Presented By Mr. Pradeepsingh B HOD OF Medical Surgical Nursing

1. COPD

2. Definition
 A disease state characterized by the
presence of airflow obstruction due to
chronic bronchitis or emphysema; the
airflow obstruction is generally
progressive, may be accompanied by
airflow hyperactivity, and may be viewed
as partially reversible.
 Includes emphysema and chronic
bronchitis

3. Definition
 COPD is an umbrella term used to
describe chronic lung diseases in which
air flow is obstructed by emphysema,
chronic bronchitis, refractory
(irreversible) asthma, and severe
bronchiectasis.

4. Prevalence
 COPD occurs in 4-6% of white males,
and 1-3% of adult white females
 The 4th most common cause of death in
the United States
 14.2 million people in U.S. have COPD
 Highest mortality rate is in white men,
and the lowest is in hispanic women.

5. Types of COPD
 Emphysema
 Permanent and destructive enlargement of airspaces
distal to the terminal bronchioles without obvious fibrosis
and with loss of normal architecture
 Always involves clinically significant airflow limitation.
 “pink puffer”
 Chronic Bronchitis
 Presence of a cough productive of sputum not attributable
to other causes on most days for at least 3 months over 2
consecutive years
 May be present in the absence of airflow limitation.
 “blue bloater”

6. COPD

8. Pathogenesis of COPD
 Increased number of activated
polymorphonuclear cells and macrophages
produce elastases (such as human leukocyte
elastase), resulting in lung destruction.
 Increased oxidative stress caused by free
radicals in cigarette smoke, the oxidants
released by phagocytes, and
polymorphonuclear leukocytes all may lead to
apoptosis or necrosis of exposed cells

9. Pathogenesis of COPD (cont.)
 Emphysema
 3 morphologic patterns:
 Centricacinar:
 focal destruction limited to the
respiratory bronchioles and the
central portions of acinus
 associated with cigarette
smoking
 most severe in the upper lobes
 Panacinar:
 involves the entire alveolus
distal to the terminal bronchiole
 develops in patients with
homozygous alpha1-antitrypsin
(AAT) deficiency
 most severe in the lower lung
zones
 Distal acinar:
 Also called paraseptal
 least common form
 involves distal airway
structures, alveolar ducts, and
sacs
 localized to fibrous septa or to
the pleura and leads to
formation of bullae (can result
in pneumothorax)
 Chronic Bronchitis
 Mucus gland enlargement
 Airway atrophy, focal
squamous metaplasia, ciliary
abnormalities, variable
amounts of airway smooth
muscle hyperplasia,
inflammation, and bronchial
wall thickening
 Respiratory bronchioles
display a mononuclear
inflammatory process, lumen
occlusion by mucous plugging,
goblet cell metaplasia, smooth
muscle hyperplasia, and
distortion due to fibrosis
 Airway walls to deform and
narrow the airway lumen

10. Risk Factors
 SMOKING!
 48 million smokers in the U.S.
 3000 new people take up smoking daily
 Nearly all patients with symptomatic
COPD are current or former smokers
 10-20% of smokers will develop
symptomatic COPD.
 In men who smoke one pack/day, the
drop in FEV1 per year was 9 mL more
than in non-smokers
 Occupational Exposures
 Dusts, gases, fumes
 Alpha1-antitrypsin deficiency
 Alpha1-antitrypsin is an important
protease inhibitor that usually presents
elastases from causing lung
destruction

11. Risk Factors
Occupations exposure
Air pollution
Genetic abnormality
Deficiency
Alpha-antitripsin
Family history
Passive smoking
Cigarette smoking
Risk factors

12. Pathophysiology
Due to causes & risk factors of the COPD
Affect ciliary cleaning mechanism of respiratory tract
Airflow is obstructed & air becomes trapped behind the obstruction
Alveoli greatly distend & lung capacity decreased
Increased accumulation of the mucus from mucus glands
Produce more irritation, infection
Damage to lung

13. Stages of COPD
Stage FEV1/FV
C Ratio
FEV1
%
Clinical Findings
At Risk >0.7 Patients who smoke, patients exposed to
high pollutants, and patients with recurrent
respiratory symptoms/infections. Give
influenza and pneumonia vaccines.
Mild < 0.7 >80 Add short-acting bronchodilator as needed
Moderate <0.7 50-80 Add regular treatment with one or more
long-acting bronchodilator and add
Pulmonary rehabilitation
Severe <0.7 30-50 Add inhaled corticosteroids if repeated
exacerbations
Very
Severe
< 0.7 <30 Add long-term oxygen if chronic respiratory
failure; Consider surgical treatments

