Step 2 CK · Internal Medicine · Pulmonology

Asthma & COPD Management

Name: Asthma & COPD Management
Creator: Veli Bakalov, MD

Step up the controller, rescue the exacerbation, and know what actually saves lives

Pulmonology·Obstructive & Airway Disease·6 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Asthma is reversible obstruction: FEV1 must rise ≥12% AND ≥200 mL after a bronchodilator; if spirometry is normal but suspicion high, a methacholine challenge (≥20% FEV1 fall) confirms it.
ICS is the asthma controller cornerstone; even mild asthma gets an ICS-containing reliever (as-needed low-dose ICS-formoterol), and a LABA is never used alone because it increases asthma deaths.
Asthma step-up: low-dose ICS → ICS-LABA → medium/high-dose ICS-LABA → add LAMA or biologic; check inhaler technique and adherence before every step-up.
Severe asthma biologics: omalizumab (anti-IgE) for allergic/high IgE; mepolizumab or benralizumab (IL-5 pathway) for eosinophilic; dupilumab (IL-4/IL-13) for type 2 disease.
Acute asthma: oxygen, albuterol + ipratropium, early systemic steroids, IV magnesium if severe; a normal or rising PaCO2, silent chest, or drowsiness means impending failure → ICU/intubation.
COPD = post-bronchodilator FEV1/FVC below 0.70; FEV1 ≥80% = GOLD 1, 50–79% = GOLD 2, 30–49% = GOLD 3, under 30% = GOLD 4; groups A/B/E by symptoms (mMRC/CAT) and exacerbations.
COPD maintenance: group A a bronchodilator, B LABA + LAMA, E LABA + LAMA plus ICS if eosinophils ≥300 or asthma overlap; never ICS monotherapy.
COPD exacerbation: albuterol/ipratropium, steroids ~5 days, antibiotics for purulent sputum or ventilation, SpO2 88–92%, BiPAP for hypercapnic acidosis (pH below 7.35).
Only smoking cessation and LTOT (resting PaO2 ≤55 or SpO2 ≤88%; ≤59 or ≤89% with cor pulmonale, polycythemia, or edema) prolong survival in COPD.

Diagnosis: reversible versus fixed obstruction

Spirometry defines both diseases. Both lower the FEV1/FVC ratio. Reversibility and the patient's profile tell them apart.

Asthma. The obstruction reverses after a bronchodilator: FEV1 must rise by ≥12% and by ≥200 mL. One without the other does not count. (The 2022 ERS/ATS standard instead defines a positive response as a rise of more than 10% of the predicted FEV1 or FVC; the 12% and 200 mL rule remains the classic exam criterion.) Asthma is variable, so spirometry between attacks may be normal. If suspicion stays high, a methacholine challenge that drops FEV1 by ≥20% confirms airway hyperresponsiveness. A negative challenge makes asthma very unlikely.

COPD. A post-bronchodilator FEV1/FVC below 0.70 (persistent airflow limitation that does not fully reverse) in a patient with risk factors, usually smoking. DLCO is reduced in emphysema because alveolar–capillary surface is destroyed. It is normal in pure chronic bronchitis and normal or high in asthma. Chronic bronchitis is a clinical diagnosis: a productive cough for ≥3 months in each of 2 consecutive years.

Asthma vs COPD

Feature	Asthma	COPD
Typical patient	Younger, atopic, episodic and variable symptoms	Older smoker with progressive dyspnea and chronic cough
Spirometry	Obstruction that reverses (FEV1 ↑ ≥12% and ≥200 mL)	Fixed obstruction: post-bronchodilator FEV1/FVC <0.70
DLCO	Normal or increased	Reduced in emphysema
Controller backbone	ICS-based; never LABA alone	LABA/LAMA-based; never ICS alone

Test every patient with COPD once for alpha-1 antitrypsin deficiency. Suspect it especially with early-onset emphysema, little or no smoking, basilar panacinar disease, or coexisting liver disease.

Chronic asthma: the controller ladder

ICS is the cornerstone. Inhaled corticosteroids treat the airway inflammation; short-acting β2-agonists (SABA, such as albuterol) only relieve bronchospasm and are the rescue drug. Current GINA guidance no longer treats even mild asthma with SABA alone. It uses an ICS-containing reliever, usually low-dose ICS-formoterol as needed.

Low-dose ICSDaily, or as-needed low-dose ICS-formoterol for mild disease.
ICS + LABALow-dose combination inhaler.
Medium/high-dose ICS-LABAIncrease the ICS dose.
Add a LAMA or a biologicFor severe, uncontrolled asthma.

SMART/MART. Formoterol works within minutes, so one ICS-formoterol inhaler can be the daily maintenance drug and the as-needed reliever (single maintenance and reliever therapy).

Never prescribe a LABA as monotherapy in asthma. A LABA without an ICS increases asthma deaths, so LABAs are always given with an ICS in one combination inhaler.

Before stepping up. Check inhaler technique and adherence, remove triggers (allergens, smoke, nonselective β-blockers), and treat comorbid rhinitis or GERD. After about 3 months of good control, step down to the lowest effective dose. Montelukast, a leukotriene receptor antagonist, is a weaker alternative controller. It is useful in aspirin-exacerbated respiratory disease and carries a boxed warning for neuropsychiatric effects.

