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COPD
Chronic Obstructive Pulmonary Disease
 a slowly progressive obstruction of the airways
 currently is 4th leading cause of death
 the 12th leading cause of disability.
 includes diseases that cause airflow obstruction
(emphysema, chronic bronchitis) or a combination of
these disorders.
 Asthma is now considered a separate disorder but can
coexist with COPD.
COPD -Pathophysiology
 Airflow limitation is progressive and is associated with
abnormal inflammatory response of the lungs to
noxious agents.
 This process causes airways to narrow  resistance to
airflow increases and expiration becomes difficult or
slow.
 The result is a mismatch between alveolar ventilation
and blood flow or perfusion  impaired gas exchange.
Noxious
Particles, gases
SMOKING!
Obstruction
(COPD)
Inflammation,
Scarring of
parenchyma &
Lumen
4
COPD versus Asthma
•Asthma is now considered a separate
reversible disorder
• No longer under the diagnosis of COPD
• Uncontrolled asthma over a
lifetime may result in COPD
• COPD is not reversible
5
CHRONIC BRONCHITIS
 A disorder of excess bronchial mucus secretion
 Productive cough
 Cigarette smoking
 Inhaled irritants
 Mucous-secreting glands and goblet cells increase in
number.
 Ciliary function is reduced, bronchial walls thicken,
bronchial airways narrow, and mucous may plug airways.
PATHO – CHRONIC
BRONCHITIS

EMPHYSEMA
 Impaired oxygen/carbon dioxide exchange
 Decreased alveolar surface area
 Hypoxemia result.
EMPHYSEMA
 Alveoli walls continue to breakdown, pulmonary
capillary bed is reduced resistance to pulmonary
blood flow is increased  forcing the ( R)
ventricle to maintain a higher pressure in the
pulmonary artery.
 Increased pulmonary artery pressure may cause
right-sided heart failure (cor pulmonale).
TYPICAL POSTUREEMPHYSEMA
RISK FACTORS
 More common in Whites than Blacks
 Affect men more frequently than women
 Affects middle-aged and older adults
 Tobacco smoke causes 80-90% of COPD cases!
 Occupational exposure
 Genetic abnormalities
Alpha1-antitrypsin deficiency
Cigarette Smoking
 affect’s the respiratory tract ciliary cleansing
mechanism
 airflow is obstructed
 irritation of the goblet cells/mucous glands 
increase mucous production
CLINICAL
MANIFESTATIONS
3 primary symptoms
 chronic cough
 sputum production
 dyspnea
 Weight loss
 Barrel chest
 Pursed lip breathing
CHARACTERISTICS CHEST
WALL
ASSESSMENT/DIAGNOSTIC
FINDINGS
 Health history
 Pulmonary function test
 Spirometry
 ABG- PCO2 >45 / PaO2 60-80
 Screening – alpha 1 – antitrypsin deficiency
 CBC – RBC/Hct.
 Key factor dx. – patient’s
history/responsiveness to bronchodilators
COLLABORATIVE
COMPLICATIONS
 Respiratory insufficiency
 Pneumonia
 Chronic atelectasis
 Pulmonary arterial hypertension (cor
pulmonale)
MEDICAL MANAGEMENT
Risk reduction –
 smoking cessation / most cost - effective intervention
nicotine replacement – gum, inhaler, nicotine patch,
positive reinforcement/patient teaching
 immunization against pneumococcal
pneumonia/influenza vaccine  reduce the risk of
respiratory infection
 Pharmacologic Therapy
MEDICAL MANAGEMENT
Bronchodilators
 Delivered –
meter-dose inhalers
dry powder inhalers
spacer holding chambers
nebulizers
DRUG THERAPY
Bronchodilators
 Beta2-Adrenergic agonists
Proventil (albuterol)
Alupent (metaproterenol)
Brethine (terbutaline)
 Anticholinergics
Atrovent (ipratropium bromide)
• Methylxanthines
Aminophylline (Phyllocontin)
Theophylline (Slo-bid; Theo-Dur)
DRUG THERAPY
Corticosteriods
• May improve the symptoms of COPD  do not slow
the decline of lung function
• Short term therapy may improve pulmonary
function and exercise tolerance .
• Long term therapy not recommended
Other medications
• antibiotics, mucolytic agents, antitussive agents,
OXYGEN THERAPY
 Long term continuous therapy, during exercise,




prevent acute dyspnea, during exacerbation
Goal to improve mental functioning and quality of
life and reduce the work load of breathing
O2 sat -90%
Low flow devices most common
COMPLICATIONS of O2 THERAPY
to much O2  CO2 retention
COPD
OTHER TREATMENTs
Surgical Management
Bullectomy
Lung Volume Reduction Surgery (LVRS)
Transplant
PATIENT EDUCATION
 Breathing exercises
 Activity pacing
 Oxygen therapy
 Nutrition therapy
 Coping measures
COpd
Nursing diagnoses
 Ineffective airway clearance
 Impaired gas exchange
 Imbalanced nutrition
 Risk for infection
Home/ Community
 Knowledge of s/s of infection
 Increase exercise tolerance and prevent further loss of
pulmonary function
 Avoid extremes of heat and cold
 Avoid stress/emotional disturbances
 Demonstrate how to use MDI prior to discharge
 Smoking cessation
 Utilize resources – home care, support groups,
organizations -> American Lung Association
ASTHMA
 Chronic inflammatory disease of the airways 
episodes of wheezing, breathlessness, chest tightness,
and coughing.
