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Chronic obstructive pulmonary disease

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This document provides information on chronic obstructive pulmonary disease (COPD). It discusses the epidemiology, definition, risk factors, pathogenesis, pathology, classification, management, and exacerbations of COPD. Key points include: cigarette smoking is the primary cause of COPD worldwide; the disease involves inflammation in the lungs from noxious particles leading to airflow limitation; emphysema and chronic bronchitis are the major pathological changes; severity is classified based on lung function tests; and management involves reducing risk factors, treating stable COPD, and managing exacerbations.

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CHRONICCHRONIC OBSTRUCTIVEOBSTRUCTIVE PULMONARY DISEASEPULMONARY DISEASE Iman Galal, MDIman Galal, MD Pulmonary Medicine DepartmentPulmonary Medicine Department Ain Shams UniversityAin Shams University
Page  2 Contents of the Lecture:Contents of the Lecture: EpidemiologyEpidemiology DefinitionDefinition Risk factorsRisk factors PathogenesisPathogenesis PathologyPathology ClassificationClassification ManagementManagement COPD exacerbationsCOPD exacerbations
Page  3 Epidemiology:Epidemiology:  Cigarette smoking is the primary cause of COPD.Cigarette smoking is the primary cause of COPD.  The WHO estimates 1.3 billion smokers worldwide,The WHO estimates 1.3 billion smokers worldwide, increasing to 2 billion by 2025.increasing to 2 billion by 2025.  In 2000, the WHO estimated 2.74 million deathsIn 2000, the WHO estimated 2.74 million deaths worldwide from COPD.worldwide from COPD.  In 1990, COPD was rankedIn 1990, COPD was ranked 1212thth as a burden of disease.as a burden of disease.  After 25 years of smoking, at least 25% of smokers without initial disease will have clinically significant COPD
Page  4 US Leading Causes of Death 2001US Leading Causes of Death 2001
Page  5 Chronic Obstructive Pulmonary Disease:Chronic Obstructive Pulmonary Disease: Chronic Obstructive Pulmonary Disease (COPD) is aChronic Obstructive Pulmonary Disease (COPD) is a preventablepreventable && treatabletreatable disease with some significantdisease with some significant extrapulmonaryextrapulmonary effects that may contribute to the severityeffects that may contribute to the severity in individual patients. Itsin individual patients. Its pulmonarypulmonary component iscomponent is characterized bycharacterized by airflow limitationairflow limitation that isthat is not fullynot fully reversible.reversible. The airflow limitation is usuallyThe airflow limitation is usually progressiveprogressive && associated with anassociated with an abnormal inflammatory responseabnormal inflammatory response ofof the lung to noxious particles or gases.the lung to noxious particles or gases. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  6 Emphysema:Emphysema:  AbnormalAbnormal permanentpermanent enlargement of the airspaces distalenlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction ofto the terminal bronchiole, accompanied by destruction of their walls without fibrosis.their walls without fibrosis.  Types:Types: (1)(1) Centrilobular (centriacinar)Centrilobular (centriacinar) (2)(2) Panlobular (panacinar)Panlobular (panacinar) (3)(3) Paraseptal (distal acinar)Paraseptal (distal acinar) (4)(4) IrregularIrregular
Page  7 Chronic bronchitis:Chronic bronchitis:  Presence ofPresence of chronic productive coughchronic productive cough forfor 3 months3 months in each ofin each of 2 successive years2 successive years in a patient in whomin a patient in whom otherother causescauses ofof chronic coughchronic cough have beenhave been excluded.excluded.
Page  8 Risk Factors:Risk Factors: Genes Exposure to particles 1. Tobacco smoke 2. Occupational dust, organic & inorganic 3. Indoor air pollution 4. Outdoor air pollution Lung growth & development Oxidative stress Gender Age Respiratory infections Previous TB Socioeconomic status Nutrition Comorbidities
Page  9 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  10 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. InflammationInflammation Small Airway DiseaseSmall Airway Disease Airway inflammationAirway inflammation Parenchymal DistructionParenchymal Distruction Decrease elastic recoilDecrease elastic recoil Loss of alveolar attachmentLoss of alveolar attachment Airflow LimitationAirflow Limitation
Page  11 Overlap of Obstructive Lung DiseaseOverlap of Obstructive Lung Disease Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  12 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. AsthmaAsthma Asthmatic AirwayAsthmatic Airway InflammationInflammation CD4-T lymphocytesCD4-T lymphocytes EosinophilsEosinophils COPD AirwayCOPD Airway InflammationInflammation CD8-T lymphocytesCD8-T lymphocytes MacrophagesMacrophages NeutrophilsNeutrophils Airflow LimitationAirflow Limitation COPDCOPD FullyFully ReversibleReversible Not FullyNot Fully ReversibleReversible
Page  13 PathologyPathology 1.1.Mucus gland hypertrophyMucus gland hypertrophy 2.2.Smooth muscle hypertrophySmooth muscle hypertrophy 3.3.Goblet cell hyperplasiaGoblet cell hyperplasia 4.4.Inflammatory infiltrateInflammatory infiltrate 5.5.Excessive mucusExcessive mucus 6.6.Squamous metaplasiaSquamous metaplasia Normal BronchialNormal Bronchial ArchitectureArchitecture COPDCOPD
Page  14 Healthy Respiratory MucosaHealthy Respiratory Mucosa  This EM shows theThis EM shows the respiratory mucosa in arespiratory mucosa in a healthy state.healthy state.  The cells are fully ciliated.The cells are fully ciliated.  The cilia beat in a co-The cilia beat in a co- ordinated fashion to moveordinated fashion to move mucus out of the airwaysmucus out of the airways (mucociliary transport).(mucociliary transport). Scanning electron micrograph showing aScanning electron micrograph showing a sheet of mucus being moved along by the ciliasheet of mucus being moved along by the cilia
Page  15 Damaged Respiratory MucosaDamaged Respiratory Mucosa  Damage to the cilia & epitheliumDamage to the cilia & epithelium occur as a result of diseaseoccur as a result of disease processes in COPD. This can alsoprocesses in COPD. This can also occur as a result of bacterialoccur as a result of bacterial damage.damage.  This slide shows the result ofThis slide shows the result of bacterial infection stripping awaybacterial infection stripping away the cilia from the mucosa.the cilia from the mucosa.  The damage to the cilia meansThe damage to the cilia means they are less effective in removingthey are less effective in removing mucus from the airwaysmucus from the airways Scanning electron micrograph showing cilialScanning electron micrograph showing cilial and epithelial damage induced by bacteriaand epithelial damage induced by bacteria
Page  16 Centriacinar EmphysemaCentriacinar Emphysema  Characterized by focal destruction limited to the respiratory bronchioles &Characterized by focal destruction limited to the respiratory bronchioles & the central portions of acinus.the central portions of acinus.  Is is associated with cigarette smoking & is most severe in the upper lobes.Is is associated with cigarette smoking & is most severe in the upper lobes.
