chronic obstructive pulmonary disease

CHRONIC CHRONIC

OBSTRUCTIVE OBSTRUCTIVE

PULMONARY DISEASEPULMONARY DISEASE

Iman Galal, MDIman Galal, MD

Pulmonary Medicine Pulmonary Medicine DepartmentDepartment

Ain Shams UniversityAin Shams University

Contents of the Lecture:Contents of the Lecture:

EpidemiologyEpidemiology

DefinitionDefinition

Risk factorsRisk factors

PathogenesisPathogenesis

PathologyPathology

ClassificationClassification

ManagementManagement

COPD exacerbationsCOPD exacerbations

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 deaths In 2000, the WHO estimated 2.74 million deaths

worldwide from COPD.worldwide from COPD.

In 1990, COPD was ranked In 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

US Leading Causes of Death 2001US Leading Causes of Death 2001

Chronic Obstructive Pulmonary Chronic Obstructive Pulmonary Disease:Disease:

Chronic Obstructive Pulmonary Disease (COPD) is a Chronic Obstructive Pulmonary Disease (COPD) is a

preventablepreventable & & treatabletreatable disease with some disease with some

significant significant extrapulmonaryextrapulmonary effects that may effects that may

contribute to the severity in individual patients. Its contribute to the severity in individual patients. Its

pulmonarypulmonary component is characterized by component is characterized by airflow airflow

limitationlimitation that is that is not fully reversible.not fully reversible. The airflow The airflow

limitation is usually limitation is usually progressiveprogressive & associated with & associated with

an an abnormal inflammatory responseabnormal inflammatory response of the lung to of the lung to

noxious particles or gases.noxious particles or gases.

Global Initiative for Chronic Obstructive Lung Disease, Global Initiative for Chronic Obstructive Lung Disease, 2008.2008.

Emphysema:Emphysema:

Abnormal Abnormal permanent permanent enlargement of the airspaces enlargement of the airspaces

distal to the terminal bronchiole, accompanied by distal to the terminal bronchiole, accompanied by

destruction of their walls without fibrosis.destruction of 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) Irregular Irregular

Chronic bronchitis:Chronic bronchitis:

Presence of Presence of chronic productive coughchronic productive cough

for for

3 months3 months in each of in each of

2 successive years2 successive years in a patient in whom in a patient in whom

other causesother causes of of chronic coughchronic cough have have

been been excluded.excluded.

Risk Factors:Risk Factors:

GenesExposure to particles

1. Tobacco smoke2. Occupational dust, organic & inorganic3. Indoor air pollution4. Outdoor air pollution

Lung growth & developmentOxidative stressGenderAgeRespiratory infectionsPrevious TBSocioeconomic statusNutritionComorbidities

Pathogenesis:Pathogenesis:




InflammationInflammation

Small Airway Small Airway

DiseaseDisease

Airway inflammationAirway inflammation

Parenchymal Parenchymal

DistructionDistructionDecrease elastic recoilDecrease elastic recoil

Loss of alveolar Loss of alveolar

attachmentattachmentAirflow LimitationAirflow Limitation

Overlap of Obstructive Lung Overlap of Obstructive Lung DiseaseDisease




AsthmaAsthma

Asthmatic Airway Asthmatic Airway

InflammationInflammation

CD4-T lymphocytesCD4-T lymphocytes

EosinophilsEosinophils

COPD Airway COPD Airway

InflammationInflammationCD8-T lymphocytesCD8-T lymphocytes

MacrophagesMacrophages

NeutrophilsNeutrophils

Airflow Airflow LimitationLimitation

COPDCOPD

Fully Fully ReversibleReversible

Not Fully Not Fully ReversibleReversible

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 Bronchial Normal Bronchial ArchitectureArchitecture

COPDCOPD

Healthy Respiratory MucosaHealthy Respiratory Mucosa

This EM shows the This EM shows the

respiratory mucosa in a respiratory mucosa in a

healthy state.healthy state.

The cells are fully The cells are fully

ciliated. ciliated.

The cilia beat in a co-The cilia beat in a co-

ordinated fashion to ordinated fashion to

move mucus out of the move mucus out of the

airways (mucociliary airways (mucociliary

transport). transport).

