OBSTRUCTIVE

DISORDER
Prepared by: Earl John S. Amado, RN, MSN
Chronic obstructive
pulmonary disease
(COPD)
COPD is a disease characterized by airflow
limitation that is not fully reversible. The
airflow limitation is usually progressive and
associated with an abnormal inflammatory
response of the lung to noxious particles or
gases, resulting in narrowing of airways,
hypersecretion of mucus, and changes in the
pulmonary vasculature.
RISK FACTORS:
-SMOKING
-Environmental pollutants
-Occupational exposure
-Genetic predisposition(Hereditary)
CLINICAL MANIFESTATION:
-Chronic cough
-Sputum production
-Dyspnea on exertion; often worsen
over time.
MEDICAL MANAGEMENT
-Smoking cessation, if appropriate.
-Bronchodilators, corticosteroids, and
other drugs (e.g. alpha1-antitrypsin
augmentation therapy, antibiotic
agents, mucolytic agents, antitussive
agents, vasodilators, narcotics).
Vaccines may also be effective.
MEDICAL MANAGEMENT
-Oxygen therapy, including nighttime
oxygen.
TWO TYPES OBTRUCTIVE AIRWAY
DISEASE IN COPD
1. Chronic bronchitis
2. Emphysema
CHRONIC BRONCHITIS

A disease of the airways, is defined as

the presence of cough and sputum
production for at least 3 months in each
of 2 consecutive years.
PATHOPHYSIOLOGY
 Causes
-Cigarette Smoking
-Respiratory Tract Infection(RTI)
-Environmental Pollutants
-Occupational Exposure to hazardous Airborne Substance
 Inflammation

Bradykinin(bronchoconstriction)
Histamine
Prostaglandin
 Fluid/Cellular Exudation

Edema of mucous membrane

Hypersecretion of mucus

Persistent Cough
Fibrotic Changes in the Airways

Bronchial Narrowing
Irreversible lung changes

Emphysema
Bronchiectasis
BLUE BLOATER
S/Sx:
• Overweight
• Elevated hemoglobin
• Peripheral edema
• Wheezing
DIAGNOSTICS
• Spirometry
• ABG:
 mild-mod hypoxemia
 Respiratory acidosis
COMPLICATION:
• RSHF(cor pulmonale)
• Pneumonia
• Pneumothorax
EMPHYSEMA

Abnormal DISTENTION of the

AIRSPACES beyond the terminal
bronchioles and destruction of the walls
of the alveoli .
PATHOPHYSIOLOGY
 Causes
-Cigarette Smoking
-Hereditary
Plasma protein abnormality,
Deficiency of alpha – 1 antitrypsin, an enzyme inhibitor
Aging Process

Disequilibrium between
ELASTASE & ATIELASTASE
Destruction of ELASTIC RECOIL

Overdistention of ALVEOLI
 Retention of CO2(Airtrapping)

Hypoxia Respiratory Acidosis

PINK PUFFER
S/Sx:
 BARREL CHEST
 Severe dyspnea
 Thin-framed body(muscle wasting)
 Purse-lip breathing
DIAGNOSTICS
• Spirometry
• CXR: hyperinflation with FLATTENED
diaphragm
• ABG:
 mild-mod hypoxemia
 Respiratory acidosis
ASSESSMENT
• Cough
• Dyspnea
• Chest pain
• Sputum production
• Wheezing
• Purse-lip breathing
• Tends to assume upright, leaning
forward position.
• Alteration in LOC
ASSESSMENT
• Alteration in skin color (Pallor or cyanosis)
• Alteration in skin temperature (cold to
touch)
• Voice changes
• Decreased metabolism
 Weakness
 Fatigue
 Anorexia
 Weight loss
ASSESSMENT

• Alteration in thoracic anatomy (Barrel

chest)
• Clubbing of fingers
• Polycythemia
INTERPROFESSIONAL
COLLABORATIVE MANAGEMENT

• Rest. To reduce oxygen demand of tissue.