14. Symptoms
 Dyspnea
 Cough (usually worse in morning, sputum production)
 Wheezing
 Cyanosis
 Right heart failure
 Weight loss, anorexia
 Frequent respiratory infections
 Production of purulent (cloudy and discolored) sputum
 Enlarged A-P diameter of chest
 Acute and chronic respiratory failure
 Weight loss
 Increased work of breathing
 Tightness of chest
 Tachypnea
 Prolonged expirations
 Pitting peripheral edema
 fatigue

15. Physical Exam
 RR, HR, O2 saturation
 Gen: Barrel-chest, accessory muscle
use
 CV: Quiet heart sounds
 Resp: Decreased breath sounds,
wheezing, rhonchi, crackles

16. Labs
 CBC:  Hgb/Hct
 ABG: pH, pCO2
Chemistry: HCO3

17. Diagnostic evaluation
 Lung function test (PFT): LFT measures how
much air person can breath in and out, how fast he/she can
breathe air out, and how well lung deliver oxygen to blood.
 Components of LFT: 1. Spirometry, post bronchodilator spirometry
, lung volumes and diffusion capacity
 CXR/ CTSCAN: These tests create pictures of the structures
inside the chest, such as heart, lungs and blood vessels. The
picture can show the signs of COPD
 ABG
 PULSE OXIMETRY
 Alpha 1 antitrypsine level: it can also cause liver diseases in
children

18. Emphysema

19. Diagnosis of COPD
 Look for secondary polycythemia:
 Hct >52% in males, Hct>47% in females
 Measure alpha1-antitrypsin levels in all
patients 40 years or younger, or in those
with family history.
 Hyperinflation see on chest x-ray
 Bullae seen on Chest x-ray or CT scan

20. Pulmonary Function Tests

21. Diagnosis of COPD – Pulmonary
Function Tests
  Forced Expiratory Volume for 1 second
(FEV1)
 FEV1/FVC (Forced Vital Capacity) ratio
  Total Lung Capacity (TLC)
  Forced Residual Capacity (FRC)
  Residual Volume (RV)
  Vital Capacity (VC)

22. Pulmonary Function Tests

23. COPD Exacerbation
 Typically manifest as increased sputum production, more purulent
sputum and worsening of dyspnea.
 Although infectious etiologies account for most exacerbations, exposure
to allergens, pollutants or inhaled irritants may also play a role.
 Bacterial infection is a factor in 70 to 75 percent of exacerbations, with
up to 60 percent caused by
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
 Antibiotic therapy has a small but important effect on clinical recovery and
outcome.
 Respiratory fluoroquinolone (Levofloxacin, Moxifloxacin)
 Ceftriaxone + azithromycin
 Short courses of systemic corticosteroids may provide important benefits
in patients with exacerbations of COPD.
 Oxygen therapy to keep saturation Between 90-93%
 Non-invasive ventilation such as BiPAP can be helpful in avoiding
intubation/mechanical ventilation.

24. Treatment of COPD
 SMOKING CESSATION!
 Short-acting bronchodilators
 Albuterol, theophylline
 Long-acting bronchodilator
 salmeterol
 Combination of anti-cholinergic and -agonist bronchodilator
 Ipratropium + albuterol (combivent)
 Tiotropium (spiriva)
 Methylxanthines (Theophylline)
 Has anti-inflammatory affect, and improves respiratory muscle function,
stimulates the respiratory center, and promotes bronchodilation
 Adverse effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia,
and seizures
 Inhaled corticosteroids
 Fluticasone (Flovent), budesonide (Pulmicort)
 Combination of Inhaled corticosteroid and long-acting -agonist
 Fluticasone + salmeterol (Advair)
 Oral Corticosteroids

25. Medical management
 Nicotine replacement therapy: Nicotine polacrilex is a
chewing gum chewing pieces come in 2 strengths(2mg ,4mg) if
person smoke 1 pack per day, he should use 4mg pieces. If person
smoke less than 1 pack per day he should use 2mg pieces. He
should chew hourly and also chew when needed. The person
should reduce the amount chewed over the next 3 months.
 Mucolytics: it not only reduce sputum but also improve sputum
clearance. Ex, guaifenesin, potassium iodide are taken orally , N-
acetycysteine is commonly taken through a nebulizer.
 Antibiotics: in people with COPD, chronic infection of lower airways
is common. Ex, amoxicilline, cefaclor or
trimethoprim/sulfamethoxazole.
 II line treatment: ex, azithromycin, clarithromycin, fluoroquinolones
 Immunization: patient with COPD should discuss influenza,
pneumococcal immunization.

