Week 2: COPD-Baydur Flashcards
Current definition of COPD
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with some significant extrapulmonary (systemic) effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases
Risk factors for COPD
- Tobacco Smoke (>20 pack-years)
- passive smoking
- air pollution
- hyperreactive airways: asthma may progress to COPD through remodelling of airways
- ethnic, racial, socioeconomic factors: men, white, poor
- bacterial infections
Bacterial infection and pathogenesis of COPD
Vicious circle hypothesis
Initiating factors: smoking, childhood respiratory disease, infection
1. impaired mucociliary clearance leads to Bacterial infection and chronic mucus hypersecretion
A inflammatory response
-leads to increased elastolytic activity
-altered elastase-anti-elastase balance
-progression of COPD
B. bacterial products lead to airway epithelial injury
-and to progression of COPD
Common bacteria: H. influenza and Chlamydia Pneumoniae
Effects of bacterial products in lower respiratory tract and COPD
- Central airways
- increased mucus secretion, decreased mucociliary clearance
- chronic mucus hypersecretion
- leads to chronic bronchitis and COPD - Peripheral airways
- cytokind secretion and neutrophil influx
- airway inflammation, thickening, fibrosis
- leads to peripheral airway obstruction and COPD - Alveoli
- PMN influx, increased elastase activity
- disruption of elastase-antielastase balance
- leads to emphysema and COPD
Genetic/Molecular factors in COPD
- COPD only develops in minority of heavy smokers. Patients with the below have faster declines in lung function
1. Alpha 1-antitrypsin deficiency - associated with panlobular emphysema
2. PMN chemokines and cytokines and MMPs produced by macrophages and neutrophils
3. polymorphisms in anti-oxidants
Clinical presentation
- smoking at least 1 pack of cigarettes a day for 20 years
- cough with mucoid to mucopurulent sputum
- dyspnea
- increased frequency of respiratory illnesses
- may have wheezing
- late symptoms/signs: hypoxemia, heart failure, weight loss, poor appetite, early satiety, secondary erythrocytosis
Exercise intolerance in COPD due to
a. Ventilatory limitation – hyperinflation, dead-space ventilation, impaired gas exchange,deconditioning, peripheral muscle dysfunction.
b. Gas exchange limitations – Hypoxemia, hypercarbia increase ventilatory demands leads to lactic acid production from fatiguing respiratory muscles.
c. cardiac dysfunction- RV hypertrophy leading to cor pulmonale leading to LV dysfunction
d. skeletal muscle dysfunction due to deconditioning, oxidative stress, inflammation, hypoxemia, chronic steroid use, weight loss
e. respiratory muscle dysfunction from chronic overload and hyperinflation
A person with emphysema looks like
- thin, weight loss
- using accessory neck muscles
- barrel chest
- tense ab muscles
- very dyspneic
- ABGs preserved until advanced phase
person with chronic bronchitis looks like
- ruddy complexion: secondary erythrocytosis
- fatigued but not dyspneic
- ABGs show hypoxemia and hypercapnia
- cor pulmonale due to hypoxemia
Findings of COPD on CXR
- hyperinflation
- flat, depressed diaphragms
- long narrow heart shadow
- increased space behind sternum seen on lateral view
- loss of vascularity( emphysema)
- thickened bronchial markings (chronic bronchitis)
PFT findings in COPD
- Spirometry: consistent with airflow obstruction with FEV1/FVC decreased
- little or no response to bronchodilators
- improves in asthma - Flow-volume curves: downward expiratory convexity (expiratory flow limitation)
- lung volumes: TLC, RV, and RV/TLC increased (indicate hyperinflation)
- DLCO:
- decreased in emphysema because of reduced alveolar surface area
- In asthma: normal or increased due to airtrapping
- chronic bronchitis: increased if increased Hct, or decreased due to mucus plugging
Findings on ABG for COPD
- hypoxemia: significant when PaO2 below 55 mmHg due to risk of developing pulmonary HTN and cor pulmonale
- hypercapnia: later in disease when FEV1 falls below 1L
Complications of COPD
- hypoxic pulmonary hypertension
- right heart failure: cor pulmonale
- frequent respiratory infections (>2/year)
- weight loss, loss of appetite
- respiratory failure with hypoxemia, hypercapnia, and respiratory acidosis
Principles of management of COPD
Smoking cessation Oxygen therapy Bronchodilators – mainly inhaled Steroids – for acute exacerbations Phosphodiesterase inhibitors Antibiotics Mechanical ventilation Surgery – lung volume reduction; transplantation Pulmonary rehabilitation