Page  17 Panacinar EmphysemaPanacinar Emphysema  It involves the entire alveolus distal to the terminal bronchiole.It involves the entire alveolus distal to the terminal bronchiole.  It is most severe in the lower lung zones & generally develops in patientsIt is most severe in the lower lung zones & generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency.with homozygous alpha1-antitrypsin (AAT) deficiency.
Page  18 Distal acinar EmphysemaDistal acinar Emphysema  Distal acinar emphysema orDistal acinar emphysema or paraseptal emphysema, is theparaseptal emphysema, is the least common form and involvesleast common form and involves distal airway structures, alveolardistal airway structures, alveolar ducts, and sacs.ducts, and sacs.  This form of emphysema isThis form of emphysema is localized to fibrous septa or tolocalized to fibrous septa or to the pleura & leads to formationthe pleura & leads to formation of bullae.of bullae.  The apical bullae may causeThe apical bullae may cause pneumothorax.pneumothorax.  Paraseptal emphysema is notParaseptal emphysema is not associated with airflowassociated with airflow obstruction.obstruction.
Page  19 EmphysemaEmphysema
Page  20 EmphysemaEmphysema EmphysemaEmphysemaNormal LungNormal Lung
Page  21 EmphysemaEmphysema EmphysemaEmphysemaNormal LungNormal Lung
Page  22 Management of COPD:Management of COPD: (1)(1) Assess and Monitor Disease.Assess and Monitor Disease. (2)(2) Reduce Risk Factors.Reduce Risk Factors. (3)(3) Manage Stable COPD.Manage Stable COPD. (4)(4) Manage Exacerbations.Manage Exacerbations.
Page  23 A) Assess & Monitor of COPD:A) Assess & Monitor of COPD: 1) Assessment of symptoms:1) Assessment of symptoms:  CoughCough  DyspneaDyspnea  Sputum productionSputum production 2) History taking:2) History taking:  Exposure to risk factors e.g., smoking, occupational or environmental.Exposure to risk factors e.g., smoking, occupational or environmental.  Pattern of symptom development.Pattern of symptom development.  History of exacerbations or previous hospitalizationsHistory of exacerbations or previous hospitalizations  Presence of comorbidities e.g., heart disease, malignancies & osteoporosisPresence of comorbidities e.g., heart disease, malignancies & osteoporosis  Appropriateness of current medical treatments.Appropriateness of current medical treatments.  Impact of disease on patients life, including limitation of activity, missed workImpact of disease on patients life, including limitation of activity, missed work  Social and family support available to the patientSocial and family support available to the patient  Possibilities for reducing risk factors, especially smoking cessationPossibilities for reducing risk factors, especially smoking cessation Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  24 MRC Dyspnea ScaleMRC Dyspnea Scale
Page  25 Chronic Cough with Normal CXRChronic Cough with Normal CXR IntrathoracicIntrathoracic  Chronic obstructive pulmonary diseaseChronic obstructive pulmonary disease  Bronchial asthmaBronchial asthma  Central bronchial carcinomaCentral bronchial carcinoma  Endobronchial tuberculosisEndobronchial tuberculosis  BronchiectasisBronchiectasis  Left sided heart failureLeft sided heart failure  Interstitial lung diseaseInterstitial lung disease  Cystic fibrosisCystic fibrosis ExtrathoracicExtrathoracic  Postnasal dripPostnasal drip  Gastroesophageal refluxGastroesophageal reflux  Drug therapy (e.g., ACE inhibitors)Drug therapy (e.g., ACE inhibitors) Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  26 Systemic manifestations of COPD:Systemic manifestations of COPD:  Skeletal muscle wastingSkeletal muscle wasting  Cachexia: loss of fat-free massCachexia: loss of fat-free mass  Lung cancer (SCLC & NSCLC)Lung cancer (SCLC & NSCLC)  Pulmonary hypertensionPulmonary hypertension  Ischaemic heart diseaseIschaemic heart disease  Congestive cardiac failureCongestive cardiac failure  OsteoporosisOsteoporosis  Normocytic anaemiaNormocytic anaemia  DiabetesDiabetes  Metabolic syndromeMetabolic syndrome  Obstructive sleep apneaObstructive sleep apnea  DepressionDepression
Page  27  Central cyanosisCentral cyanosis  Hyperinflated chestHyperinflated chest  Increased resting respiratory rate with shallow breathingIncreased resting respiratory rate with shallow breathing  Pursed-lip breathingPursed-lip breathing  Respiratory distressRespiratory distress  Lower limb edemaLower limb edema  Difficulty in detection of heart apexDifficulty in detection of heart apex  Resonant bare area of the heartResonant bare area of the heart  Downward displacement of the liverDownward displacement of the liver  Distant breath soundsDistant breath sounds  Wheezy chestWheezy chest Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. 3) Physical Examination:3) Physical Examination:
Page  28 Hyperinflation in COPD:Hyperinflation in COPD:
Page  29 4) Spirometric Classification of COPD:4) Spirometric Classification of COPD: Severity Based on Post-Bronchodilator FEV1Severity Based on Post-Bronchodilator FEV1 StageStage Stage IStage I MildMild FEV1/FVC < 0.70 FEV1 ≥ 80% predicted Stage IIStage II ModerateModerate FEV1/FVC < 0.70 50% ≤ FEV1 < 80% predicted Stage IIIStage III SevereSevere FEV1/FVC < 0.70 30% ≤ FEV1 < 50% predicted Stage IVStage IV VeryVery SevereSevere FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  30 5) Bronchodilator Reversibility Testing:5) Bronchodilator Reversibility Testing: PreparationPreparation  Patients should be clinically stable & free from respiratory infection.Patients should be clinically stable & free from respiratory infection.  Patients should not have taken inhaled short-acting bronchodilators in thePatients should not have taken inhaled short-acting bronchodilators in the previous 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustainedprevious 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustained release theophylline in the previous 24 hrs.release theophylline in the previous 24 hrs. SpirometrySpirometry  FEV1 should be measured before a bronchodilator is given.FEV1 should be measured before a bronchodilator is given.  The bronchodilator should be given by metered dose inhaler through a spacerThe bronchodilator should be given by metered dose inhaler through a spacer device or by nebulizer.device or by nebulizer.  Possible dosage protocols are 400 gPossible dosage protocols are 400 g ββ2-agonist, up to 160 g anticholinergic, or2-agonist, up to 160 g anticholinergic, or the two combined.the two combined.  FEV1 should be measured again 10-15 minutes after a short-actingFEV1 should be measured again 10-15 minutes after a short-acting bronchodilator is given; 30-45 minutes after the combination.bronchodilator is given; 30-45 minutes after the combination. ResultsResults  Increase in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 isIncrease in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 is considered significant.considered significant. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  31 6) Lung Volumes:6) Lung Volumes: The three volumes most relevant to COPD are forced vital capacity (FVC), residual volume (RV), & total lung capacity (TLC).
