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COPD (Obstr­uctive Disease)

Typical symptoms indica­­tive of disease of large airways (dyspnea, cough, and sputum produc­tion) with evidence of irreve­rsible air­flow obstru­ction (FEV/FVC < 0.70).
Can be asympt­omatic. Any combin­ation of cough, sputum, and dyspnea (on exertion or at rest depending on severity). Depends on relative contri­butions of chronic bronchitis and emphysema. Most patients have MIXED features of both.
Risk Factors
Smoking (90% of cases), alpha1­-an­tit­rypsin deficiency (risk is even worse with smoking), enviro­nmental factors (second hand smoke), and chronic asthma.
Get PFTs (FEV/FVC < 0.70), CXR, A1A level in patients with a personal or family history of premature emphysema (<5­0yo), and ABG (shows chronic pCO2 retention and decreased PO2). COPD leads to respir­atory acidosis with metabolic alkalosis as compen­sation.
Low sensit­ivity for diagnosing COPD. Only severe, advanced shows hyperi­nfl­ation, flattened diaphragm, enlarged retros­ternal space, and diminished vascular markings.
Measure peak expiratory flow rate using peak flow meter. If <35­0L/min, get PFTs to test for obstru­ction.
Pulmonary Function Tests
• Definitive diagnostic test. FEV1 (the amount of air that can be forced out of the lungs in 1s) is decreased.
TLC, RV, and FRV are increased (air trapping). Although the TLC is increased, the air is not useful because it is RV (no gas exchange). Decreased vital capacity.
• Best prognostic indicator for COPD
• The best predictor of FEV1 is pack years of smoking
• PaO2 falls when FEV1 is < 50%
• When FEV1 is < 25% chronic retention of C02 occurs
• Cor pulmonale occurs only after prolonged reduction in FEV1 (< 25%) with severe, chronic hypoxemia.
• Prolonged forced expiratory time.
Timed full exhalation of VC >6sec.
• During auscul­tation, end-ex­pir­atory wheezes on forced expira­tion, decreased breath sounds, or inspir­atory crackles.
• Tachypnea, tachyc­ardia, cyanosis, use of accessory respir­atory muscles, hyperr­eso­nance on percus­sion, and signs of cor pulmonale.
Serial FEV1 measur­ements have high predictive value. Watch pulse oximetry and exercise tolerance too.
• acute exacer­bations (most common causes are infection, noncom­pliance and heart disease), secondary polycy­themia (Hct>55% in men or >47% in women) compen­sating to chronic hypoxemia, cor pulmonale, pulmonary HTN.


• Permanent enlarg­ement of small airway spaces distal to terminal bronch­ioles due to destru­ction of alveolar walls.
• Decreased elastic recoil means increased compli­ance, increased TLC, RV (air trapping), so the TC (or FVC) is decreased!
• Air trapping leads to dynamic hyperi­n­f­lation resulting in large auto-PEEP (intrinsic PEEP).
• Thin patients with severe dyspnea, hyperi­nflated chests, decreased vascular markings, moderate oxygen desatu­ration.
Pathop­hys­iology of Emphysema
• Destru­ction of alveolar walls (impaires gas exchange) due to relative excess in protease (elastase) activity or relative deficiency of antipr­otenase (alpha­1-a­nti­try­psin) activity in the lung.
Elastase is released from PMNs and macrop­hages and digests human lung. This is inhibited by alpha1­-an­tit­rypsin.
• Tobacco smoke increases the number of activated PMNs and macrop­hages, inhibits A1A, and increases oxidative stress on lung by free radical produc­tion.
Pink Puffers
Tend to be thin due to increased energy expend­iture during breathing. When sitting, they tend to lean forward, barrel chest (increased AP diameter). Tachypnea with prolonged expiration through pursed lips. Patient is distressed and uses accessory muscles (esp. strap muscles in the neck).
Centri­lobular Emphysema
most common type, typically seen in smokers. Destru­ction is limited to respir­atory bronch­ioles (proximal acini) with little changed distal acini. Predil­ection for upper lung zones.
Panlobular Emphysema
Panlobular Emphysema: seen in patients with alpha1­-an­tit­rypsin deficiency. Destru­ction involves both proximal and distal acini. Predil­ection for lung bases.

GOLD Criteria

• GOLD I =mild: FEV1 <80% predicted
• GOLD 2 =moderate: FEV1 <50­--79% predicted
• GOLD 3 =severe: FEV1 3 <9% predicted
• GOLD 4=very severe: FEV1 < 30% predicted
Severity of symptoms
• A=fewer symptoms, low risk of exacerbations
• B = more symptoms, low risk
• C = fewer symptoms, high risk
• D =more symptoms, high risk


• SABAs as needed in all patients.
• LABAs in modera­te-­to-very severe stages (reduce exacer­bations and hospit­ali­zat­ions) when SABAs fail to control.
ICS is recomm­ended in patients with GOLD 3-4 disease (FEV1< 50%). Reduce exacer­bat­ions, improved lung function, QoL. But increased risk for PNA. Should be combined with LABAs.
• Combin­ation LABA + ICS is more e effective at reducing exacer­bations associated with an increased risk of PNA.
• GOLD 3-4 patients may benefit from roflum­ilast, a phosph­odi­est­erase-4 inhibitor for bronch­itis, not emphysema.

Chronic Bronchitis

• Chronic cough productive of sputum for at least 3 months per year for at least 2 consec­utive years.
• Due to hypers­ecr­etion of mucus and structural changes in the large airway­/tr­ach­eob­ron­chial tree
• Bronch­ova­scular markings, flattened diaphragm, and normal DLCO.
Pathop­hys­iology of Chronic Bronchitis
Excess mucus production narrows the airways. Productive cough. Inflam­mation and scarring in airways, enlarg­ement in mucous glands, and smooth muscle hyperp­lasia lead to obstru­ction.
Blue Bloaters
• Predom­inantly chronic bronch­itis, overweight and cyanotic (secondary to hyperc­apnia and hypoxemia).
• Chronic cough and sputum produc­tion.
• Signs of cor pulmonale may be present in severe or long-s­tanding disease.
• Respir­atory rate is normal or slightly increased, no apparent distress, no use of accessory muscles.

Acute Exacer­bation

• Persistent increase in dyspnea not relieved with bronch­odi­lators. Increased sputum production and cough are common.
• Can lead to acute respir­atory failure requiring hospit­ali­zation and possibly mechanical ventil­ation. •
Pulmonary infection is one of the main precip­itants.
• CXR shows hyperi­nfl­ation. ABG shows hypoxia, hyperc­arbia, and respir­atory acidosis.
Treatment of Acute Exacer­bation
• bronch­odi­lators (beta agonist and/or antich­oli­ner­gics), systemic cortic­ost­eroids (methy­lpr­edn­iso­lone) when hospit­alized, antibi­otics (azith­romycin or levofl­oxacin), supple­mental oxygen, noninv­asive positive pressure ventil­ation (BIPAP or CPAP), and intubation if necessary (only severe CO2 retent­ion). NO INHALED CORTIC­OST­EROIDS.

Oxygen Therapy

• Improves survival and quality of life in patients. Some need continuous oxygen, while others only require it during exertion or sleep. Get ABG to determine need.
• Criteria: PaO2 55, SaO2<88%, or PaO2 55-59 plus polycy­themia or cor pulmonale.
• Long standing hypoxemia may lead to pulmonary HTN and cor pulmonale.
• Continuous oxygen therapy for >18 hr/day has been shown to reduce mortality
• Hypoxemia is due to V/Q mismat­ching therefore responsive to low flow oxygen (2-3L/­min). If not responsive to oxygen, consider shunt.

Smoking Cessation

Most important interv­ention.
• Disease progre­ssion is accele­rated by continued smoking and can be greatly slowed by its cessation. Around age 35, FEV1 decreases approx­imate 25-30m­L/yr. In smokers, the decline is faster (3-4x). If a smoker quits, the rate of decline slows to normal.
• Smoking does not completely reverse. Respir­atory symptoms improve within 1 year of quitting.
Smoking cessation and oxygen therapy are the only interv­entions shown to reduce mortality.


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