• From Tintinalli (Chapter 69): Epidemiology, pathophysiology, clinical features, diagnosis, severity assessment, management (SABA, ipratropium, magnesium, corticosteroids, heliox, NIV, intubation), disposition
• From GINA 2026: Track 1/Track 2 stepwise therapy, AIR therapy, MART, new acute flowcharts, anaphylaxis co-presentation rule, biologics, oxygen targets

ASTHMA - 20 Mark Short Note

1. Definition and Epidemiology

• Affects ~8% of the U.S. population; most common chronic disease of childhood (9% prevalence)
• ~50% of cases develop before age 10 years; another one-third by age 40
• Annual global burden: >250,000 deaths; >300 million affected worldwide
• (Tintinalli, Chapter 69)

2. Pathophysiology

• Smooth muscle contraction (bronchospasm)
• Vascular congestion and bronchial wall edema
• Thick mucous plugs containing serum proteins, eosinophils, and cellular debris

1. Early phase (0-2 hrs): IgE-dependent mast cell degranulation → histamine, leukotrienes C4/D4, tryptase, prostaglandins → bronchospasm
2. Late phase (4-8 hrs): T-helper cell and eosinophil-mediated inflammation → sustained bronchoconstriction, mucosal edema

• Viral respiratory infections (most common - 40-80% in adults, 80% in children)
• Exercise, cold air, environmental allergens (mold, dust mites, cockroaches, animal dander)
• NSAIDs, aspirin, beta-blockers
• Occupational exposures, tobacco smoke, stress, hormonal changes
• (Tintinalli, Chapter 69)

3. Clinical Features

• Tachypnea, tachycardia
• Prolonged expiration, expiratory wheezing
• Use of accessory muscles (sternocleidomastoid, intercostals)
• Air trapping causing hyperinflation
• Pulsus paradoxus (>10 mmHg) - indicates severe obstruction
• Diminished breath sounds (silent chest) - life-threatening sign indicating near-complete obstruction

• Increased airway resistance
• Decreased maximum expiratory flow rates
• Air trapping and increased airway pressure
• Barotrauma risk
• V/Q mismatch → hypoxemia → hypercarbia (late, ominous sign)
• Increased work of breathing → respiratory muscle fatigue → ventilatory failure

4. Diagnosis

1. Characteristic symptom pattern (variable respiratory symptoms - wheeze, dyspnea, cough, chest tightness)
2. Evidence of variable expiratory airflow limitation:
   • Bronchodilator reversibility: FEV1 increase ≥12% AND ≥200 mL from baseline after SABA (traditional ATS/ERS 2005 criterion); GINA 2026 notes that the newer 2022 criterion (>10% of predicted FEV1) may reduce underdiagnosis, especially in young males
   • Peak expiratory flow (PEF) variability: >10% diurnal variation on ≥2 days/week
   • Bronchial provocation test (if spirometry normal)
   • FeNO ≥40 ppb in adults (supports eosinophilic airway inflammation)

• Pulse oximetry (SpO2)
• Peak flow measurement (PEFR): expressed as % predicted or % personal best
• ABG (rarely needed - reserved for SpO2 <92% or severe/deteriorating cases)
• CXR: useful to exclude pneumonia, pneumothorax, foreign body (not routine in uncomplicated asthma)
• ECG: sinus tachycardia common; right heart strain pattern in severe cases

• COPD, cardiac asthma (pulmonary edema), vocal cord dysfunction
• Foreign body aspiration, anaphylaxis, pulmonary embolism, epiglottitis

5. Severity Assessment

GINA Classification of Asthma Control:

ED Severity Classification (Tintinalli):

6. Management in the Emergency Department

A. Oxygen

• Target SpO2 93-95% in adults/adolescents, 94-98% in children (GINA 2026)
• Deliver via nasal cannula or face mask
• Avoid hyperoxia - liberal O2 worsens V/Q mismatch and hypercapnia in severe asthma

B. Short-Acting Beta-2 Agonists (SABAs)

• Salbutamol (albuterol) - first-line bronchodilator
• Inhaled via MDI + spacer or nebulizer (equivalent efficacy)
• Mild-moderate: 2-4 puffs (100 mcg/puff) q20 min x 3, then reassess
• Severe: continuous or frequent (q20-30 min) nebulization
• GINA 2026: Emphasizes conservative SABA dosing and safety prompts - patients should seek medical care if needing >a specified threshold of inhalations in 24 hours

