Chronic Obstructive Pulmonary Disease
Dr .Mohammad Kharraz MD InternistArab-Jordanian-Palestinian Board
Definition of COPD
Chronic Obstructive Pulmonary Disease is a preventable and treatable disease with some significant extrapulmonary effects.
The pulmonary component is characterized by airflow limitation that is not fully reversible.
Healthy Alveolus
COPD
Chronic Obstructive Pulmonary Disease (COPD)
The airflow limitation in COPD is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases
Severe COPD leads to respiratory failure, hospitalization and eventually death from suffocation
1990 2020Ischaemic heart diseaseCerebrovascular diseaseLower resp infectionDiarrhoeal diseasePerinatal disordersCOPDTuberculosisMeaslesRoad Traffic AccidentsLung Cancer
Stomach CancerHIVSuicide
6th
3rd
COPD Mortality Worldwide
Source: Murray & Lopez. Lancet 1997
COPD Mortality increased 22% over the last decade.
COPD is the third most common cause of death for both men and women worldwide.
About 13.9% of the U.S. adult population (25+ years) have been diagnosed with COPD*
An estimated 15-19% of COPD cases are work-related**
24 million other adults have evidence of troubled breathing, indicating COPD is under diagnosed by up to 60%***
*Braman, S. Update on the ATS Guidelines for COPD. Medscape Pulmonary Medicine. 2005;9(1):1. **CDC programs in Brief– Workplace Health and Safety-Work-related Lung Diseases.
www.cdc.gov/programs/workpl18.htm ***COPD Fact Sheet. Oct 2003. www/lungusa.org
Obstructive Lung Disease
EMPHYSEMACHRONIC BRONCHITIS
ASTHMABRONCHECTASISCYSTIC FIBROSIS
BULLOUS LUNG DISEASE
Causes Most cases of COPD occur as a result of long-term exposure to lung
irritants that damage the lungs and the airways
The most common irritant that causes COPD is cigarette smoke
In rare cases, a genetic condition called alpha-1 antitrypsin deficiency may play a role in causing COPD
Risk Factors for COPD
Nutrition
Infections
Socio-economic status
Aging Populations
Other risk factors
About 20% or more of all COPD in USA occur in never-smokers.
Childhood recurrent viral infections and childhood Asthma contribute to increase risk of developing COPD in the future.
Tuberculosis can result in airflow obstruction secondary to destruction of lung tissue.
Hereditary factors
Data show that relatives of patients with COPD have a higher prevalence of the disease ,that cannot be attributed to environmental factors.
Best documented genetic influence is hereditary deficiency of alfa-1-antitrypsin :
-COPD at age <45.-non-smoker.
-basilar lung disease.-concurrent liver disease.
Pathology Central airways shows mucous gland hypertrophy and goblet
cell metaplasia.
Peripheral airway shows smooth muscle hypertrophy, peribronchial fibrosis, luminal occlusion by mucus and enlarged lymphoid follicles.
Alveoli enlarged by loss of the alveolar walls with evidence of persistent inflammation with neutrophils in the airway lumen and macrophage in the airway wall.
Normal versus Diseased Bronchi
Comorbid conditions commonly observed in PTs with COPD
CVD, AF,CHF,MIHigh cholesterol
GERDDepression
OsteoporosisDM
Glaucoma Erectile dysfunction
High blood pressureArthritis
CataractsSleep apnea
StrokeCancer
Diagnosis of COPD
Guidelines from both American College of Physicians and GOLD define airflow obstruction as postbrochodilator FEV1/FEV ratio less than 70%.
Spirometry is essential for diagnosis of COPD.
Testing should not be performed in asymptomatic peoples as screening intervention.
Classification of COPD Severity by Spirometry
Stage I: Mild FEV1/FVC < 0.70 GOLD 1 FEV1 > 80% predicted
Stage II: Moderate FEV1/FVC < 0.70 GOLD 2 50% < FEV1 < 80% predicted
Stage III: Severe FEV1/FVC < 0.70GOLD 3 30% < FEV1 < 50% predicted
Stage IV: Very Severe FEV1/FVC < 0.70GOLD 4 FEV1 < 30% predicted or
FEV1 < 50% predicted plus chronic respiratory failure
Physiology Reduced forced expiratory flow ( FEV1) FEV1/Forced vital capacity ( FVC) ratio less than 0.7 Lung compliance is increased in emphysema. Loss of elastic recoil in emphysema which result in alteration
in lung compliance.