 Most episodes of asthma ”attacks” are brief
 Acute episodes usually reverse either spontaneously or
with treatment
ASTHMA
 Affects more than 22 million people
 Accounts for more than 497, 000 hospitalizations
annually
 Common chronic disease of children – occurs at any age
 More common in women than men
 Patients may experience symptom – free periods
alternating with acute exacerbations  last from
minutes to hours, to days.
ASTHMA
Pathophysiology
 airways are in a persistent state of inflammation
 during this period, neutrophils, and lymphocytes play
a role in the inflammation of asthma.
 when activated they produce chemicals that enhance
the inflammatory response  increase blood flow,
vasoconstriction
 inflammation progresses  airway edema,
bronchoconstriction and mucous secretion - narrows
the airway
ASTHMA
CONT’D
 resistance increases, limiting airflow and increasing
the work of breathing.
 trapped air mixes with inspired air in the alveoli 
affecting gas exchange  hypoxemia
 hypoxemia  hyperventilation  decrease in PaCO2
 respiratory alkalosis
ASTHMA
 Predisposing factors/Triggers:
o exposure to allergens
o inhaled irritants
o respiratory tract infection
o stress, medications, exercise
ASTHMA
Clinical manifestations
 Chest tightness, non-productive cough, dyspnea,
wheezing
 Often occurs at night or early in morning
 Onset
 Attack may subside rapidly or persist for hours/days
 During an attack
ASTHMA
Assessment/Diagnostic findings
 Episodic symptoms of airflow obstruction
 Positive family history
 Pulmonary function test
 ABGs
ASTHMA
Preventive Measures
 Avoiding allergens/environmental triggers
 Modifying home environment
 Early treatment of respiratory tract infection
ASTHMA
Medical Management /Medications therapy
 Quick relief medications
 Long acting medications
ASTHMA
Quick relief medications
 Beta2- agonists
 albuterol (Proventil) /levalbuterol (Xopenex)
 Administered by MDI/DPI
 Act within minutes
 Tachycardia, nervousness and muscle tremors
 Monitor v/s prior to, during, and after treatment
ASTHMA
Anticholinergic medications
 Prevent bronchoconstriction
 Ipratropium bromide (Atrovent), Tiotropium bromide
(Spriva)
 Administered by MDI/inhaler
 Act more slowly than adrenergic stimulants
ASTHMA
Systemic Corticosteroids
 Solu-Medrol, Prednisone
 very potent and effective anti-inflammatory
 alleviate symptoms, improve airway function
 initially used – inhaled form  side effect thrush
 side effects
ASTHMA
Long-term medications
Methylxanthines -Theophylline
 Relaxes bronchial smooth muscle
 Monitor serum theophylline levels (10-20ug/mL)
Mast Cell Stablizers
 Cromolyn sodium(Intal), nedrocromil(Tilade)
 Decreases inflammation, prevents bronchospasm
effects
 Monitor for coughing, skin rash, unpleasant taste
ASTHMA
Leukotriene Modifiers
 Montelukast (Singulair), zafirlukast (Accolate)
 Oral medications – reduces the inflammatory
response in asthma, improves lung function
 Affects the metabolism and secretion of other
medication – warfarin, theophylline
 May cause liver toxicity
 Administer with meals
ASTHMA
Management of Exacerbations
 Early treatment and education
 Quick – acting beta 2 adrenergic agonist
 Systemic corticosteroids’
 Oxygen supplementation
 Antibiotics
 Peak Flow Monitoring
ASTHMA
Peak expiratory flow monitoring
 measures the highest airflow during a forced
expiration
 establishes the patient’s personal best or normal PERF
 value is used to evaluate the severity of airway
obstruction
 Traffic signals are used for simplicity –
green (80 to 100%)
yellow 50-80%
red 50 % or less
ASTHMA
Nursing management – depends on severity of
symptoms
 Acute asthma attacks cause – fear as breathing
becomes more difficult  hypoxemia
 Priority during an attack – improve airway clearance
and reduce fear and anxiety
 Teach about prevention of future attacks and home
management
ASTHMA
 Ineffective airway clearance
 Anxiety
 Community based - care
STATUS ASTHMATICUS
 Severe /persistent asthma that does not respond to
routine treatment
 Without aggressive therapy  respiratory failure
 Attacks can occur with little or no warning  can
progress rapidly to asphyxiation