C. Anticholinergics (Ipratropium Bromide)

• Add to SABA in moderate-severe asthma
• Ipratropium 0.5 mg nebulized q20 min x 3, then q2-4h
• Reduces hospital admissions when combined with SABA in the ED
• Mechanism: blocks muscarinic receptors → reduces vagal bronchoconstriction and secretions
• (Tintinalli, Chapter 69)

D. Systemic Corticosteroids

• Indication: All moderate-severe acute asthma; if no rapid response to SABA
• Oral prednisone: 40-80 mg/day (equivalent efficacy to IV for most patients)
• IV methylprednisolone: 60-125 mg for severe/unable to take oral
• Onset: Begins in 4-6 hours
• Effect: Suppress late-phase inflammatory response, potentiate beta-agonist effect
• Duration: 5-7 day course (taper not needed for short courses)
• GINA 2026: Emphasizes OCS stewardship - optimizing ICS-containing therapy to reduce OCS dependence

E. Magnesium Sulfate (IV)

• Indication: Severe acute asthma not responding to initial treatment; SpO2 <92%
• Dose: 2 g IV over 20 min (single dose)
• Mechanism: Inhibits calcium-mediated smooth muscle contraction
• Reduces hospital admissions; safe adjunct
• Nebulized isotonic magnesium may also be beneficial
• (Tintinalli, Chapter 69)

F. Heliox (Helium-Oxygen)

• 70:30 or 80:20 helium/oxygen mixture
• Reduces turbulent flow in obstructed airways; lowers work of breathing
• Useful as a bridge in severe asthma when conventional therapies failing
• Delivers aerosolized medications more effectively to distal airways
• Caution: Cannot be used if FiO2 >30% is needed

G. Ketamine

• Sub-dissociative or dissociative doses (0.5-2 mg/kg IV)
• Bronchodilator properties (stimulates catecholamine release)
• Preferred induction agent if intubation needed in severe bronchospasm

H. Non-Invasive Ventilation (NIV/BiPAP)

• Consider in severe asthma with respiratory fatigue before frank failure
• Reduces intubation rate as a temporizing measure
• (Tintinalli, Chapter 69)

I. Endotracheal Intubation and Mechanical Ventilation

• Indications (Tintinalli): Respiratory arrest, failure of NIV/medical therapy, altered consciousness, rising PaCO2 with fatigue
• RSI: Ketamine preferred (bronchodilatory); succinylcholine or rocuronium for paralysis
• Ventilator strategy (permissive hypercapnia):
  • Low respiratory rate (10-14/min) and tidal volumes to allow complete exhalation
  • Prolonged expiratory time (I:E ratio 1:3 to 1:5)
  • Accept PaCO2 50-70 mmHg to avoid auto-PEEP and barotrauma
  • External PEEP low initially (avoid worsening air trapping)

J. GINA 2026 - Anaphylaxis Co-presenting with Asthma (NEW RULE)

• If features of anaphylaxis AND asthma are present simultaneously:
  • Step 1: Give EPINEPHRINE (IM or intranasal) FIRST
  • Step 2: Then give bronchodilators
  • (Intranasal route is NOT suitable for small children)

7. Stepwise Long-Term Management (GINA 2026)

Track 1 (Preferred): ICS-Formoterol Anti-Inflammatory Reliever (AIR) Therapy

Track 2 (Alternative): ICS-SABA Anti-Inflammatory Reliever

• Step 1: As-needed combination low-dose ICS-SABA for symptom relief (if Track 1 unavailable, or patient stable on current therapy)
• Steps 2-5: Daily maintenance ICS-LABA + as-needed ICS-SABA as reliever

Step 5 - Severe/Difficult-to-Treat Asthma (GINA 2026 Updates):

• Add-on LAMA (e.g., tiotropium): Reduces exacerbations but reduction is far less than biologics; useful when biologics unavailable
• Biologic therapies (new in GINA 2026):
  • Anti-IgE: Omalizumab (now generic anti-IgE added)
  • Anti-IL-5: Mepolizumab, reslizumab, benralizumab
  • Anti-IL-4/13: Dupilumab
  • Anti-TSLP: Tezepelumab
  • Depemokimab (new anti-IL-5 biologic added in 2026)
  • A table of non-asthma indications for the four biologic classes was newly added