Page  32 7) Exercise Testing:7) Exercise Testing: Measurement COPD VO2max Decreased Anaerobic threshold Normal/decreased/indeterminate Peak HR Decreased, Normal in mild O2 pulse Normal or decreased (VE/MVV) X 100 Increased VE/VCO2 (at AT) Increased VD/VT Increased PaO2 Variable P(A-a)O2 Variable, usually increased
Page  33 8) Arterial Blood Gases:8) Arterial Blood Gases:  In advanced COPD, measurement of ABGs should be performed in stableIn advanced COPD, measurement of ABGs should be performed in stable patients with FEV1 < 50% predicted or with clinical signs of respiratorypatients with FEV1 < 50% predicted or with clinical signs of respiratory failure or right heart failure.failure or right heart failure.  Changes in arterial blood gas tensions take time to occur. Thus, 20-30Changes in arterial blood gas tensions take time to occur. Thus, 20-30 minutes should pass before rechecking the gas tensions when the FIO2minutes should pass before rechecking the gas tensions when the FIO2 has been changed, e.g., during assessment for domiciliary oxygen therapy.has been changed, e.g., during assessment for domiciliary oxygen therapy.  Adequate pressure must be applied at the arterial puncture site for atAdequate pressure must be applied at the arterial puncture site for at least one minute, as failure to do so can lead to painful bruising.least one minute, as failure to do so can lead to painful bruising. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  34 9) Chest X ray:9) Chest X ray:
Page  35 Differential Diagnosis of COPD:Differential Diagnosis of COPD: DiagnosisDiagnosis Suggestive FeaturesSuggestive Features COPDCOPD Onset in mid-life.Onset in mid-life. Symptoms slowly progressive.Symptoms slowly progressive. Long history of tobacco smoking.Long history of tobacco smoking. Dyspnea during exercise.Dyspnea during exercise. Largely irreversible airflow limitation.Largely irreversible airflow limitation. AsthmaAsthma Onset early in life (often childhood).Onset early in life (often childhood). Symptoms vary from day to day.Symptoms vary from day to day. Symptoms at night/early morning.Symptoms at night/early morning. Allergy, rhinitis, and/or eczema also present.Allergy, rhinitis, and/or eczema also present. Family history of asthma.Family history of asthma. Largely reversible airflow limitation.Largely reversible airflow limitation. CongestiveCongestive Heart FailureHeart Failure Fine basilar crackles on auscultation.Fine basilar crackles on auscultation. Chest X-ray shows dilated heart, pulmonary edemaChest X-ray shows dilated heart, pulmonary edema Pulmonary function tests indicate volume restriction, not airflowPulmonary function tests indicate volume restriction, not airflow limitation.limitation. BronchiectasiBronchiectasi ss Onset all agesOnset all ages Chest X-ray shows lung infiltrate.Chest X-ray shows lung infiltrate. Microbiological confirmation.Microbiological confirmation.
Page  36 B) Reduce Risk Factors:B) Reduce Risk Factors: 1.1. SmokingSmoking 2.2. Occupational exposureOccupational exposure 3.3. Indoor/Outdoor air pollutionIndoor/Outdoor air pollution
Page  37 Smoking Cessation:Smoking Cessation: ASK:ASK: Identify all tobacco users at every visit.Identify all tobacco users at every visit. ADVISE:ADVISE: Strongly urge all tobacco users to quit.Strongly urge all tobacco users to quit. ASSESS:ASSESS: Willingness to make a quit attempt.Willingness to make a quit attempt. ASSIST:ASSIST: Aid the patient in quitting.Aid the patient in quitting. ARRANGE:ARRANGE: Schedule follow-up contact.Schedule follow-up contact.
Page  38 COPD Risk & Smoking CessationCOPD Risk & Smoking Cessation Adapted from Fletcher C et al. Br Med J. 1977;1:1645–1648. Stopped smokingStopped smoking at 45 (mild COPD)at 45 (mild COPD) Stopped smokingStopped smoking at 65 (severe COPD)at 65 (severe COPD)
Page  39 C) Manage Stable COPD:C) Manage Stable COPD:  Pharmacological therapyPharmacological therapy  Long-term oxygen therapyLong-term oxygen therapy  Pulmonary rehabilitationPulmonary rehabilitation  NutritionNutrition  SurgerySurgery
Page  40 Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. C) Manage Stable COPDC) Manage Stable COPD::
Page  41 Pharmacological TherapyPharmacological Therapy::  The medications for COPD currently available can reduce or abolish symptoms, increase exercise capacity, reduce the number and severity of exacerbations, and improve health status.  At present, no treatment has been shown to modify the rate of decline in lung function.  The inhaled route is preferred.
Page  42 Pharmacological TherapyPharmacological Therapy:: BronchodilatorsBronchodilators  Three types of bronchodilators are available:Three types of bronchodilators are available: 1.1. β-agonistsβ-agonists 2.2. Anticholinergic drugsAnticholinergic drugs 3.3. Methylxanthines.Methylxanthines. β-agonistsβ-agonists  Salbutamol (Ventolin)Salbutamol (Ventolin)  Sameterol (Servent)Sameterol (Servent)  Formoterol (Foradil)Formoterol (Foradil)  TerbutalinTerbutalin AnticholinergicsAnticholinergics  Ibrtropuim bromideIbrtropuim bromide (Atrovent)(Atrovent)  Tiotropuim bromideTiotropuim bromide (Spiriva)(Spiriva) MethylxanthineMethylxanthine  AminophyllineAminophylline (Uniphylline,(Uniphylline, Quibron, Theo SR)Quibron, Theo SR)
Page  43 Pharmacological TherapyPharmacological Therapy:: Inhaled CorticosteroidsInhaled Corticosteroids  Types of Inhaled Corticosteroids (ICS):Types of Inhaled Corticosteroids (ICS):  Beclomethasone dipropionate (Clenil)Beclomethasone dipropionate (Clenil)  Fluticasone propionate (Flexotide)Fluticasone propionate (Flexotide)  Budesonide (Meflonide)Budesonide (Meflonide)  Ciclesonide (Alvesco)Ciclesonide (Alvesco)
Page  44 Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy  Three types of bronchodilators are available:Three types of bronchodilators are available: 1.1. Meter dose inhalerMeter dose inhaler 2.2. DiskusDiskus 3.3. TubuhalerTubuhaler 4.4. AerolizerAerolizer 5.5. HandihalerHandihaler 6.6. NebulizerNebulizer
Page  45 Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy
Page  46 C) Manage Stable COPD:C) Manage Stable COPD: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  47 Long-term Oxygen Therapy:Long-term Oxygen Therapy:  Long-term oxygen therapy (LTOT) improves survival, exercise, sleep and cognitive performance.  Physiological indications for oxygen include an arterial oxygen tension (Pa,O2) <55 mmHg guided by ABGs.  The therapeutic goal is to maintain Sa,O2 >90% during rest, sleep and exertion.  If oxygen was prescribed during an exacerbation, recheck ABGs after 30–90 days.
