When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

Asthma -GINA Stepwise Therapy -RoundsRx

🚨 Acute Exacerbation

Severity Grading

Severity	Features	PEF	SpO₂ on RA	Disposition
Mild–Moderate	Speaks in sentences, RR < 30, HR < 120, alert	> 50% predicted	> 92%	ED treat & reassess; discharge if responsive
Severe	Speaks in phrases or words, accessory muscle use, RR > 30, HR > 120, agitated	< 50% predicted	< 92%	Admit; consider ICU if no response in 1h
Life-threatening / near-fatal	Silent chest, drowsy/confused, bradycardia, cyanosis, paradoxical chest/abdomen, exhaustion	< 33% predicted (or unable)	< 90%	ICU. Prepare for intubation.
"Quiet chest" is the most dangerous sign, no air movement = no wheeze. Rising PaCO₂ on a tiring asthmatic is impending arrest, not a relief.

Don't Confuse the Protocol with AECOPD

⚠️ Same drugs, different protocol. Treating an AECOPD patient like an asthmatic (q20 min × 3 albuterol + 100% O₂) induces hypercapnia and hypoxic-drive crash. The first three decisions diverge:

Decision	Acute asthma	AECOPD
Albuterol frequency	q20 min × 3 in first hour, front-loaded	q1–4 h scheduled, no q20 min loading
Continuous nebs (albuterol)	Yes for severe (albuterol 10–15 mg/hr via large-volume nebulizer)	Rarely; intermittent dosing works and chronic patients don't tolerate continuous
Ipratropium duration	First 3 nebs only (ceiling effect, Rodrigo 2005)	Continued throughout admission (often DuoNeb q4–6 h)
O₂ target	93–95%	88–92% (controlled O₂, avoid hypercapnic respiratory failure) AVOID, 2010
Steroids	Prednisone 40–60 mg × 5 d	Prednisone 40 mg × 5 d REDUCE, 2013
Antibiotics	Usually NO	YES if Anthonisen ≥ 2 of 3 (↑ dyspnea, sputum volume, sputum purulence)
NIV	Bridge only, low threshold to intubate	First-line for hypercapnic exacerbation (strong evidence; 65% relative reduction in intubation, 46% reduction in mortality per Cochrane meta-analysis, Osadnik 2017)
IV magnesium	2 g IV over 20 min for severe (per 3Mg, 2013)	Not standard, weak evidence
Decompensation tempo	Hours	Days

What's the same: dose per neb (albuterol 2.5–5 mg, ipratropium 0.5 mg), DuoNeb formulation, steroid burst with no taper if ≤ 5 days, sit upright. Full AECOPD protocol →

Acute Treatment Protocol

First 5 min

Assess & stabilize. ABCs, SpO₂, ECG, IV access, peak flow if able. Apply O₂ to keep SpO₂ 93–95% (avoid hyperoxia, target is 93–95% per BTS). Sit upright. Continuous monitoring.

First hour (SABA × the whole hour)

Albuterol 2.5–5 mg nebulized q20 min throughout the first hour (3 back-to-back doses minimum; can keep stacking q20 min while assessing response).

For severe / poor response, switch to continuous nebulization 10–15 mg/hr via large-volume nebulizer, can run uninterrupted for an hour or more.

Ipratropium 0.5 mg added to first 3 nebs only, no added benefit beyond that Rodrigo, 2005.

Systemic corticosteroids early (4–6h to take effect): prednisone 40–60 mg PO or methylprednisolone 60–125 mg IV. PO and IV equivalent if patient tolerating PO Rowe, 2001.

Reassess at 60 min: PEF, accessory muscle use, ability to speak. SABA continues throughout, the q20 min schedule is the floor, not the ceiling.

1 hour: severe / no response

Magnesium sulfate 2 g IV over 20 min (smooth muscle relaxation, reduced admissions in severe exacerbations) 3Mg, 2013.
Watch out for: some EMR order sets default to a 30–60 min infusion, change the rate to 20 min (the 3Mg trial protocol).

Epinephrine 0.3–0.5 mg IM (1:1000) if anaphylactic component, peri-arrest, or unable to deliver inhaled bronchodilator effectively (silent chest).

Trial of NIV (BiPAP): start IPAP 10–12 / EPAP 4–5, titrate IPAP up by 2 q5–10 min (typical target 15–20) to RR < 25 and accessory muscle relief. Reassess at 1–2 h. Worsening pH, rising PaCO₂, drowsiness, or no clinical improvement = intubate, do NOT persist.