8. Status Asthmaticus

• Maximize all bronchodilator therapies (SABA, ipratropium, IV magnesium)
• IV or IM epinephrine/terbutaline (subcutaneous - reserved for severe refractory cases)
• Early consideration of NIV
• ICU admission; prepare for mechanical ventilation
• Consider IV ketamine infusion as bronchodilatory agent
• Near-fatal asthma: Respiratory arrest → RSI with ketamine, permissive hypercapnia strategy (Tintinalli)

9. Disposition

• Reliever inhaler (ICS-formoterol in GINA Track 1 preferred)
• Short course oral corticosteroids (5-7 days)
• Written asthma action plan (GINA 2026 - mandatory for all patients)
• Ensure correct inhaler technique before discharge
• Education on trigger avoidance

10. Summary of Key GINA 2026 Updates

• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th Edition, Chapter 69 - "Acute Asthma and Status Asthmaticus" (Goto & Hasegawa)
• GINA 2026 Strategy Report (published May 5, 2026)
• GINA 2026 Key Highlights - Guideline Central

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) - 20 Mark Short Note

1. Definition and Epidemiology

• Third leading cause of death in the United States; women now account for >50% of COPD-related deaths
• ~10% global prevalence; >3 million deaths annually worldwide
• Vastly underdiagnosed - majority of patients never have spirometry performed
• (Tintinalli, Chapter 70)

2. Risk Factors

3. Pathophysiology

• Loss of elastic recoil
• Narrowing and collapse of small airways
• Mucous stasis and bacterial colonization in bronchi

• Chronic bronchitis ("Blue Bloater"): Productive cough for ≥3 months/year for ≥2 consecutive years; mucus hypersecretion, airway edema, prominent hypoxemia
• Emphysema ("Pink Puffer"): Destruction of alveolar walls; hyperinflation; barrel chest; pursed-lip breathing to generate intrinsic PEEP

4. Diagnosis

Spirometry (Mandatory for Diagnosis)

• Pre-bronchodilator spirometry can be used to exclude a diagnosis of COPD (GOLD 2026)
• GOLD 2026 emphasis: Spirometry must be interpreted alongside clinical characteristics and imaging findings when estimating disease burden and prognosis

GOLD Spirometric Severity Grading (Tintinalli Table 70-1, GOLD GRADE):

Supporting investigations:

• CXR: Hyperinflation, flattened diaphragm, increased AP diameter, bullae (emphysema); helpful to exclude pneumonia/pneumothorax
• ABG: Determines degree of hypoxemia (PaO2) and ventilatory failure (PaCO2); essential in acute exacerbations
• ECG: Right heart strain, RAD, P pulmonale, RBBB in severe disease
• FBC: Polycythemia (chronic hypoxemia); anemia (worsens dyspnea)
• CT thorax: Gold standard for emphysema quantification; identifies bullae, bronchiectasis; not routine in ED

5. Clinical Features

• Tachypnea; use of accessory muscles; pursed-lip exhalation
• Expiratory wheeze; prolonged expiratory time
• Hyperinflated chest ("barrel chest") - AP diameter increased
• Diminished breath sounds
• Coarse crackles (secretions in chronic bronchitis)
• Lower extremity edema (cor pulmonale/right heart failure)
• Cyanosis; asterixis (CO2 narcosis in severe hypercapnia)

6. GOLD ABE Assessment Framework (GOLD 2026 - KEY UPDATE)

Symptom Assessment Tools:

• mMRC Dyspnoea Scale (0-4): mMRC ≥2 = significant dyspnea
• CAT (COPD Assessment Test): Score 0-40; CAT ≥10 = significant impact

7. Stable COPD Pharmacotherapy (GOLD 2026)

Initial Treatment (Treatment-naive patients):

Follow-up / Escalation:

• Persistent dyspnea on monotherapy: Escalate to LABA + LAMA
• Persistent exacerbations on LABA + LAMA: Add ICS → Triple therapy (LABA + LAMA + ICS) - especially if eosinophils ≥100-300 cells/µL
• Persistent exacerbations despite triple therapy: Consider roflumilast (PDE4 inhibitor) if FEV1 <50% + chronic bronchitis; azithromycin (in ex-smokers); or biologic therapy in select cases

Drug classes:

• SABAs: Salbutamol, terbutaline - quick relief
• SAMAs: Ipratropium bromide - reduce secretions + bronchodilate
• LABAs: Salmeterol, formoterol, indacaterol - 12-24h duration
• LAMAs: Tiotropium, umeclidinium, aclidinium, glycopyrronium - reduce exacerbations, improve lung function
• ICS: Fluticasone, budesonide - add only when indicated (eosinophils ≥100; recurrent exacerbations); not as monotherapy in COPD
• Triple inhalers (LABA/LAMA/ICS): Single-inhaler combinations (e.g., fluticasone/umeclidinium/vilanterol)

Non-pharmacological (GOLD 2026 emphasis):

• Smoking cessation - single most effective intervention; slows FEV1 decline
• Pulmonary rehabilitation - improves exercise capacity, symptoms, and QoL across all GOLD grades
• Vaccination: Influenza (annual), pneumococcal (PPSV23 + PCV20), COVID-19, RSV vaccine - GOLD 2026 places increased emphasis on vaccination against respiratory viral infections
• Long-term oxygen therapy (LTOT): Only when resting PaO2 ≤55 mmHg or SpO2 ≤88% (improves survival in severe resting hypoxemia); NOT routinely for moderate desaturation
• Lung volume reduction (surgical/bronchoscopic): Selected severe emphysema
• Lung transplantation: End-stage disease

8. Acute Exacerbation of COPD (AECOPD)

Definition (GOLD 2026):

Common Causes:

• Viral infections (rhinovirus, influenza, RSV) - most common
• Bacterial infections (H. influenzae, S. pneumoniae, M. catarrhalis, Pseudomonas in severe COPD)
• Environmental pollutants/cold air
• Unknown cause in ~1/3 of cases

Mimics to exclude:

GOLD 2026 Severity Classification - Rome Proposal (NEW):

9. Emergency Department Management of AECOPD

A. Oxygen Therapy

• Target SpO2 88-92% (Tintinalli) to avoid hypercapnic respiratory failure (hypoxic ventilatory drive theory)
• Deliver via controlled Venturi mask (preferred) - delivers precise FiO2 (24%, 28%, 35%)
• Hyperoxia worsens hypercarbia by Haldane effect and V/Q mismatch - avoid SpO2 >92-94%
• Check ABG if SpO2 <92% or clinical deterioration - essential to detect CO2 retention

B. Short-Acting Bronchodilators (SABDs)

• SABA (salbutamol/albuterol) ± SAMA (ipratropium) - first-line for all moderate/severe exacerbations (GOLD 2026)
• MDI + spacer or nebulizer (equivalent efficacy; MDI + spacer preferred in non-severe cases)
• Ipratropium 0.5 mg q4-6h nebulized; salbutamol 2.5-5 mg q4-6h
• Combination SABA + SAMA (Duoneb) superior to either alone

C. Systemic Corticosteroids

• Indicated for moderate/severe AECOPD
• Oral prednisolone 40 mg/day for 5 days (GOLD 2026 - shorter courses equally effective)
• IV methylprednisolone 40-125 mg if unable to take orally
• Benefits: shorter hospital stay, faster FEV1 improvement, reduced treatment failure
• Taper not needed for ≤5 day courses
• Caution: Hyperglycemia (especially in diabetics), immunosuppression

D. Antibiotics

• Indications (GOLD 2026): Purulent sputum (change in sputum color is most specific indicator), documented prior bacterial lung infection, those requiring ventilatory support
• Duration: 5 days (GOLD 2026)
• Choice based on local resistance patterns:
  • Outpatient/mild-moderate: Amoxicillin, doxycycline, or azithromycin
  • Severe/Pseudomonas risk (frequent exacerbations, severe COPD, recent hospitalization): Ciprofloxacin or anti-Pseudomonal beta-lactam
• Methylxanthines (theophylline/aminophylline): NOT recommended due to increased side-effect profile without proven additional benefit (GOLD 2026)

E. Non-Invasive Ventilation (NIV / BiPAP)

• Indication: Acute or acute-on-chronic hypercapnic respiratory failure
  • pH <7.35 AND PaCO2 >45 mmHg
  • Moderate-severe dyspnea with accessory muscle use/paradoxical breathing
• High-flow nasal therapy (HFNT): Alternative adjunct in select patients - improves gas exchange and reduces work of breathing (new GOLD 2026 emphasis)
• NIV reduces intubation rate, hospitalization duration, and improves survival (GOLD 2026)
• Contraindications: vomiting, facial trauma, unable to protect airway, hemodynamic instability, respiratory arrest