Page  48 Long-term Oxygen Therapy:Long-term Oxygen Therapy:
Page  49 RehabilitationRehabilitation For the lungs to get more airFor the lungs to get more air PURSED-LIP BREATHINGPURSED-LIP BREATHING (like breathing out slowly into a straw)(like breathing out slowly into a straw) INHALEINHALE EXHALEEXHALE
Page  50 RehabilitationRehabilitation Sit comfortablySit comfortably && relax your shouldersrelax your shoulders Put one hand on yourPut one hand on your abdomen. Now inhaleabdomen. Now inhale slowly through yourslowly through your nose. (Push yournose. (Push your abdomen out while youabdomen out while you breathe in)breathe in) Then push in yourThen push in your abdominal musclesabdominal muscles and breathe out usingand breathe out using the pursed-lipthe pursed-lip techniquetechnique For the lungs to get more airFor the lungs to get more air DIAPHRAGMATIC BREATHINGDIAPHRAGMATIC BREATHING
Page  51 Nutrition:Nutrition:  Weight loss & depletion of fat-free mass (FFM) may be observed inWeight loss & depletion of fat-free mass (FFM) may be observed in stable COPD patients.stable COPD patients.  Being underweight is associated with an increased mortality risk.Being underweight is associated with an increased mortality risk.  Criteria to define weight loss are:Criteria to define weight loss are: Weight loss >10% in the past 6 months or >5% in the past month.Weight loss >10% in the past 6 months or >5% in the past month.  Nutritional therapy may only be effective if combined with exercise orNutritional therapy may only be effective if combined with exercise or other anabolic stimuli.other anabolic stimuli. UnderweightUnderweight BMI <21 kgBMI <21 kg··mm-2-2 ;age >50 yrs;age >50 yrs Normal weightNormal weight BMI <21–25 kgBMI <21–25 kg··mm-2-2 OverweightOverweight BMI <30 kgBMI <30 kg··mm-2-2 ObeseObese BMIBMI ≥≥30 kg30 kg··mm-2-2
Page  52 Lung Volume Reduction In EmphysemaLung Volume Reduction In Emphysema ↓ ↓ ↑ ↑ ↑ ↑ ↓ ↑ ↑ ↓ ↓ ↓
Page  53 What's a COPD Exacerbation?What's a COPD Exacerbation?  An exacerbation of COPD is defined as an event in theAn exacerbation of COPD is defined as an event in the natural course of the disease characterized by a change innatural course of the disease characterized by a change in the patients baseline dyspnea, cough, and/or sputum that isthe patients baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, andbeyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patientmay warrant a change in regular medication in a patient with underlying COPD.with underlying COPD. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
Page  54 Anthonisen's Typing of COPD ExacerbationAnthonisen's Typing of COPD Exacerbation Cardinal SignsCardinal Signs Worsening dyspnea, increase in sputum volume & purulenceWorsening dyspnea, increase in sputum volume & purulence Other SignsOther Signs Upper respiratory tract infection in past 5 days, fever without otherUpper respiratory tract infection in past 5 days, fever without other apparent cause, wheezing, increase cough & increase respiratoryapparent cause, wheezing, increase cough & increase respiratory rate or heart rate by 20% above baselinerate or heart rate by 20% above baseline All 3 cardinal symptomsAll 3 cardinal symptoms Type 1 (SEVERE)Type 1 (SEVERE) 2 of 3 cardinal symptoms2 of 3 cardinal symptoms Type 2 (MODERATE)Type 2 (MODERATE) 1 of 3 cardinal symptoms1 of 3 cardinal symptoms Type 3 (MILD)Type 3 (MILD)
Page  55 Causes of COPD ExacerbationsCauses of COPD Exacerbations
Page  56 D) Manage Exacerbations:D) Manage Exacerbations: Assessment of COPD ExacerbationsAssessment of COPD Exacerbations Medical HistoryMedical History  Severity of FEV1Severity of FEV1  Duration of worsening or newDuration of worsening or new symptomssymptoms  Number of previousNumber of previous (exacerbations/hospitalizations)(exacerbations/hospitalizations)  ComordibitiesComordibities  Present treatment regimenPresent treatment regimen Signs of SeveritySigns of Severity  Use of accessory respiratoryUse of accessory respiratory musclesmuscles  Paradoxical chest wall movementsParadoxical chest wall movements  Worsening or new central cyanosisWorsening or new central cyanosis  Peripheral edemaPeripheral edema  Hemodynamic instabilityHemodynamic instability  Signs of right heart failureSigns of right heart failure  Reduced alertnessReduced alertness
Page  57 Indications for Hospitalization in AECB:Indications for Hospitalization in AECB:  Marked increase in symptoms, e.g. sudden development of restingMarked increase in symptoms, e.g. sudden development of resting dyspnea.dyspnea.  Severe underlying COPDSevere underlying COPD  Onset of new physical signs (e.g., cyanosis, peripheral edema)Onset of new physical signs (e.g., cyanosis, peripheral edema)  Failure of exacerbation to respond to initial medical managementFailure of exacerbation to respond to initial medical management  Significant comorbidities.Significant comorbidities.  Frequent exacerbations.Frequent exacerbations.  Newly occurring arrhythmias.Newly occurring arrhythmias.  Diagnostic uncertainty.Diagnostic uncertainty.  Older age.Older age.  Insufficient home support.Insufficient home support.
Page  58 Indications for ICU admission in AECB:Indications for ICU admission in AECB:  Severe dyspnea that responds inadequately to initialSevere dyspnea that responds inadequately to initial emergency therapy.emergency therapy.  Changes in mental status (Confusion, lethargy, coma).Changes in mental status (Confusion, lethargy, coma).  Persistent or worsening hypoxemia (PaO2<40 mmHg),Persistent or worsening hypoxemia (PaO2<40 mmHg), and/or severe/worsening hypercapnia (PaCO2>60 mmHg),and/or severe/worsening hypercapnia (PaCO2>60 mmHg), and/or severe/worsening acidosis (pH<7.25) despiteand/or severe/worsening acidosis (pH<7.25) despite supplemental oxygen & non-invasive ventilation.supplemental oxygen & non-invasive ventilation.  Need for invasive mechanical ventilation.Need for invasive mechanical ventilation.  Hemodynamic instability – need for vasopressors.Hemodynamic instability – need for vasopressors.