Refractory / ICU

IV terbutaline (selective β₂): 0.25 mg SQ q20 min × 3, OR IV load 10 mcg/kg over 10 min → 0.4–6 mcg/kg/min infusion. Watch for tachyarrhythmia, hyperglycemia, lactic acidosis (β₂-driven, do NOT mistake for sepsis).

Ketamine for refractory bronchospasm: 0.5–1 mg/kg IV bolus, then 0.5–2 mg/kg/hr infusion. Direct bronchodilator + dissociative sedation. Bridge to intubation or buy time on NIV. Goyal, 2013 (review)

Heliox 70:30 or 80:20 helium:O₂. Lower density gas = lower turbulent flow = less work of breathing. Useful as a bridge; FiO₂ ceiling is the trade-off (cannot use if SpO₂ requirement > 30%).

Avoid: sedatives without airway control (worsens hypercapnia), aminophylline (no benefit, more toxicity), high-dose beta-blockers, NSAIDs in aspirin-sensitive asthma.

Drug Side Effects to Anticipate

Drug	Common (most patients)	Watch for / cautions
Albuterol (SABA)	Tachycardia, fine tremor, anxiety	Hypokalemia (β₂ shifts K⁺ into cells, repeat BMP after continuous nebs), lactic acidosis (β₂-driven type B, do NOT mistake for sepsis), hyperglycemia, QT prolongation at high cumulative doses, paradoxical bronchospasm (rare).
Ipratropium	Dry mouth, metallic taste	Mydriasis / acute angle-closure glaucoma if mask leaks into eye (use mouthpiece or seal mask). Urinary retention in elderly men with BPH. Avoid in true peanut/soy allergy (older formulations).
Prednisone / Methylprednisolone	Hyperglycemia, insomnia, mood lability, increased appetite	Anticipate insulin needs in diabetics (BG often jumps 100–200 within 24 h). Steroid psychosis at high doses or in elderly. HTN, fluid retention. GI upset (consider PPI if high-risk). No taper needed for ≤ 5 days.
Magnesium sulfate IV	Flushing, warmth, mild nausea	Hypotension with rapid infusion (the main reason for 20–60 min run-time). Diminished deep tendon reflexes at level > 4 mEq/L; respiratory depression / arrhythmia at > 8–10. Reduce dose in renal failure (accumulates, monitor reflexes).
Epinephrine IM	Palpitations, tachycardia, tremor, anxiety, HTN, headache	Arrhythmia and ischemia risk in elderly / CAD, but life-threatening asthma overrides relative contraindications. IM (not IV) for asthma; IV epi is for arrest only. Avoid mixing with beta-blocker on board if alternatives exist (unopposed alpha can spike BP).
IV / SQ Terbutaline	Tachycardia, tremor, palpitations	Tachyarrhythmias (continuous tele required), hypokalemia, lactic acidosis (β₂-driven), hyperglycemia, myocardial ischemia in CAD. Check ECG and electrolytes q2–4h on infusion.
Ketamine	Hypertension, tachycardia (often beneficial here), increased secretions, nystagmus	Laryngospasm (rare but dangerous in asthma, paradoxical airway compromise). Co-administer glycopyrrolate 0.2 mg IV to dry secretions. Emergence reactions on awakening (treat with low-dose midazolam). Theoretical ICP concern in TBI but not a contraindication in modern practice.
Heliox	None directly (inert gas)	FiO₂ ceiling: ratio is fixed (70:30 or 80:20), so cannot use if patient needs more O₂ than that delivers. Voice changes (Donald Duck effect) is harmless but disconcerting. Bridge only, does not treat the underlying obstruction.

Two electrolyte traps with high-dose β₂ therapy (continuous albuterol, IV terbutaline, or both):

(1) Hypokalemia. β₂ activation drives Na/K-ATPase, shifting K⁺ into cells. Can drop serum K⁺ by 0.5–1 mEq/L within hours. Repeat BMP and replace.