F. Invasive Mechanical Ventilation

• Indications (Tintinalli):
  • Respiratory or cardiac arrest
  • Failure of NIV or NIV contraindicated
  • Altered mental status / inability to protect airway
  • Hemodynamic instability
• Ventilator strategy:
  • Controlled-mode ventilation initially
  • Allow adequate expiratory time (prevent auto-PEEP/dynamic hyperinflation)
  • Permissive hypercapnia acceptable
  • Low PEEP initially; titrate cautiously

G. Additional Measures

• Treat precipitating causes (antibiotics for pneumonia, anticoagulation for PE)
• Diuretics if congestive heart failure component
• Bronchodilator nebulization through ventilator circuit if intubated
• DVT prophylaxis (hospitalized patients)

10. Indications for Hospital Admission (Tintinalli + GOLD 2026)

• SpO2 <90% or significant hypoxemia/hypercarbia on ABG
• Severe dyspnea not responding to initial ED treatment
• Altered mental status
• Inability to ambulate, eat, or care for self
• Uncertain diagnosis
• Significant comorbidities (heart failure, pulmonary embolism, arrhythmia)
• Insufficient home support
• Failure of outpatient management

• Severe dyspnea not responding to initial therapy
• Hemodynamic instability
• pH <7.25 despite NIV
• Impaired consciousness, need for intubation
• Severe hypoxemia (PaO2/FiO2 <200)

11. Disposition and Post-Exacerbation Care (GOLD 2026)

• Exacerbation recovery takes 4-6 weeks; some patients never return to pre-exacerbation functional state
• Follow-up within 4-6 weeks of discharge (GOLD recommendation)
• Reassess and optimize maintenance therapy at follow-up
• At discharge: if ≥1 moderate/severe exacerbation + elevated eosinophils → add ICS to dual bronchodilator regimen
• Written discharge action plan; inhaler technique education
• Ensure smoking cessation counseling
• Address vaccination status

12. Summary of Key GOLD 2026 Updates

• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th Edition, Chapter 70 - "Chronic Obstructive Pulmonary Disease" (Craig G. Bates)
• GOLD 2026 Strategy Report - Key Changes (published November 2025 / effective 2026)
• GOLD 2026 Summary - Guideline Central
• GOLD 2026 Updates - CHEST Physician
• University of Minnesota Pharmacy - GOLD 2026 Analysis

RESPIRATORY FAILURE: TYPES AND MANAGEMENT IN THE EMERGENCY DEPARTMENT

20-Mark Short Note based on Tintinalli's Emergency Medicine: A Comprehensive Study Guide (9th Ed.)

1. Definition

• Hypoxemic (Type 1): PaO2 <60 mmHg on room air
• Hypercapnic (Type 2): PaCO2 >45 mmHg with acidosis (pH <7.35)

2. Types of Respiratory Failure

TYPE 1 - Hypoxemic Respiratory Failure (Oxygenation Failure)

• Definition: Hypoxia without hypercapnia (PaO2 <60 mmHg; normal or low PaCO2)
• Mechanism: Conditions that affect oxygenation but not necessarily ventilation - primarily V/Q mismatch, diffusion impairment, or intrapulmonary shunting
• Pathophysiology:
  • V/Q mismatch: most common mechanism - areas of lung are perfused but poorly ventilated
  • Shunt: deoxygenated blood bypasses ventilated alveoli (e.g., atelectasis, consolidation)
  • Diffusion impairment: thickened alveolar-capillary membrane
  • Low FiO2 (high altitude) - rare in clinical settings

TYPE 2 - Hypercapnic (Ventilatory) Respiratory Failure

• Definition: Hypoxia with hypercapnia (PaCO2 >45 mmHg) and respiratory acidosis
• Mechanism: Inadequate alveolar ventilation (hypoventilation) - the lungs cannot excrete CO2 at the rate it is produced
• Pathophysiology:
  • Reduced respiratory drive (CNS depression)
  • Neuromuscular weakness (cannot generate adequate minute ventilation)
  • Increased airway resistance or decreased compliance (increased work → muscle fatigue)
  • Increased dead space (V/Q mismatch where areas are ventilated but not perfused)

Additional Clinical Types (Functional Classification)

3. Clinical Features

• Dyspnea, breathlessness
• Weakness, fatigue
• Chest tightness or pain
• Confusion, altered mentation (anxiety → confusion → obtundation → coma)

