What it is:Progressive, largely irreversible airflow limitation from years of noxious exposure (almost always tobacco smoke) causing two overlapping problems: chronic bronchitis(mucus-hypersecreting, inflamed airways with a productive cough on most days for 3+ months, 2+ years running) and emphysema(destroyed alveolar walls, no fibrosis, just lost surface area). Most patients have both in some mix.
The core problem:Inflammation narrows and plugs small airways while destroyed alveolar walls rob the lung of elastic recoil. Air gets trapped, the chest hyperinflates, and the diaphragm flattens into a mechanically disadvantaged, easily fatigued muscle. None of that reverses with a bronchodilator, which is why "not fully reversible" is baked into the definition.
What you do about it:Stop smoking (the only intervention that changes the trajectory), pick a bronchodilator strategy based on symptom burden and exacerbation history using the GOLD ABE system, add inhaled steroid only when eosinophils and exacerbation history justify the pneumonia risk, and vaccinate relentlessly.
Brauer's framing: the reliever inhaler is not the treatment.Albuterol makes patients feel better in the moment, but the maintenance bronchodilator (a LAMA and/or LABA) is what actually reduces exacerbations and hospitalizations. Patients who lean on their rescue inhaler and skip their maintenance inhaler have it exactly backwards, and that misconception is worth correcting at every visit. Heavy SABA use (more than a canister every 1-2 months, or daily use) is itself a marker of poor control, not a harmless habit.
Two classification questions get asked about every COPD patient, and they're independent of each other: what does the lung look like(phenotype) and how obstructed is it(GOLD spirometric grade). A separate question, symptom/risk group, is covered under Diagnosis and drives therapy.
| Phenotype | Classic picture | Mechanism |
|---|---|---|
| Chronic bronchitis("blue bloater") | Productive cough, cyanotic, often overweight, cor pulmonale earlier | Goblet cell hyperplasia, mucus gland hypertrophy, impaired ciliary clearance |
| Emphysema("pink puffer") | Thin, barrel chest, pursed-lip breathing, quiet chest | Alveolar wall destruction, loss of elastic recoil, air trapping, no fibrosis |
"Pink puffer / blue bloater" is a presentation pattern, not a diagnostic category on its own, and most real patients are a blend. The exam-relevant point is that emphysema has no fibrosis(that's what separates it from other interstitial lung diseases) and that chronic bronchitis is a clinical diagnosis by history(cough + sputum, most days, 3 months a year, 2 years running), not a spirometry number.
| Grade | Severity | Postbronchodilator FEV1 % predicted |
|---|---|---|
| GOLD 1 | Mild | ≥80% |
| GOLD 2 | Moderate | 50-79% |
| GOLD 3 | Severe | 30-49% |
| GOLD 4 | Very severe | <30% |
FEV1/FVC confirms COPD; FEV1 % predicted grades its severity.The ratio (FEV1/FVC <70%, unitless) is the actual measured value and doesn't get "percent predicted." The FEV1 used to assign GOLD grade 1-4 ispercent predicted, compared against a reference population. Two different numbers, two different jobs. Also: GOLD grade(spirometry) is not the same thing as GOLD groupA/B/E (symptoms + exacerbation risk) - grade tells you how obstructed the airways are, group tells you what drug to start.
Cigarette smoke (or occupational dust, biomass fuel, or rarely inherited alpha-1 antitrypsin deficiency) activates neutrophils, macrophages, and CD8+ lymphocytes in the airway. They dump TNF-α, IL-8, and leukotriene B4 into the tissue, driving chronic inflammation across the airways, the pulmonary vessels, and the lung parenchyma itself. Unlike asthma's eosinophil/mast cell-driven, often-reversible inflammation, COPD's inflammatory pattern is neutrophilic and self-perpetuating.
Smoke also generates oxidants that damage lung proteins and lipids directly and, critically, inhibit antiprotease activity. Neutrophil elastase is normally kept in check by alpha-1 antitrypsin (AAT). When AAT is overwhelmed (heavy smoke exposure) or genetically deficient, elastase runs unopposed and chews through alveolar walls. That's the direct mechanistic link between smoking, inherited AAT deficiency, and emphysema, and it's why guidelines now recommend testing every COPD patient for AAT deficiency at least once.