26.  Treatment of A-1 antitrypsin deficiency:
replacement of missing or inactive AAT by
injection can help prevent progression of
associated emphysema.
 Non pharmacologic therapy:
 1. Nebulization
 Oxygen therapy
 Removing bronchial secretions
 Exercises

27. Treatment of COPD (cont.)
 Oxygen Therapy
 Continous oxygen has been shown to cut mortality in half or
decrease morbidity when compared with non-continous
oxygen
 Continuous (24 hours/day)
 Resting Pa02 of 55 mm HG, or Resting oxygen saturation < 88%
 Resting Pa02 of 56-59 mmHg or Oxygen Sat. <89% in presence of
dependent edema (suggestive of CHF), P pulmonale on ECG (P
wave more than 3 mm in inferior leads) or cor pulmonale, or
erythrocytosis (Hct > 56)
 Noncontinuous
 During exercise – when PaO2 is < 55 mmHg or Oxygen sat. < 88%
with low level of exercise.
 During sleep if Pa02 is < 55 mmHg or Sa02 less than 88% with
associated complications such as pulmonary hypertension, daytime
somnolence, cardiac arrythmias.

28. Treatment of COPD (cont.)
 Pulmonary Rehabilitation
 Aimed at keeping patient conditioned with exercise,
perception of dyspnea, quality of life and self-efficacy.
 Surgery
 Bullectomy
 Resection of large bullae compressing normal lung
 Lung volume reduction surgery
 Pneumonectomy of nonuniform emphysematous lung
 Double lung transplantation
 Can be life-saving, but is costly, can be lack of donor
availability and requires lifelong immunosuppression.

29. Take Home Points
 Smoking is the number one cause of
COPD!
 If smoking is stopped once COPD
diagnosed, the progression of disease
can slow down.
 Treat COPD exacerbations with
antibiotics and possibly with steroids.
 Continuous oxygen is shown to decrease
morbidity and mortality in COPD

30. COMPLICATIONS
 Respiratory insufficiency
 Respiratory failure
 Pneumonia
 Atelectasis
 Pneumothorax
 Hypoxemia
 Respiratory acidosis
 Cardiac failure
 Status asthmaticus

31. Nursing diagnosis
 Ineffective airway clearance r/t bronchoconstriction, increased
mucus production
 Impaired gas exchange r/t decreased ventilations
 Ineffective breathing pattern r/t shortness of breath
 Imbalanced nutrition less than body requirement r/t increased
work of breathing, air swallowing
 Activity intolrence r/t fatigue, inadequate oxygenation &
dyspnea
 Anxiety r/t acute breathing difficulties and fear of suffocation
 Deficient knowledge r/t regarding condition, treatment, self
care and discharged needs lack of information's.

32. BRONCHIAL ASTHMA
 It is a chronic (long term) lung diseases
that inflames and narrow the airways.
 Asthma is reversible, obstractive airway
diseases.
 There is a narrowing of bronchial lumen
characterized by wheezing & diffculty in
breathing.

33. Types of asthma /causes
1. Allergic asthma (extrinsic asthma): triggered
by allergens, such as pet dander, house dust,
feathers, food , pollen ---------inhalation of
specific allergens-------- hyper immune
response (type 1 hypersensitivity)------- IgE
bind to mast cells in the bronchial mucosa------
-- bronchospasm ----- airway obstruction --
--- mucus secretions

34. 2.Non-allergic asthma
 This type of asthma is triggered by irritants in
the air that are not related to allergens.
 Example- air pollution, cold, heat, weather
changes, fumes, wood , cigarette smoke, room
deodorants, household cleaning product,
perfumes, RTI, change in temp.
 Stress, physical exertion, drugs- aspirin
NSAIDs

35. 3. Mixed asthma
 It has both allergic and non allergic
asthma.
 Cough variant asthma
4. Cough-variant asthma: CVA is a
characterized by one symptom, a
persistent dry cough
5. Exercise induced asthma: it effects
people during or after physical activity.

36. 6. Nocturnal asthma: It is characterized
by asthma symptoms that worsen at
night. However, certain triggers- such as
heartburn, pet dander, dust & mites can
cause those symptoms to worsen at
night while sleeping.
7. Occupational asthma: It is induced by
triggers that exist in a person’s
workplace. Irritants & allergens include
dusts, dyes, gases, fumes, animal
proteins, & rubber latex, industries-
manufacturing, textiles, farming &
woodworking.

