Transcript Chronic Obstructive Pulmonary Disease

Chronic Obstructive
Pulmonary Disease
E. Sevda Özdoğan MD
Chest diseases
COPD
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COPD is a disease state characterized
by airflow limitation that is not fully
reversible. The airflow limitation is
usually both progressive and associated
with
an
abnormal
inflammatory
response of the lungs to noxious
particles or gases.
Terminology
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Chronic Bronchitis
Defined as the presence of cough and sputum production
for at least 3 months in each of 2 consecutive years, is not
necessarily associated with airflow limitation.
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Emphsema
Irreversibl dilatation and destruction of the airways distal
to terminal bronchie (without fibrosis)
– Centrlobular emphysema (respiratory bronchioles)
– Panlobular emphsema (resp. Br+alv ductus and
alveolus)
RİSK FACTORS İN COPD
Environmental
 Smoking (active, passive)
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Occupational exposures
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Responsible from 80-90% of COPD)
RR for Chronic bronchitis among
smokers is 50 %, COPD 15-20 %
Miners (kadmiyum,silica)
bakers, construction, wood workers
Grain dust
Wool
Air pollution
Social factors
Dietary factors
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Low Antioxidans and vitamin
(A,C,E;Mg)
High salt
Host related
 Genetic factors (%1)
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Alfa-1 antitripsin deficiency
(otozomal recessive)
Family history
Age
Childhood viral infections
(RSV,Adenovirüs)
 Bronchial hyperreactivity
 Atophy
 Low birth weight
Pathophysiological
Mechanisms
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Inflammation
 Protease-antiprotease imbalance
 Oxydative stress
CELLULAR MECHANISMS OF COPD
Cigarette smoke
Alveolar macrophage
?
CD8+
lymphocyte
MCP-1
Neutrophil chemotactic factors
Cytokines (IL-8)
Mediators (LTB4) 4))
Neutrophil
PROTEASE
INHIBITORS
-
Neutrophil elastase
Cathepsins
PROTEASES
Matrix metalloproteinases
Alveolar wall destruction
(Emphysema)
Mucus hypersecretion
(Chronic bronchitis)
Diagnosis of COPD
EXPOSURE TO RISK
FACTORS
SYMPTOMS
cough
sputum
dyspnea
tobacco
occupation
indoor/outdoor pollution
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Physical examination
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Prolonged expiration (>6 sec),
Barrel chest
Accesory muscle activity, pursed lip respiration
Cyanosis
Wheesing, ronchus silent chest
Corpulmonale signs
Flapping tremor
Diagnosis of COPD
EXPOSURE TO RISK
FACTORS
SYMPTOMS
cough
sputum
dyspnea
tobacco
occupation
indoor/outdoor pollution
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SPIROMETRY
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FEV1/FVC<%70
 FEV1 is used for
the classification
of severity
 Decreased FEF
25-75 (MMFR)
Decreased DLCO
DLCO/VA in
emphysema
Air trapping
and
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Reversibility test (-)
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Chest radiology
– Normal
– Emphysema
– Pulmonary hypertension
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Blood gas
Measurement of arterial blood gas tension should be
considered in all patients with FEV1 < 40% predicted or
clinical signs suggestive of respiratory failure or right heart
failure.
 Routine blood tests:
– Polistemia
– Liver function abnormality
– Renal function abnormalities
 ECG:
– Axis changes due to diafragmatic flattening or
right ventricular hypertrophy
– P pulmonale
– Right bundle block
– İmpaired R progression
 Alfa-1
antitripsin deficiency tests:
– COPD before the age of 45
– Family history
– Nonsmokers
– Panlobular emphysema in the lower lobes
Pulmonary Hypertension in
COPD
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Decreased pulmonary vascularity
 Hypoxemia-pulmonary vasoconstruction
 Polistemia and increased blood viscosity
 Pulmonary thrombosis
 Hypoxemia- decreased renal blood supplyfluid retantion
Physical signs of Corpulmonale
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Cyanosis
 Peripheral edema (Pretibial)
 Enlarged liver
 Venous enlargement on the neck
 Conjunctival hyperemia
Radiologic signs of corpulmonale
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Cardiomegaly
 Increased vascular arborization
 Enlarged pulmonary artery of right hilum
(over 14-16 mm)
 Enlargement in main pulmonary artery
 Costophrenic dullness- pleural effusion
Objectives of COPD
Management
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Prevent disease progression
 Relieve symptoms
 Improve exercise tolerance
 Improve health status
 Prevent and treat exacerbations
 Prevent and treat complications
 Reduce mortality
 Minimize side effects from treatment
Reduce Risk Factors
• Reduction of total personal exposure to tobacco
smoke, occupational dusts and chemicals, and
indoor and outdoor air pollutants are important
goals to prevent the onset and progression of
COPD.
