GRAND ROUNDS 01 · DISEASE EDUCATION

Asthma

Reversible airflow obstruction — spasm, swelling, secretions

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Asthma = chronic airway inflammation with hyper-reactive smooth muscle → reversible, episodic airflow obstruction. Three lesions choke the lumen at once: bronchospasm · mucosal edema · mucus plugging. The obstruction is expiratory — air traps, the lung hyperinflates.

1Pathophysiologytrigger → cascade

1Trigger — allergen, virus, cold air, exercise, smoke → mast-cell & eosinophil activation.

2Inflammation — histamine, leukotrienes → mucosal edema + goblet-cell mucus.

3Bronchospasm — smooth-muscle constriction narrows the airway further.

4Air trapping — expiratory obstruction → hyperinflation, auto-PEEP, ↑ work of breathing.

5Fatigue — muscles tire → hypoventilation → rising CO₂ → respiratory failure.

2Presentation

Classic: wheeze (expiratory), cough, chest tightness, dyspnea — episodic, worse at night / with triggers, reversible.

Look for the work: accessory muscles, tripoding, prolonged expiration, ↑ RR & HR, pulsus paradoxus, speaking in short phrases.

Ominous: silent chest (no air moving), exhaustion, drowsiness, cyanosis, bradycardia, hypotension — peri-arrest.

SSeveritygrade the attack

GRADE	SPEAKS	SpO₂ · PEF	SIGN
Mild	sentences	>95% · >70%	end-exp wheeze
Moderate	phrases	92–95% · 50–70%	loud wheeze, ↑WOB
Severe	words	<92% · 33–50%	accessory, HR>120
Life-threat	can't	<92% · <33%	silent chest, ↓GCS, brady

A normal or rising PaCO₂ in a tiring asthmatic is a near-fatal sign — not reassurance.

TTriggersfind & remove

Viral URIAllergensExercise Cold airSmoke · pollutionAspirin / NSAIDs β-blockersStressGERD

6Differentialnot all that wheezes

COPD exacerbation
CHF / cardiac "asthma"
Anaphylaxis
Foreign body
Pneumonia / bronchiolitis
Pulmonary embolism
Vocal-cord dysfunction
Tension pneumothorax

PSpecial Populations

PEDSViral-triggered, weight-based dosing, deceptively well — then crash fast. Fewer wheezes ≠ better.

AERDAspirin-exacerbated: asthma + nasal polyps + NSAID reaction. Avoid NSAIDs.

PREGTreat aggressively — maternal hypoxia harms the fetus. Most inhalers & steroids are safe.

▲The Airwaynormal vs the asthma attack
bronchiole cross-section

WHAT CHOKES THE LUMEN smooth muscle · edema · mucus

Spasm

Smooth-muscle constriction. β₂-agonists reverse it.

Edema

Inflammatory swelling. Steroids reverse it (slow).

Mucus

Goblet-cell plugs. Hydration, time; not suction-able.

4Diagnosticsit's clinical — confirm & trend

Bedside: auscultation (wheeze → silent = worse), SpO₂, PEF % predicted (trend response), work of breathing.

Capnography: a shark-fin upslope = obstruction; watch the number & shape for response.

ABG trend (the key story): early respiratory alkalosis (low CO₂, tachypnea) → a "normalizing" CO₂ → rising CO₂ = the patient is tiring. CXR only to exclude pneumothorax / pneumonia.

CAPNOGRAPHY — THE SHARK FIN EtCO₂ vs time

▲Air Trappingwhy the chest hyperinflates

EXPIRATORY OBSTRUCTION → HYPERINFLATION the macro picture

5Treatmentfirst-line → refractory · per protocol

Oxygen — titrate to SpO₂ 93–95% (don't over-oxygenate). Sit up, calm, coach.

SABA albuterol — continuous neb (± MDI+spacer). Reverses spasm.

SAMA ipratropium added ×3 in severe — additive bronchodilation.

Steroids early — prednisone PO or methylprednisolone IV. Treats edema (hours).

Magnesium 2 g IV over 20 min (severe) — smooth-muscle relaxant.

Epinephrine IM 0.3–0.5 mg 1:1000 — near-fatal / not moving air.

Adjuncts: IV/neb magnesium, epinephrine gtt, ketamine, heliox, NIV trial.

CChronic ControlGINA step-up · outpatient

STEP	CONTROLLER
1–2	Low-dose ICS (or ICS-formoterol as needed)
3	Low-dose ICS-LABA
4	Medium/high ICS-LABA ± LAMA
5	Add-on LAMA / biologic · specialist referral

Reliever every visit; step up if uncontrolled, down when stable. Check inhaler technique & adherence first.

7Critical Proceduresthe airway is a trap

⚠ Intubation is dangerous here

NIV first in the cooperative patient — offloads work, buys time for drugs.
Intubate for exhaustion, silent chest, ↓GCS — not a number alone.
Ketamine is the induction agent — it bronchodilates; large ETT.
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

Rising CO₂ = fatigue, not calm. The "normalizing" gas is the trap.
Silent chest is an emergency — no wheeze because no air moves.
Steroids early — they fix the edema hours later; don't delay.
Wheeze isn't specific — CHF, anaphylaxis, foreign body all wheeze.
Don't over-bag / over-ventilate post-tube — auto-PEEP arrest.
Pulsus paradoxus >10 mmHg tracks severity.

REMEMBER — Spasm · Edema · Mucus. β-agonist + steroid + magnesium. Rising CO₂ = tiring. If tubed & crashing → DISCONNECT, let them exhale.

DDisposition

ADMIT / ICU

Incomplete response · PEF <50–70% after Rx
Persistent hypoxia / rising CO₂
Prior near-fatal / intubation
Exhaustion, silent chest

DISCHARGE

Good response, PEF >70%
Steroid course + inhaler
Action plan + follow-up
Technique taught

Sheet

Asthma

Series / No.

GRAND ROUNDS 01

Part No.

CC-GR-01

Rev

Status

EDUCATION REFERENCE — NOT A PROTOCOL. VERIFY LOCALLY.

SOURCES: GINA Global Strategy for Asthma (2024) · BTS/SIGN Asthma Guideline · NAEPP EPR-3 · Marino, The ICU Book (obstructive ventilation, auto-PEEP); 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.