(2) Type B lactic acidosis (β₂-driven). Mechanism: β₂ stimulation → ↑ adenylyl cyclase → ↑ intracellular cAMP → activates glycogenolysis (liver, muscle) and glycolysis → pyruvate generated faster than mitochondria can oxidize it → excess pyruvate is shunted to lactate via LDH. Also ↑ lipolysis adds to the metabolic load. This is aerobic glycolysis, NOT tissue hypoxia, so the lactate is not a marker of hypoperfusion. Increased work of breathing in severe asthma adds a smaller contribution from respiratory muscle lactate. Lewis 1986; Manthous 2001

Lactate often climbs to 4–8 mmol/L on continuous β₂ therapy. Do NOT chase it with fluids, broad-spectrum antibiotics, or pressors. It resolves over hours as the β₂ drip comes down. The diagnostic clue: lactate rises while the patient is otherwise improving (better PEF, dropping HR, normalizing BP).

Intubation in Status Asthmaticus

⚠️ Indications

Cardiac or respiratory arrest
Decreased level of consciousness, exhaustion, inability to maintain effort
Rising PaCO₂ despite maximal therapy and NIV trial (not the absolute number, but the trend)
Refractory hypoxia (SpO₂ < 90% on max O₂ + NIV)
Hemodynamic instability not responding to fluids

Step	Choice	Why
Pre-oxygenate	NRB + nasal cannula 15 L apneic O₂	Asthmatics desat fast, FRC is shrunken with air trapping. HFNC if available.
Resuscitate before intubate	500–1000 mL NS bolus, push-dose epi/phenylephrine ready	Positive-pressure ventilation drops preload severely in air-trapped patients. Pre-empt hypotension.
Induction	Ketamine 1.5–2 mg/kg IV	Drug of choice. Bronchodilator, preserves BP, dissociative. Avoid propofol (drops BP) and etomidate (no bronchodilation).
Paralytic	Rocuronium 1.2 mg/kg IV	Avoid succinylcholine if hyperK risk (severe acidosis can shift K⁺ up). Rocuronium reversible with sugammadex.
Tube size	Largest that fits (8.0–9.0 in adults)	Reduces airway resistance and allows bronchoscopy / pulmonary toilet.

Post-Intubation Vent Strategy: Permissive Hypercapnia

The killer is dynamic hyperinflation (breath stacking → auto-PEEP). Each breath adds to trapped volume because expiration is incomplete. Auto-PEEP raises intrathoracic pressure, drops venous return, and causes PEA arrest within minutes of intubation. Goal: let air out before pushing more air in.

Setting	Target	Why
Mode	Volume control (AC/VC)	Predictable Vt, lets you measure plateau and auto-PEEP precisely.
Tidal volume	6–8 mL/kg IBW	Smaller Vt = less hyperinflation. Don't try to "blow off" CO₂ with bigger breaths.
Respiratory rate	6–10 breaths/min	Long expiratory time. Slow rate is the single most important setting.
I:E ratio	1:4 to 1:5	Inspiratory time 0.8–1.0 s, leave the rest for exhalation.
Inspiratory flow	80–100 L/min (high)	Deliver Vt fast so most of cycle is exhalation.
PEEP	0–5 cm H₂O (low or zero)	Adding extrinsic PEEP can worsen hyperinflation. Some titrate to ~80% of measured auto-PEEP if patient is triggering.
Plateau pressure	< 30 cm H₂O	Reflects alveolar pressure; high plateau = barotrauma + hypotension risk. Peak pressure can be high (resistance) and that's OK if plateau is fine.
pH / PaCO₂	Accept pH ≥ 7.15–7.20, any PaCO₂	Permissive hypercapnia. Don't chase normocarbia, that's how you kill the patient.
Sedation	Deep + paralytic if needed	Ventilator dyssynchrony in asthma is fatal. Continue inhaled bronchodilators in-line with circuit.

Sudden post-intubation hypotension → think auto-PEEP first. Disconnect from vent for 30–60 seconds and let the lungs deflate, BP usually recovers within seconds. If not: tension pneumothorax (needle decompression), or acidosis-driven cardiovascular collapse (bicarb, fluids, epi).

Disposition

Discharge if: PEF > 70% predicted, symptom improvement, can speak in full sentences, SpO₂ > 94% on RA. Send with: prednisone 40 mg × 5 days (no taper needed for ≤ 5 days), albuterol PRN, step up controller if needed.
Admit if: PEF < 50% after treatment, persistent hypoxia, unable to speak in sentences, prior near-fatal asthma, high-risk features.

💊 Chronic Stepwise Therapy (GINA 2023)

Stepwise Approach

Key 2023 GINA change: SABA-only rescue is no longer recommended as monotherapy for ANY severity. All patients should have an ICS-containing regimen -either as-needed ICS-formoterol (Track 1) or regular low-dose ICS + SABA rescue (Track 2).

