive/Non-invasive blood gas monitoring
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RT Role in COPD (cont.)
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Follow up:
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
Smoking cessation
Pulmonary rehab
Long-term oxygen therapy
Invasive/Non-invasive ventilatory support
Advocacy
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