• Smoking cessation is the single most effective-and
cost-effective- intervention to reduce the risk of
developing COPD and stop its progression
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Vaccines:
– Influenza vaccines reduce serious illness
and death in COPD patients by 50%. Give
once (in Autumn) each year.
– Pneumococcal vaccine
Pharmacologic treatment
Can improve and prevent symptoms,
 Reduce the frequency and severity of
exacerbations,
 Improve health status,
 Improve exercise tolerance.
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Bronchodilators
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These medications are central to symptom
management in COPD.
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Short acting beta agonists
LABA
Anticholinergics (long and short acting)
Theophyline
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Regular treatment with long-acting bronchodilators is
more effective and convenient than treatment with
short-acting bronchodilators, but more expensive.
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Combining drugs with different mechanisms and
durations of action may increase the degree of
bronchodilation for equivalent or lesser side effects.
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Theophylline is effective in COPD, but due to its
potential toxicity inhaled bronchodilators are
preferred when available.
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Regular treatment with inhaled
glucocorticosteroids is not always necessary
only appropriate for patients with:
– symptomatic improvement and a documented
spirometric response to inhaled
glucocorticosteroids or
– If FEV1 < 50% predicted and repeated
exacerbations (for example, 3 in the last three
years).
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Antibiotics: Not recommended except for
treatment of infectious exacerbations and
other bacterial infections.
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Mucolytic (Mucokinetic, Mucoregulator)
Agents: Patients with viscous sputum may
benefit from mucolytics, but overall benefits
are very small.
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Antitussives: Regular use contraindicated in
stable COPD.
If Corpulmonale is formed:
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Diuretics
 Anticoagulation
 Flebotomy (if Htc>55)
Manage Exacerbations
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Exacerbations:
– Increased dyspnea
– Increased cough and sputum
– Purulance in sputum
(Sometimes drowsiness, high fever etc)
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The most common causes of an exacerbation are
infection of the tracheobronchial tree (80%) and; s
pneumonia; h influensae; m catarrhalis; are the most
common pathogens (viruses less common)
Main Causes of exacerbations
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Tracheobronchial
infections
Air pollution
Pneumonia
Pulmonary embolism
Pneumothorax
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Thorax trauma
Code fractures
Beta blockers narcotic
use
Arhytmia
Cardiac failure
Manage Exacerbations in the
Emergency Department
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Oxygen (cautious)
 Short acting beta agonist and/or
anticholinergic inhalation (Spacer or
nebulisation)
 Iv Teophyline (5-6 mg/kg in 20 min, 0.5 mg/kg/hr infusion)
 Iv steroid in severe attack
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Antibiotics (iv, oral)
 Check fluid imbalance, nutrition
 Treat concomitant disease (Corpulmonale, px
etc)
 Prophylactic anticoagulation
 Noninvasive (BİPAP) and invasive mechanic
ventilation
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Noninvasive intermittent positive pressure
ventilation (NIIPPV) in acute exacerbations
improves blood gases and pH, reduces inhospital mortality, decreases the need for
invasive mechanical ventilation and intubation,
and decreases the length of hospital stay
Severe Exacerbation
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Cyanosis
RR>25
HR>110/dk
Somnolence
Severe deteoriation in PFT
Pneumonia, pneumotorax
Confusion, coma, arrest
PO2<50, PCO2>70, pH<7.35
Intensive care
indication
Hospitalization Indications
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Severe attack
No response to 4-6 hours of treatment
İmpared sleep and feeding due to dyspnea
İnsufficient care at home
>3 attack with hospitalization in one year
Concomitant severe disease
Deteoriated mental functions
Increased hypoxemia or hypercapnia
Non-Pharmacologic Treatment
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Rehabilitation
 Oxygen therapy
 Surgical interventions
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Rehabilitation programs should include, at a
minimum:
– Exercise training
– Nutrition counseling
– Education.
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The goals of pulmonary rehabilitation are to reduce
symptoms, improve quality of life, and increase
participation in everyday activities.
Oxygen Therapy
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The long-term administration of oxygen (>15 hours per day) to
patients with chronic respiratory failure increases survival and
has a beneficial impact on pulmonary arterial pressure,
polycythemia (hematocrit > 55%), exercise capacity, lung
mechanics, and mental state.
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The goal of long-term oxygen therapy is to increase the baseline
PaO2 at rest to at least 60 mm Hg at sea level, and/or produce
SaO2 at least 90%, which will preserve vital organ function by
ensuring an adequate delivery of oxygen.
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Low flow rates 2-3lt/min should be given
Surgical Treatments
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Bullectomy, lung volume reduction
surgery (LVRS) and lung transplantation
may be considered in carefully selected
patients with Stage IV: Very Severe
COPD.
COPD IS NOT ASTHMA !
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Different causes
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Different inflammatory cells
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Different mediators
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Different inflammatory consequences
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Different response to treatment
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