Read the pathophysiology and the drug list writes itself. Muscarinic antagonists and beta agoniststarget the neural/receptor side of bronchoconstriction and mucus tone, not the inflammation. Inhaled corticosteroidstarget the inflammatory cascade itself, which is why they help exacerbations (an inflammatory event) more than they help baseline airflow. Roflumilastdirectly blocks the same PDE4 pathway driving TNF-α and IL-8 release. AAT augmentationreplaces the exact protein that's missing. Nothing here regenerates destroyed alveoli or reverses fibrosis-free emphysematous change; that's the ceiling on what any of these drugs can do.
Destroyed elastic recoil plus small-airway narrowing means air gets trapped on exhalation. Functional residual capacity (FRC)rises, the chest hyperinflates, and the diaphragm flattens into a shortened, mechanically disadvantaged muscle that fatigues fast, especially during an exacerbation. A flattened diaphragm also shortens inhalation time, which is a big part of why dyspnea gets worse as disease progresses even when the underlying obstruction hasn't changed that day.
Advanced disease develops a low ventilation/perfusion (V/Q) ratio: alveoli are underventilated relative to how well they're perfused. PaO2 falls chronically (initially with exertion, eventually at rest), and some patients become chronic CO2 retainers whose central respiratory drive has blunted to rising CO2 - their kidneys compensate by retaining bicarbonate, so pH looks deceptively normal until an acute insult tips them into decompensated respiratory acidosis. Chronic hypoxemia and vascular remodeling raise pulmonary artery pressure, and sustained pulmonary hypertension drives right ventricular hypertrophy: cor pulmonale.
COPD isn't just a lung disease. Chronic inflammation and deconditioning drive skeletal muscle wasting, cachexia, osteoporosis, anemia, and increased cardiovascular event risk. This is part of why pulmonary rehabilitation (exercise training, not just breathing exercises) is a guideline-level recommendation and not an afterthought.
Cough and sputum typically show up years beforedyspnea does. That order matters: a patient with a smoking history and a chronic productive cough who "doesn't feel short of breath yet" is often earlier in the disease, not disease-free.
| Category | Findings |
|---|---|
| Early / mild | Chronic cough, sputum production; exam may be entirely normal |
| Progressive | Exertional dyspnea, decreased exercise tolerance, chest tightness, wheeze |
| Advanced exam findings | Barrel chest (hyperinflation), pursed-lip expiration, accessory muscle use, shallow rapid breathing, cyanosis of mucous membranes |
Asthma symptoms are classically variable(better and worse across days, triggers, seasons) and often start in childhood. COPD symptoms are chronic and progressive- a slow downward slope over years, not a flare-and-remit pattern - in a patient usually over 40 with a smoking or occupational exposure history. When both patterns overlap in the same patient, treat the asthma component first: ICS goes in the initial regimen regardless of eosinophil count or exacerbation history.
Diagnosis requires all three: compatible symptoms, a history of exposure (smoking, occupational, biomass fuel), and spirometric confirmation. None of the three alone is sufficient.
| Tool | What it measures | Low-burden cutoff |
|---|---|---|
| CAT(COPD Assessment Test) | Comprehensive symptom impact, 8 items | <10 = low symptom burden |
| mMRC(modified Medical Research Council) | Breathlessness only, grades 0-4 | <2 (i.e., grade 0-1) = low symptom burden |
A change of 2+ points on CAT is considered clinically meaningful when tracking a patient over time.
Before you treat "another COPD exacerbation," rule out pneumonia, pulmonary embolism, acute heart failure, and pneumothorax. All four can present with acute worsening dyspnea in a COPD patient and none of them respond to a steroid burst and an inhaler bump.
Guideline pharmacotherapy is chosen by GOLD group (A, B, or E), not by spirometric grade and not by symptoms alone. This replaced the older four-quadrant ABCD system used in the 2022-era guideline (still what your handbook chapter describes) - group C and D collapsed into a single group E, because the data show exacerbation history predicts future risk regardless of how symptomatic the patient feels day to day.
| Group | Exacerbation history | Symptom burden | Initial therapy |
|---|---|---|---|
| A | 0-1 moderate, no hospitalization | mMRC 0-1 / CAT <10 (low) | A bronchodilator (short- or long-acting) |
| B | 0-1 moderate, no hospitalization | mMRC ≥2 / CAT ≥10 (high) | LAMA + LABAdual bronchodilator |
| E | ≥2 moderate, or ≥1 leading to hospitalization | Any | LAMA + LABA; add ICS upfront if eosinophils ≥300 cells/µL |
The 2026 update Brauer flagged lowered the group-E exacerbation threshold further: even one moderate exacerbationin the past year is now enough to flag elevated future risk, tightening what used to require two moderate or one hospitalization. The rationale is observational data showing that even a single moderate exacerbation raises the odds of the next one. Expect the threshold for "high risk" to keep getting more conservative as evidence accumulates - the underlying logic (exacerbation history is the single best predictor of future exacerbations) hasn't changed.
