CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
DR.ALTAF AL-KAMISH
Definition
 COPD is characterised by Persistent airflow limitation that is usually
progressives, not reversible and does not change markedly over several
months.
 The disease is predominantly caused by smoking.
 estimates suggest that 384 million people worldwide suffer from moderate to
severe disease 2010.
 more than 3 million deaths (5% of deaths globally
 Chronic bronchitis: is a clinical diagnosis defined by
excessive secretion of bronchial mucus and is manifested
by daily productive cough for 3 months or more in at least
2 consecutive years.
 Emphysema: is a pathologic diagnosis that denotes
abnormal permanent enlargement of air spaces distal to
the terminal bronchiole, with destruction of their walls
and without obvious fibrosis
Risk factors
 Cigarette smoking is clearly the most important cause of COPD . It is
estimated that 80% of patients seen for COPD have significant exposure to
tobacco smoke.
 The remaining 20% frequently have a combination of exposures to
environmental tobacco smoke, occupational dusts and chemicals, and indoor
air pollution from biomass fuel used for cooking and heating in poorly
ventilated buildings.
 Outdoor air pollution, airway infection, familial factors, and allergy have also
been implicated in chronic bronchitis, and hereditary factors (deficiency of
alpha-1-antiprotease [alpha-1-antitrypsin]) have been implicated
Clinical Findings
 Symptoms :
 excessive cough.
 sputum production.
 shortness of breath.
 Dyspnea.
 Exacerbations Often including increased dyspnea, an increased frequency or
severity of cough, increased sputum volume or change in sputum character.
 These exacerbations are commonly precipitated by infection (more often viral
than bacterial) or environmental factors.
signs
 Signs of respiratory disease tend to appear as COPD progresses.
 normal,
 Cyanosis.,an elevate respiratory rate at rest in mild disease.
 Hyper inflated chest (increased antero- posterior diameter of the chest wall).
 intercostal in drawing.
 diminished breath sounds.
 prolongation of the expiratory phase of respiration
 wheeze is usually heard during expiration
 Late course inspiratory crackles .
 faint heart sounds (due to hyper inflated lungs).
Laboratory Findings
 CBC.
 Serum electrolytes .
 RFT
 LFT.
 ECG P Pulmonal .
 Echocardiography. Pulmonary HTN.
 PFT
 provides objective information about pulmonary function
and assesses the response to therapy.
 COPD can be diagnosed when forced expiratory volume in
1 second/forced vital capacity (FEV1/FVC) <0.7 and FEV1
< 80% predictedI
 f the FEV1 is ≥80% predicted of normal, a diagnosis of
COPD should only be made in the presence of typical
respiratory symptoms.
Normal volume/time tracing
obstructive ventilatory defect
;
Flow/volume
Imaging
 Plain radiographs are insensitive for the diagnosis of
emphysema; they show hyperinflation with flattening of
the diaphragm or peripheral arterial deficiency.
 CT of the chest, particularly using high-resolution CT, is
more sensitive and specific than plain radiographs for its
diagnosis.
Chest X-ray showing typical changes of
chronic obstructive pulmonary disease
High-resolution computed tomogram of the chest
showing widespread upper lobe emphysematous bullae
GOLD CLASSIFICATION
 MILD: FEV1 ≥ 80%.
 Moderate : FEV1 50–79%.
 Severe : FEV1 30–49% .
 Very severe : FEV1 < 30% (or when< 50% with
respiratory failure
Complication
 Acute bronchitis.
 pneumonia.
 pulmonary thromboembolism.
 atrial dysrhythmias .
 Pulmonary hypertension
TREATMENT
 1. Smoking cessation
 2. Home oxygen therapy
 Resting pao2<or=55.
 O2 sat (SaO2)<88%
 Pao2<or=59mmHg O2Sat <or=89% with
 Corpulmonale
 Erythrocytosis.
(
GOLD
)
guidelines for treatment of COPD
 Corticosteroids-
 :Inhaler corticosteroids
 reduction in the frequency of COPD exacerbations
 an increase functional status
 Systemic corticosteroids:
 Only used in COPD EXACERPATION..
 Theophylline is one of the oldest oral therapeutic agents available for the
treatment of COPD .
Non-invasive ventilation (NIV)
 Non-invasive ventilation (NIV) reduces mortality and the need for intubation in
patients with a respiratory acidosis (pH < 7.35 and PaCO2 > 6 kPa)
 NIV should be considered within the first 60 minutes of hospital arrival in all
patients in whom a respiratory acidosis persists despite maximum medical
therapy
 NIV should be initiated only by trained staff; monitoring should include
respiratory rate, arterial blood gases, pulse oximetry, synchrony and compliance
 NIV should be continued until the underlying acute cause has
 resolved
 All patients should have a clear plan recorded and agreed upon
 in the event of NIV failure
الانسداد الرئوي لطلاب التمريض في المستشفى
الانسداد الرئوي لطلاب التمريض في المستشفى

الانسداد الرئوي لطلاب التمريض في المستشفى

  • 1.