• Position: Semi to High Fowler’s
• Teaching: PURSE-LIP BREATHING
• Increase fluid intake. To liquify mucus
secretions.
• Good oral care. To remove sputum and
prevent infection.
INTERPROFESSIONAL
COLLABORATIVE MANAGEMENT

• Diet:
 High Calorie – Source of energy
 high Protein(CHON) – helps maintain
integrity of alveolar walls.
 low Carbohydrates(CHO) – Limits CO2
production.
INTERPROFESSIONAL
COLLABORATIVE MANAGEMENT
• O2 therapy 1-3 lpm. The safest amount is
2 lpm.
 Do not give high concentration of O2, The
drive for breathing may be depressed.
 Consistent high CO2 in blood causes
damage in medulla oblongata.
Chemoreceptors in the carotid and aortic
bodies take up the work of breathing. The
stimulus for the peripheral chemoreceptor
is low oxygen levels in the blood.
INTERPROFESSIONAL
COLLABORATIVE MANAGEMENT
• Avoid Cigarette smoking, alcohol,
environmental pollutants, These inhibit
muco-ciliary function.
• CPT – Percussion, Vibration, Postural
drainage.
• Bronchial Hygiene measure.
 Steam inhalation
 Aerosol inhalation
 Medimist inhalation
EMPHYSEMA/CHRONIC BRONCHITIS
MANAGEMANT

MEDICATIONS:
• Bronchodilators
 Beta-2 agonists (ALBUTEROL,
SALBUTAMOL, SALMETEROL,
TERBUTALINE)
 Anticholinergics (IPRATROPIUM)
 Long-acting anticholinergic
(TIOTROPIUM(Spiriva))
EMPHYSEMA/CHRONIC BRONCHITIS
MANAGEMANT

MEDICATIONS:
• Steroid (BUDESONIDE, FLUTICASONE,
BECLOMETHASONE(Beclovent),
METHYLPREDNISONE(Solu-Medrol))
• Methylxanthines (THEOPHYLLINE,
AMINOPHYLLINE)
• Leukotriene antagonists(MONTELUKAST)
• Antimicrobials – if infection is present
EMPHYSEMA/CHRONIC BRONCHITIS
MANAGEMANT

COR PULMONALE
• Hypertrophy of the right side of heart, with
or without heart failure, resulting from
pulmonary hypertension,
• It is caused by diseases affecting the lungs
or pulmonary blood vessels.
Bronchiectasis
A chronic, irreversible dilation of the bronchi
and bronchioles.
CAUSES OF BRONCHIECTASIS

• Airway obstruction
• Diffuse airway injury
• Pulmonary infections and obstruction of
the bronchus or complications of long-term
pulmonary infections
• Genetic disorders such as cystic fibrosis
• Abnormal host defense (eg, ciliary
dyskinesia or humoral immunodeficiency)
• Idiopathic causes
CAUSES OF BRONCHIECTASIS

• People may be predisposed to

bronchiectasis as a result of recurrent
respiratory infections in early childhood:
-Measles
-Influenza
-Tuberculosis
-Immunodeficiency disorders.
PATHOPHYSIOLOGY
 Causes:
-Airway obstruction
-Diffuse airway injury
-Pulmonary infections
-Genetic disorders such as cystic fibrosis
-Abnormal host defense
-Idiopathic

Destruction of elastic and muscular structure supporting

bronchial wall
Reduced ability to clear mucus from the lungs
Decrease expiratory flow

Clinical manifestation
CLINICAL MANIFESTATION

 Persistent or recurrent cough with

production of purulent sputum may exceed
500 ml/day(hallmark of bronchiectasis)
 Dyspnea
 Wheezing
 Pleuritic chest pain
 Hemoptysis
 Crackles/ Rales
DIAGNOSTIC STUDIES

 Chest X-Ray
 High Resolution CT Scan(HRCTS) – Gold
standard for diagnosing bronchiectasis
 Bronchoscopy
 Sputum studies
 Pulmonary function studies
INTERPROFESSIONAL
COLLABORATIVE MANAGEMENT
• Antibiotics
• Bronchodilator therapy(to prevent
bronchospasm)
• Beta-2 antagonist.(to stimulate muco-
ciliary clearance)
• Mucolytic agents.
• Anti-inflammatory agents.
• Pneumococcal and influenza vaccinations.
• Rest, Good nutrition, adequate hydration.
• CPT with postural drainage.
Bronchial asthma
Asthma is a chronic inflammatory disease of the
airways characterized by hyperresponsiveness,
mucosal edema, and mucus production. Allergy
is the strongest factor for the development of
asthma. The most common chronic disease of
childhood, can begin at any age.
RISK FACTORS:
-Family history
-Allergy (strongest factor)
-Chronic exposure to airway irritants or allergens
(eg, grass, weed pollens, mold, dust, or
animals).
COMMON ALLERGENS

 Grass  Histamine-rich
 Tree foods
 Weeds  Eggs
 Pollens  Sea foods
 Molds  Snack foods
 Dust
 Roaches
 Cat/Dog danders
TRIGGERS OF ACUTE ASTHMA ATTACKS