Group A is officially "any bronodilator," but trial data (the 2017 tiotropium-in-early-COPD trial) showed a LAMA reduces first-exacerbation risk even in these low-risk patients. So while albuterol PRN alone is technically compliant with Group A, starting a LAMA is the stronger answer if the patient is willing.
Escalation depends on whichproblem persists: dyspnea despite adequate technique/adherence, or ongoing exacerbations.
Every major triple-therapy trial (IMPACT, ETHOS) showed increased pneumonia riskwith ICS-containing regimens, concentrated in patients with lower eosinophil counts. The WISDOM trial showed ICS could be tapered out of a stable LAMA+LABA+ICS regimen without a meaningful rise in exacerbations. Net message: ICS benefit in COPD is exacerbation reduction in the right (eosinophilic) phenotype, not a default add-on for breathlessness, and it should come off the regimen if it isn't clearly earning its keep.
symptom reliefmarks drugs with no proven exacerbation or mortality benefit, used purely for symptom control.
| Short-acting β2-agonists (SABA) - rescue, all GOLD groups | ||
| Albuterol (ProAir, Proventil, Ventolin) | MDI/DPI/nebulizer, every 4-6 h PRN rescue | |
| Levalbuterol (Xopenex) | Nebulizer q6-8h or MDI q4-6h PRN; single R-isomer, no proven advantage over albuterol, costs more | |
| Short-acting muscarinic antagonist (SAMA) | ||
| Ipratropium (Atrovent) | MDI 4x/day PRN or nebulizer 3-4x/day PRN; slower onset (15-20 min) than albuterol | |
| Long-acting β2-agonists (LABA) - no titration, effective dose from the start | ||
| Formoterol (Perforomist) | Nebulizer q12h | |
| Arformoterol (Brovana) | Nebulizer q12h | |
| Salmeterol (Serevent) | DPI q12h; slower onset (15-20 min) | |
| Indacaterol (Arcapta) | DPI once daily | |
| Olodaterol (Striverdi) | Soft mist once daily | |
| Long-acting muscarinic antagonists (LAMA) - no titration | ||
| Tiotropium (Spiriva Handihaler/Respimat) | Once daily; slowest onset of the class (~80 min) but longest duration | |
| Umeclidinium (Incruse Ellipta) | Once daily | |
| Aclidinium (Tudorza) | DPI twice daily; widest therapeutic index (fastest plasma hydrolysis) | |
| Glycopyrrolate (Seebri, Lonhala) | Twice daily | |
| LAMA + LABA combinations | ||
| Umeclidinium/vilanterol (Anoro Ellipta) | Once daily | |
| Tiotropium/olodaterol (Stiolto Respimat) | Once daily | |
| Glycopyrrolate/formoterol (Bevespi Aerosphere) | Twice daily | |
| Glycopyrrolate/indacaterol (Utibron Neohaler) | Twice daily | |
| ICS + LABA combinations - not preferred initial regimen; use if eos ≥300 or asthma overlap | ||
| Budesonide/formoterol (Symbicort) | Twice daily | |
| Fluticasone furoate/vilanterol (Breo Ellipta) | Once daily | |
| Fluticasone propionate/salmeterol (Advair) | Twice daily | |
| Mometasone/formoterol (Dulera) | Twice daily | |
| Triple therapy: LAMA + LABA + ICS | ||
| Fluticasone furoate/umeclidinium/vilanterol (Trelegy Ellipta) | Once daily; only triple approved for both COPD and asthma | |
| Budesonide/glycopyrronium/formoterol (Breztri Aerosphere) | Twice daily; COPD only, mortality signal in ETHOS at the 320 mcg budesonide dose | |
| Oral therapy | ||
| Roflumilast (Daliresp) | 250 mcg daily x4 weeks | then 500 mcg daily maintenance |
| Azithromycin | 250 mg daily or500 mg 3x/week, chronic use in non-smokers with recurrent exacerbations | |
| Theophylline ER | 200 mg BID start | titrate to 400-900 mg/day; goal level 8-15 mcg/mL |
| Acute exacerbation | ||
| Prednisone (or equivalent) | 40 mg PO daily x5 days | |
| Alpha-1 antitrypsin augmentation (confirmed AAT deficiency only) | ||
| AAT (Prolastin-C, Aralast, Zemaira, Glassia) | 60 mg/kg IV weekly; keeps trough above protective threshold of 10 µmol/L; roughly $50,000+/year | |
Acetylcholine released from parasympathetic (vagal) nerves acts on airway smooth muscle to cause bronchoconstriction and on mucus glands to increase secretion, working mainly through M3receptors postsynaptically. M2receptors sit presynaptically on the same nerve terminal and normally act as a brake, inhibiting further ACh release.
