GRAND ROUNDS 02 · DISEASE EDUCATION

COPD

Fixed airflow limitation — emphysema + chronic bronchitis
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COPD = chronic airflow limitation from noxious exposure (smoking #1) — persistent inflammation destroys alveoli (emphysema) and plugs airways (chronic bronchitis). Obstruction is largely irreversible & progressive. Expiratory airflow limitation → air trapping → dynamic hyperinflation, auto-PEEP, ↑ work of breathing.
1Pathophysiologyexposure → cascade
1Noxious exposure — tobacco smoke (#1), biomass, occupational dust; α1-antitrypsin deficiency in the young.
2Inflammation — neutrophils, macrophages, protease/antiprotease imbalance → tissue destruction.
3Emphysema — septal destruction → lost surface area + loss of elastic recoil & airway tethering.
4Chronic bronchitis — goblet hyperplasia, mucus plugging, small-airway fibrosis & narrowing.
5Airflow limitation + air trapping — expiratory collapse → dynamic hyperinflation, auto-PEEP, ↑ WOB.
6Chronic gas failure — V/Q mismatch → hypoxemia, chronic hypercapnia; pulmonary vasoconstriction → cor pulmonale.
2Presentation

Chronic: progressive dyspnea (worse on exertion), chronic productive cough, wheeze, prolonged expiration, pursed-lip breathing, accessory muscles, barrel chest.

The EXACERBATION: acute ↑ dyspnea + ↑ sputum volume + ↑ sputum purulence (Anthonisen). Often infection-triggered (viral/bacterial).

Ominous: exhaustion, drowsiness / CO₂ narcosis, asterixis, cyanosis, silent chest, hemodynamic collapse — peri-arrest.

▲Phenotypestwo classic pictures — most overlap
Pink Puffer
emphysema-predominant · type A
  • Thin, barrel chest, tachypneic
  • Pursed-lip breathing, ↑ WOB
  • Near-normal SpO₂ / PaCO₂ (long)
  • "Fighting to oxygenate"
Blue Bloater
chronic-bronchitis-predominant · type B
  • Overweight, cyanotic, cough
  • CO₂ retainer, hypoxemic
  • Cor pulmonale → peripheral edema
  • Blunted respiratory drive
SSeveritygrade the exacerbation
GRADEWORK / GASACTION
Mild↑ dyspnea, speaks freelySABA ± abx PO
Moderate↑ WOB, SpO₂ <92%Nebs + steroids + abx
Severeaccessory, hypercapnia+ controlled O₂, NIV
Resp failurepH<7.35, ↓GCS, narcosisNIV → intubate

Grade the pH, not the CO₂ alone — a high CO₂ with near-normal pH is compensated & chronic; a falling pH = acute decompensation.

6Differentialnot every dyspneic wheeze is COPD
  • Acute heart failure / flash
  • Pneumonia
  • Pulmonary embolism
  • Pneumothorax
  • Asthma (reversible)
  • ACS / arrhythmia
  • Bronchiectasis
  • Lung cancer / effusion
CComorbid LoadCOPD is a systemic disease
HEARTCor pulmonale, CAD, arrhythmia — dyspnea is often cardiac + pulmonary together.
GASChronic hypoxemia → polycythemia, pulmonary hypertension; consider home O₂.
SYSMuscle wasting, osteoporosis, depression, ↑ VTE risk in exacerbation.
▲The Alveolusnormal vs emphysema
+ chronic-bronchitis airway
EMPHYSEMA — SEPTAL DESTRUCTION alveolar cluster · lost surface area
NORMAL many small sacs · thin septa · big area EMPHYSEMA few large floppy spaces · walls destroyed · air trapped ① septal destruction → lost surface area ② airway collapse on exhalation (no cartilage support) ③ air trapping → hyperinflation THE OTHER HALF — CHRONIC BRONCHITIS Mucus plugging + small-airway fibrosis narrow the lumen → chronic productive cough & wheeze. Inflamed wall, goblet hyperplasia. COPD = emphysema + this.
Emphysema
Septa destroyed → lost recoil & surface area. Irreversible.
Chronic Bronchitis
Mucus + airway fibrosis. Cough & sputum ≥3 mo/yr ×2 yr.
Result
Expiratory airflow limitation → air trapping, hyperinflation.
4Diagnosticsclinical + SpO₂ · watch acute-on-chronic

Bedside: exam & WOB, SpO₂ (know the baseline), ECG/troponin (cardiac overlap), CXR (pneumonia/pneumothorax), capnography.

ABG — the key story: chronic CO₂ retention with metabolic compensation (↑ HCO₃⁻, near-normal pH). Acute-on-chronic = CO₂ climbs faster than the kidney compensates → pH falls = decompensation.