  • 2.
    Definition  COPD ischaracterised by Persistent airflow limitation that is usually progressives, not reversible and does not change markedly over several months.  The disease is predominantly caused by smoking.  estimates suggest that 384 million people worldwide suffer from moderate to severe disease 2010.  more than 3 million deaths (5% of deaths globally
  • 3.
     Chronic bronchitis:is a clinical diagnosis defined by excessive secretion of bronchial mucus and is manifested by daily productive cough for 3 months or more in at least 2 consecutive years.  Emphysema: is a pathologic diagnosis that denotes abnormal permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of their walls and without obvious fibrosis
  • 4.
    Risk factors  Cigarettesmoking is clearly the most important cause of COPD . It is estimated that 80% of patients seen for COPD have significant exposure to tobacco smoke.  The remaining 20% frequently have a combination of exposures to environmental tobacco smoke, occupational dusts and chemicals, and indoor air pollution from biomass fuel used for cooking and heating in poorly ventilated buildings.  Outdoor air pollution, airway infection, familial factors, and allergy have also been implicated in chronic bronchitis, and hereditary factors (deficiency of alpha-1-antiprotease [alpha-1-antitrypsin]) have been implicated
  • 5.
    Clinical Findings  Symptoms:  excessive cough.  sputum production.  shortness of breath.  Dyspnea.  Exacerbations Often including increased dyspnea, an increased frequency or severity of cough, increased sputum volume or change in sputum character.  These exacerbations are commonly precipitated by infection (more often viral than bacterial) or environmental factors.
  • 6.
    signs  Signs ofrespiratory disease tend to appear as COPD progresses.  normal,  Cyanosis.,an elevate respiratory rate at rest in mild disease.  Hyper inflated chest (increased antero- posterior diameter of the chest wall).  intercostal in drawing.  diminished breath sounds.  prolongation of the expiratory phase of respiration  wheeze is usually heard during expiration  Late course inspiratory crackles .  faint heart sounds (due to hyper inflated lungs).
  • 9.
    Laboratory Findings  CBC. Serum electrolytes .  RFT  LFT.  ECG P Pulmonal .  Echocardiography. Pulmonary HTN.  PFT
  • 10.
     provides objectiveinformation about pulmonary function and assesses the response to therapy.  COPD can be diagnosed when forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) <0.7 and FEV1 < 80% predictedI  f the FEV1 is ≥80% predicted of normal, a diagnosis of COPD should only be made in the presence of typical respiratory symptoms.
  • 11.
  • 12.
  • 13.
  • 14.
    Imaging  Plain radiographsare insensitive for the diagnosis of emphysema; they show hyperinflation with flattening of the diaphragm or peripheral arterial deficiency.  CT of the chest, particularly using high-resolution CT, is more sensitive and specific than plain radiographs for its diagnosis.
  • 15.
    Chest X-ray showingtypical changes of chronic obstructive pulmonary disease
  • 16.
    High-resolution computed tomogramof the chest showing widespread upper lobe emphysematous bullae
  • 17.
    GOLD CLASSIFICATION  MILD:FEV1 ≥ 80%.  Moderate : FEV1 50–79%.  Severe : FEV1 30–49% .  Very severe : FEV1 < 30% (or when< 50% with respiratory failure
  • 18.
    Complication  Acute bronchitis. pneumonia.  pulmonary thromboembolism.  atrial dysrhythmias .  Pulmonary hypertension
  • 19.
    TREATMENT  1. Smokingcessation  2. Home oxygen therapy  Resting pao2<or=55.  O2 sat (SaO2)<88%  Pao2<or=59mmHg O2Sat <or=89% with  Corpulmonale  Erythrocytosis.
  • 20.
  • 21.
     Corticosteroids-  :Inhalercorticosteroids  reduction in the frequency of COPD exacerbations  an increase functional status  Systemic corticosteroids:  Only used in COPD EXACERPATION..  Theophylline is one of the oldest oral therapeutic agents available for the treatment of COPD .
  • 22.
    Non-invasive ventilation (NIV) Non-invasive ventilation (NIV) reduces mortality and the need for intubation in patients with a respiratory acidosis (pH < 7.35 and PaCO2 > 6 kPa)  NIV should be considered within the first 60 minutes of hospital arrival in all patients in whom a respiratory acidosis persists despite maximum medical therapy  NIV should be initiated only by trained staff; monitoring should include respiratory rate, arterial blood gases, pulse oximetry, synchrony and compliance  NIV should be continued until the underlying acute cause has  resolved  All patients should have a clear plan recorded and agreed upon  in the event of NIV failure