⚠️ SMART/MART is outpatient only. It relies on patient self-titration (extra puffs of the same ICS-formoterol inhaler when symptomatic). For an admitted or ED patient with an acute exacerbation, use nebulized SABA + ipratropium + systemic steroids ± IV magnesium (see Acute Management tab). Start or resume SMART at discharge, not during the acute episode.

✅ Before stepping up therapy, check the 4 T's: Technique (watch them use the inhaler, > 50% use it wrong), Adherence (refill history, are they actually taking it), Triggers (occupational, allergens, smoking, ASA/NSAIDs), Comorbidities (GERD, chronic rhinosinusitis, vocal cord dysfunction, OSA, obesity). Most "uncontrolled" asthma is one of these, not true treatment failure.

Step	Track 1 (Preferred)	Track 2 (Alternative)	Notes
Step 1 (Mild intermittent)	As-needed low-dose ICS-formoterol (e.g., budesonide-formoterol PRN)	Low-dose ICS whenever SABA used	No more SABA-only. SYGMA, 2018: PRN budesonide-formoterol was superior to SABA alone for severe exacerbation prevention.
Step 2 (Mild persistent)	As-needed low-dose ICS-formoterol	Daily low-dose ICS + SABA PRN	ICS reduces exacerbations, hospitalizations, and death from asthma. This is the foundation. START, 2003
Step 3 (Moderate)	Low-dose ICS-formoterol maintenance + reliever (MART / SMART therapy)	Low-dose ICS-LABA + SABA PRN	MART (GINA term) = SMART therapy (NHLBI / US term) = Single (or Same) Maintenance And Reliever Therapy. One inhaler used for both daily controller and as-needed rescue. Reduces severe exacerbations vs traditional ICS-LABA + SABA PRN. FACET, 1997
Step 4 (Moderate-severe)	Medium-dose ICS-formoterol maintenance + reliever	Medium/high-dose ICS-LABA + SABA PRN	Consider adding LAMA (tiotropium) if uncontrolled. Single-inhaler triple therapy (ICS/LABA/LAMA) reduces exacerbations vs ICS/LABA. CAPTAIN, 2020 · TRIMARAN/TRIGGER, 2019 · SHINE, 2014
Step 5 (Severe)	Refer to specialist. High-dose ICS-LABA + LAMA. Phenotype: eosinophilic → add biologic (anti-IgE, anti-IL5, anti-IL4R). Low-dose OCS as last resort.		Biologics: omalizumab (Xolair) anti-IgE; mepolizumab (Nucala) / benralizumab (Fasenra) anti-IL-5; dupilumab (Dupixent) anti-IL-4Rα; tezepelumab (Tezspire) anti-TSLP. See Medications tab for trial citations and indication criteria.

Asthma vs COPD -Key Differences

Feature	Asthma	COPD
Exacerbation tempo	Fast. Can go from "talking in sentences" to silent chest / peri-arrest in hours. Less reserve, acute bronchospasm on top of baseline normal lungs.	Slow. Usually builds over days. Patients tolerate higher PaCO₂ at baseline (chronic CO₂ retention).
Time to intubation	Sooner. Asthmatics tire and crash quickly once accessory muscles fail. NIV trial is shorter (1–2 h max), low threshold to intubate if not improving.	Later. NIV (BiPAP) avoids intubation in > 80% of COPD exacerbations strong NIV evidence base. Can support on NIV for many hours to days.
NIV response	Less validated. Used as a bridge, not a definitive therapy. If pH or PaCO₂ trending the wrong way at 1–2 h, intubate.	First-line for acute hypercapnic exacerbation (pH < 7.35, PaCO₂ > 45). Reduces intubation, mortality, and length of stay.
Age of onset	Usually childhood / young adult	Usually > 40, smoker
Reversibility	Reversible (FEV₁ improves ≥ 12% + 200 mL post-bronchodilator)	Irreversible (FEV₁/FVC stays < 0.70)
Inflammation	Eosinophilic (Th2, IgE-mediated)	Neutrophilic (CD8+, macrophages)
ICS role	Cornerstone of therapy	Add-on only if eos ≥ 300