CO₂-retainer O₂ caution: over-oxygenation worsens hypercapnia — target SpO₂ 88–92%, don't chase 100%.

ABG — READ THE pH, NOT THE CO₂ ALONE acute vs chronic
pH 7.40 chronic: ↑CO₂ · ↑HCO₃⁻ · pH ~normal compensated — this is their baseline acute-on-chronic: pH FALLS → NIV
▲Air Trappingwhy the chest hyperinflates
EXPIRATORY OBSTRUCTION → HYPERINFLATION the macro picture
NORMAL domed diaphragm HYPERINFLATED flat diaphragm · barrel chest · trapped air can't exhale

Dynamic hyperinflation & auto-PEEP: each breath stacks on trapped air → the resting lung volume climbs. The flattened diaphragm loses mechanical advantage → ↑ work of breathing, and intrinsic PEEP raises the threshold to trigger a breath — a vicious cycle that drives the muscles to fatigue.

5Treatmentthe exacerbation · per protocol
Controlled O₂ → SpO₂ 88–92%. Venturi 24–28%. Titrate — don't drown the retainer.
SABA + SAMA albuterol + ipratropium nebs (air-driven if retainer).
Steroids prednisone 40 mg PO ×5 d (or IV) — shortens the exacerbation.
Antibiotics if ↑ purulence (≥2 Anthonisen) — e.g. amoxicillin/doxycycline per protocol.
NIV (BiPAP) — first-line for hypercapnic acidosis pH 7.25–7.35. STRONG evidence.
Adjuncts: treat the trigger (CHF, PE, pneumonia); VTE prophylaxis.
Intubate if NIV fails / pH <7.25, ↓GCS, can't protect airway, arrest.
BBaseline / ChronicGOLD · outpatient
GROUPMAINTENANCE
AA bronchodilator (LABA or LAMA)
BLABA + LAMA
ELABA+LAMA (± ICS if eos↑)
AllStop smoking · vaccines · rehab · O₂ if hypoxemic

Smoking cessation & long-term O₂ (chronic hypoxemia) are the only interventions that change mortality.

7Critical ProceduresNIV first · the vent is a trap
⚠ Hypercapnic failure — NIV, then ventilate slow
  • NIV is first-line for pH 7.25–7.35 hypercapnic acidosis — reduces intubation & mortality (strong evidence).
  • Give controlled O₂ — don't withhold it, but don't over-oxygenate the retainer (88–92%).
  • Ventilate slow: low RR, long expiratory time, permissive hypercapnia — let them exhale.
  • Auto-PEEP kills: breath-stacking → ↓ venous return / barotrauma. If they arrest → DISCONNECT the circuit, press the chest, let air out.
PPitfalls & Pearls
  • Don't withhold O₂ — but don't over-oxygenate. Target 88–92% in a retainer.
  • Read the pH, not the CO₂. High CO₂ + normal pH = chronic & compensated.
  • NIV early in hypercapnic acidosis — waiting costs intubations.
  • Hunt the trigger — pneumonia, PE, CHF, pneumothorax, ischemia.
  • Auto-PEEP arrest post-tube → disconnect & let them exhale.
REMEMBER — Controlled O₂ 88–92% · SABA+SAMA nebs · Steroids · Antibiotics if purulent · NIV early for pH<7.35. Tubed & crashing → DISCONNECT, long expiratory time.
DDisposition
ADMIT / ICU
  • Acidosis / NIV need, ↓GCS
  • New hypoxemia / hypercapnia
  • Failed outpatient Rx; comorbid PE/pneumonia
DISCHARGE
  • Good response, back to baseline
  • Steroid ± antibiotic course
  • Inhalers + smoking cessation + f/u
Sheet
COPD
Series / No.
GRAND ROUNDS 02
Part No.
CC-GR-02
Rev
A
Status
EDUCATION REFERENCE — NOT A PROTOCOL. VERIFY LOCALLY.

SOURCES: GOLD Global Strategy for the Diagnosis, Management & Prevention of COPD (2025 Report) · BTS/ICS Guideline for Ventilatory Management of Acute Hypercapnic Respiratory Failure (NIV) · Austin et al., BMJ 2010 (titrated O₂, 88–92%) · Anthonisen criteria (antibiotics) · Marino, The ICU Book (auto-PEEP, obstructive ventilation); Tintinalli, Emergency Medicine. Doses educational — not medical advice & not a protocol; reference for trained clinicians only. Verify all drugs, doses & treatments against local protocol & current guidelines. Full disclaimer: crashcard.co/legal. © 2026 Claustrum LLC d/b/a Crash Card · crashcard.co · Printed in Minnesota.