A non-selective antagonist blocks the presynaptic M2 brake along with the postsynaptic M3 receptor. Losing the M2 brake means moreACh gets dumped into the synapse, which can compete off the antagonist at M3 and blunt the bronchodilation you were trying to achieve. Modern LAMAs (tiotropium, umeclidinium, glycopyrrolate, aclidinium) are relatively M3-selective and dissociate slowly from M3 once bound, which is the actual mechanism behind their long duration of action, not just formulation tricks.
Systemic absorption is low with inhaled use, so classic anticholinergic effects (dry mouth, blurred vision, urinary retention, constipation) are uncommon, though not zero, and inhaled anticholinergics can rarely precipitate acute narrow-angle glaucoma. The most consistent complaint is dry mouth.
Onset varies:aclidinium, glycopyrrolate, and umeclidinium act in 5-15 minutes; tiotropium takes about 80 minutes. None of the LAMAs are appropriate for acute rescue use, ever, regardless of onset speed - that's a labeling and evidence issue, not just a pharmacokinetic one. Ipratropium (the SAMA) is technically faster than tiotropium but still slower than albuterol (15-20 min vs 5 min), so it's often better used scheduled or added to albuterol than relied on alone for rescue.
β2-adrenergic receptors on airway smooth muscle raise intracellular cAMP, relaxing the muscle. Selectivity for β2 over β1 is never complete, so tachycardia and palpitations remain possible, especially at higher doses or in patients sensitive to catecholamine effects.
Cardioselective beta blockers (metoprolol, bisoprolol, atenolol, nebivolol, betaxolol, acebutolol, esmolol) are not contraindicatedin COPD and should still be used when there's a clear cardiac indication (post-MI, HFrEF, etc). What they are notis a COPD treatment: the BLOCK-COPD trial added metoprolol to COPD patients without a cardiac indication and found no reduction in exacerbations, plus more hospitalizations. Don't start a beta blocker to treat COPD, but don't stop a cardioselective one a patient needs for their heart just because they also have COPD.
LABA monotherapy is fine in COPD. That's different from asthma, where LABA monotherapy carries a mortality signal and the drug must be paired with an ICS. If a COPD patient also has asthma, treat the asthma overlap with ICS-containing therapy regardless of eosinophils or exacerbation count.
ICS reduce capillary permeability, block proteolytic enzyme release from leukocytes, and inhibit prostaglandin synthesis, i.e. they blunt the inflammatory cascade rather than relaxing smooth muscle directly. That's why their proven benefit in COPD is exacerbation reduction, not day-to-day symptom improvement, and why ICS monotherapy has no rolein COPD (it's never studied or recommended without a paired bronchodilator).
| Eosinophils | Interpretation |
|---|---|
| ≥300 cells/µL | Strong ICS responders; NNT ≈8.6 to prevent one exacerbation vs LAMA+LABA alone |
| 100-300 cells/µL | Modest benefit possible; NNT ≈46 - weigh against pneumonia risk |
| <100 cells/µL | ICS unlikely to prevent exacerbations; avoid regardless of exacerbation frequency |
The trial arc that built this rule:FLAME showed LABA+LAMA beat LABA+ICS outright on exacerbations, ending routine LABA+ICS as first-line COPD therapy. IMPACT and ETHOS then showed triple therapy (LAMA+LABA+ICS) beats dual therapy on exacerbations and, notably, showed a mortality benefitin more severe, higher-eosinophil populations - but at the cost of measurably more pneumonia. WISDOM showed that in patients not clearly benefiting, ICS can be tapered back out of a triple regimen without a rebound in exacerbations.