37. Due to etiological factors
Reversible and diffuse airway
inflammation
Hyper responsiveness of
airways Air flow limitation
Swelling of membranes that line
the airways (mucosal edema)
Contraction of the bronchial
smooth muscles
(bronchospasms )
Bronchial muscles and mucus
glands enlarges
Production of thick, tenacious
sputum
Alveoli hyper inflate
Wheezing, cough, Dyspnea,
chest tightness

38. CLINICAL FEATURES
 Coughing: A persistent cough, the cough may be dry or wet and
might worsen, early in the morning
 Wheezing: wheezing is a whistling noise heard during breathing
 Chest tightness: this may feel like something is squeezing or
sitting on chest. As muscles surrounding the airways constrict,
patient may experience a feeling of tightness in the chest.
 Shortness of breath: shortness of breath id the feeling that a
barely finished before another is needed.
 Mucus production : many people with asthma produce excessive,
thick mucus that obstructs the airways, which can lead to
coughing.

39. Other clinical features
 Restlessness prolonged expiratory phase
Dry, hacking & non-productive Hypoxemia
cough widened pulse pressure
 Fever of 100 degree fatigue
 Chest & abdominal pain difficulty talking and walking
 Headache status asthmaticus:
 Diaphoresis
 Central cyanosis
 Nasal flaring
 Mental confusion
 ARF
 Irritable
 Vomiting

40. Diagnostic evaluation
 Spirometer
 Peak Expiratory Flow (PEF): it measures the ability to push air out of
the lungs or how fast air can be exhaled
 Pulse oxymetry
 Methacholine challenge: methacholine will cause mild constriction of
airway
 Nitric oxide test: it measures the amount of a gas called nitrous oxide
in breath. If airways are inflamed- a sign of asthma –may have higher
than normal nitric oxide level
 CXR
 Allergy blood testing
 ABG
 CBC
 Sputum culture
 Sputum cytology

41. Asthma zone -NHLBI
 Green zone: “ Doing well”
 Yellow zone: “asthma is getting worse”
 Red zone: “ medical alert”

42. MANAGEMNT
 A voidance of triggers: The patient is
instructed to identify and avoid asthma
triggers, the patient can use
bronchodilator or mast cell inhibitors MDI
 Using vinyl matters
 Maintenance in door humidity
 Smoking and secondary smoke
discouraged

43.  These drugs should be avoided
-Asprin, NSAIDs, Beta blockers- propranolol, metoprolol
PHARMACOLOGIC THERAPY:
Long term control medications:
Inhaled corticosteroid: to relieve airway inflammation and swelling
ex: fluticasone, budesonide, mometasone, beclomethsone,
 Patients may need to use these medications for several days to
weeks
Leukotriene modifiers: It reduce inflammation, these are 2nd line of
defence against astrhma ex; ZILEUTON(Zyflo), Zafirlukast,
montelukast(Singulair)
Long acting beta agonists(LABA’s): This class of drugs is
chemically related to adrenaline. Inhaled LABA’s work to keep
breathing passages open for 12h or lonnger.
 they relax the muscles of breathing passgage. They may also
reduce the inflammation

44.  Ex: LABA’s Salmeterol( serevent), formoterol( Foradil)
Methylxanthines: These are the another group of controller
medications useful in the treatment of asthma
 This group of medications is chemically related to caffeine.
 It works as a long acting bronchodilators
 ex: Theophylline, aminopahylline
Combination inhalers: ex: fluticasone+ salmeterol and
Formoterol + Budesonide these medications contain a LABA
along with corticosteroid
Cromolyn sodium: Cromolyn sodium is prevent the release of
chemicals that cause asthma related inflammation.
Omalizumab: it belongs to a newer class of agents that works with
the bodys immune system. Asthma who have an elevated level of
immnogloblines E (IgE) an allergy antibodys the drug is given by
injections. This agents inhibits IgE binding to cells that release
chemicals, this binding prevents relase of these mediators

45.  Short acting Beta agonists: It is used for rescue medications,
inhaled work rapidly., within a minutes, to open the breathing
passages, and effects usually lasts for four hours.
 Ex: albuterol, levalbuterol, pirbuterol,(Maxair Auto inhaler)
ANTICHOLINRGICS: This drugs used for rescue medications during
asthma attacks. Inhaled drugs open the airway passage. Ex,
Ipratropium bromide(Atrovent)
Oral & IV corticosteroids: ex, Prednisone and methylprednisolone
 Bronchial thermoplasty
 Breathing techniques
 Relaxation techniques
 Acupuncture:

46. Self care at home
 A void trigger
 Use air conditioner
 Reduce pet dander
 Clean regularly
 Get regular exercises
 Maintain a health weight
 Eat fruits and vegetables
 Do not take cough medicines

47. Nursing Diagnosis
 Impaired gas exchange r/t altered O2 supply, obstruction of
airway
 Ineffective airway clearance r/t bronchospasm
 Ineffective breathing pattern r/t bronchospasm
 Imbalanced nutrition less than body requirement r/t dyspnea,
sputum production
 Risk for increasing attack of respiratory distress r/t exposures
allergens