• Tachypnea, hyperpnea
• Accessory muscle use (sternocleidomastoid, intercostals, scalenes)
• Paradoxical abdominal breathing (diaphragmatic fatigue)
• Nasal flaring, tracheal tug
• Intercostal/subcostal/suprasternal retractions
• Cyanosis (late, unreliable)
• Wheezing (obstructive), stridor (upper airway obstruction), silent chest (critical obstruction)

• Bounding pulse, plethoric face, warm peripheries (vasodilation from CO2 retention)
• Asterixis (CO2 narcosis - flapping tremor)
• Drowsiness, headache (raised ICP from cerebral vasodilation)
• Papilledema in extreme cases

4. Assessment in the ED

• Pulse oximetry (SpO2): Continuous monitoring; target SpO2 94-98% in most patients; 88-92% in known COPD/Type 2 failure
• ABG (Arterial Blood Gas): Definitive assessment of PaO2, PaCO2, pH, HCO3-; mandatory in suspected Type 2 failure and whenever SpO2 <92%
• Respiratory rate and effort: Subjective gauge - the patient's visible work of breathing
• Capnography (ETCO2): Non-invasive estimate of PaCO2; useful in monitoring ventilated/pre-intubation patients
• CXR: Consolidation, pulmonary edema, pneumothorax, pleural effusion
• ECG: Right heart strain, dysrhythmias
• Point-of-care US (POCUS): Pleural effusion, pneumothorax, B-lines (pulmonary edema), cardiac function

5. Emergency Management - Step-by-Step Approach

STEP 1: Position and Initial Stabilization

• Sit patient upright (reduces work of breathing, improves FRC)
• Continuous monitoring: SpO2, ECG, ETCO2, RR, BP
• IV access; blood for ABG, CBC, BMP, cardiac enzymes, BNP/proBNP
• Identify and treat precipitating cause simultaneously

STEP 2: Oxygen Delivery - Escalating Strategy

• Delivers humidified, heated oxygen at flow rates up to 60 L/min
• Provides modest positive pressure effect while decreasing work of breathing
• Best used in patients with hypoxia and intact respiratory drive (non-hypercapnic failure)
• Alternative to invasive ventilation: indicated when SpO2 <92% and RR >22 breaths/min (excluding bullous lung disease and pneumothorax)
• Key evidence: HFNC may improve mortality in patients with non-hypercapnic acute hypoxemic respiratory failure compared to NIPPV and conventional supplemental oxygen (Tintinalli, Table 28-4)
• Also used as pre-oxygenation bridge before intubation ("apneic oxygenation")
• Flush-rate oxygenation (wall O2 at 40-60 L/min) - alternative bridge to other ventilation methods

STEP 3: Non-Invasive Positive-Pressure Ventilation (NIPPV/NIV)

• Reduces work of breathing
• Improves pulmonary compliance
• Recruits and stabilizes atelectatic alveoli
• Decreases intubation rate, ICU LOS, and mortality (especially in COPD + acute cardiogenic pulmonary edema)

• Cooperative with intact airway reflexes
• Intact ventilatory effort
• Able to tolerate mask

• Absent or agonal respiratory effort
• Impaired/absent gag reflex
• Altered mental status (significant)
• Severe maxillofacial trauma or potential basilar skull fracture
• Life-threatening epistaxis
• Bullous lung disease
• Use with caution in hypotension (positive pressure → reduced venous return → worsen cardiac output)

• Air trapping
• Increased intrathoracic pressure → decreased venous return, afterload reduction, cardiac output reduction, hypotension
• Pulmonary barotrauma

• IPAP: 10-14 cm H2O (titrate for comfort and tidal volume)
• EPAP/PEEP: 4-8 cm H2O
• FiO2: titrate to target SpO2

STEP 4: Endotracheal Intubation and Invasive Mechanical Ventilation

• Respiratory or cardiac arrest
• Failure of HFNC and NIPPV
• Contraindications to NIPPV
• Severe altered mental status / inability to protect airway
• Refractory hypoxemia (SpO2 <88-90% despite maximal non-invasive therapy)
• Progressive respiratory acidosis (pH <7.25) despite NIV
• Hemodynamic instability
• Impending upper airway obstruction