Other adverse effects:oral candidiasis and hoarseness (counsel rinse-and-spit after every dose), skin bruising; at higher chronic doses, osteoporosis, cataracts, and adrenal suppression become concerns, so use the lowest effective dose.
Roflumilastis an oral PDE4 inhibitor, same anti-inflammatory pathway (TNF-α, IL-8) as the airway inflammation itself. Reserved for patients with the chronic bronchitis phenotype and FEV1 <50%who keep exacerbating despite triple therapy, or as an ICS-sparing option in low-eosinophil patients. Start low (250 mcg daily x4 weeks) before the maintenance dose (500 mcg daily) because GI intolerance (diarrhea, nausea, weight loss, decreased appetite) is common early and often transient. Do not combine with theophylline- same mechanistic pathway, additive toxicity without added benefit. Watch for neuropsychiatric effects (insomnia, anxiety, new or worsening depression, rarely suicidality); avoid in patients with a mental health history.
Chronic azithromycin(250 mg daily or 500 mg three times weekly) reduces exacerbation frequency through anti-inflammatory, not just antimicrobial, effects, but is reserved for non-smokerswith recurrent exacerbations despite optimal therapy. The tradeoffs are real: macrolide-resistant bacterial colonization, hearing loss with prolonged use, and QT prolongation risk.
Biologics(dupilumab, mepolizumab) are newer entrants, indicated when eosinophils are ≥300 cells/µL andthe patient has had 2+ moderate or 1+ severe exacerbation despite optimized inhaled therapy. Dupilumab's COPD indication is specifically for the chronic bronchitis phenotype. Think of these as the eosinophilic-severe-exacerbator escalation tier, analogous to how biologics are used in severe eosinophilic asthma.
Theophylline inhibits phosphodiesterase (raising cAMP) and may modestly improve dyspnea, exercise tolerance, and respiratory drive, but its role has shrunk to near-irrelevance now that LABAs and LAMAs exist, because of a brutal combination of a narrow therapeutic window (8-15 mcg/mL), major CYP interactions, and wide interpatient dosing variability. Clearance falls (needing lower doses) with advanced age, pneumonia, heart failure, liver dysfunction, and drugs like cimetidine, macrolides, and fluoroquinolones. Clearance rises (needing higher doses) with smoking, hyperthyroidism, and enzyme inducers like phenytoin and rifampin.
Reserve it for patients who can't use inhaled bronchodilators at all, and get a pulmonology referral if you're seriously considering it. It should generally be avoided during acute exacerbationsgiven the toxicity risk and lack of proven benefit in that setting.
For patients with confirmed AAT deficiency-associated emphysema, augmentation replaces the missing antiprotease with pooled human AAT (Prolastin-C, Aralast, Aralast-NP, Zemaira, Glassia), dosed at 60 mg/kg IV weekly to keep trough levels above the protective threshold of 10 µmol/L. It does not reverse existing damage; the goal is slowing further loss. It's also expensive (over $50,000/year), which matters for counseling and access conversations, and it does nothing to replace smoking cessation, which remains essential even in genetically driven disease.
An exacerbation is an acute change from baselinein dyspnea, cough, or sputum, severe enough to change management. Usually triggered by viral or bacterial infection or an environmental irritant, and typically evolves over days (up to about 14). Some patients never fully return to their prior baseline afterward, which is part of why exacerbation history is such a strong predictor of future risk.
The three cardinal symptoms are worsening dyspnea, increased sputum volume, and increased sputum purulence.Count how many are present to stage severity.
| Stage | Definition |
|---|---|
| Mild (type 1) | 1 cardinal symptom plus a supporting sign (URI in past 5 days, unexplained fever, increased wheeze/cough, or resp/heart rate >20% above baseline) |
| Moderate (type 2) | 2 cardinal symptoms |
| Severe (type 3) | All 3 cardinal symptoms |
Defined by an acute drop in PaO2 of 10-15 mmHg, or any acute rise in PaCO2 that drops serum pH to ≤7.3. Watch for restlessness, confusion, tachycardia, diaphoresis, cyanosis, hypotension, and irregular breathing as clinical clues something has crossed from "exacerbation" into "respiratory failure."
