Respiratory

Asthma exacerbation: ED and inpatient CCS-style management

Clinical Overview and When to Suspect Asthma Exacerbation

— Asthma affects ~8% of US adults and ~7% of children; exacerbations drive >1.5 million ED visits/year.

— Mortality concentrated in patients with prior intubation, recent hospitalization, frequent SABA use, low socioeconomic access, and African American/Puerto Rican demographics.

— Known asthmatic with increased SABA use (>2 canisters/month is a red flag), nocturnal awakenings, viral URI prodrome, or peak flow <80% personal best.

— New-onset wheezing in an atopic patient (eczema, allergic rhinitis, family history) — but consider mimics first (see chunks 13–14).

— Viral URI (most common in adults and kids), allergen exposure, NSAID/aspirin (AERD), beta-blocker, cold air, exercise, smoke, menses, GERD, poor controller adherence.

— Prior intubation or ICU admission for asthma.

— ≥2 hospitalizations or >3 ED visits in past year.

— Hospitalization or ED visit in past month.

— Use of >2 SABA canisters/month.

— Current/recent oral corticosteroid use.

— Low socioeconomic status, illicit drug use, major psychiatric/psychosocial comorbidity.

— Food allergy in a patient with asthma.

Step 3 management: On the CCS, the first three orders for any suspected asthma exacerbation are continuous pulse oximetry, supplemental O2 to keep SpO2 92–96%, and nebulized albuterol-ipratropium — before you order a chest x-ray or ABG. Move the clock forward after initiating treatment, then reassess. Do not delay bronchodilators to obtain "confirmatory" testing — asthma exacerbation is a clinical diagnosis.

Definition: Acute or subacute worsening of airflow obstruction in a patient with known or suspected asthma, characterized by progressive dyspnea, cough, wheeze, chest tightness, and a fall in PEF or FEV1 from baseline.

Epidemiology and burden:

When to suspect an exacerbation in the ED:

Common triggers to elicit immediately:

Risk factors for fatal/near-fatal asthma — memorize these:

Presentation Patterns and Key History

— Slow-onset (Type 1, ~80%): days of worsening symptoms, viral trigger, mucus plugging predominant, slower response to therapy.

— Sudden-asphyxic (Type 2, ~20%): minutes-to-hours, allergen or NSAID trigger, bronchospasm predominant, responds faster to bronchodilators but higher mortality risk.

— Baseline control: daytime symptoms/week, night awakenings/month, SABA use, controller regimen and adherence, last PFTs/peak flow personal best.

— Exacerbation history: prior intubations, ICU stays, ED visits and hospitalizations in past year, last oral steroid burst.

— Current episode: time of onset, triggers, home treatments tried, response.

— Medications: ICS dose, LABA, LTRA, biologic (omalizumab, mepolizumab, dupilumab, benralizumab, tezepelumab), recent oral steroids, beta-blockers, NSAIDs, ACEi.

— Comorbidities: allergic rhinitis, nasal polyps (think AERD), GERD, obesity, OSA, vocal cord dysfunction, pregnancy.

— Inability to speak in full sentences.

— Diaphoresis, agitation, somnolence.

— Symptoms despite home nebs/multiple SABA puffs.

— Prior intubation for asthma (single strongest predictor of future fatal asthma).

Board pearl: A patient with asthma, nasal polyps, and an NSAID-triggered exacerbation has AERD (Samter triad) — avoid all COX-1 inhibitors, consider aspirin desensitization once stable, and add a leukotriene receptor antagonist (montelukast) or 5-LOX inhibitor (zileuton) to controller therapy.

Key distinction: "Wheezing" is not synonymous with asthma. In an older smoker without prior asthma diagnosis, anchor only after excluding COPD exacerbation, CHF ("cardiac asthma"), PE, and upper-airway obstruction — history alone often discriminates them.

Classic symptom tetrad: dyspnea, wheezing, cough (often nocturnal), chest tightness — typically episodic and reversible.

Tempo matters — two patterns:

Targeted ED history (get it while nebs run):

Red-flag historical features for impending respiratory failure:

Physical Exam Findings and Severity Assessment

— Mild–moderate: speaks in full sentences, prefers sitting, no accessory muscle use, RR <30, HR <120, SpO2 >90% on room air, PEF >50% predicted/personal best.

— Severe: speaks in phrases, sits forward (tripod), accessory muscle use, RR ≥30, HR ≥120, SpO2 <90%, PEF <50%, pulsus paradoxus >25 mmHg.

— Life-threatening / impending arrest: drowsy, confused, silent chest (no air movement), paradoxical thoracoabdominal motion, bradycardia, cyanosis, absent pulsus paradoxus due to respiratory muscle fatigue.

— Expiratory wheeze is typical; biphasic wheeze suggests more severe obstruction.

— A quiet chest in a distressed patient is ominous — too little airflow to generate wheeze.

— Focal findings (unilateral wheeze, dullness, asymmetric breath sounds) → think pneumothorax, mucus plug atelectasis, foreign body, or pneumonia.

— Sinus tachycardia is expected; bradycardia in a hypoxic asthmatic = peri-arrest.

— Altered mental status = hypercapnic narcosis until proven otherwise.

— >70% predicted/personal best: mild.

— 40–69%: moderate.

— <40%: severe.

— <25% or unable to perform: life-threatening.