Scanning electron micrograph showing Scanning electron micrograph showing a sheet of mucus being moved along by a sheet of mucus being moved along by

the ciliathe cilia

Damaged Respiratory Damaged Respiratory MucosaMucosa

Damage to the cilia & Damage to the cilia & epithelium occur as a result epithelium occur as a result of disease processes in COPD. of disease processes in COPD. This can also occur as a This can also occur as a result of bacterial damage. result of bacterial damage.

This slide shows the result of This slide shows the result of bacterial infection stripping bacterial infection stripping away the cilia from the away the cilia from the mucosa.mucosa.

The damage to the cilia The damage to the cilia means they are less effective means they are less effective in removing mucus from the in removing mucus from the airwaysairwaysScanning electron micrograph showing Scanning electron micrograph showing

cilial and epithelial damage induced by cilial and epithelial damage induced by bacteriabacteria

Centriacinar EmphysemaCentriacinar Emphysema

Characterized by focal destruction limited to the respiratory Characterized by focal destruction limited to the respiratory

bronchioles & the central portions of acinus. bronchioles & the central portions of acinus. Is is associated with cigarette smoking & is most severe in the Is is associated with cigarette smoking & is most severe in the

upper lobes. upper lobes.

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 It is most severe in the lower lung zones & generally develops

in patients with homozygous alpha1-antitrypsin (AAT) in patients with homozygous alpha1-antitrypsin (AAT)

deficiency. deficiency.

Distal acinar EmphysemaDistal acinar Emphysema

Distal acinar emphysema or Distal acinar emphysema or

paraseptal emphysema, is paraseptal emphysema, is

the least common form and the least common form and

involves distal airway involves distal airway

structures, alveolar ducts, structures, alveolar ducts,

and sacs. and sacs. This form of emphysema is This form of emphysema is

localized to fibrous septa or localized to fibrous septa or

to the pleura & leads to to the pleura & leads to

formation of bullae. formation of bullae. The apical bullae may cause The apical bullae may cause

pneumothorax. pneumothorax. Paraseptal emphysema is Paraseptal emphysema is

not associated with airflow not associated with airflow

obstruction. obstruction.

EmphysemaEmphysema

EmphysemaEmphysema

EmphysemaEmphysemaNormal Normal LungLung

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.

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 & Presence of comorbidities e.g., heart disease, malignancies &

osteoporosisosteoporosis Appropriateness of current medical treatments.Appropriateness of current medical treatments. Impact of disease on patients life, including limitation of activity, Impact of disease on patients life, including limitation of activity,

missed work 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


MRC Dyspnea ScaleMRC Dyspnea Scale

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)


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

Central cyanosis Central cyanosis Hyperinflated chestHyperinflated chest Increased resting respiratory rate with shallow breathingIncreased resting respiratory rate with shallow breathing Pursed-lip breathing Pursed-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 liver Downward displacement of the liver Distant breath soundsDistant breath sounds Wheezy chestWheezy chest


3) Physical Examination:3) Physical Examination:

Hyperinflation in COPD:Hyperinflation in COPD:

4) Spirometric Classification of 4) Spirometric Classification of COPD: COPD:

Severity Based on Post-Bronchodilator FEV1Severity Based on Post-Bronchodilator FEV1

StageStage

Stage IStage I MildMildFEV1/FVC < 0.70

FEV1 ≥ 80% predicted

Stage IIStage II ModerateModerateFEV1/FVC < 0.70

50% ≤ FEV1 < 80% predicted

Stage Stage IIIIII SevereSevere

FEV1/FVC < 0.70

30% ≤ FEV1 < 50% predicted

Stage Stage IVIV

Very Very SevereSevere

FEV1/FVC < 0.70

FEV1 < 30% predicted or FEV1 < 50% predicted

plus chronic respiratory failure


5) Bronchodilator Reversibility 5) Bronchodilator Reversibility Testing: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 Patients should not have taken inhaled short-acting bronchodilators in

the previous 6 hrs, long-acting bronchodilator in the previous 12 hrs, the previous 6 hrs, long-acting bronchodilator in the previous 12 hrs, or sustained release theophylline in the previous 24 hrs.or sustained 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 The bronchodilator should be given by metered dose inhaler through

a spacer device or by nebulizer.a spacer device or by nebulizer. Possible dosage protocols are 400 g Possible dosage protocols are 400 g ββ2-agonist, up to 160 g 2-agonist, up to 160 g

anticholinergic, or the two combined.anticholinergic, or the two combined. FEV1 should be measured again 10-15 minutes after a short-acting FEV1 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 Increase in FEV1 both > 200 ml & 12% above pre-bronchodilator

FEV1 is considered significant.FEV1 is considered significant.