Page  59 Management of COPD ExacerbationManagement of COPD Exacerbation
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Chronic obstructive pulmonary disease

  • 1. CHRONICCHRONIC OBSTRUCTIVEOBSTRUCTIVE PULMONARY DISEASEPULMONARY DISEASE Iman Galal, MDIman Galal, MD Pulmonary Medicine DepartmentPulmonary Medicine Department Ain Shams UniversityAin Shams University
  • 2. Page  2 Contents of the Lecture:Contents of the Lecture: EpidemiologyEpidemiology DefinitionDefinition Risk factorsRisk factors PathogenesisPathogenesis PathologyPathology ClassificationClassification ManagementManagement COPD exacerbationsCOPD exacerbations
  • 3. Page  3 Epidemiology:Epidemiology:  Cigarette smoking is the primary cause of COPD.Cigarette smoking is the primary cause of COPD.  The WHO estimates 1.3 billion smokers worldwide,The WHO estimates 1.3 billion smokers worldwide, increasing to 2 billion by 2025.increasing to 2 billion by 2025.  In 2000, the WHO estimated 2.74 million deathsIn 2000, the WHO estimated 2.74 million deaths worldwide from COPD.worldwide from COPD.  In 1990, COPD was rankedIn 1990, COPD was ranked 1212thth as a burden of disease.as a burden of disease.  After 25 years of smoking, at least 25% of smokers without initial disease will have clinically significant COPD
  • 4. Page  4 US Leading Causes of Death 2001US Leading Causes of Death 2001
  • 5. Page  5 Chronic Obstructive Pulmonary Disease:Chronic Obstructive Pulmonary Disease: Chronic Obstructive Pulmonary Disease (COPD) is aChronic Obstructive Pulmonary Disease (COPD) is a preventablepreventable && treatabletreatable disease with some significantdisease with some significant extrapulmonaryextrapulmonary effects that may contribute to the severityeffects that may contribute to the severity in individual patients. Itsin individual patients. Its pulmonarypulmonary component iscomponent is characterized bycharacterized by airflow limitationairflow limitation that isthat is not fullynot fully reversible.reversible. The airflow limitation is usuallyThe airflow limitation is usually progressiveprogressive && associated with anassociated with an abnormal inflammatory responseabnormal inflammatory response ofof the lung to noxious particles or gases.the lung to noxious particles or gases. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 6. Page  6 Emphysema:Emphysema:  AbnormalAbnormal permanentpermanent enlargement of the airspaces distalenlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction ofto the terminal bronchiole, accompanied by destruction of their walls without fibrosis.their walls without fibrosis.  Types:Types: (1)(1) Centrilobular (centriacinar)Centrilobular (centriacinar) (2)(2) Panlobular (panacinar)Panlobular (panacinar) (3)(3) Paraseptal (distal acinar)Paraseptal (distal acinar) (4)(4) IrregularIrregular
  • 7. Page  7 Chronic bronchitis:Chronic bronchitis:  Presence ofPresence of chronic productive coughchronic productive cough forfor 3 months3 months in each ofin each of 2 successive years2 successive years in a patient in whomin a patient in whom otherother causescauses ofof chronic coughchronic cough have beenhave been excluded.excluded.
  • 8. Page  8 Risk Factors:Risk Factors: Genes Exposure to particles 1. Tobacco smoke 2. Occupational dust, organic & inorganic 3. Indoor air pollution 4. Outdoor air pollution Lung growth & development Oxidative stress Gender Age Respiratory infections Previous TB Socioeconomic status Nutrition Comorbidities
  • 9. Page  9 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 10. Page  10 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. InflammationInflammation Small Airway DiseaseSmall Airway Disease Airway inflammationAirway inflammation Parenchymal DistructionParenchymal Distruction Decrease elastic recoilDecrease elastic recoil Loss of alveolar attachmentLoss of alveolar attachment Airflow LimitationAirflow Limitation
  • 11. Page  11 Overlap of Obstructive Lung DiseaseOverlap of Obstructive Lung Disease Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 12. Page  12 Pathogenesis:Pathogenesis: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. AsthmaAsthma Asthmatic AirwayAsthmatic Airway InflammationInflammation CD4-T lymphocytesCD4-T lymphocytes EosinophilsEosinophils COPD AirwayCOPD Airway InflammationInflammation CD8-T lymphocytesCD8-T lymphocytes MacrophagesMacrophages NeutrophilsNeutrophils Airflow LimitationAirflow Limitation COPDCOPD FullyFully ReversibleReversible Not FullyNot Fully ReversibleReversible
  • 13. Page  13 PathologyPathology 1.1.Mucus gland hypertrophyMucus gland hypertrophy 2.2.Smooth muscle hypertrophySmooth muscle hypertrophy 3.3.Goblet cell hyperplasiaGoblet cell hyperplasia 4.4.Inflammatory infiltrateInflammatory infiltrate 5.5.Excessive mucusExcessive mucus 6.6.Squamous metaplasiaSquamous metaplasia Normal BronchialNormal Bronchial ArchitectureArchitecture COPDCOPD
  • 14. Page  14 Healthy Respiratory MucosaHealthy Respiratory Mucosa  This EM shows theThis EM shows the respiratory mucosa in arespiratory mucosa in a healthy state.healthy state.  The cells are fully ciliated.The cells are fully ciliated.  The cilia beat in a co-The cilia beat in a co- ordinated fashion to moveordinated fashion to move mucus out of the airwaysmucus out of the airways (mucociliary transport).(mucociliary transport). Scanning electron micrograph showing aScanning electron micrograph showing a sheet of mucus being moved along by the ciliasheet of mucus being moved along by the cilia
  • 15. Page  15 Damaged Respiratory MucosaDamaged Respiratory Mucosa  Damage to the cilia & epitheliumDamage to the cilia & epithelium occur as a result of diseaseoccur as a result of disease processes in COPD. This can alsoprocesses in COPD. This can also occur as a result of bacterialoccur as a result of bacterial damage.damage.  This slide shows the result ofThis slide shows the result of bacterial infection stripping awaybacterial infection stripping away the cilia from the mucosa.the cilia from the mucosa.  The damage to the cilia meansThe damage to the cilia means they are less effective in removingthey are less effective in removing mucus from the airwaysmucus from the airways Scanning electron micrograph showing cilialScanning electron micrograph showing cilial and epithelial damage induced by bacteriaand epithelial damage induced by bacteria
  • 16. Page  16 Centriacinar EmphysemaCentriacinar Emphysema  Characterized by focal destruction limited to the respiratory bronchioles &Characterized by focal destruction limited to the respiratory bronchioles & the central portions of acinus.the central portions of acinus.  Is is associated with cigarette smoking & is most severe in the upper lobes.Is is associated with cigarette smoking & is most severe in the upper lobes.
  • 17. Page  17 Panacinar EmphysemaPanacinar Emphysema  It involves the entire alveolus distal to the terminal bronchiole.It involves the entire alveolus distal to the terminal bronchiole.  It is most severe in the lower lung zones & generally develops in patientsIt is most severe in the lower lung zones & generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency.with homozygous alpha1-antitrypsin (AAT) deficiency.
  • 18. Page  18 Distal acinar EmphysemaDistal acinar Emphysema  Distal acinar emphysema orDistal acinar emphysema or paraseptal emphysema, is theparaseptal emphysema, is the least common form and involvesleast common form and involves distal airway structures, alveolardistal airway structures, alveolar ducts, and sacs.ducts, and sacs.  This form of emphysema isThis form of emphysema is localized to fibrous septa or tolocalized to fibrous septa or to the pleura & leads to formationthe pleura & leads to formation of bullae.of bullae.  The apical bullae may causeThe apical bullae may cause pneumothorax.pneumothorax.  Paraseptal emphysema is notParaseptal emphysema is not associated with airflowassociated with airflow obstruction.obstruction.
