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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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