CCS pearl: On the CCS, after your first round of nebulizers and steroids, re-examine the patient (advance the clock 20–30 minutes, then "physical exam, respiratory" and "peak expiratory flow") before deciding on disposition. The exam-and-PEF reassessment is what unlocks "discharge home" vs "admit" vs "ICU" pathways.

Board pearl: Disappearance of pulsus paradoxus and of wheezing in a previously severe asthmatic is not improvement — it's respiratory muscle exhaustion. Prepare for intubation.

General appearance — fastest triage tool:

Pulmonary exam pearls:

Cardiovascular and neuro:

Pulsus paradoxus: drop in SBP >12 mmHg during inspiration; correlates with severity but is operator-dependent and often skipped in real practice.

Peak expiratory flow (PEF) — bedside severity tool:

Diagnostic Workup — Initial Labs, Imaging, ECG

— Indications: severe distress, SpO2 <92% on supplemental O2, altered mental status, no improvement after initial therapy, suspicion of hypercapnia.

— Expected pattern: early exacerbation → respiratory alkalosis with hypocapnia (PaCO2 <35) from tachypnea.

— Ominous pattern: "normal" or elevated PaCO2 (≥42) in a tachypneic, distressed asthmatic = fatigue and impending failure → prepare for NIV or intubation.

— Order when: first episode of wheezing, fever, focal exam findings, suspected pneumothorax/pneumomediastinum, failure to respond, or planned admission.

— Typical findings: hyperinflation, flattened diaphragms; look for complications (pneumothorax, pneumomediastinum, infiltrate, atelectasis from mucus plug).

— Mild leukocytosis common (stress demargination + steroids).

— Watch for hypokalemia from beta-agonists and steroids — replete proactively.

— Hyperglycemia from systemic steroids — anticipate, especially in diabetics.

Step 3 management: A "normal" ABG with PaCO2 of 40 in an asthmatic with RR 36 and accessory muscle use is not reassuring — it is the inflection point toward respiratory failure. The next order is prepare for intubation / call ICU, not "recheck ABG in 30 minutes."

The exacerbation is a clinical diagnosis — testing is for severity assessment, complications, and ruling out mimics, not for confirmation.

Pulse oximetry: continuous; titrate O2 to SpO2 93–95% (avoid hyperoxia, which can worsen V/Q mismatch and raise PaCO2 in severe obstruction).

Peak expiratory flow (PEF) or FEV1: obtain before and after each bronchodilator round when feasible.

Arterial blood gas — selective, not routine:

Chest x-ray — not routine:

ECG: in older patients, comorbid cardiac disease, or to exclude ischemia/arrhythmia masquerading as dyspnea. Expect sinus tachycardia; may show transient right heart strain.

CBC, BMP:

Viral testing / influenza-COVID PCR: during respiratory virus season or if febrile; influenza-positive patients with asthma get oseltamivir.

Diagnostic Workup — Advanced or Confirmatory Studies

— Spirometry (outpatient or post-stabilization): FEV1/FVC <0.70 with ≥12% and ≥200 mL bronchodilator reversibility confirms asthma. Avoid in acute exacerbation — use PEF instead at bedside.

— Bronchoprovocation testing (methacholine, mannitol, exercise): for suspected asthma with normal baseline spirometry, in stable outpatients only. A negative methacholine challenge has high negative predictive value.

— FeNO (fractional exhaled nitric oxide): elevated (>50 ppb adults, >35 ppb children) supports Th2/eosinophilic inflammation; guides ICS responsiveness and biologic selection.

— Serum total IgE, allergen-specific IgE, skin prick testing: for phenotyping and biologic candidacy (omalizumab requires elevated IgE).

— Peripheral eosinophil count: ≥300/µL supports eosinophilic phenotype → candidates for anti–IL-5 (mepolizumab, reslizumab, benralizumab) or anti–IL-4Rα (dupilumab).

— D-dimer / CTPA if PE plausible (pleuritic pain, hemoptysis, unilateral leg swelling, no clear asthma history).

— BNP / echocardiogram if cardiac asthma (CHF) is in differential — bilateral crackles, S3, JVD, orthopnea.

— Laryngoscopy / flow-volume loop for vocal cord dysfunction (VCD): inspiratory wheeze/stridor, throat tightness, paradoxical vocal fold motion, poor response to bronchodilators, often young female with anxiety or athletes.

— High-resolution CT chest: for suspected bronchiectasis, ABPA, or atypical features.

— Aspergillus IgE, total IgE >1000, peripheral eos, central bronchiectasis: ABPA in poorly controlled asthma.

Key distinction: Asthma vs COPD — asthma is reversible (≥12%/200 mL post-bronchodilator FEV1 increase), often atopic, episodic, with normal DLCO. COPD has fixed obstruction, smoking history, reduced DLCO (emphysema), and incomplete reversibility. Asthma–COPD overlap (ACO) has features of both — treat as asthma first (ICS-containing regimen mandatory).

Board pearl: Never order methacholine challenge during an acute exacerbation — it can precipitate severe bronchospasm.

When the diagnosis is unclear, expand the workup after stabilizing:

When mimics are on the table:

Risk Stratification and First-Line Management Logic

— 1. Oxygen to SpO2 93–95% (nasal cannula or simple mask).

— 2. Inhaled SABA + SAMA: albuterol 2.5–5 mg nebulized + ipratropium 0.5 mg nebulized, every 20 min × 3 doses, OR continuous albuterol 10–15 mg/hr in severe.

