Last reviewed: March 2026
Contents
MDM Templates
Asthma Exacerbation
Patient with acute asthma exacerbation given ***, wheezing, and respiratory distress. Known history of asthma with *** prior exacerbations. Never intubated / previously intubated for asthma. No history of ICU admission for asthma. Home medications include ***. Presentation less concerning for pneumonia, heart failure, pulmonary embolism, foreign body airway obstruction, or anaphylaxis. Vital signs demonstrate ***, oxygen saturation *** on room air.
Mild — responding to initial treatment:
No signs of impending ventilatory failure including altered mental status, silent chest, or paradoxical breathing. Patient improved after albuterol, ipratropium, and systemic steroids. Speaking in full sentences with good air movement on reassessment.
Plan: Discharge with 5-day prednisone course and albuterol MDI. Counsel on SMART inhaler use if not already prescribed.
Disposition: Discharge with return precautions for worsening dyspnea, inability to speak in full sentences, or chest pain. Follow up with PCP within 48 hours for reassessment and step-up therapy discussion.
Moderate — incomplete response, observation:
Minimal improvement after repeated bronchodilator treatments and systemic steroids over *** hours. Still with accessory muscle use and wheezing but no signs of impending ventilatory failure. No AMS, no silent chest.
Plan: IV methylprednisolone 125 mg, continued nebulized bronchodilators q1-2h, IV magnesium sulfate 2 g over 20 minutes.
Disposition: Observation admission for continued treatment and airway monitoring. If no improvement over 6-8 hours, escalate to inpatient admission.
Severe — admit:
Worsening despite aggressive bronchodilator therapy, IV steroids, and IV magnesium. Persistent accessory muscle use, SpO2 *** on supplemental O2, difficulty speaking in full sentences. Labs: ***. CXR: ***.
Plan: Continuous nebulized albuterol, IV methylprednisolone 125 mg q6h, consider epinephrine 0.3 mg IM, initiate BiPAP if tolerating.
Disposition: Admit to medicine/stepdown for continued intensive therapy and monitoring.
Critical — ICU:
Status asthmaticus with signs of impending ventilatory failure: SpO2 ≤90% despite high-flow O2, altered mental status, silent chest, or paradoxical breathing. Labs: ***. Blood gas: ***. CXR: ***.
Plan: Continuous nebulized albuterol, IV methylprednisolone 2 mg/kg, epinephrine 0.3 mg IM, BiPAP trial vs intubation (see vent management below). Consider ketamine 0.5 mg/kg IV bolus for bronchodilation if peri-intubation.
Disposition: MICU admission for impending or actual respiratory failure.
Clinical Education
ED Treatment Ladder
| Severity | Agents | Dosing |
| All patients | Albuterol | 2.5 mg neb or 4-8 puffs MDI q20min × 3, then q1-4h |
| Ipratropium | 0.5 mg neb with first 3 albuterol treatments | |
| Systemic steroids | Prednisone 40-60 mg PO or methylprednisolone 125 mg IV | |
| Moderate-severe | Magnesium sulfate | 2 g IV over 20 min (single dose) |
| Continuous albuterol | 10-15 mg/hr nebulized | |
| Refractory / critical | Epinephrine | 0.3 mg IM (1 mg/mL solution), may repeat q20min |
| BiPAP | IPAP 10-15, EPAP 5, titrate to work of breathing | |
| Ketamine (dissociative dose) | 0.5-1 mg/kg IV if peri-intubation (limited evidence)[6] |
Ipratropium is first 3 treatments only — there is no benefit to continued dosing beyond the initial hour in adults.[1] Onset of systemic steroids is 1-2 hours regardless of PO vs IV route, so give early.[2]
SMART Therapy
Budesonide-formoterol (Symbicort) as both maintenance and rescue is now preferred over SABA-only rescue. GINA 2024 recommends against SABA-only treatment at any step — all patients with asthma should have an ICS-containing controller.[3] Formoterol is a long-acting beta-agonist with rapid onset (1-3 minutes), making it effective as a rescue inhaler while simultaneously delivering an anti-inflammatory dose of budesonide.
SMART = Single Maintenance And Reliever Therapy. Budesonide-formoterol 80/4.5 mcg, 1-2 puffs as needed for rescue and 1-2 puffs twice daily for maintenance. This approach reduces exacerbations by 60% compared to SABA-only rescue per the MANDALA and SYGMA trials.[4] On discharge from the ED, counsel patients on SMART if they are currently using albuterol only — this is a high-yield intervention point.
Steroid Pearls
PO and IV steroids reach equal efficacy at the same time — onset is 1-2 hours regardless of route.[2] Reserve IV for patients who are vomiting or too dyspneic to swallow. Prednisone 40-60 mg PO is appropriate for most ED patients.