  • 22. Page  22 Management of COPD:Management of COPD: (1)(1) Assess and Monitor Disease.Assess and Monitor Disease. (2)(2) Reduce Risk Factors.Reduce Risk Factors. (3)(3) Manage Stable COPD.Manage Stable COPD. (4)(4) Manage Exacerbations.Manage Exacerbations.
  • 23. Page  23 A) Assess & Monitor of COPD:A) Assess & Monitor of COPD: 1) Assessment of symptoms:1) Assessment of symptoms:  CoughCough  DyspneaDyspnea  Sputum productionSputum production 2) History taking:2) History taking:  Exposure to risk factors e.g., smoking, occupational or environmental.Exposure to risk factors e.g., smoking, occupational or environmental.  Pattern of symptom development.Pattern of symptom development.  History of exacerbations or previous hospitalizationsHistory of exacerbations or previous hospitalizations  Presence of comorbidities e.g., heart disease, malignancies & osteoporosisPresence of comorbidities e.g., heart disease, malignancies & osteoporosis  Appropriateness of current medical treatments.Appropriateness of current medical treatments.  Impact of disease on patients life, including limitation of activity, missed workImpact of disease on patients life, including limitation of activity, missed work  Social and family support available to the patientSocial and family support available to the patient  Possibilities for reducing risk factors, especially smoking cessationPossibilities for reducing risk factors, especially smoking cessation Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 24. Page  24 MRC Dyspnea ScaleMRC Dyspnea Scale
  • 25. Page  25 Chronic Cough with Normal CXRChronic Cough with Normal CXR IntrathoracicIntrathoracic  Chronic obstructive pulmonary diseaseChronic obstructive pulmonary disease  Bronchial asthmaBronchial asthma  Central bronchial carcinomaCentral bronchial carcinoma  Endobronchial tuberculosisEndobronchial tuberculosis  BronchiectasisBronchiectasis  Left sided heart failureLeft sided heart failure  Interstitial lung diseaseInterstitial lung disease  Cystic fibrosisCystic fibrosis ExtrathoracicExtrathoracic  Postnasal dripPostnasal drip  Gastroesophageal refluxGastroesophageal reflux  Drug therapy (e.g., ACE inhibitors)Drug therapy (e.g., ACE inhibitors) Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 26. Page  26 Systemic manifestations of COPD:Systemic manifestations of COPD:  Skeletal muscle wastingSkeletal muscle wasting  Cachexia: loss of fat-free massCachexia: loss of fat-free mass  Lung cancer (SCLC & NSCLC)Lung cancer (SCLC & NSCLC)  Pulmonary hypertensionPulmonary hypertension  Ischaemic heart diseaseIschaemic heart disease  Congestive cardiac failureCongestive cardiac failure  OsteoporosisOsteoporosis  Normocytic anaemiaNormocytic anaemia  DiabetesDiabetes  Metabolic syndromeMetabolic syndrome  Obstructive sleep apneaObstructive sleep apnea  DepressionDepression
  • 27. Page  27  Central cyanosisCentral cyanosis  Hyperinflated chestHyperinflated chest  Increased resting respiratory rate with shallow breathingIncreased resting respiratory rate with shallow breathing  Pursed-lip breathingPursed-lip breathing  Respiratory distressRespiratory distress  Lower limb edemaLower limb edema  Difficulty in detection of heart apexDifficulty in detection of heart apex  Resonant bare area of the heartResonant bare area of the heart  Downward displacement of the liverDownward displacement of the liver  Distant breath soundsDistant breath sounds  Wheezy chestWheezy chest Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. 3) Physical Examination:3) Physical Examination:
  • 28. Page  28 Hyperinflation in COPD:Hyperinflation in COPD:
  • 29. Page  29 4) Spirometric Classification of COPD:4) Spirometric Classification of COPD: Severity Based on Post-Bronchodilator FEV1Severity Based on Post-Bronchodilator FEV1 StageStage Stage IStage I MildMild FEV1/FVC < 0.70 FEV1 ≥ 80% predicted Stage IIStage II ModerateModerate FEV1/FVC < 0.70 50% ≤ FEV1 < 80% predicted Stage IIIStage III SevereSevere FEV1/FVC < 0.70 30% ≤ FEV1 < 50% predicted Stage IVStage IV VeryVery SevereSevere FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 30. Page  30 5) Bronchodilator Reversibility Testing:5) Bronchodilator Reversibility Testing: PreparationPreparation  Patients should be clinically stable & free from respiratory infection.Patients should be clinically stable & free from respiratory infection.  Patients should not have taken inhaled short-acting bronchodilators in thePatients should not have taken inhaled short-acting bronchodilators in the previous 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustainedprevious 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustained release theophylline in the previous 24 hrs.release theophylline in the previous 24 hrs. SpirometrySpirometry  FEV1 should be measured before a bronchodilator is given.FEV1 should be measured before a bronchodilator is given.  The bronchodilator should be given by metered dose inhaler through a spacerThe bronchodilator should be given by metered dose inhaler through a spacer device or by nebulizer.device or by nebulizer.  Possible dosage protocols are 400 gPossible dosage protocols are 400 g ββ2-agonist, up to 160 g anticholinergic, or2-agonist, up to 160 g anticholinergic, or the two combined.the two combined.  FEV1 should be measured again 10-15 minutes after a short-actingFEV1 should be measured again 10-15 minutes after a short-acting bronchodilator is given; 30-45 minutes after the combination.bronchodilator is given; 30-45 minutes after the combination. ResultsResults  Increase in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 isIncrease in FEV1 both > 200 ml & 12% above pre-bronchodilator FEV1 is considered significant.considered significant. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 31. Page  31 6) Lung Volumes:6) Lung Volumes: The three volumes most relevant to COPD are forced vital capacity (FVC), residual volume (RV), & total lung capacity (TLC).