— 3. Systemic corticosteroids within 1 hour: prednisone 40–60 mg PO or methylprednisolone 40–80 mg IV. Oral = IV in efficacy if patient can swallow.

— 4. Consider IV magnesium sulfate 2 g over 20 min for severe exacerbation (PEF <40%) not responding to initial therapy.

— Good response (PEF >70%, sustained ≥60 min, no distress): observe 60 min, then discharge with steroid taper and asthma action plan.

— Incomplete response (PEF 40–69%, mild–moderate symptoms): continue treatment, admit to ward.

— Poor response (PEF <40%, severe symptoms, rising PaCO2): ICU admission, consider NIV/intubation.

— Heliox (70:30 He:O2): improves laminar flow; bridge in severe obstruction (limits FiO2 delivery — not for hypoxic patients).

— IV magnesium: reasonable in severe; cheap, safe, modest benefit.

— Ketamine (1–2 mg/kg IV): bronchodilator properties; useful as induction agent for intubation.

— Epinephrine IM (0.3–0.5 mg of 1:1000): reserved for anaphylaxis or peri-arrest asthma; not first-line.

CCS pearl: On the CCS, the canonical "severe asthma exacerbation" order set in the first 15 minutes: Oxygen, continuous pulse oximetry, IV access, albuterol-ipratropium nebulizer, methylprednisolone IV, magnesium sulfate IV, PEF, then advance clock 30 minutes and reassess. Do not waste a clock-advance ordering a chest x-ray before treatment is running.

Initial severity classification drives the entire algorithm (mild–moderate vs severe vs life-threatening — see chunk 3).

The "first hour" bundle for moderate–severe exacerbation:

Reassess at 60 minutes — this is the decision node:

Adjuncts for refractory disease:

Pharmacotherapy — First-Line Drug Regimen

— Nebulized 2.5–5 mg every 20 min × 3 doses, then every 1–4 hours as needed. Continuous nebulization 10–15 mg/hr for severe.

— MDI with spacer (4–8 puffs every 20 min) is equivalent to nebulizer in cooperative patients — useful in pandemics to limit aerosolization.

— Side effects: tachycardia, tremor, hypokalemia, hyperglycemia, lactic acidosis (transient, benign type B from beta-agonism).

— 0.5 mg nebulized with each albuterol dose for the first hour in moderate–severe exacerbations. Reduces hospitalization rates.

— Not continued beyond the ED — no proven inpatient/outpatient benefit in asthma.

— Prednisone 40–60 mg PO daily × 5–7 days is standard for adults; no taper needed if course ≤7 days and patient not on chronic steroids.

— Methylprednisolone 40–80 mg IV q6–12h if NPO or severe.

— Dexamethasone 6–12 mg PO/IM × 1–2 doses is non-inferior in mild-moderate exacerbations and improves adherence (especially pediatrics).

— Onset of action 4–6 hours — give early, do not wait for response.

— Bronchial smooth muscle relaxant; use in severe exacerbation refractory to first-hour therapy or with PEF <40%.

— Caution: hypotension, areflexia at high levels.

— Start or continue ICS at discharge for every patient — reduces relapse and readmission.

— Budesonide-formoterol as SMART therapy (single inhaler maintenance and reliever) is now preferred over SABA-only rescue per GINA for Steps 1–5.

Step 3 management: Discharge prescription for an asthma exacerbation = prednisone 50 mg × 5 days + ICS-formoterol inhaler + spacer + written asthma action plan + PCP follow-up in 1–4 weeks. Missing the ICS is the most commonly tested error.

Short-acting beta-2 agonist (SABA): albuterol

Short-acting muscarinic antagonist (SAMA): ipratropium

Systemic corticosteroids — the disease-modifying drug:

Magnesium sulfate IV 2 g over 20 min:

Inhaled corticosteroids (ICS) at discharge — do NOT skip:

Procedures and Advanced Management — Ventilatory Support

— Consider in severe exacerbation with hypercapnia, accessory muscle use, RR >25, but only in alert, cooperative patients without imminent arrest.

— Evidence weaker in asthma than COPD — use as a bridge while medical therapy works, not as a definitive solution.

— Typical settings: IPAP 8–12, EPAP 3–5; titrate.

— Cardiopulmonary arrest or peri-arrest.

— Severe AMS, exhaustion, silent chest.

— Worsening hypercapnia/acidosis despite maximal therapy.

— Hypoxia refractory to high-flow O2.

— Ketamine 1–2 mg/kg IV is induction of choice (bronchodilator, preserves hemodynamics).

— Rocuronium 1.2 mg/kg for paralysis.

— Use largest-bore ETT (8.0+ in adults) to reduce resistance and facilitate suctioning.

— Pre-oxygenate aggressively; expect hypotension on positive-pressure ventilation due to auto-PEEP.

— Low tidal volume (6 mL/kg ideal body weight).

— Low RR (8–12) to allow full exhalation.

— Long expiratory time (I:E 1:4 or 1:5).

— Plateau pressure <30 cm H2O.

— Accept PaCO2 50–80, pH ≥7.20 — goal is avoiding barotrauma, not normalizing gases.

— Displacement of tube, Obstruction (mucus plug), Pneumothorax, Equipment failure, Stacking (auto-PEEP) → disconnect from vent and let patient exhale.