🧪 Workup

Workup

Spirometry -FEV₁/FVC <0.70 + reversibility
Peak flow variability >20%
Methacholine challenge -if normal PFTs + suspected asthma
FeNO >25ppb → eosinophilic inflammation
CBC eosinophils -biologic selection
IgE -omalizumab candidacy
Allergy testing
CXR to exclude other diagnoses

💊 Medications

Medications

Drug	Dose	Route	Notes
Fluticasone/salmeterol	100–500/50 BID	DPI	ICS/LABA, Steps 3–4
Budesonide/formoterol	80–160/4.5	DPI	SMART/MART (controller + reliever)
Tiotropium Respimat	2.5 mcg 2 puffs daily	Inhaler	LAMA add-on, Steps 4–5
Prednisone	40–60 mg × 5 d	PO	Exacerbation, no taper needed

Biologic Selection (Step 5 / Severe Asthma)

Pick by phenotype. Eos high or atopic → IL-5 / IL-4R / IgE class. Phenotype unclear or eos low → tezepelumab. All are SQ injections at outpatient pulm or allergy clinic.

Biologic	Target	Use when	Dose	Key trials
Omalizumab (Xolair)	Anti-IgE	Moderate-severe allergic asthma, age ≥ 6, IgE 30–700 IU/mL + perennial aeroallergen sensitivity (skin test or specific IgE +)	75–375 mg SQ q2–4wk (weight + IgE based)	INNOVATE 2005 EXTRA 2011
Mepolizumab (Nucala)	Anti-IL-5	Severe eosinophilic asthma, age ≥ 6, eos ≥ 150 at start OR ≥ 300 in past 12 mo, ≥ 2 exacerbations/yr on high-dose ICS-LABA	100 mg SQ q4wk (adult); 40 mg (peds 6–11)	DREAM 2012 MENSA 2014 SIRIUS 2014
Benralizumab (Fasenra)	Anti-IL-5Rα (ADCC, depletes eos)	Severe eosinophilic asthma, age ≥ 12, eos ≥ 300 (some sources ≥ 150), uncontrolled on high-dose ICS-LABA	30 mg SQ q4wk × 3 doses, then q8wk	SIROCCO 2016 CALIMA 2016 ZONDA 2017
Dupilumab (Dupixent)	Anti-IL-4Rα (blocks IL-4 + IL-13)	Moderate-severe asthma, age ≥ 6, eos ≥ 150 OR FeNO ≥ 25, especially with atopic dermatitis / CRSwNP / EoE. Also OCS-dependent asthma regardless of phenotype	200–300 mg SQ q2wk (after 400–600 mg load)	QUEST 2018 VENTURE 2018
Tezepelumab (Tezspire)	Anti-TSLP (upstream alarmin)	Severe asthma, age ≥ 12, uncontrolled on high-dose ICS-LABA, regardless of eos or IgE. The choice when phenotype is unclear or biomarkers are low	210 mg SQ q4wk	NAVIGATOR 2021 SOURCE 2022

Quick decision tree:

Allergic + IgE 30–700 + perennial allergen + → omalizumab
Eos ≥ 300 alone → mepolizumab or benralizumab (q8wk wins on adherence)
Eos ≥ 150 + atopic comorbidity (AD, CRSwNP, EoE) → dupilumab (treats all simultaneously)
OCS-dependent regardless of biomarkers → dupilumab (VENTURE) or benralizumab (ZONDA)
Eos low / phenotype unclear / non-Type 2 → tezepelumab (only biologic with proven non-Type 2 efficacy)

📋 On Rounds

Why can't you give a LABA alone in asthma?

SMART Trial, 2006 (Salmeterol Multicenter Asthma Research Trial) was stopped early because salmeterol monotherapy increased asthma-related deaths. The mechanism: LABAs provide bronchodilation but do NOT address the underlying eosinophilic inflammation. Patients feel better (less bronchospasm) but the inflammation silently worsens → sudden severe exacerbation → death. LABAs must ALWAYS be paired with ICS in asthma.

What is the biggest danger of intubating an asthmatic?

Dynamic hyperinflation (breath stacking → auto-PEEP → hemodynamic collapse). Severe bronchospasm means air goes in but can't get out fast enough before the next breath. Each breath adds to the trapped volume (auto-PEEP) → intrathoracic pressure rises → venous return drops → cardiac output crashes → PEA arrest. Prevention: low respiratory rate (8–12), prolonged expiratory time (I:E 1:4 to 1:5), permissive hypercapnia (accept high CO₂).

Why did GINA remove SABA-only as first-line rescue?