Biologics for severe asthma

Drug	Target	Phenotype
Omalizumab	Anti-IgE	Allergic asthma with high IgE
Mepolizumab	Anti-IL-5	Eosinophilic
Benralizumab	IL-5 pathway (anti-IL-5 receptor; depletes eosinophils)	Eosinophilic
Dupilumab	Anti-IL-4/IL-13 (blocks the shared IL-4 receptor α)	Type 2 inflammation

Biologics are add-ons for severe asthma that stays uncontrolled on high-dose ICS-LABA. Choose by phenotype (IgE level, blood eosinophils).

Acute asthma exacerbation

Treatment. Give oxygen, an inhaled SABA (albuterol, repeated or continuous) plus ipratropium, and early systemic corticosteroids; oral prednisone works as well as IV. Add IV magnesium sulfate for a severe attack, and escalate to ICU care for a poor response. At discharge, finish a short oral steroid course and start or step up an ICS-containing controller.

Reading the blood gas. Early in an attack, hyperventilation drives PaCO2 low (respiratory alkalosis). A PaCO2 that is normal or rising in a patient who is still tachypneic (for example, climbing from 30 to 45 mmHg) means the respiratory muscles are tiring and respiratory failure is close. It does not mean the patient is improving.

Silent chest: too little airflow to generate a wheeze
Inability to speak
Altered mental status: drowsiness or confusion
Normal or rising PaCO2 despite tachypnea

Any of these red flags means preparing for ICU care and intubation. After intubation, use a low rate and a long expiratory time to avoid air trapping (auto-PEEP).

Stable COPD: grade, group, and maintenance

Two separate axes. The GOLD grade describes airflow severity by FEV1 % predicted. The group (A, B, or E) reflects symptom burden (mMRC dyspnea scale or CAT score) and exacerbation history, and it determines initial therapy.

≥80%GOLD 1 (mild)

50–79%GOLD 2 (moderate)

30–49%GOLD 3 (severe)

<30%GOLD 4 (very severe)

GOLD groups and initial maintenance therapy

Group	Defined by	Initial maintenance
A	0–1 moderate exacerbations (none hospitalized); few symptoms (mMRC 0–1, CAT <10)	A bronchodilator
B	0–1 moderate exacerbations (none hospitalized); more symptoms (mMRC ≥2, CAT ≥10)	LABA + LAMA
E	≥2 moderate exacerbations, or ≥1 leading to hospitalization, in the past year	LABA + LAMA; add ICS if eosinophils ≥300 or asthma overlap

Avoid ICS monotherapy in COPD. ICS also raises pneumonia risk in COPD, so use it only where it helps.

Escalation. If a patient on LABA + LAMA keeps having exacerbations, step up to triple therapy (add ICS) when eosinophils are ≥100. If eosinophils are lower, add roflumilast or azithromycin (see below).

COPD exacerbation

Controlled oxygenTitrate to SpO2 88–92%; check an ABG.
Short-acting bronchodilatorsAlbuterol and ipratropium.
Systemic corticosteroidsAbout 5 days (prednisone 40 mg daily); longer courses add side effects without benefit.
Antibiotics when indicatedIncreased sputum purulence and volume, or any ventilated patient.
BiPAP for hypercapnic acidosispH <7.35 with a raised PaCO2.

Why not more oxygen? Over-oxygenation worsens hypercapnia. Relieving hypoxic vasoconstriction sends blood to poorly ventilated units, which worsens V/Q mismatch. By the Haldane effect, oxygenated hemoglobin also unloads CO2. Aim for 88–92%, not 100%.

Antibiotics (Anthonisen criteria). The cardinal symptoms are more dyspnea, more sputum volume, and more sputum purulence. Treat when all three are present, when two are present and one is purulence, or when the patient needs noninvasive or invasive ventilation. The usual culprits are H. influenzae, Moraxella catarrhalis, and S. pneumoniae. Common choices are amoxicillin-clavulanate, doxycycline, or a macrolide, given for 5–7 days.

BiPAP. In acute hypercapnic respiratory acidosis (pH <7.35), noninvasive positive-pressure ventilation lowers intubation rates and mortality; a drowsy but arousable patient still qualifies. Intubate if the patient cannot protect the airway, is unstable, or worsens on NIV.

Survival and prevention

Two interventions prolong life. Smoking cessation is the single most important intervention because it slows the accelerated decline in FEV1. The other is long-term oxygen therapy (LTOT), which improves survival only in resting hypoxemia and should be worn at least 15 hours a day.

PaO2 ≤55mmHg at rest (SpO2 ≤88%) qualifies for LTOT

PaO2 ≤59mmHg (SpO2 ≤89%) qualifies if cor pulmonale, polycythemia, or edema

Oxygen is not prescribed for dyspnea alone. Without resting hypoxemia it does not prolong life.

Vaccination: yearly influenza and pneumococcal vaccines
Pulmonary rehabilitation: improves dyspnea, exercise tolerance, and quality of life, but not FEV1
Roflumilast (oral PDE-4 inhibitor): reduces exacerbations in selected frequent exacerbators with severe airflow limitation and chronic bronchitis; causes diarrhea and weight loss
Azithromycin (daily): reduces exacerbations in selected frequent exacerbators; watch for QT prolongation and hearing loss
Lung volume reduction surgery: helps carefully chosen patients with upper-lobe-predominant emphysema; lung transplant is the option for end-stage disease