Changes in end expiratory lung volume and increase residual volume result in a lower, flatter diaphragm and more horizontal rib cage which will impair the inspiratory muscles ability to develop pressure and increase the overall work of breathing.
Flattening of the diaphragm redirects the axis of shortening of skeletal muscle and produce paradoxical in drawing of the lower rib cage
Gas exchange Arterial Hypoxemia which become clinically significant when
the PO2 fall below 60 mmHg Arterial Hypercapnia due to increase dead space and reduce
alveolar ventilation
Pulmonary circulation Hypoxic vasoconstriction with increase in the pulmonary
artery pressure Treatment with oxygen prevents disease progression and
reduce pulmonary artery pressure
SYMPTOMScough
sputum shortness of breath
EXPOSURE TO RISKFACTORS tobacco
occupationindoor/outdoor pollution
SPIROMETRY
Diagnosis of COPD
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Volume Measuring Spirometer
Flow Measuring Spirometer
Desktop Electronic Spirometers
Small Hand-held Spirometers
Spirometry
Predicted Normal Values
Predicted Normal Values
Age Height Sex Ethnic Origin
Affected by :
Criteria for Normal Post-bronchodilator Spirometry
FEV1: % predicted > 80%
FVC: % predicted > 80%
FEV1/FVC: > 0.7 - 0.8, depending on age
Spirometric Diagnosis of COPD COPD is confirmed by post–bronchodilator FEV1/FVC < 0.7
Post-bronchodilator FEV1/FVC measured 15 minutes after 400µg salbutamol or equivalent
Bronchodilator Reversibility Testing
Provides the best achievable FEV1 (and FVC)
Helps to differentiate COPD from asthma
Must be interpreted with clinical history - neither asthma nor COPD are diagnosed on spirometry alone
When to refer to PulmonologistDisease onset before 40 years age .
Rapidly progressive course of diseaseSevere COPD despite optimal treatment
Need for oxygen therapyDiagnostic uncertainty
Confirmed or suspected alpha 1 antitrypsin deficiency
Management
Reduce symptomsPrevent exacerbationsEnhance quality of life
Reduce disease morbidity and mortality
Medications Bronchodilators:
Inhaled short acting anticholinergicInhaled short acting B2 –agonists
Inhaled long acting anticholinergics
Methylxanthine
Oral phosphodiesterase -4 inhibitor Roflumilast
Anti -inflamatory agentsInhaled and oral steroids
Recently FDA approved an inhaled long acting B2- agonist Indacaterol (arcapta) for once daily maintenance treatment of airflow obstruction in pt with COPD.
Roflumilast is indicated to reduce the risk and frequency of exacerbations or to improve symptoms with severe COPD.Its not indicated for the relief of acute bronchospasm or rescue therapy.
Not indicated in the treatment of emphysema.
Antibiotics Indicated to treat exacerbations ;
Increased dyspneaSputum volume
Sputum purulenceSevere exacerbation of COPD requiring
mechanical ventilation
Respiratory fluoroquinolones or Third generation cephalosporin plus macrolide
Influenza and pneumococcal vaccine are recommended for pts with COPD.
Smoking cessation
Pulmonary rehabilitation;Can be considered in all pts with
FEV1<50%.Involves education,nutritional counseling,
excersize training.
Oxygen therapy
Indicated for pts who have resting hypoxia , defined as arterial Po2 of 55 mmHg or lower arterial oxygen saturation of 88%.
Duration of oxygen therapy not less than 15 hours daily.
Oxygen therapy improves survival, hemodynamics, excersize capacity and mental status
Noninvasive positive pressure ventilation in pts with COPD exacerbation
Improve respiratory acidosisIncrease pH
Decrease the need for endotracheal intubation
Reduce arterial Pco2 ,respiratory rate, length of hospital stay and mortality.
Lung volume reduction surgery
Resecting up to 30% of diseased or non functioning parynchyma to reduce hyperinflation and allow the remaining lung to function more efficiently.
LVRS indicated in pts with advanced COPD FEV1<45% and >20% and Dlco> 20%.
Lung trasplantation
For patients with very advanced COPD.The leading cause of long term morbidity at 5
years posttransplant is chronic allograft rejection ( bronchiolitis obliterance).