ALLERGEN AIR POLLUTANTS

INHALATION  Exhaust fumes
 Animal danders  Perfumes
 House dust mite  Oxidants
 Cockroaches  Sulfur dioxides
 Pollens  Cigarette smoke
 Molds  Aerosol spray
TRIGGERS OF ACUTE ASTHMA ATTACKS
• Viral Upper Respiratory Infection
• Sinusitis
• Exercise and cold dry air
• Drugs(e.g. ASA, NSAIDSs, beta adrenergic
blockers.
• Occupational exposure
 Metal salt
 Wood and vegetable dust
 Industrial chemicals
 Pharmaceutical agents
TRIGGERS OF ACUTE ASTHMA ATTACKS

• Food additives
 Sulfites
 Beer, wine, dried fruits, shrimp, processed
potatoes, chip
 Monosodium glutamate(MSG)
 Tartrazine (Yellow dye no. 5)
TRIGGERS OF ACUTE ASTHMA ATTACKS

• Hormones, menses
• Gastroesophageal reflux disease
• Stress(Psychological/emotional)
 Crying
 Laughing
 Anger
 Fear
PATHOPHYSIOLOGY
 Allergy
Inflammation

Mast cells, macrophages, eosinophils, neutrophils, T & B

lymphocytes, epithelial cells of the airway become involve
 Most cells degranulate

Histamine, Prostaglandin, Leukotrienes, Interleukin 4 & 5,

Nitric oxide

A. Bronchospasm
 Bronchoconstriction
B. Edema of mucous membrane
C. Hypersecretion of mucus

Narrowing of Airways
Increase work of breath
 Tends to sit up, Restlessness, Tachypnea/ dyspnea,
Tachycardia, Flaring of alae nasi, Diaphoresis, Cold
clammy skin, Wheezing, Retractions, Pallor - cyanosis

Exhaustion
Slow, shallow respiration (Hypoventilation)

Retenbtion of CO2(airtrapping)
Hypoxia Respiratory Acidosis
CLINICAL MANIFESTATION

 wheezing (first on expiration, then later, on

inspiration).
 Cough (thick, tenacious, white, gelatinous
mucus)
 Dyspnea
 Chest tightness
 Prolonged expiration(1:3 or 1:4)
 Sit up and slightly bend forward using
accessory muscle of respiration.
CLINICAL MANIFESTATION
 Signs of hypoxemia
 Restlessness
 Increased anxiety
 Inappropriate behavior
 Increased pulse, BP, pulsus paradoxus
 Difficulty to speak in complete sentences.
 Increased RR (>30bpm) with use of ace.
Muscles.
 Hyperresonance on percussion of the
chest.
CLINICAL MANIFESTATION

NOTE:
 Diminish or Absent breath sounds
 Significant decrease in air
movement(exhaustion)
 Atelectasis or pneumothorax
 Severe Diminish breath sounds(“Silent
chest”)
 Ominous sign, indicating severe and
impending respiratory failure.
CLINICAL MANIFESTATION

NOTE:
 A severe, continuous reaction, “STATUS
ASTHMATICUS”, may occur.
 Does not respond to conventional therapy.
 Attack last longer than 24 hours.
 Life-threatening and places the pt. at risk
for developing respiratory failure.
 “The longer it last, the worse it gets, and
the worse it gets, the longer it last.
CLINICAL MANIFESTATION

NOTE:
Causes of Status asthmaticus
 Viral illness
 Ingestion of ASA or NSAID
 Emotional stress
 Environmental pollutant or other allergen
exposure.
 Abrupt DC of drug therapy(Corticosteroids)
 Overuse of aerosol medications.
 Ingestion of beta-adrenergic blockers.
Assessment and Diagnostic Methods
• Family, environment, and occupational
history is essential.
• During acute episodes
 Sputum and blood test
 Pulse oximetry
 ABGs
 hypocapnia and respiratory alkalosis, and
pulmonary function (forced expiratory
volume [FEV] and forced vital capacity
[FVC] decreased) tests are performed.
Medical Management
Pharmacologic Therapy
There are two classes of medications
 Long-acting control
 Quick-relief medications(as well as
combination products).
 Short-acting beta2-adrenergic agonists
 Anticholinergics
 Corticosteroids: metered-dose inhaler (MDI)
 Leukotriene modifiers inhibitors/
antileukotrienes
 Methylxanthines
Nursing Management

• Assess the patient’s respiratory status by

monitoring the severity of symptoms, breath
sounds, peak flow, pulse oximetry, and vital
signs.
• Obtain a history of allergic reactions to
medications before administering
medications.
• Identify medications the patient is currently
taking.
Nursing Management

• Administer medications as prescribed and

monitor the patient’s responses to those
medications; medications may include an
antibiotic if the patient has an underlying
respiratory infection.
• Administer fluids if the patient is dehydrated.
• Assist with intubation procedure, if required.
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