SYGMA 1 & 2, 2018 showed that PRN budesonide-formoterol (ICS-formoterol used only as rescue) reduced severe exacerbations by 64% compared to SABA-only. SABA treats bronchospasm but not the underlying inflammation -patients using only SABA have worse outcomes even if they feel fine between episodes. The paradigm shift: even the mildest asthma has ongoing airway inflammation that needs anti-inflammatory therapy.

A patient on maximum ICS/LABA still has poorly controlled asthma. What are the next steps before adding a biologic?

Before escalating to Step 5 (biologics), always reassess the basics -"treatable traits": (1) Inhaler technique: 70-80% of patients use inhalers incorrectly -observe return demonstration. Spacer for MDIs. (2) Adherence: check refill records -are they actually using the controller? (3) Triggers: allergens (pets, dust mites, mold), occupational exposures, GERD, sinusitis, NSAID/ASA sensitivity

Clinical Examples

📋 Case 1, Acute Severe Asthma Exacerbation

Patient: 22F, moderate persistent asthma on medium-dose ICS/LABA (non-adherent), presents with acute dyspnea, wheezing, and inability to speak in full sentences after URI exposure.

Key findings: HR 124, RR 32, SpO2 88% on RA. Peak flow 120 L/min (predicted 450). Accessory muscle use, paradoxical breathing. ABG: pH 7.38, pCO2 40 (ominous, should be low in acute asthma).

Management:

Continuous albuterol nebulization + ipratropium 500 mcg neb q20min x 3
Methylprednisolone 125 mg IV (or prednisone 60 mg PO if tolerating)
Magnesium sulfate 2g IV over 20 minutes (for severe exacerbation not responding to initial therapy)
If worsening: BiPAP 12/5 as bridge; prepare for intubation with ketamine (bronchodilator properties)
Post-stabilization: prednisone 40 mg x 5 days, restart ICS/LABA, check technique

Teaching point: A normal or rising pCO2 in acute asthma is an ominous sign. Patients with severe bronchospasm should be hyperventilating (low pCO2). A "normal" pCO2 of 40 means the patient is tiring and respiratory failure is imminent. Rowe et al., 2000

📋 Case 2, Step-Up Therapy Evaluation in Clinic

Patient: 35M, moderate persistent asthma on fluticasone/salmeterol 250/50 BID. Reports nocturnal symptoms 4x/week, rescue inhaler use daily, 2 ED visits in past 6 months. ACT score 12 (poorly controlled).

Key findings: Spirometry: FEV1 68% predicted, 14% improvement post-bronchodilator. FeNO 58 ppb (elevated, suggests eosinophilic inflammation). Blood eos 480/mcL.

Management:

Before escalating: assess inhaler technique (observed return demo, incorrect MDI technique identified, corrected with spacer)
Check adherence: pharmacy records show only 40% refill rate, counsel on importance
Trigger assessment: cat at home, no mattress encasement, exercise in cold air
If still uncontrolled after fixing above: Step 5, add tiotropium (Spiriva Respimat)
If refractory: biologic evaluation, eos 480 + FeNO 58 = Type 2 high → consider dupilumab (Dupixent) or mepolizumab (Nucala)

Teaching point: Before adding expensive biologics, fix the basics: 70-80% of patients use inhalers incorrectly, and non-adherence is the most common reason for "refractory" asthma. Always check technique, adherence, and triggers before escalating GINA steps. SYGMA 1 & 2, 2018

📋 Case 3, Near-Fatal Asthma with Intubation

Patient: 19M, severe persistent asthma, prior ICU admission x 2, presents in extremis. Unable to speak, minimal air movement ("silent chest"), altered consciousness.

Key findings: HR 140, RR 8 (bradypneic, pre-arrest), SpO2 78%, GCS 10. ABG: pH 7.12, pCO2 85, pO2 52. Peak flow unmeasurable.

Management:

Emergent RSI: ketamine 2 mg/kg (bronchodilator) + rocuronium 1.2 mg/kg
Ventilator settings: low RR (10-12), long expiratory time (I:E 1:4-1:5), low tidal volume
Permissive hypercapnia (accept pCO2 60-80 as long as pH > 7.20)
If PEA arrest post-intubation: disconnect from vent, compress chest to release trapped air (auto-PEEP)
Continuous albuterol via ETT + IV methylprednisolone 125 mg q6h + consider IV epinephrine drip

Teaching point: The "silent chest" with bradypnea is pre-respiratory arrest. After intubation, the greatest danger is dynamic hyperinflation (breath stacking → auto-PEEP → decreased venous return → PEA arrest). If a patient crashes post-intubation, disconnect from the ventilator and manually decompress. Permissive hypercapnia saves lives in status asthmaticus.