Give antibiotics if the patient has all 3 cardinal symptoms, OR 2 cardinal symptoms with increased sputum purulenceas one of them, OR requires mechanical ventilationregardless of symptoms. Sputum culture is often unhelpful because many COPD patients are chronically colonized between exacerbations; purulence (a clinical, visual assessment) is doing the real diagnostic work here, not the culture.
| Risk category | Likely organisms | Recommended |
|---|---|---|
| Uncomplicated(<4 exacerbations/yr, no comorbidity) | S. pneumoniae, H. influenzae, M. catarrhalis, H. parainfluenzae; resistance uncommon | Macrolide, 2nd/3rd-gen cephalosporin, or doxycycline |
| Complicated(age ≥65 and >4 exacerbations/yr, or comorbid illness) | Above plus drug-resistant pneumococci, β-lactamase-producing H. influenzae/M. catarrhalis | Amoxicillin/clavulanate or a respiratory fluoroquinolone (levofloxacin, gemifloxacin, moxifloxacin) |
| MDR risk(chronic steroids, hospitalization or antibiotics in past 90 days, long-term care resident) | Above plus P. aeruginosa | Levofloxacin, or IV antipseudomonal β-lactam/cephalosporin if hospitalized |
TMP/SMX(rising pneumococcal resistance), amoxicillin alone and first-generation cephalosporins(too vulnerable to β-lactamase), and erythromycin(insufficient H. influenzaecoverage) are all specifically called out as inadequate empiric choices here, even though they show up as reasonable options in other respiratory infections.
This is where a lot of "treatment failure" actually lives. A patient on the textbook-correct regimen who can't operate the device correctly is, functionally, untreated. Before escalating therapy for persistent symptoms or exacerbations, confirm technique and adherence first.
| Patient issue | Better fit |
|---|---|
| Low inspiratory flow / low FVC / dysfunctional breathing | HFA with spacer, soft mist inhaler, or nebulizer (not a DPI - it needs forceful inhalation to disperse the powder) |
| Arthritis or motor deficits limiting HFA actuation | DPI or a breath-activated device; spacer chamber if staying on HFA |
| Poor adherence | Once-daily device to cut pill/puff burden |
| Memory or coordination issues | Fewest possible preparation/administration steps |
Wrong posture, forgetting to exhale fully before actuating, wrong inhalation speed (aerosol wants slow and steady, powder wants forceful and deep - opposite techniques, easy to swap by habit), firing before or after starting to inhale instead of during, not holding breath 5-10 seconds after, and skipping the rinse-and-spit after ICS. A dirty or clogged spacer is an underrated, easily-fixed cause of "my inhaler stopped working."
Most DPIs use pharmaceutical lactose carrier with the milk protein component removed, so contamination risk is very low even in milk-protein allergy and lactose intolerance, despite package inserts still listing milk-protein allergy as a caution. In practice most specialists remain comfortable prescribing DPIs to these patients; switch device types only if the patient actually reacts.
Inhaler cost derails adherence constantly. Practical levers: manufacturer copay coupons (commercial insurance) or patient assistance programs (some now accept Medicare patients), consolidating to a single combination inhaler instead of several separate devices, checking the Medicare Prescription Payment Plan and Extra Help/Low-Income Subsidy for Medicare patients, and turning off pharmacy autofill for PRN inhalers like albuterol so copays aren't wasted on unused refills.
| Parameter | When | Watching for |
|---|---|---|
| Spirometry (FEV1) | Annually, and with any therapy change | Rate of decline; a rapid faller may need reassessment of phenotype/diagnosis |
| CAT or mMRC | Every visit | Symptom trajectory; CAT change ≥2 points is meaningful |
| Exacerbation count/severity | Every visit, look back 12 months | GOLD group reclassification and escalation triggers |
| Blood eosinophils | At escalation decision points; repeat, don't rely on one draw | ICS candidacy - is the patient still ≥300, 100-300, or <100? |
| Inhaler technique | Every visit, especially before escalating therapy | Device errors masquerading as drug failure |
| SpO2 / ABG | Baseline if advanced disease; during any exacerbation | Criteria for long-term oxygen therapy; CO2 retention |
| Theophylline level(if used) | 1-2x/year at steady state, or with dose/interacting drug change | Target 8-15 mcg/mL; narrow window |
| Vaccination status | Every visit | Influenza (annual), pneumococcal, COVID-19, and consider pertussis, shingles, RSV |