• Preoxygenation: HFNC or non-rebreather mask at 15 L/min for ≥3 min; maintain HFNC during apneic phase
• Induction: Ketamine (1-2 mg/kg) preferred in bronchospasm/hypotension; propofol (1-2 mg/kg) in normovolemic patients; etomidate (0.3 mg/kg) for hemodynamic stability
• Paralytic: Succinylcholine (1.5 mg/kg) or rocuronium (1.2 mg/kg)
• Confirm placement: direct visualization + waveform capnography (gold standard) + bilateral breath sounds + CXR

STEP 5: Mechanical Ventilation Settings

• Volume Control (VC): Set VT is delivered regardless of patient effort; inspiratory flow over time delivers the target volume; monitor peak and plateau pressures
• Pressure Control (PC): Set pressure is delivered; VT varies with compliance/resistance; monitor tidal volumes
• Synchronous Intermittent Mandatory Ventilation (SIMV): Allows spontaneous breaths between mandatory breaths; set rate guarantees minimum minute ventilation

STEP 6: Disease-Specific Ventilation Strategies

A. ARDS / Severe Hypoxemic Failure (Type 1)

• Low VT: 6 mL/kg ideal body weight (max 8 mL/kg)
• Limit plateau pressure to ≤30 cm H2O
• Higher PEEP (8-15 cm H2O or higher) to recruit collapsed alveoli and improve FRC
• Permissive hypercapnia: Accept higher PaCO2 (to 50-60 mmHg) to avoid volutrauma
• High FiO2 initially with PEEP titration (ARDSNet PEEP-FiO2 tables)
• Prone positioning for severe ARDS (PaO2/FiO2 <150) - reduces mortality
• Deep sedation often required (patients need to accommodate lung-protective strategy)

B. Obstructive Lung Disease (Asthma/COPD - Type 2 + dynamic hyperinflation)

• High airway resistance → very high peak pressures (but plateau may be normal)
• Dynamic hyperinflation (auto-PEEP): Incomplete exhalation before next breath → progressive air trapping → rising lung volumes → barotrauma + pneumothorax + hypotension

• Low respiratory rate (8-12 breaths/min) to maximize expiratory time
• Prolonged I:E ratio (1:3 to 1:5)
• Low VT (6-8 mL/kg)
• Permissive hypercapnia - accept PaCO2 50-70 mmHg
• Keep PEEP low initially (auto-PEEP already present; external PEEP may worsen trapping)
• Monitor expiratory flow limb on ventilator; end-expiratory hold to measure intrinsic PEEP
• Avoid increasing RR if PaCO2 is high - counterproductive; shortens expiratory time

STEP 7: Sedation of the Intubated Patient

• Patients with severe hypoxemic or hypercapnic failure often need deeper sedation to accommodate lung-protective ventilation
• Patients intubated for airway protection alone may require less sedation
• Target analgesia before targeting sedation (pain → agitation → dyssynchrony → ventilator-induced lung injury)
• Use standardized scales: Richmond Agitation-Sedation Scale (RASS); target RASS −2 to 0 in the ED
• Avoid continuous benzodiazepine infusions - associated with higher mortality, increased delirium, prolonged sedation
• Prefer propofol (short-acting, titratable) or dexmedetomidine for sedation; fentanyl for analgesia

6. Causes of Upper Airway Obstruction (Tintinalli Table 28-1)

7. Summary: Management Algorithm for Respiratory Failure in the ED

Respiratory Failure Suspected
        ↓
ABG + SpO2 + Clinical Assessment
        ↓
Type 1 (Hypoxemic)?         Type 2 (Hypercapnic)?
    ↓                               ↓
Optimise O2:                Support Ventilation:
Nasal Cannula                BiPAP / NIV
      ↓                           ↓
HFNC (if SpO2 <92%, RR >22)   If fail → Intubate
      ↓                           ↓
If fail → Intubate + MV     MV: Low RR, Long I:E,
  (Lung protective)          Permissive hypercapnia

8. Quick Reference Table: NIPPV vs. HFNC vs. Invasive Ventilation

• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th Edition
  • Chapter 28: "Noninvasive Airway Management" (Carlson & Wang)
  • Chapter 29B: "Mechanical Ventilation" (Lentz, Atchinson & Roginski)
  • Chapter 29A: "Tracheal Intubation"
  • Chapter 30: "Surgical Airways"
  • Chapter 70: "Chronic Obstructive Pulmonary Disease" (Bates)