📣 Sample Presentation

One-Liner

"Ms. Brown is a 24-year-old with moderate persistent asthma on medium-dose ICS/LABA (Advair 250/50 BID) presenting to clinic with continued nocturnal symptoms 3×/week and rescue inhaler use 4×/week. Poorly controlled."

Key Points to Cover on Rounds

Poorly controlled asthma on Step 4 therapy. Before escalating: (1) Inhaler technique assessed -incorrect MDI technique identified, corrected with spacer education and observed return demo. (2) Adherence: admits missing doses 2-3×/week -counseled. (3) Trigger assessment: cat at home (allergen), no mattress encasement (dust mites), GERD symptoms (omeprazole started). (4) Spirometry today: FEV₁ 72%, 15% improvement post-bronchodilator. If still uncontrolled after optimizing technique/adherence/triggers → Step 5: add tiotropium (Spiriva Respimat) or refer for biologic evaluation (check eosinophils, FeNO, IgE). Asthma Action Plan provided. Plan: return in 6 weeks.

Monitoring

Spirometry at dx, 3-6mo, then q1-2y
ACT ≤19 = not controlled
Exacerbation frequency
FeNO trending
Inhaler technique -observe every visit
Adherence -refill records

⚡ Summary

Summary

Step Therapy

Step 1: PRN low-dose ICS-formoterol. Step 2: daily low-dose ICS. Step 3: medium ICS/LABA. Step 4: high ICS/LABA. Step 5: add LAMA, biologic, or OCS.

Before Escalating

Check: inhaler technique (70-80% incorrect), adherence, trigger avoidance, comorbidities (GERD, sinusitis, VCD). Fix these first.

Biologics

High eos → mepolizumab (Nucala), benralizumab (Fasenra). High IgE + allergic → omalizumab (Xolair). Type 2 inflammation → dupilumab (Dupixent). Phenotype-agnostic → tezepelumab (Tezspire).

Acute Exacerbation

Albuterol neb q20 min × 3, ipratropium, systemic steroids (prednisone 40-60 mg × 5 days). MgSO₄ 2g IV if severe. Assess peak flow.

Action Plan

Green (well): continue controller. Yellow (worsening): increase ICS, start OCS, use rescue. Red (emergency): call 911, albuterol, start OCS.

Asthma vs COPD

Asthma: reversible obstruction, normal DLCO, younger, atopic. COPD: fixed obstruction, low DLCO, older, smoking. ACO: features of both → treat with ICS + bronchodilators.

📄 One Pager

Pulmonology · One Pager

Asthma

Step therapy: low-dose ICS → ICS/LABA → add LAMA → biologic. Before escalating: check technique, adherence, triggers. Acute: albuterol + steroids. Action plan for all patients.

🧪 Diagnosis

Variable airflow obstruction + symptoms (wheeze, dyspnea, cough, chest tightness). Spirometry: FEV₁/FVC < 0.70 with significant reversibility (≥ 12% AND ≥ 200 mL). Normal DLCO distinguishes from emphysema.

🚨 Acute Exacerbation

Albuterol neb q20 min × 3 + ipratropium. Systemic steroids: prednisone 40-60 mg × 5 days. MgSO₄ 2g IV if severe. Peak flow or FEV₁ to assess response. If not improving → ICU.

💊 Stepwise Chronic Management

Step 1: PRN low-dose ICS-formoterol. Step 2: daily low-dose ICS. Step 3: medium ICS/LABA. Step 4: high ICS/LABA ± LAMA. Step 5: add biologic (based on eos, FeNO, IgE). Before escalating: fix technique + adherence + triggers.

💊 Key Drugs

Albuterol2 puffs q4-6h PRN

Fluticasone/salmeterol250/50 BID

Prednisone40-60 mg × 5d (exacerbation)

Dupilumab200-300 mg SQ q2wk (biologic)

⚠️ Pitfalls

Incorrect inhaler technique (70-80% use incorrectly -observe return demo)
SABA-only treatment (all persistent asthma needs a controller)
Not checking eos/FeNO before biologics
Missing VCD (vocal cord dysfunction mimics asthma)