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).

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

8) Arterial Blood Gases:8) Arterial Blood Gases:

In advanced COPD, measurement of ABGs should be performed in In advanced COPD, measurement of ABGs should be performed in stable patients with FEV1 < 50% predicted or with clinical signs of stable patients with FEV1 < 50% predicted or with clinical signs of respiratory failure or right heart failure. respiratory failure or right heart failure.

Changes in arterial blood gas tensions take time to occur. Thus, Changes in arterial blood gas tensions take time to occur. Thus, 20-30 minutes should pass before rechecking the gas tensions 20-30 minutes should pass before rechecking the gas tensions when the FIO2 has been changed, e.g., during assessment for when the FIO2 has been changed, e.g., during assessment for domiciliary oxygen therapy. domiciliary oxygen therapy.

Adequate pressure must be applied at the arterial puncture site for Adequate pressure must be applied at the arterial puncture site for at least one minute, as failure to do so can lead to painful bruising.at least one minute, as failure to do so can lead to painful bruising.


9) Chest X ray:9) Chest X ray:

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.

Congestive Congestive 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 airflow Pulmonary function tests indicate volume restriction, not airflow limitation.limitation.

BronchiectasBronchiectasisis

Onset all agesOnset all ages

Chest X-ray shows lung infiltrate.Chest X-ray shows lung infiltrate.

Microbiological confirmation.Microbiological confirmation.

High local prevalence of tuberculosisHigh local prevalence of tuberculosis

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

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.

COPD Risk & Smoking CessationCOPD Risk & Smoking Cessation

Adapted from Fletcher C et al. Br Med J. 1977;1:1645–1648.

Stopped smoking Stopped smoking at 45 (mild COPD)at 45 (mild COPD)

Stopped smoking Stopped smoking at 65 (severe COPD)at 65 (severe COPD)

C) Manage Stable COPD:C) Manage Stable COPD:

Pharmacological therapyPharmacological therapy

Long-term oxygen therapyLong-term oxygen therapy

Pulmonary rehabilitationPulmonary rehabilitation

NutritionNutrition

SurgerySurgery


C) Manage Stable COPDC) Manage Stable COPD::

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.

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 Salbutamol

(Ventolin)(Ventolin)

Sameterol (Servent)Sameterol (Servent)

Formoterol (Foradil)Formoterol (Foradil)

TerbutalinTerbutalin

AnticholinergicsAnticholinergics

Ibrtropuim Ibrtropuim

bromide (Atrovent)bromide (Atrovent)

Tiotropuim Tiotropuim

bromide (Spiriva)bromide (Spiriva)

MethylxanthineMethylxanthine

Aminophylline Aminophylline

(Uniphylline, (Uniphylline,

Quibron, Theo Quibron, Theo

SR)SR)

Pharmacological TherapyPharmacological Therapy: : Inhaled CorticosteroidsInhaled Corticosteroids

Types of Inhaled Corticosteroids (ICS): Types of Inhaled Corticosteroids (ICS):

Beclomethasone dipropionate Beclomethasone dipropionate

(Clenil)(Clenil)

Fluticasone propionate (Flexotide)Fluticasone propionate (Flexotide)

Budesonide (Meflonide)Budesonide (Meflonide)

Ciclesonide (Alvesco)Ciclesonide (Alvesco)

Pharmacological TherapyPharmacological Therapy:: Aerosol Aerosol TherapyTherapy

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

Pharmacological TherapyPharmacological Therapy:: Aerosol Aerosol TherapyTherapy

C) Manage Stable COPD:C) Manage Stable COPD:


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.