CCS pearl: Once a severe asthmatic is intubated on the CCS, your next three orders are arterial line, continuous capnography, and ICU admission. Order chest x-ray to confirm ETT placement and exclude pneumothorax. Then advance clock 30 minutes and reassess plateau pressures and auto-PEEP.

Non-invasive ventilation (NIV / BiPAP):

Indications for intubation:

Intubation technique (high-risk procedure):

Ventilator strategy — "permissive hypercapnia":

If sudden deterioration on ventilator — "DOPES":

ECMO: salvage therapy for refractory respiratory failure with reversible cause — early transfer to ECMO center if available.

Special Populations — Elderly and Renal/Hepatic Impairment

— Up to 10% of older adults have asthma; often labeled "COPD" erroneously.

— Higher mortality from exacerbations due to comorbidities, polypharmacy, atypical presentation (cough or dyspnea on exertion rather than wheeze).

— Beta-blocker interaction: non-selective beta-blockers (propranolol, nadolol) can trigger bronchospasm — switch to cardioselective (metoprolol, bisoprolol) if cardiac indication is compelling; cardioselective beta-blockers are generally safe in stable asthma.

— Inhaler technique is frequently poor — assess and use spacers or breath-actuated devices; arthritis impairs MDI use.

— Cardiac comorbidity: SABA-induced tachycardia and hypokalemia may precipitate arrhythmia or ischemia — telemetry advisable.

— Albuterol, ipratropium, ICS, prednisone: no dose adjustment needed.

— Magnesium sulfate: reduce dose or avoid in severe CKD (CrCl <30) due to risk of magnesium toxicity (areflexia, respiratory depression, cardiac arrest).

— Theophylline (largely obsolete): narrow therapeutic index; monitor levels, hepatic dosing required.

— Montelukast: rare hepatotoxicity (and neuropsychiatric black-box warning: agitation, depression, suicidal ideation).

— Zileuton: contraindicated in active liver disease; monitor LFTs monthly × 3, then quarterly.

— Prednisone: hepatic conversion to prednisolone — in severe hepatic failure, use prednisolone directly.

— NSAIDs (AERD), ACEi cough mimic, beta-blockers, sedatives masking distress.

Board pearl: A 72-year-old with HFrEF and asthma needs a beta-blocker for guideline-directed heart failure therapy — use metoprolol succinate or bisoprolol (cardioselective) at the lowest effective dose and monitor PEF. Withholding beta-blockade entirely is the wrong answer when cardiac benefit is established.

Step 3 management: Renal failure + severe asthma exacerbation → use IV magnesium cautiously (1–2 g over 30 min) with neuro checks, or skip it entirely if CrCl <30.

Elderly asthmatics — underdiagnosed and undertreated:

Renal impairment:

Hepatic impairment:

Polypharmacy red flags in older adults:

Special Populations — Pregnancy and Pediatrics

— Uncontrolled asthma is far more dangerous to the fetus than asthma medications.

— Safe in pregnancy: albuterol, ipratropium, budesonide (preferred ICS), beclomethasone, salmeterol, formoterol, montelukast, systemic prednisone (oral steroids associated with mild risk of cleft lip/palate in first trimester, low birth weight, preeclampsia — but benefit outweighs risk in severe exacerbation).

— Maintain SpO2 ≥95% (fetal hypoxia threshold is lower than maternal).

— Magnesium sulfate is safe.

— Continuous fetal monitoring for viable gestation (≥24 weeks) during severe exacerbation.

— Severity scored with PRAM or PASS scores (work of breathing, air entry, wheeze, O2 sat, mental status).

— First-line: albuterol MDI with spacer + mask (4–8 puffs every 20 min) is equivalent to nebulizer and preferred.

— Ipratropium with albuterol for moderate–severe.

— Dexamethasone 0.6 mg/kg PO × 1–2 doses preferred over prednisone (better palatability, adherence, shorter course).

— Magnesium sulfate 25–50 mg/kg IV for severe.

— Avoid theophylline, sedatives.

— Disposition: discharge if sustained good response 60 min after last neb; admit if PEF <70% or persistent hypoxia.

— Distinguish viral bronchiolitis (RSV, <2 yrs, first wheeze) from asthma — bronchodilators not routinely effective in bronchiolitis.

— Modified Asthma Predictive Index: major (parental asthma, atopic dermatitis, allergen sensitization) + minor criteria predict future asthma in wheezy preschoolers.

Board pearl: Budesonide is the inhaled corticosteroid with the most pregnancy safety data (former Category B); when starting a new ICS in pregnancy, choose budesonide.

Step 3 management: Pregnant asthmatic in ED with severe exacerbation → same regimen as non-pregnant adult (O2, neb albuterol-ipratropium, IV/PO steroids, magnesium), plus continuous fetal heart monitoring after 24 weeks and OB consult. Withholding steroids "because of pregnancy" is the tested error.

Pregnancy — "treat asthma as you would in any adult":

Pediatric exacerbation (≤12 years):

Infant/toddler wheeze:

Complications and Adverse Outcomes

— Pneumothorax / pneumomediastinum from high intrathoracic pressures, severe coughing, or barotrauma on the ventilator — sudden chest pain, subcutaneous emphysema, asymmetric breath sounds, tracheal deviation (tension PTX → needle decompression immediately).

— Mucus plugging → atelectasis — focal consolidation on CXR, may need bronchoscopy if persistent.

— Respiratory failure with hypercapnia and acidosis.