  • 32. Page  32 7) Exercise Testing:7) Exercise Testing: Measurement COPD VO2max Decreased Anaerobic threshold Normal/decreased/indeterminate Peak HR Decreased, Normal in mild O2 pulse Normal or decreased (VE/MVV) X 100 Increased VE/VCO2 (at AT) Increased VD/VT Increased PaO2 Variable P(A-a)O2 Variable, usually increased
  • 33. Page  33 8) Arterial Blood Gases:8) Arterial Blood Gases:  In advanced COPD, measurement of ABGs should be performed in stableIn advanced COPD, measurement of ABGs should be performed in stable patients with FEV1 < 50% predicted or with clinical signs of respiratorypatients with FEV1 < 50% predicted or with clinical signs of respiratory failure or right heart failure.failure or right heart failure.  Changes in arterial blood gas tensions take time to occur. Thus, 20-30Changes in arterial blood gas tensions take time to occur. Thus, 20-30 minutes should pass before rechecking the gas tensions when the FIO2minutes should pass before rechecking the gas tensions when the FIO2 has been changed, e.g., during assessment for domiciliary oxygen therapy.has been changed, e.g., during assessment for domiciliary oxygen therapy.  Adequate pressure must be applied at the arterial puncture site for atAdequate pressure must be applied at the arterial puncture site for at least one minute, as failure to do so can lead to painful bruising.least one minute, as failure to do so can lead to painful bruising. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 34. Page  34 9) Chest X ray:9) Chest X ray:
  • 35. Page  35 Differential Diagnosis of COPD:Differential Diagnosis of COPD: DiagnosisDiagnosis Suggestive FeaturesSuggestive Features COPDCOPD Onset in mid-life.Onset in mid-life. Symptoms slowly progressive.Symptoms slowly progressive. Long history of tobacco smoking.Long history of tobacco smoking. Dyspnea during exercise.Dyspnea during exercise. Largely irreversible airflow limitation.Largely irreversible airflow limitation. AsthmaAsthma Onset early in life (often childhood).Onset early in life (often childhood). Symptoms vary from day to day.Symptoms vary from day to day. Symptoms at night/early morning.Symptoms at night/early morning. Allergy, rhinitis, and/or eczema also present.Allergy, rhinitis, and/or eczema also present. Family history of asthma.Family history of asthma. Largely reversible airflow limitation.Largely reversible airflow limitation. CongestiveCongestive Heart FailureHeart Failure Fine basilar crackles on auscultation.Fine basilar crackles on auscultation. Chest X-ray shows dilated heart, pulmonary edemaChest X-ray shows dilated heart, pulmonary edema Pulmonary function tests indicate volume restriction, not airflowPulmonary function tests indicate volume restriction, not airflow limitation.limitation. BronchiectasiBronchiectasi ss Onset all agesOnset all ages Chest X-ray shows lung infiltrate.Chest X-ray shows lung infiltrate. Microbiological confirmation.Microbiological confirmation.
  • 36. Page  36 B) Reduce Risk Factors:B) Reduce Risk Factors: 1.1. SmokingSmoking 2.2. Occupational exposureOccupational exposure 3.3. Indoor/Outdoor air pollutionIndoor/Outdoor air pollution
  • 37. Page  37 Smoking Cessation:Smoking Cessation: ASK:ASK: Identify all tobacco users at every visit.Identify all tobacco users at every visit. ADVISE:ADVISE: Strongly urge all tobacco users to quit.Strongly urge all tobacco users to quit. ASSESS:ASSESS: Willingness to make a quit attempt.Willingness to make a quit attempt. ASSIST:ASSIST: Aid the patient in quitting.Aid the patient in quitting. ARRANGE:ARRANGE: Schedule follow-up contact.Schedule follow-up contact.
  • 38. Page  38 COPD Risk & Smoking CessationCOPD Risk & Smoking Cessation Adapted from Fletcher C et al. Br Med J. 1977;1:1645–1648. Stopped smokingStopped smoking at 45 (mild COPD)at 45 (mild COPD) Stopped smokingStopped smoking at 65 (severe COPD)at 65 (severe COPD)
  • 39. Page  39 C) Manage Stable COPD:C) Manage Stable COPD:  Pharmacological therapyPharmacological therapy  Long-term oxygen therapyLong-term oxygen therapy  Pulmonary rehabilitationPulmonary rehabilitation  NutritionNutrition  SurgerySurgery
  • 40. Page  40 Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008. C) Manage Stable COPDC) Manage Stable COPD::
  • 41. Page  41 Pharmacological TherapyPharmacological Therapy::  The medications for COPD currently available can reduce or abolish symptoms, increase exercise capacity, reduce the number and severity of exacerbations, and improve health status.  At present, no treatment has been shown to modify the rate of decline in lung function.  The inhaled route is preferred.
  • 42. Page  42 Pharmacological TherapyPharmacological Therapy:: BronchodilatorsBronchodilators  Three types of bronchodilators are available:Three types of bronchodilators are available: 1.1. β-agonistsβ-agonists 2.2. Anticholinergic drugsAnticholinergic drugs 3.3. Methylxanthines.Methylxanthines. β-agonistsβ-agonists  Salbutamol (Ventolin)Salbutamol (Ventolin)  Sameterol (Servent)Sameterol (Servent)  Formoterol (Foradil)Formoterol (Foradil)  TerbutalinTerbutalin AnticholinergicsAnticholinergics  Ibrtropuim bromideIbrtropuim bromide (Atrovent)(Atrovent)  Tiotropuim bromideTiotropuim bromide (Spiriva)(Spiriva) MethylxanthineMethylxanthine  AminophyllineAminophylline (Uniphylline,(Uniphylline, Quibron, Theo SR)Quibron, Theo SR)
  • 43. Page  43 Pharmacological TherapyPharmacological Therapy:: Inhaled CorticosteroidsInhaled Corticosteroids  Types of Inhaled Corticosteroids (ICS):Types of Inhaled Corticosteroids (ICS):  Beclomethasone dipropionate (Clenil)Beclomethasone dipropionate (Clenil)  Fluticasone propionate (Flexotide)Fluticasone propionate (Flexotide)  Budesonide (Meflonide)Budesonide (Meflonide)  Ciclesonide (Alvesco)Ciclesonide (Alvesco)
  • 44. Page  44 Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy  Three types of bronchodilators are available:Three types of bronchodilators are available: 1.1. Meter dose inhalerMeter dose inhaler 2.2. DiskusDiskus 3.3. TubuhalerTubuhaler 4.4. AerolizerAerolizer 5.5. HandihalerHandihaler 6.6. NebulizerNebulizer
  • 45. Page  45 Pharmacological TherapyPharmacological Therapy:: Aerosol TherapyAerosol Therapy
  • 46. Page  46 C) Manage Stable COPD:C) Manage Stable COPD: Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 47. Page  47 Long-term Oxygen Therapy:Long-term Oxygen Therapy:  Long-term oxygen therapy (LTOT) improves survival, exercise, sleep and cognitive performance.  Physiological indications for oxygen include an arterial oxygen tension (Pa,O2) <55 mmHg guided by ABGs.  The therapeutic goal is to maintain Sa,O2 >90% during rest, sleep and exertion.  If oxygen was prescribed during an exacerbation, recheck ABGs after 30–90 days.