A 5-day course of prednisone 40 mg daily is sufficient — there is no benefit to longer courses or tapers for typical exacerbations.[5] Dexamethasone 12 mg PO × 2 days is an alternative with better compliance, though evidence is strongest for prednisone. A short steroid burst after discharge reduces readmission by approximately 3-fold.[2]
Magnesium & Adjuncts
IV magnesium sulfate 2 g over 20 minutes for moderate-severe exacerbations. Most beneficial in patients with FEV1 <25% predicted at presentation. Reduces admission rates in severe asthma (NNT ~4) but has minimal effect in mild-moderate disease.[7] Single dose only — no benefit to repeated dosing.
Epinephrine 0.3 mg IM is an underused option for refractory bronchospasm or patients with very poor air movement who are not responding to nebulized therapy. It is not just for anaphylaxis — beta-2 agonism provides bronchodilation independent of the inhaled route. Also consider terbutaline 0.25 mg SC as an alternative.
Ketamine evidence is weak. Small case series and one RCT showed no benefit for subdissociative ketamine (0.1-0.3 mg/kg) as an adjunct bronchodilator.[6] However, it remains a reasonable induction agent at dissociative doses (1-2 mg/kg) when intubation is necessary — it preserves respiratory drive and has bronchodilatory properties.
BiPAP in Asthma
Early BiPAP can prevent intubation in severe asthma. NIPPV reduces work of breathing, improves gas exchange, and buys time for pharmacotherapy to work. One RCT demonstrated significant improvement in FEV1 and reduced hospitalization rates with early BiPAP use in acute severe asthma.[8]
| Setting | Value | Notes |
| IPAP | 10-15 cmH₂O | Start low, titrate to comfort and work of breathing |
| EPAP | 5 cmH₂O | Counteracts auto-PEEP; avoid going too high |
| FiO₂ | Titrate to SpO₂ ≥92% | Most asthmatics don’t need high FiO₂ unless severe |
Do not delay intubation for a BiPAP trial if the patient has AMS, is unable to protect their airway, or is in frank respiratory failure. BiPAP is for the patient who is tiring but still alert and cooperative. Run nebulized albuterol through the BiPAP circuit simultaneously.
Ventilator Management
The intubated asthmatic is at high risk for barotrauma and hemodynamic collapse. Air trapping (auto-PEEP/breath stacking) is the primary danger — it increases intrathoracic pressure, decreases venous return, and can cause PEA arrest. The strategy is to allow exhalation time and tolerate hypercapnia.[9]
| Parameter | Target | Rationale |
| Mode | Volume control (AC/VC) | Guarantees tidal volume delivery; monitor peak and plateau pressures |
| Tidal volume | 6-8 mL/kg IBW | Lower volumes reduce air trapping |
| Respiratory rate | 10-12 breaths/min | Low rate maximizes expiratory time |
| I:E ratio | ≥1:3 to 1:4 | Long expiratory phase prevents stacking |
| PEEP | 0-5 cmH₂O | Extrinsic PEEP adds to auto-PEEP; keep low or zero |
| Plateau pressure | <30 cmH₂O | High plateau = air trapping; disconnect and allow full exhalation if rising |
| pCO₂ | Permissive hypercapnia | Tolerate pCO₂ 60-80 if pH >7.15; do NOT chase the CO₂ |
If the patient arrests post-intubation, disconnect from the vent and manually compress the chest to empty trapped air. Auto-PEEP causing PEA is the most common cause of peri-intubation arrest in asthmatics — this is not a time for epi and chest compressions alone. Also ensure adequate sedation and paralysis — patient-ventilator dyssynchrony worsens air trapping.[9]
References
- Rodrigo GJ, Castro-Rodriguez JA. Anticholinergics in the treatment of children and adults with acute asthma: a systematic review with meta-analysis. Thorax. 2005;60(9):740-746. PubMed
- Rowe BH, Spooner C, Ducharme FM, et al. Early emergency department treatment of acute asthma with systemic corticosteroids. Cochrane Database Syst Rev. 2001;(1):CD002178. PubMed
- Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. 2024 Report. GINA
- Beasley R, Holliday M, Reddel HK, et al. Controlled trial of budesonide-formoterol as needed for mild asthma (Novel START). N Engl J Med. 2019;380(21):2020-2030. PubMed
- National Heart, Lung, and Blood Institute. 2020 Focused Updates to the Asthma Management Guidelines: Expert Panel Report 4. J Allergy Clin Immunol. 2020;146(6):1217-1270. PubMed
- Jat KR, Chawla D. Ketamine for management of acute exacerbations of asthma in children. Cochrane Database Syst Rev. 2012;(11):CD009293. PubMed
- Kew KM, Kirtchuk L, Michell CI. Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department. Cochrane Database Syst Rev. 2014;(5):CD010909. PubMed
- Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest. 2003;123(4):1018-1025. PubMed
- Leatherman JW, McArthur C, Shapiro RS. Effect of prolongation of expiratory time on dynamic hyperinflation in mechanically ventilated patients with severe asthma. Crit Care Med. 2004;32(7):1542-1545. PubMed
tydotphrase.com 