— Hypoxic-ischemic brain injury in delayed recognition of peri-arrest asthma.

— Tachyarrhythmias from beta-agonists, hypokalemia, hypoxia.

— Demand ischemia in patients with CAD.

— Auto-PEEP–induced hypotension in mechanically ventilated patients (high intrathoracic pressure → reduced venous return) — disconnect from vent, allow exhalation, fluid bolus.

— Hypokalemia, hyperglycemia, lactic acidosis from beta-agonists.

— Hypomagnesemia, hypophosphatemia from steroids + nutrition shifts.

— Short-term: hyperglycemia, insomnia, mood changes, hypertension.

— Cumulative bursts (≥4/year or >1 g prednisone-equivalent lifetime): osteoporosis, cataracts, adrenal suppression, metabolic syndrome, infection risk.

— Airway remodeling → fixed obstruction.

— Decline in lung function.

— Increased mortality risk after each subsequent severe exacerbation.

— Critical illness myopathy if neuromuscular blockers + steroids used >48 hours.

— Delirium, deconditioning.

Key distinction: Sudden chest pain + asymmetric breath sounds + hypotension in a ventilated asthmatic = tension pneumothorax (clinical diagnosis, decompress immediately — do not wait for chest x-ray). Asymmetric findings + stable vitals = consider PTX vs mucus plug atelectasis (CXR appropriate).

Board pearl: Lactic acidosis from continuous high-dose albuterol can be alarming (lactate 4–8 mmol/L) but is benign Type B and resolves with dose reduction — do not broaden antibiotics or pursue sepsis workup based on lactate alone in this context.

Respiratory complications:

Cardiovascular:

Metabolic:

Iatrogenic from systemic steroids:

Long-term consequences of recurrent exacerbations:

Post-extubation:

When to Escalate — ICU, Consultation, Inpatient Triage

— Sustained PEF ≥70% predicted/personal best for ≥60 min after last bronchodilator.

— SpO2 ≥94% on room air.

— Minimal symptoms, normal mental status, able to ambulate.

— Reliable home environment, follow-up secured, no high-risk features.

— Incomplete response (PEF 40–69%), persistent symptoms.

— Requiring frequent bronchodilators (every 1–2 hours).

— High-risk features (prior intubation, recent hospitalization, poor adherence, comorbidities).

— Inadequate home support.

— PEF <40% despite therapy, persistent severe symptoms.

— Hypercapnia (PaCO2 ≥42 in an exacerbation), acidemia (pH <7.35).

— Altered mental status, exhaustion.

— Need for NIV or intubation.

— Hemodynamic instability.

— Pulmonology: ICU admissions, refractory exacerbations, recurrent ED visits, consideration of biologics, ABPA workup.

— Allergy/Immunology: severe atopic disease, biologic candidacy, immunotherapy.

— Critical care: any intubated or NIV-dependent patient.

— OB: pregnant patients with severe exacerbation or ICU admission.

— Continue scheduled SABA (every 4 hours, with PRN), inhaled steroid, oral/IV corticosteroid.

— Stop ipratropium after ED (no inpatient benefit).

— Asthma education, inhaler technique, action plan before discharge.

— Screen and treat triggers: GERD, allergic rhinitis, OSA.

CCS pearl: On the CCS, the trigger to "admit to ICU" is rising or normalizing PaCO2 in a tachypneic patient, OR altered mental status, OR need for continuous nebulization beyond the ED. Order ICU admission, then continue therapy and monitor.

Step 3 management: Never discharge an asthma patient from the ED without (1) an oral steroid course, (2) an ICS-containing inhaler with technique demonstrated, (3) a written asthma action plan, and (4) follow-up within 1–4 weeks. Missing any of these is testable.

Discharge home from ED — criteria (all met):

Admit to ward (general medicine):

Admit to ICU:

Consultations to consider:

Inpatient management priorities:

Key Differentials — Same-Category (Obstructive Airway) Causes

— Smoking history, age >40, fixed obstruction on PFTs, reduced DLCO, hypoxemia at baseline.

— Triggered by infection, air pollution, non-adherence.

— Treatment overlap (SABA, SAMA, steroids) but antibiotics indicated for Anthonisen criteria (increased dyspnea + sputum volume + sputum purulence), and target SpO2 88–92% (not 93–95%).

— Features of both; usually older patients with smoking history but atopy and reversibility.

— Treat with ICS-containing therapy (not LABA monotherapy).

— Infants <2 years, RSV most common, fine crackles + wheeze.

— Supportive care; bronchodilators not routinely effective.

— Chronic productive cough, recurrent infections, HRCT shows airway dilation/tree-in-bud.

— Triggered by Pseudomonas, NTM; needs airway clearance and targeted antibiotics.

— Poorly controlled asthmatic, central bronchiectasis, total IgE >1000, eosinophilia, Aspergillus-specific IgE+.

— Treat with prednisone + itraconazole.

— Inspiratory stridor (not expiratory wheeze), throat/neck tightness, poor SABA response, young women, athletes, often anxiety- or exercise-triggered.

— Diagnosis: laryngoscopy during episode shows paradoxical adduction.

— Treatment: speech therapy, anxiolytics, treat GERD/postnasal drip.

— Stridor or "barking" cough, monophonic wheeze, positional symptoms.

— Sudden onset, unilateral wheeze, focal hyperinflation; pediatrics especially.