  • 48. Page  48 Long-term Oxygen Therapy:Long-term Oxygen Therapy:
  • 49. Page  49 RehabilitationRehabilitation For the lungs to get more airFor the lungs to get more air PURSED-LIP BREATHINGPURSED-LIP BREATHING (like breathing out slowly into a straw)(like breathing out slowly into a straw) INHALEINHALE EXHALEEXHALE
  • 50. Page  50 RehabilitationRehabilitation Sit comfortablySit comfortably && relax your shouldersrelax your shoulders Put one hand on yourPut one hand on your abdomen. Now inhaleabdomen. Now inhale slowly through yourslowly through your nose. (Push yournose. (Push your abdomen out while youabdomen out while you breathe in)breathe in) Then push in yourThen push in your abdominal musclesabdominal muscles and breathe out usingand breathe out using the pursed-lipthe pursed-lip techniquetechnique For the lungs to get more airFor the lungs to get more air DIAPHRAGMATIC BREATHINGDIAPHRAGMATIC BREATHING
  • 51. Page  51 Nutrition:Nutrition:  Weight loss & depletion of fat-free mass (FFM) may be observed inWeight loss & depletion of fat-free mass (FFM) may be observed in stable COPD patients.stable COPD patients.  Being underweight is associated with an increased mortality risk.Being underweight is associated with an increased mortality risk.  Criteria to define weight loss are:Criteria to define weight loss are: Weight loss >10% in the past 6 months or >5% in the past month.Weight loss >10% in the past 6 months or >5% in the past month.  Nutritional therapy may only be effective if combined with exercise orNutritional therapy may only be effective if combined with exercise or other anabolic stimuli.other anabolic stimuli. UnderweightUnderweight BMI <21 kgBMI <21 kg··mm-2-2 ;age >50 yrs;age >50 yrs Normal weightNormal weight BMI <21–25 kgBMI <21–25 kg··mm-2-2 OverweightOverweight BMI <30 kgBMI <30 kg··mm-2-2 ObeseObese BMIBMI ≥≥30 kg30 kg··mm-2-2
  • 52. Page  52 Lung Volume Reduction In EmphysemaLung Volume Reduction In Emphysema ↓ ↓ ↑ ↑ ↑ ↑ ↓ ↑ ↑ ↓ ↓ ↓
  • 53. Page  53 What's a COPD Exacerbation?What's a COPD Exacerbation?  An exacerbation of COPD is defined as an event in theAn exacerbation of COPD is defined as an event in the natural course of the disease characterized by a change innatural course of the disease characterized by a change in the patients baseline dyspnea, cough, and/or sputum that isthe patients baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, andbeyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patientmay warrant a change in regular medication in a patient with underlying COPD.with underlying COPD. Global Initiative for Chronic Obstructive Lung Disease, 2008.Global Initiative for Chronic Obstructive Lung Disease, 2008.
  • 54. Page  54 Anthonisen's Typing of COPD ExacerbationAnthonisen's Typing of COPD Exacerbation Cardinal SignsCardinal Signs Worsening dyspnea, increase in sputum volume & purulenceWorsening dyspnea, increase in sputum volume & purulence Other SignsOther Signs Upper respiratory tract infection in past 5 days, fever without otherUpper respiratory tract infection in past 5 days, fever without other apparent cause, wheezing, increase cough & increase respiratoryapparent cause, wheezing, increase cough & increase respiratory rate or heart rate by 20% above baselinerate or heart rate by 20% above baseline All 3 cardinal symptomsAll 3 cardinal symptoms Type 1 (SEVERE)Type 1 (SEVERE) 2 of 3 cardinal symptoms2 of 3 cardinal symptoms Type 2 (MODERATE)Type 2 (MODERATE) 1 of 3 cardinal symptoms1 of 3 cardinal symptoms Type 3 (MILD)Type 3 (MILD)
  • 55. Page  55 Causes of COPD ExacerbationsCauses of COPD Exacerbations
  • 56. Page  56 D) Manage Exacerbations:D) Manage Exacerbations: Assessment of COPD ExacerbationsAssessment of COPD Exacerbations Medical HistoryMedical History  Severity of FEV1Severity of FEV1  Duration of worsening or newDuration of worsening or new symptomssymptoms  Number of previousNumber of previous (exacerbations/hospitalizations)(exacerbations/hospitalizations)  ComordibitiesComordibities  Present treatment regimenPresent treatment regimen Signs of SeveritySigns of Severity  Use of accessory respiratoryUse of accessory respiratory musclesmuscles  Paradoxical chest wall movementsParadoxical chest wall movements  Worsening or new central cyanosisWorsening or new central cyanosis  Peripheral edemaPeripheral edema  Hemodynamic instabilityHemodynamic instability  Signs of right heart failureSigns of right heart failure  Reduced alertnessReduced alertness
  • 57. Page  57 Indications for Hospitalization in AECB:Indications for Hospitalization in AECB:  Marked increase in symptoms, e.g. sudden development of restingMarked increase in symptoms, e.g. sudden development of resting dyspnea.dyspnea.  Severe underlying COPDSevere underlying COPD  Onset of new physical signs (e.g., cyanosis, peripheral edema)Onset of new physical signs (e.g., cyanosis, peripheral edema)  Failure of exacerbation to respond to initial medical managementFailure of exacerbation to respond to initial medical management  Significant comorbidities.Significant comorbidities.  Frequent exacerbations.Frequent exacerbations.  Newly occurring arrhythmias.Newly occurring arrhythmias.  Diagnostic uncertainty.Diagnostic uncertainty.  Older age.Older age.  Insufficient home support.Insufficient home support.
  • 58. Page  58 Indications for ICU admission in AECB:Indications for ICU admission in AECB:  Severe dyspnea that responds inadequately to initialSevere dyspnea that responds inadequately to initial emergency therapy.emergency therapy.  Changes in mental status (Confusion, lethargy, coma).Changes in mental status (Confusion, lethargy, coma).  Persistent or worsening hypoxemia (PaO2<40 mmHg),Persistent or worsening hypoxemia (PaO2<40 mmHg), and/or severe/worsening hypercapnia (PaCO2>60 mmHg),and/or severe/worsening hypercapnia (PaCO2>60 mmHg), and/or severe/worsening acidosis (pH<7.25) despiteand/or severe/worsening acidosis (pH<7.25) despite supplemental oxygen & non-invasive ventilation.supplemental oxygen & non-invasive ventilation.  Need for invasive mechanical ventilation.Need for invasive mechanical ventilation.  Hemodynamic instability – need for vasopressors.Hemodynamic instability – need for vasopressors.
  • 59. Page  59 Management of COPD ExacerbationManagement of COPD Exacerbation

Editor's Notes

  • #15: Average adult inspires and expires around 6 litres of air from the lungs every minute The mucociliary escalator is the primary mechanism within the lungs It beigns in the nose and extends throughout the respiratory tract This esculator is contiually active, therefore propelling foreign matter out of the respiratory tract
  • #16: Cigarette smoke compromises the action of the cilla and results in mucus being retained for longer periods Thus increasing risk of infection, the causing symptoms such as productive cough and thus gives rise to an obstructive pattern.
  • #22: Dilation of alveolar wall ↓ alveolar capillary network, loss of guy rope effect ↓ lung tissue elasticity Caused by smoking » irritation » inflammation » neutrophils and macrophages » release neutrophil elastase (type of proteases)
  • #32: The forced vital capacity is the maximum volume of air which can be forcibly expelled after inhaling as deeply as possible. Not all of the air in the lungs is removed when measuring the vital capacity. The amount remaining is called the residual volume. The total lung capacity is the combination of the forced vital capacity and residual volume. While most of the measured lung volumes or capacities change to some degree with COPD, residual volume usually increases quite markedly. This increase is the result of the weakened airways collapsing before all the normally expired air can leave the lungs. The increased residual volume makes breathing even more difficult and labored.
  • #53: Remove hyperinflated areas of lung: Improve V/Q matching Reduce resting length of respiratory muscles Reduce Dynamic Hyperinflation