Long-term Oxygen Therapy:Long-term Oxygen Therapy:

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

RehabilitationRehabilitation

Sit comfortably Sit comfortably & &

relax your shoulders relax your shoulders

Put one hand on your Put one hand on your abdomen. Now inhale abdomen. Now inhale slowly through your slowly through your

nose. (Push your nose. (Push your abdomen out while abdomen out while

you breathe in) you breathe in)

Then push in your Then push in your abdominal muscles abdominal muscles

and breathe out and breathe out using the pursed-lip using the pursed-lip

techniquetechnique

For the lungs to get more airFor the lungs to get more air

DIAPHRAGMATIC BREATHINGDIAPHRAGMATIC BREATHING

Nutrition:Nutrition: Weight loss & depletion of fat-free mass (FFM) may be observed in stable COPD Weight loss & depletion of fat-free mass (FFM) may be observed in stable COPD

patients.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 or other Nutritional therapy may only be effective if combined with exercise or other anabolic stimuli.anabolic stimuli.

UnderweightUnderweight BMI <21 kgBMI <21 kg··mm-2-2;age >50 ;age >50 yrsyrs

Normal Normal weightweight

BMI <21–25 kgBMI <21–25 kg··mm-2-2

OverweightOverweight BMI <30 kgBMI <30 kg··mm-2-2

Obese Obese BMI BMI 30 kg30 kg··mm-2-2

Lung Volume Reduction In Lung Volume Reduction In EmphysemaEmphysema

What's a COPD Exacerbation?What's a COPD Exacerbation?

An exacerbation of COPD is defined as an event in An exacerbation of COPD is defined as an event in

the natural course of the disease characterized by the natural course of the disease characterized by

a change in the patients baseline dyspnea, cough, a change in the patients baseline dyspnea, cough,

and/or sputum that is beyond normal day-to-day and/or sputum that is beyond normal day-to-day

variations, is acute in onset, and may warrant a variations, is acute in onset, and may warrant a

change in regular medication in a patient with change in regular medication in a patient with

underlying COPD.underlying COPD.


Anthonisen's Typing of COPD ExacerbationAnthonisen's Typing of COPD Exacerbation

Cardinal Signs Cardinal 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 Upper respiratory tract infection in past 5 days, fever without

other apparent cause, wheezing, increase cough & increase other apparent cause, wheezing, increase cough & increase

respiratory rate or heart rate by 20% above baseline respiratory rate 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)

Causes of COPD Causes of COPD ExacerbationsExacerbations

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 new Duration 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 respiratory Use of accessory respiratory musclesmuscles

Paradoxical chest wall Paradoxical chest wall movementsmovements

Worsening or new central Worsening or new central cyanosiscyanosis

Peripheral edemaPeripheral edema Hemodynamic instabilityHemodynamic instability Signs of right heart failureSigns of right heart failure Reduced alertnessReduced alertness

Indications for Hospitalization in AECB:Indications for Hospitalization in AECB:

Marked increase in symptoms, e.g. sudden development of resting Marked 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.

Indications for ICU admission in AECB:Indications for ICU admission in AECB:

Severe dyspnea that responds inadequately to initial Severe dyspnea that responds inadequately to initial

emergency therapy.emergency therapy.

Changes in mental status (Confusion, lethargy, Changes in mental status (Confusion, lethargy,

coma).coma).

Persistent or worsening hypoxemia (PaO2<40 Persistent or worsening hypoxemia (PaO2<40

mmHg), and/or severe/worsening hypercapnia mmHg), and/or severe/worsening hypercapnia

(PaCO2>60 mmHg), and/or severe/worsening (PaCO2>60 mmHg), and/or severe/worsening

acidosis (pH<7.25) despite supplemental oxygen & acidosis (pH<7.25) despite supplemental oxygen &

non-invasive ventilation.non-invasive ventilation.

Need for invasive mechanical ventilation.Need for invasive mechanical ventilation.

Hemodynamic instability – need for vasopressors.Hemodynamic instability – need for vasopressors.

Management of COPD ExacerbationManagement of COPD Exacerbation

Thank YouThank You

chronic obstructive pulmonary disease

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