Key distinction: Wheeze is expiratory and polyphonic in asthma; stridor is inspiratory and monophonic in VCD or upper-airway obstruction. Mislabeling VCD as refractory asthma leads to inappropriate steroid courses and intubations.

Board pearl: A young female athlete with "exercise-induced asthma" who fails albuterol and has inspiratory throat tightness has VCD until proven otherwise — order laryngoscopy and refer for speech therapy.

COPD exacerbation:

Asthma–COPD overlap (ACO):

Bronchiolitis (pediatric/viral):

Bronchiectasis:

ABPA (allergic bronchopulmonary aspergillosis):

Vocal cord dysfunction (paradoxical vocal fold motion):

Tracheomalacia / central airway obstruction:

Foreign body aspiration:

Key Differentials — Other-Category Causes of Acute Dyspnea/Wheeze

— Orthopnea, PND, JVD, S3, bilateral crackles, lower-extremity edema, BNP elevated, CXR with cephalization/Kerley B lines.

— Wheeze from peribronchial edema can mimic asthma — don't miss this in older patients without prior asthma.

— Treatment is diuresis + afterload reduction, not bronchodilators.

— Sudden dyspnea, pleuritic pain, hemoptysis, unilateral leg swelling, tachycardia.

— Risk: malignancy, immobilization, OCPs, recent surgery, pregnancy.

— Wells score → D-dimer or CTPA.

— Urticaria, angioedema, hypotension, GI symptoms within minutes of exposure.

— Treatment: IM epinephrine first, then antihistamines, steroids, fluids — not nebulizers alone.

— Sudden pleuritic pain, decreased breath sounds, hyperresonance, tracheal deviation in tension.

— Tall thin young males or known lung disease.

— Fever, focal crackles, productive cough, focal infiltrate on CXR.

— May coexist with and trigger an asthma exacerbation.

— Stridor, voice change, drooling, tripoding.

— ACEi-induced angioedema (lip/tongue swelling, hours to days after dose), epiglottitis, retropharyngeal abscess, foreign body.

— Smoke, chlorine, ammonia exposure; carbon monoxide poisoning (cherry-red, headache, normal SpO2 — use co-oximetry).

Key distinction: Bilateral wet crackles + orthopnea + edema = CHF, not asthma. SABA worsens tachycardia and ischemia; the right answer is IV furosemide, nitrates, and NIV.

Step 3 management: Any "asthma exacerbation" not responding to standard therapy → broaden the differential. Order CXR, BNP, ECG, troponin, D-dimer or CTPA, and reconsider PE, CHF, pneumothorax, and anaphylaxis before doubling down on more albuterol.

Cardiogenic ("cardiac asthma" / acute decompensated heart failure):

Pulmonary embolism:

Anaphylaxis:

Pneumothorax (spontaneous or tension):

Pneumonia:

Upper-airway obstruction / angioedema:

Toxic/inhalational injury:

Carcinoid syndrome: flushing, diarrhea, bronchospasm — rare but classic.

Secondary Prevention, Discharge Medications, Long-Term Plan

— Oral corticosteroid course: prednisone 40–60 mg daily × 5–7 days (no taper if ≤7 days). Dexamethasone 12 mg × 1–2 doses is an alternative.

— Inhaled corticosteroid (ICS) or ICS-LABA: start or step up at discharge — every patient leaves on an ICS-containing controller. SABA-only treatment is no longer acceptable per GINA.

— SMART therapy: budesonide-formoterol used as both controller and reliever — preferred Step 1–5 strategy in GINA 2023+.

— Spacer with MDI — improves drug delivery, reduces oral candidiasis.

— Asthma action plan — written, color-coded (green/yellow/red zones) based on symptoms and PEF.

— Step 1–2: low-dose ICS-formoterol PRN.

— Step 3: low-dose ICS-formoterol daily + PRN (MART).

— Step 4: medium-dose ICS-formoterol MART.

— Step 5: add-on LAMA (tiotropium), refer for phenotyping, consider biologic.

— Omalizumab (anti-IgE): allergic asthma, IgE elevated.

— Mepolizumab, reslizumab, benralizumab (anti–IL-5 / receptor): eosinophilic asthma (eos ≥300).

— Dupilumab (anti–IL-4Rα): Th2-high, also for atopic dermatitis/CRSwNP.

— Tezepelumab (anti-TSLP): broad — works regardless of phenotype.

— Smoking cessation (active and secondhand) — most impactful intervention.

— Annual influenza vaccine, pneumococcal vaccine (PCV20 or PCV15+PPSV23), COVID-19 boosters.

— Avoid NSAIDs in AERD.

— Allergen mitigation (dust mite covers, pet dander, mold).

— Treat GERD, allergic rhinitis, OSA, obesity.

Step 3 management: Every asthma exacerbation discharge note must specify the ICS dose, the spacer, the action plan, and PCP/pulmonology follow-up timing. Discharging on SABA alone is a guideline violation and a tested error.

Discharge medication bundle (memorize for CCS and MCQs):

Step-up therapy (GINA stepwise approach):

Biologics (specialty referral):

Trigger reduction:

Follow-Up, Monitoring, and Counseling

— PCP visit within 1–4 weeks after ED visit or hospitalization — confirms recovery, reinforces controller, reviews technique.

— Pulmonology referral within 4–6 weeks for: ICU admission, ≥2 ED visits/year, ≥1 hospitalization/year, suspected biologic candidacy, refractory disease, diagnostic uncertainty.

— Repeat PEF or spirometry at follow-up to document recovery and update personal best.

— Daytime symptoms (>2 days/week = uncontrolled).

— Night awakenings (>2/month = uncontrolled).

— SABA use (>2 days/week or >1 canister/month = uncontrolled).

— Activity limitation.

— PEF or FEV1 trend.

— Exacerbations in past 12 months.

— Most common errors: not exhaling before MDI, failing to coordinate actuation with inhalation, not holding breath 10 seconds.

— Spacer use solves most coordination issues.

— DPI requires forceful inhalation — confirm patient can generate flow.

— Pharmacy refill records: <50% of expected refills predicts exacerbation.

— Address cost (generic ICS, formulary alternatives, patient assistance).

— Consider for moderate–severe asthma with deconditioning, post-ICU recovery, or coexisting COPD.

— Recognize yellow-zone symptoms (PEF 50–80%): increase SABA or ICS-formoterol, start oral steroid if no improvement in 24–48 hours.

— Red zone (PEF <50% or severe symptoms): take SABA, start oral steroids, seek emergency care.

Board pearl: The single most cost-effective intervention to prevent future exacerbations is improving inhaler technique and adherence, not adding new medications. Always check the inhaler before stepping up therapy.

Step 3 management: Persistent uncontrolled symptoms despite Step 4 ICS-LABA → check adherence and technique → check for comorbidities (GERD, OSA, rhinitis, obesity) → then phenotype for biologic, in that order.

Follow-up cadence:

Monitoring parameters at each visit (ACT or ACQ score):

Inhaler technique — recheck at every visit:

Adherence counseling:

Pulmonary rehabilitation:

Self-management education:

Ethical, Legal, and Patient Safety Considerations

— Up to 50% of asthma readmissions stem from poor ED-to-PCP handoff: no controller prescribed, no follow-up scheduled, no action plan given, no inhaler technique verified.

— Mandatory elements before discharge: medication reconciliation, written action plan, follow-up appointment (or warm handoff), patient teach-back.

— Communicate ICU admission and intubation history to PCP and pulmonology explicitly — these patients are at the highest mortality risk.

— Biologic therapy: discuss cost (often >$30,000/year), injection logistics, adverse effects, alternatives.

— Intubation in severe asthma: when feasible, discuss prognosis and code status — but do not delay life-saving intubation for prolonged discussions in peri-arrest patients; presumed consent applies.

— Pregnancy: explicitly counsel that treating asthma is safer than not treating it; document discussion.

— Adolescents often manage their own inhalers; assess directly, not only via parent.

— School asthma action plans — coordinate with school nurse; ensure access to rescue inhaler at school per state law.

— Asthma mortality is 3× higher in Black Americans and Puerto Ricans; drivers include access, housing/environmental exposures, and structural racism. Screen for social determinants (housing, mold, smoke exposure, food insecurity) and connect to resources.

— Occupational asthma: report to state public health where applicable; remove patient from exposure (baker's asthma, isocyanates, latex).

— Suspected child abuse/neglect if recurrent severe exacerbations with poor caregiver follow-through despite resources — mandatory reporting per state law.

— Avoid sedatives/opioids in non-intubated asthmatics — risk respiratory depression.

— Boarding asthmatics in the ED without controller initiation contributes to readmission — start ICS in the ED.

Step 3 management: Failure to prescribe an ICS at discharge after an asthma exacerbation is a documented patient-safety event in many institutions — treat it as a near-miss and address systematically (order set, EHR prompt, pharmacist review).

Transition-of-care safety:

Informed consent and shared decision-making:

Pediatric and adolescent autonomy:

Health equity:

Mandatory considerations:

Patient safety in the ED:

High-Yield Associations and Rapid-Fire Clinical Facts

— Samter triad (AERD): asthma + nasal polyps + NSAID/aspirin sensitivity → avoid COX-1, consider aspirin desensitization, add LTRA.

— Churg-Strauss (EGPA): asthma + eosinophilia + vasculitis (mononeuritis multiplex, sinusitis, ANCA often p-ANCA/MPO+).

— ABPA: asthma + central bronchiectasis + IgE >1000 + Aspergillus sensitization + eosinophilia.

— Non-selective beta-blockers (propranolol, timolol eye drops!), aspirin/NSAIDs (in AERD), ACE inhibitors (cough, not true bronchospasm), adenosine (transient bronchospasm — avoid in asthmatics during stress testing).

— Eosinophilia + asthma → think eosinophilic phenotype, ABPA, EGPA, parasites.

— Curschmann spirals (mucus casts) and Charcot-Leyden crystals (eosinophil lysozyme) on sputum = classic asthma.

— FeNO ≥50 ppb → Th2-high, ICS-responsive.

Board pearl: When you see "asthma + nasal polyps" on the stem, the answer is almost always aspirin/NSAID avoidance, and the next-best test or treatment relates to AERD management (LTRA, aspirin desensitization).

Triads and syndromes:

Drug triggers — memorize:

Lab/finding associations:

Vaccines: annual flu, COVID, pneumococcal (PCV20 or PCV15→PPSV23) for asthmatics on ICS or with severe disease.

Pregnancy: budesonide preferred ICS; ~1/3 worsen, 1/3 improve, 1/3 unchanged.

Occupational asthma: isocyanates (auto body), flour (bakers), latex, animal dander, grain dust — symptoms improve on weekends/vacation.

Cold air, exercise: consider exercise-induced bronchoconstriction — pretreat with SABA 15 min before activity or use ICS-formoterol PRN.

GERD, OSA, obesity, allergic rhinitis = the "asthma comorbidity cluster" — treating each improves control.

Mortality predictors: prior intubation > recent hospitalization > >2 SABA canisters/month > psychiatric/SES factors.

SMART therapy: budesonide-formoterol as both controller and reliever — preferred for most adults/adolescents (GINA).

Magnesium toxicity signs: areflexia, respiratory depression, hypotension — treat with IV calcium gluconate.

Auto-PEEP in ventilated asthmatics → hypotension → disconnect from vent.

Board Question Stem Patterns

— 25-year-old, prior intubation, in ED tachypneic, accessory muscles, ABG: pH 7.38, PaCO2 41, PaO2 65 on 4 L NC.

— Trap: "normal" PaCO2 is reassuring. Answer: prepare for intubation — this is a pre-arrest gas.

— 68-year-old smoker with new dyspnea, bilateral crackles + wheeze, JVD, BNP 1200.

— Trap: wheeze ≠ asthma. Answer: IV furosemide + NIV for cardiogenic pulmonary edema.

— 22-year-old runner, episodic stridor and shortness of breath during races, no response to albuterol, normal PFTs at rest.

— Answer: laryngoscopy for vocal cord dysfunction; treatment is speech therapy.

— Took ibuprofen for headache, severe wheeze in 30 min, polyps on exam.

— Answer: AERD; avoid NSAIDs, add montelukast, consider aspirin desensitization.

— 28 weeks pregnant, severe exacerbation, "is it safe to give steroids?"

— Answer: Yes — give systemic corticosteroids, nebulizers, magnesium; uncontrolled asthma is more harmful to fetus.

— Poorly controlled despite "two inhalers."

— Answer: Observe inhaler technique with spacer before stepping up therapy.

— Resolved exacerbation, what do you prescribe?

— Answer: Oral prednisone × 5 days + ICS-containing inhaler + spacer + action plan + follow-up 1–4 weeks.

— Intubated asthmatic, hypotension, high peak pressures.

— Answer: Disconnect from vent (auto-PEEP), check tube position, exclude pneumothorax (DOPES).

— Frequent exacerbations on Step 4, eos 600.

— Answer: Refer for anti–IL-5 biologic (mepolizumab/benralizumab).

Key distinction: Many "asthma exacerbation" stems are actually testing your ability to recognize mimics (PE, CHF, anaphylaxis, VCD, pneumothorax) — always pause and reconsider before doubling down on bronchodilators.

Step 3 management: The correct discharge answer almost always includes the ICS — it is the most tested error.

Stem 1 — "The young woman with ICU asthma":

Stem 2 — "The wheezing older smoker":

Stem 3 — "The athlete with throat tightness":

Stem 4 — "The asthmatic with nasal polyps and an NSAID":

Stem 5 — "The pregnant asthmatic":

Stem 6 — "The kid with the spacer-free MDI":

Stem 7 — "Discharge from the ED":

Stem 8 — "Sudden deterioration on the vent":

Stem 9 — "Refractory eosinophilic asthma":

One-Line Recap

Asthma exacerbation is a clinical diagnosis treated immediately with oxygen to SpO2 93–95%, repeated nebulized albuterol-ipratropium, systemic corticosteroids within the first hour, IV magnesium for severe disease, and early escalation to NIV/intubation when hypercapnia, exhaustion, or altered mentation appear — with every discharge requiring an oral steroid course, an ICS-containing controller, a spacer, a written action plan, and follow-up within 1–4 weeks.

— First 60 minutes: O2, neb SABA+SAMA q20 min × 3, systemic steroids within 1 hour, IV magnesium 2 g if severe — then reassess at 60 min with PEF and exam.

— Pre-arrest clues: silent chest, drowsiness, normal/rising PaCO2 in a tachypneic patient, paradoxical breathing — these mandate immediate ICU and intubation prep, not another round of nebs.

— Intubation strategy: ketamine induction, large-bore ETT, permissive hypercapnia (low Vt 6 mL/kg, low RR 8–12, long expiratory time, plateau <30); for sudden deterioration on vent, work the DOPES mnemonic — Displacement, Obstruction, Pneumothorax, Equipment, Stacking (auto-PEEP, disconnect from circuit).

— Discharge bundle (every patient): prednisone 40–60 mg × 5–7 days (or dexamethasone), ICS or ICS-formoterol with spacer, written asthma action plan, inhaler-technique teach-back, PCP follow-up in 1–4 weeks, pulmonology referral for ICU stay/recurrent exacerbations/biologic candidacy.

— Always reconsider the differential when response is poor: PE, CHF ("cardiac asthma"), anaphylaxis, vocal cord dysfunction, pneumothorax, foreign body, COPD/ACO, AERD, ABPA, EGPA.

Board pearl: If you remember only one thing — a "normal" PaCO2 in a severely tachypneic, distressed asthmatic is a sign of impending respiratory failure, not improvement. Prepare to intubate.

Step 3 management: No asthma patient should leave the ED or hospital on a SABA alone — an ICS-containing controller is mandatory, and its absence is the single most testable patient-safety error in this topic.

High-yield recap bullets: