Asthma in ICU (Status Asthmaticus)

Quick Answer

Quick Answer: Status asthmaticus is acute severe asthma refractory to initial bronchodilator therapy, representing a life-threatening emergency requiring ICU admission. The pathophysiology centres on dynamic hyperinflation and auto-PEEP, which cause respiratory failure and haemodynamic compromise.

Immediate management:

1. High-flow oxygen (target SpO₂ 92-95%)
2. Continuous nebulised salbutamol + ipratropium bromide
3. IV hydrocortisone 200 mg or methylprednisolone 60-125 mg
4. IV magnesium sulfate 2 g over 20 minutes
5. Escalate to IV salbutamol if refractory

If intubation required:

• Permissive hypercapnia is the cornerstone strategy
• Low respiratory rate (8-10/min), low tidal volume (6-8 mL/kg)
• Prolonged I:E ratio (1:3 to 1:5)
• Target plateau pressure <30 cmH₂O
• Monitor and minimise auto-PEEP
• Disconnect circuit if sudden hypotension (auto-PEEP relief)

Red flags: Silent chest, inability to speak, confusion, bradycardia, normocapnia/hypercapnia on ABG = impending arrest.

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CICM Exam Focus

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Key Points (10)

Key Points: 1. Status asthmaticus is acute severe asthma unresponsive to standard bronchodilator therapy, with features of life-threatening or near-fatal asthma

2. Dynamic hyperinflation occurs when insufficient expiratory time leads to progressive air trapping and increased end-expiratory lung volume
3. Auto-PEEP (intrinsic PEEP) is the positive alveolar pressure at end-expiration due to trapped air - the key physiological derangement to monitor and manage
4. Silent chest indicates severe bronchospasm with minimal air entry - an ominous pre-arrest sign
5. Normocapnia or hypercapnia on ABG in acute severe asthma indicates respiratory muscle fatigue and impending respiratory failure
6. Post-intubation hypotension is usually due to auto-PEEP reducing venous return - disconnect from ventilator as first intervention
7. Permissive hypercapnia is the cornerstone of mechanical ventilation - accept PaCO₂ up to 80-100 mmHg and pH down to 7.15-7.20 to avoid dynamic hyperinflation
8. Ventilator settings: low RR (8-10), low VT (6-8 mL/kg), high inspiratory flow (80-100 L/min), I:E ratio 1:3-1:5, plateau pressure <30 cmH₂O
9. IV magnesium sulfate 2 g is first-line adjunct for life-threatening asthma; IV salbutamol and aminophylline are second-line options
10. ECMO is highly effective for refractory status asthmaticus (survival ~83%) due to the reversible nature of the disease [1,2,3]

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Red Flags

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Definition and Classification

Definitions [4,5]

Status asthmaticus (acute severe asthma, life-threatening asthma):

• Severe acute asthma that fails to respond adequately to initial standard bronchodilator therapy
• Requires intensive monitoring and treatment beyond standard ED/ward care
• Represents a medical emergency with significant mortality risk

Life-threatening asthma (UK/Australian classification):

• Any one of:
  • SpO₂ <92%
  • PaO₂ <60 mmHg (8 kPa)
  • Normal or elevated PaCO₂ (35-45 mmHg)
  • Silent chest
  • Cyanosis
  • Feeble respiratory effort
  • Bradycardia or arrhythmia
  • Hypotension
  • Exhaustion, confusion, or coma
  • Peak expiratory flow (PEF) <33% predicted

Near-fatal asthma:

• Respiratory arrest requiring mechanical ventilation, OR
• PaCO₂ >50 mmHg with respiratory acidosis, OR
• Requiring ICU admission

Severity Classification

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Epidemiology

Global and Australian Data [6,7,8]

Risk Factors for Fatal or Near-Fatal Asthma [9,10]

Patient Factors:

• Previous near-fatal asthma or ICU admission
• Previous intubation for asthma
• ≥3 ED visits or ≥2 hospitalisations in past year
• Poor perception of symptom severity (blunted perception)
• Non-adherence to preventer therapy
• Overuse of SABA (>3 canisters/year)
• Poor access to healthcare
• Low socioeconomic status
• Psychosocial factors (depression, anxiety, denial)
• Food allergy (anaphylaxis risk)

Disease Factors:

• Brittle asthma (type 1: wide PEF variability; type 2: sudden attacks)
• Aspirin-exacerbated respiratory disease (AERD)
• Allergic bronchopulmonary aspergillosis (ABPA)
• Frequent oral corticosteroid courses

Australian/NZ Specific Context

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Pathophysiology

Underlying Mechanisms [15,16,17]

Acute severe asthma involves three key pathological processes:

1. Bronchoconstriction

Mechanism:

• Allergen, irritant, or infection triggers IgE-mediated mast cell degranulation
• Release of histamine, leukotrienes (C4, D4, E4), prostaglandins
• Direct bronchial smooth muscle contraction
• Rapid onset (minutes to hours)

Clinical effect:

• Increased airway resistance
• Prolonged expiratory time constant
• Wheezing (becomes silent when severe)

2. Airway Inflammation and Oedema

Mechanism:

• Eosinophilic inflammation (most asthma phenotypes)
• Mucosal oedema and increased vascular permeability
• Epithelial shedding
• Inflammatory mediator release (IL-4, IL-5, IL-13)

Clinical effect:

• Further airway narrowing
• Takes hours to days to resolve (steroid responsive)
• Contributes to mucus hypersecretion

3. Mucus Plugging

Mechanism:

• Goblet cell hyperplasia and hypersecretion
• Thick, tenacious mucus
• Impaired mucociliary clearance
• Formation of mucus plugs (Curschmann spirals, Charcot-Leyden crystals)

Clinical effect:

• Airway obstruction (may be refractory to bronchodilators)
• Regional atelectasis and V/Q mismatch
• Major cause of sudden death in some autopsy studies

Dynamic Hyperinflation and Auto-PEEP [18,19,20]

Exam Detail: #### The Physiology of Dynamic Hyperinflation

Normal expiration:

• Expiratory time sufficient for complete exhalation
• End-expiratory lung volume = Functional Residual Capacity (FRC)
• Alveolar pressure returns to zero (atmospheric) at end-expiration

In severe asthma:

• Markedly increased airway resistance (R)
• Prolonged expiratory time constant (τ = R × C)
• Expiration cannot complete before next inspiration begins
• Incomplete exhalation → air trapping → progressive hyperinflation

Consequences of Dynamic Hyperinflation:

Measuring Auto-PEEP

End-expiratory hold manoeuvre:

1. Ensure patient is paralysed/deeply sedated (no spontaneous efforts)
2. Press "expiratory hold" button on ventilator
3. Wait for equilibration (2-3 seconds)
4. Read total PEEP
5. Auto-PEEP = Total PEEP - Set PEEP

Example:

• Set PEEP: 5 cmH₂O
• Total PEEP (on hold): 18 cmH₂O
• Auto-PEEP: 18 - 5 = 13 cmH₂O

Target: Minimise auto-PEEP (ideally <5-10 cmH₂O)

Flow-Volume Loop Changes

In obstructive disease:

• Expiratory limb shows reduced flow at all lung volumes
• Scooped appearance (concave shape)
• Flow does not return to zero before inspiration (incomplete exhalation)

Time Constant Concept

τ (time constant) = Resistance × Compliance

In severe asthma:
- Resistance: ↑↑↑ (10-fold or more)
- Compliance: Normal to slightly ↓ (hyperinflation)
- τ markedly prolonged (seconds vs. normal 0.5s)

Time to exhale 95% of tidal volume = 3τ
Normal: 3 × 0.5 = 1.5 seconds
Severe asthma: 3 × 3 = 9 seconds or more

This explains why adequate expiratory time is critical in mechanical ventilation.

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Clinical Assessment

History [21,22]

Presenting Symptoms:

• Progressive dyspnoea
• Wheeze (may be absent if severe - "silent chest")
• Chest tightness
• Cough (often non-productive, may be paroxysmal)
• Difficulty speaking
• Diaphoresis
• Anxiety, sense of impending doom

Triggering Factors:

• Viral upper respiratory tract infection (most common)
• Allergen exposure (pollen, dust mite, pets, moulds)
• Exercise
• Cold air
• Irritants (smoke, pollution, cleaning products)
• Medications (NSAIDs, beta-blockers)
• Emotional stress
• Poor medication adherence (most important risk factor)

Key History Points:

• Duration and progression of current attack
• Response to home nebulisers/inhalers
• Previous ICU admissions or intubations (major red flag)
• Usual medications and recent changes
• Recent oral steroid courses
• Allergies and anaphylaxis history
• Comorbidities (cardiac disease, COPD overlap)
• Social circumstances affecting adherence

Physical Examination

General Appearance:

• Distress level (can speak in sentences/phrases/words/none?)
• Posture (tripod position, unable to lie flat)
• Diaphoresis
• Cyanosis
• Use of accessory muscles (sternocleidomastoid, intercostals)
• Paradoxical abdominal movement (diaphragm fatigue)

Vital Signs:

• Tachypnoea (RR >25 indicates severity)
• Tachycardia (HR >110 indicates severity)
• Pulsus paradoxus (>10 mmHg = severe, >25 mmHg = critical)
• Hypoxaemia (SpO₂ <92% on room air)
• Hypotension (late sign, impending arrest)

Chest Examination:

• Wheeze (polyphonic expiratory wheeze is classic)
• Silent chest (NO wheeze = ominous, minimal air movement)
• Prolonged expiratory phase
• Hyperinflated chest
• Reduced breath sounds

Mental Status:

• Agitation/anxiety (hypoxaemia, distress)
• Confusion/drowsiness (hypercapnia - critical sign)
• Decreased level of consciousness (impending arrest)

Severity Assessment Scoring

Clinical Pearl: #### BTS/SIGN Severity Classification

Moderate Acute Asthma:

• Increasing symptoms
• PEF 50-75% best or predicted
• No features of severe asthma

Acute Severe Asthma (any of):

• PEF 33-50% best or predicted
• Respiratory rate ≥25/min
• Heart rate ≥110/min
• Inability to complete sentences in one breath

Life-Threatening Asthma (any of):

• PEF <33% best or predicted
• SpO₂ <92%
• PaO₂ <60 mmHg (8 kPa)
• Normal or raised PaCO₂
• Silent chest
• Cyanosis
• Feeble respiratory effort
• Bradycardia
• Arrhythmia
• Hypotension
• Exhaustion/confusion/coma

Near-Fatal Asthma:

• Raised PaCO₂ and/or requiring mechanical ventilation with raised inflation pressures

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Investigations

Arterial Blood Gas [23,24]

Interpretation in acute asthma:

Key points:

• Normal PaCO₂ in a distressed asthmatic is a RED FLAG (they should be hyperventilating)
• Metabolic acidosis with elevated lactate is common (β-agonist effect, NOT necessarily tissue hypoxia)
• Repeat ABG after treatment to assess trajectory

Lactic Acidosis in Asthma:

• β₂-agonists stimulate glycolysis → Type B lactic acidosis
• Can reach 4-8 mmol/L with IV salbutamol
• Does NOT indicate shock if haemodynamically stable
• Resolves with cessation of salbutamol
• Do not chase lactate with fluids if patient is well-perfused [25]

Other Investigations

Bedside:

• Peak expiratory flow (if patient can perform) - serial measurements valuable
• ECG: sinus tachycardia, possible RV strain, arrhythmias
• Continuous SpO₂ monitoring
• Blood glucose (stress response, steroids)

Laboratory:

• FBC: leukocytosis (steroids, stress, infection)
• U&E: hypokalaemia (β-agonists, steroids) - monitor closely
• Magnesium: may be low, affects bronchial smooth muscle
• Troponin: if cardiac history or significant hypoxia
• Blood cultures: if infection suspected

Imaging:

CXR findings in acute asthma:

• Hyperinflation (>10 posterior ribs visible, flat diaphragms)
• Peribronchial cuffing
• Usually NO consolidation (if present, consider infection, aspiration)
• Pneumothorax (complication)
• Pneumomediastinum (complication)
• Mucus plugging → segmental atelectasis

Venous Blood Gas

• Acceptable alternative for trend monitoring
• VBG PaCO₂ typically 5-8 mmHg higher than arterial
• Useful for serial assessments
• If VBG shows elevated CO₂ and low pH, obtain ABG for accurate values

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Initial Management

Immediate Resuscitation [26,27,28]

Algorithm

Clinical Pathway

Status Asthmaticus - Initial Management

Simultaneous Actions (First 15 minutes):

1. Oxygen:

   • High-flow oxygen via Hudson mask (15 L/min) if SpO₂ <92%
   • Target SpO₂ 92-95% (avoid hyperoxia)
   • Continuous pulse oximetry

2. Inhaled bronchodilators:

   • Continuous nebulised salbutamol 5 mg (can give back-to-back)
   • Add ipratropium bromide 500 mcg (single dose or q4h)
   • Oxygen-driven nebuliser (6-8 L/min)

3. Systemic corticosteroids:

   • IV hydrocortisone 200 mg, OR
   • IV methylprednisolone 60-125 mg, OR
   • PO prednisolone 50 mg (if can swallow)
   • Critical: Start within first hour

4. Monitoring:

   • Continuous ECG, SpO₂
   • Arterial blood gas
   • Establish IV access
   • Continuous reassessment

Bronchodilator Therapy [29,30]

Inhaled Short-Acting Beta-2 Agonists (SABA)

Salbutamol (Ventolin):

• Nebulised: 5 mg in 4 mL saline, driven by oxygen 6-8 L/min
• Continuous nebulisation: 5-10 mg/hour
• MDI with spacer: 4-8 puffs, repeat every 15-20 min (less effective if severe)

Mechanism:

• β₂-receptor agonist → adenylyl cyclase activation → ↑cAMP
• Bronchial smooth muscle relaxation
• Inhibition of mast cell mediator release
• Improved mucociliary clearance

Side effects:

• Tachycardia
• Tremor
• Hypokalaemia (monitor K⁺)
• Lactic acidosis (Type B)
• Arrhythmias (rare)

Inhaled Short-Acting Muscarinic Antagonist (SAMA)

Ipratropium bromide (Atrovent):

• Nebulised: 500 mcg with first 1-3 salbutamol doses
• MDI: 4-8 puffs

Mechanism:

• Muscarinic receptor (M3) antagonist
• Blocks vagally-mediated bronchoconstriction
• Additive effect with SABA in severe asthma
• Less effective than SABA as monotherapy

Systemic Corticosteroids [31,32]

Evidence:

• Reduce mortality, hospitalisation, and relapse
• Reduce airway inflammation and oedema
• Effect onset: 4-6 hours (not immediate)
• No evidence IV better than PO if can swallow

Dosing:

Duration: 5-7 days (weaning not required for short courses)

IV Magnesium Sulfate [33,34]

3Mg Trial (PMID: 23725650):

• IV MgSO₄ reduces hospital admission in severe acute asthma
• Improves PEF and FEV₁
• Safe with few side effects

Dosing:

• 2 g (8 mmol) IV over 20 minutes
• Can repeat once after 30-60 minutes if inadequate response

Mechanism:

• Calcium antagonist → bronchial smooth muscle relaxation
• Inhibits mast cell degranulation
• Inhibits acetylcholine release at neuromuscular junction

Side effects:

• Flushing, warmth
• Hypotension (if given too rapidly)
• Nausea
• Rarely: respiratory depression, hyporeflexia (if Mg >4 mmol/L)

Contraindications:

• Severe renal impairment (use with caution)
• Myasthenia gravis
• Heart block

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Escalation Therapies

IV Salbutamol [35,36]

Indication:

• Life-threatening asthma not responding to nebulised therapy
• Severe bronchospasm with poor air entry (drug not reaching airways)
• Bridge to intubation

Dosing:

• Loading: 200 mcg (4 mL of 50 mcg/mL) slow IV bolus
• Infusion: 5-20 mcg/min (start low, titrate to effect)
• Prepare: 5 mg in 500 mL 0.9% saline = 10 mcg/mL

Monitoring:

• Continuous ECG (arrhythmias)
• Serial potassium (hypokalaemia common - supplement aggressively)
• Lactate (Type B lactic acidosis expected)

Evidence:

• Limited evidence of benefit over continuous nebulisation [35]
• Reserved for patients with very poor air entry
• Watch for tachyarrhythmias and hypokalaemia

Aminophylline [37,38]

Cochrane Review (PMID: 11059434):

• No significant benefit in hospital stay or lung function when added to optimal SABA therapy
• Significantly increased adverse effects (nausea, vomiting, arrhythmias)
• Narrow therapeutic index

Use:

• Consider in refractory cases not responding to other therapies
• More useful in some patients with COPD-asthma overlap

Dosing:

• Loading: 5 mg/kg IV over 20-30 minutes (omit if taking oral theophylline)
• Maintenance: 0.5-0.7 mg/kg/hour infusion
• Check theophylline level at 4-6 hours (target 10-20 mg/L)

Toxicity:

• Narrow therapeutic index (10-20 mg/L)
• Nausea, vomiting
• Tachycardia, arrhythmias
• Seizures (at high levels)
• Drug interactions (CYP1A2)

Ketamine [39,40]

Mechanism:

• NMDA receptor antagonist
• Direct bronchial smooth muscle relaxation
• Sympathomimetic effects (catecholamine release)
• Maintains respiratory drive

Role in status asthmaticus:

• Induction agent for intubation (preserves bronchomotor tone)
• Continuous infusion as bronchodilator (limited evidence)
• Sedation with bronchodilatory properties

Dosing:

• Induction: 1-2 mg/kg IV
• Infusion: 0.5-2 mg/kg/hour (for sedation/bronchodilation)

Evidence:

• Limited RCT evidence in adults
• Case series suggest benefit in refractory cases [39]
• Low side effect profile in ICU setting
• Consider early in patients with refractory bronchospasm

Side effects:

• Hypersecretion (may worsen mucus plugging - consider antisialagogue)
• Emergence phenomena (less relevant in ICU with ongoing sedation)
• Tachycardia, hypertension

Heliox [41,42]

Mechanism:

• Helium-oxygen mixture (typically 70:30 or 80:20)
• Low density → promotes laminar flow in narrow airways
• Reduces work of breathing
• May improve nebuliser drug delivery

Evidence:

• Cochrane review (PMID: 16855961): Limited evidence
• May improve PEF and reduce dyspnoea
• Greatest benefit in severe obstruction with turbulent flow
• Bridge to allow time for steroids to work

Limitations:

• Cannot use high FiO₂ (helium must be >60% for effect)
• Requires specific delivery system
• Not widely available in all ICUs
• Expensive

Volatile Anaesthetic Agents [43,44]

Agents: Sevoflurane, isoflurane

Mechanism:

• Direct bronchial smooth muscle relaxation
• Reduce airway responsiveness
• Potent bronchodilators

Use:

• Rescue therapy in refractory bronchospasm
• Requires anaesthetic machine or specialised ICU vaporiser
• Gas scavenging system required

Evidence:

• Case reports and series show benefit in refractory cases
• No RCT evidence

Practical issues:

• Requires specialised equipment
• Pollution concerns (scavenging)
• Need for experienced staff
• Cardiovascular effects (hypotension)

ECMO [45,46,47]

Indications:

• Refractory hypercapnic respiratory failure despite optimal ventilation
• Life-threatening acidosis (pH <7.15) not responding to therapy
• Haemodynamic collapse from auto-PEEP
• Impending cardiac arrest

Evidence:

• ELSO registry (PMID: 24713915): ~83% survival in asthma patients
• Highest survival of all ECMO indications due to reversibility
• VV-ECMO for respiratory failure
• VA-ECMO if cardiac arrest/severe haemodynamic compromise

Key points:

• Asthma is an excellent ECMO indication (reversible disease)
• Early consideration in refractory cases
• Allows "lung rest" while bronchospasm and inflammation resolve
• Often rapid weaning once asthma controlled

Australian context:

• ECMO retrieval services available (Victoria, NSW, Queensland)
• Contact early if considering ECMO
• Transport logistics for regional patients

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Mechanical Ventilation

Decision to Intubate [48,49]

Indications for intubation:

• Respiratory arrest or impending arrest
• Deteriorating conscious level (hypercapnic encephalopathy)
• Exhaustion with rising PaCO₂ despite maximal therapy
• Severe hypoxaemia (SpO₂ <85%) despite high-flow oxygen
• Haemodynamic instability

Caution:

• Intubation in status asthmaticus is HIGH RISK
• May precipitate cardiac arrest from auto-PEEP
• Senior airway management essential
• Have plan for post-intubation hypotension

Intubation Technique [50]

Clinical Pearl: #### Safe Intubation in Status Asthmaticus

Pre-intubation:

1. Senior, experienced operator (consultant-level if possible)
2. Preoxygenation (if patient tolerates)
3. IV access, fluids running
4. Vasopressor ready (push-dose adrenaline)
5. Consider manual ventilation to assess resistance before paralysis

Induction:

• Ketamine 1-2 mg/kg IV (bronchodilator, maintains BP) - preferred
• OR propofol 1-2 mg/kg (risk of hypotension)
• Rocuronium 1.2 mg/kg (rapid paralysis, can reverse with sugammadex)
• Avoid suxamethonium if hyperkalaemic (rare in asthma)

During intubation:

• Use 7.5-8.0 mm ETT (allows bronchoscopy if needed for mucus plugs)
• Confirm placement with capnography

Immediately post-intubation:

1. Start with conservative settings (RR 8-10, low VT)
2. Allow prolonged expiration
3. Monitor for hypotension (common - auto-PEEP)
4. If hypotensive: disconnect from circuit 20-30 seconds
5. Consider push-dose adrenaline 10-20 mcg if hypotensive

Ventilator Settings [51,52,53]

Exam Detail: #### Mechanical Ventilation Strategy in Status Asthmaticus

Goals:

1. Maintain oxygenation (SpO₂ 88-92%)
2. Minimise dynamic hyperinflation and auto-PEEP
3. Accept permissive hypercapnia
4. Avoid barotrauma

Recommended Settings:

Pressure Targets:

Inspiratory Flow Rate and Waveform

High inspiratory flow (80-100 L/min):

• Shortens inspiratory time (Ti)
• Lengthens expiratory time (Te)
• Allows more time for exhalation
• May increase peak pressure (but not plateau)

Square (constant) vs decelerating waveform:

• Square waveform: Shorter Ti for given VT
• Decelerating: More even distribution, but longer Ti
• Either acceptable; focus on ensuring adequate Te

Permissive Hypercapnia [54,55]

Rationale:

• Accepting high PaCO₂ allows lower minute ventilation
• Lower MV → less air trapping → less auto-PEEP → less haemodynamic compromise and barotrauma

Acceptable targets:

• PaCO₂: Up to 80-100 mmHg (some cases higher)
• pH: Down to 7.15-7.20 (lower if slowly rising and stable)
• Avoid rapid changes

Buffering:

• Generally NOT recommended
• Sodium bicarbonate may worsen CO₂ (paradoxical intracellular acidosis)
• Consider only if pH <7.10 and haemodynamic instability
• THAM (tris-hydroxymethyl aminomethane) is alternative buffer

Contraindications to severe hypercapnia:

• Raised intracranial pressure
• Severe cardiac arrhythmias
• Pregnancy (relative - avoid fetal acidosis)

PEEP Management

External PEEP in asthma - controversial:

Recommendation:

• Start with PEEP 0-5 cmH₂O
• Measure auto-PEEP
• If auto-PEEP high, focus on reducing minute ventilation first
• In paralysed patient: minimize external PEEP
• In spontaneously breathing: some external PEEP may help overcome triggering threshold

Monitoring During Ventilation [56]

Continuous:

• Airway pressures (peak, plateau)
• Waveforms (flow, pressure)
• SpO₂, EtCO₂
• Haemodynamics

Periodic:

• Auto-PEEP (end-expiratory hold) - at least hourly during acute phase
• ABG (every 1-4 hours based on severity)
• Electrolytes (K⁺, Mg²⁺) - every 4-6 hours

Waveform analysis:

Post-Intubation Hypotension [57]

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Complications

Barotrauma [58,59]

Pneumothorax:

• Occurs in 5-10% of ventilated asthmatics
• High risk due to hyperinflation
• May present as sudden deterioration, hypotension
• Tension pneumothorax mimics auto-PEEP haemodynamically

Signs:

• Sudden rise in peak and plateau pressures
• Haemodynamic instability
• Asymmetric chest movement/air entry
• Subcutaneous emphysema

Management:

• High index of suspicion
• Immediate needle decompression if unstable
• Chest drain insertion

Pneumomediastinum:

• Air tracking along bronchovascular bundles
• Often benign, may not require intervention
• CXR: lucent line along mediastinum
• May present with chest pain, neck swelling

Myopathy [60,61]

Acute Quadriplegic Myopathy (Critical Illness Myopathy):

• Risk factors: corticosteroids + NMBAs
• Flaccid weakness, often diffuse
• Elevated CK (variable)
• EMG/NCS for diagnosis

Prevention:

• Minimise NMBA use (first 24-48 hours only if needed)
• Avoid prolonged high-dose steroids
• Early mobilisation when stable

ICU-Acquired Weakness:

• Combination of CIP (polyneuropathy) and CIM (myopathy)
• May prolong weaning and rehabilitation
• Monitor with daily sedation holds and weakness assessment

Arrhythmias [62]

Risk factors:

• Hypokalaemia (β-agonists, steroids)
• Hypoxaemia
• β-agonist toxicity
• Aminophylline toxicity
• Pre-existing cardiac disease

Common arrhythmias:

• Sinus tachycardia (most common, usually benign)
• Atrial fibrillation/flutter
• Ventricular ectopy
• VT (rare, usually with severe electrolyte disturbance)

Management:

• Correct hypokalaemia aggressively (target K⁺ >4.0 mmol/L)
• Correct hypomagnesaemia
• Reduce β-agonist dose if significant tachyarrhythmia
• Avoid aminophylline if arrhythmias

Lactic Acidosis [25]

Mechanism:

• β₂-agonists stimulate Na⁺/K⁺-ATPase and glycolysis
• Increased lactate production (Type B lactic acidosis)
• NOT due to tissue hypoperfusion

Characteristics:

• Lactate often 4-8 mmol/L with IV salbutamol
• Patient haemodynamically stable
• Normal/supranormal cardiac output
• Resolves with cessation of β-agonists

Pitfall:

• Do NOT fluid resuscitate for β-agonist-induced lactate
• Do NOT assume shock based on lactate alone
• Assess perfusion clinically

Hypokalaemia [63]

Mechanism:

• β₂-agonists activate Na⁺/K⁺-ATPase → intracellular K⁺ shift
• Corticosteroids → renal K⁺ loss
• Can be severe and rapid

Management:

• Monitor K⁺ every 2-4 hours during aggressive therapy
• Replace aggressively (40-80 mmol over 2-4 hours via central line if severe)
• Target K⁺ >4.0 mmol/L in ICU

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Weaning from Mechanical Ventilation [64,65]

Prerequisites for Weaning

Clinical improvement:

• Reduced wheeze on auscultation
• Decreasing peak and plateau pressures
• Decreasing auto-PEEP (<5 cmH₂O)
• Improving ABG (resolving respiratory acidosis)
• Able to trigger ventilator appropriately

Resolution of dynamic hyperinflation:

• Flow returning to zero before next breath (on waveform)
• Able to tolerate lower inspiratory flow without air trapping
• Expiratory time constant normalising

Weaning Strategy

Spontaneous Breathing Trials (SBT):

• PSV 5-8 cmH₂O + PEEP 5 cmH₂O
• Or T-piece trial
• Duration 30-120 minutes

Criteria for successful SBT:

• RR <30, no distress
• SpO₂ ≥92%
• Haemodynamically stable
• No significant increase in wheeze

Extubation considerations:

• May require ongoing bronchodilators post-extubation
• NIV post-extubation in selected cases
• Continue steroids for 5-7 day course
• Early mobilisation

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Prognosis and Outcomes [66,67,68]

Mortality

Predictors of Poor Outcome

• Previous near-fatal asthma or ICU admission
• Delayed presentation or treatment
• Older age and comorbidities
• Longer duration of mechanical ventilation
• Development of MODS
• Pneumothorax or other barotrauma

Long-Term Outcomes

• 50-70% have persistent symptoms at 1 year
• 30% have reduced lung function
• High risk of recurrence if triggers not addressed
• Psychological impact (anxiety, PTSD) common
• ICU-acquired weakness may affect rehabilitation

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Australian Guidelines

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SAQ Practice Questions

SAQ 1: Mechanical Ventilation in Status Asthmaticus (15 marks)

Stem: A 28-year-old woman with a history of asthma is intubated in the Emergency Department for status asthmaticus after failing to respond to nebulised bronchodilators, IV corticosteroids, and IV magnesium. She has become increasingly drowsy with an ABG showing pH 7.18, PaCO₂ 85 mmHg, PaO₂ 72 mmHg on FiO₂ 0.6.

Post-intubation, she becomes hypotensive with BP 70/40 mmHg.

Questions:

a) What is the most likely cause of post-intubation hypotension in this patient? (2 marks)

b) Describe your immediate management of this hypotensive episode. (3 marks)

c) Outline the optimal ventilator settings for mechanical ventilation in status asthmaticus. (5 marks)

d) Define permissive hypercapnia and explain its rationale in this condition. (3 marks)

e) How would you monitor for and quantify auto-PEEP? (2 marks)

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Model Answer:

a) Cause of post-intubation hypotension (2 marks)

The most likely cause is dynamic hyperinflation with auto-PEEP (intrinsic PEEP) leading to:

• Increased intrathoracic pressure
• Reduced venous return to the right heart
• Decreased cardiac output
• Hypotension

Other causes to consider:

• Tension pneumothorax (barotrauma)
• Induction agent effects (propofol)
• Pre-existing hypovolaemia
• Anaphylaxis (rare)

b) Immediate management of hypotension (3 marks)

1. Disconnect the patient from the ventilator circuit for 20-30 seconds

   • Allow complete passive exhalation
   • Relieves auto-PEEP and restores venous return
   • Observe for blood pressure recovery

2. If blood pressure improves:

   • Confirms auto-PEEP as cause
   • Reconnect with more conservative ventilator settings
   • Lower respiratory rate, lower tidal volume, longer expiratory time

3. If blood pressure does NOT improve:

   • Consider bilateral needle decompression for tension pneumothorax
   • Administer push-dose adrenaline 10-20 mcg IV
   • Fluid bolus (cautiously)
   • Arrange CXR when stable

c) Optimal ventilator settings (5 marks)

Targets:

• Plateau pressure <30 cmH₂O (NOT peak pressure)
• Auto-PEEP <10 cmH₂O (ideally <5)
• Accept elevated PaCO₂

d) Permissive hypercapnia (3 marks)

Definition: Permissive hypercapnia is a ventilatory strategy that deliberately accepts elevated arterial carbon dioxide levels (PaCO₂) to avoid the harmful effects of aggressive mechanical ventilation.

Targets:

• PaCO₂: Accept up to 80-100 mmHg (even higher in some cases)
• pH: Accept down to 7.15-7.20

Rationale:

1. Lower minute ventilation reduces dynamic hyperinflation and auto-PEEP
2. Less auto-PEEP → reduced risk of barotrauma
3. Less auto-PEEP → improved haemodynamics (better venous return)
4. Avoids excessively high airway pressures
5. The underlying disease is reversible - patient will eventually clear CO₂ once bronchospasm resolves

Contraindications:

• Raised intracranial pressure
• Severe cardiac arrhythmias
• Pregnancy (relative)

e) Monitoring and quantifying auto-PEEP (2 marks)

End-expiratory hold manoeuvre:

1. Ensure patient is deeply sedated/paralysed (no spontaneous respiratory effort)
2. Press "expiratory hold" button on ventilator
3. Hold for 2-3 seconds to allow pressure equilibration
4. Read the total PEEP displayed

Calculation: Auto-PEEP = Total PEEP (measured) - Set PEEP (external)

Example:

• Set PEEP: 5 cmH₂O
• Total PEEP on hold: 18 cmH₂O
• Auto-PEEP: 18 - 5 = 13 cmH₂O

Additional monitoring:

• Observe expiratory flow waveform - flow should return to zero before next breath
• If flow does not reach zero = incomplete exhalation = air trapping

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SAQ 2: Escalation Therapy in Refractory Status Asthmaticus (15 marks)

Stem: A 35-year-old male with severe asthma is admitted to ICU intubated and ventilated. Despite optimised ventilation with permissive hypercapnia (RR 8, VT 350 mL, I:E 1:4), continuous nebulised salbutamol, IV hydrocortisone, and IV magnesium sulfate, he remains severely bronchospastic with plateau pressures of 35 cmH₂O, auto-PEEP of 20 cmH₂O, and pH 7.08 with PaCO₂ 130 mmHg.

Questions:

a) List four escalation therapies you would consider in this patient. (4 marks)

b) For IV salbutamol, describe the dosing, administration, and monitoring requirements. (3 marks)

c) Describe the role and evidence for ketamine in refractory status asthmaticus. (3 marks)

d) What is the role of ECMO in status asthmaticus? What outcomes would you expect? (3 marks)

e) What complications would you monitor for in this patient receiving aggressive beta-agonist therapy? (2 marks)

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Model Answer:

a) Four escalation therapies (4 marks)

1. IV salbutamol - Continuous infusion to bypass poor inhaled drug delivery in severely obstructed airways

2. IV aminophylline - Phosphodiesterase inhibitor; narrow therapeutic index, limited evidence but may be tried in refractory cases

3. Ketamine - NMDA receptor antagonist with bronchodilatory properties; useful for sedation and as adjunct bronchodilator

4. Heliox - Helium-oxygen mixture (70:30 or 80:20); reduces turbulent flow and work of breathing; may improve drug delivery

5. Volatile anaesthetic agents - Sevoflurane or isoflurane; potent bronchodilators; require anaesthetic machine or specialised vaporiser

6. ECMO - Extracorporeal membrane oxygenation for refractory respiratory failure; allows lung rest while disease resolves

b) IV salbutamol dosing and monitoring (3 marks)

Dosing:

• Loading dose: 200 mcg (4 mL of 50 mcg/mL) slow IV bolus over 2-3 minutes
• Infusion: 5-20 mcg/min
• Preparation: 5 mg in 500 mL 0.9% saline = 10 mcg/mL
• Titrate to effect (clinical response, wheeze reduction)

Monitoring:

• Continuous ECG (tachyarrhythmias)
• Serial potassium every 2-4 hours (severe hypokalaemia expected)
• Serial lactate (Type B lactic acidosis expected)
• Blood glucose (hyperglycaemia)
• Clinical response (breath sounds, plateau pressures, auto-PEEP)

Administration:

• Via central venous catheter if available
• Separate line or compatibility confirmed
• Do not stop abruptly - wean when improving

c) Ketamine in refractory status asthmaticus (3 marks)

Mechanism:

• NMDA receptor antagonist
• Direct bronchial smooth muscle relaxation (independent of beta-receptors)
• Sympathomimetic effects (catecholamine release) → bronchodilation
• Maintains respiratory drive (unlike other sedatives)
• Analgesic properties

Role:

• Induction agent for intubation (preferred in asthma - maintains bronchomotor tone)
• Continuous infusion for sedation with bronchodilatory benefit
• Adjunct therapy in refractory bronchospasm

Evidence:

• Limited RCT evidence in adults (mostly case series)
• PMID: 24108241 - Case series showing benefit in children
• Generally considered safe in ICU setting
• Reasonable option given favourable side effect profile

Dosing:

• Induction: 1-2 mg/kg IV
• Infusion: 0.5-2 mg/kg/hour

Considerations:

• Hypersecretion (may worsen mucus plugging) - consider glycopyrrolate
• Emergence phenomena (less relevant with ongoing sedation)

d) Role of ECMO and expected outcomes (3 marks)

Role:

• VV-ECMO (veno-venous) for refractory hypercapnic respiratory failure
• Provides oxygenation and CO₂ removal independent of lungs
• Allows "lung rest" with very low ventilator settings
• Buys time for bronchospasm and inflammation to resolve

Indications in status asthmaticus:

• Refractory hypercapnic acidosis (pH <7.15) despite optimal ventilation
• Haemodynamic instability from auto-PEEP
• Barotrauma or impending barotrauma
• Impending or actual cardiac arrest

Expected outcomes:

• Survival approximately 83% (ELSO registry, PMID: 24713915)
• One of the highest survival rates among all ECMO indications
• Excellent outcomes due to reversible nature of disease
• Often rapid weaning once bronchospasm controlled (days)
• Most patients make full recovery

Australian context:

• ECMO retrieval services available in major centres
• Early contact with ECMO service (Victoria, NSW, Queensland)

e) Complications of aggressive beta-agonist therapy (2 marks)

1. Hypokalaemia

   • β₂-agonists activate Na⁺/K⁺-ATPase → intracellular K⁺ shift
   • Can be severe and rapid (K⁺ <2.5 mmol/L)
   • Risk of arrhythmias
   • Requires aggressive replacement (target K⁺ >4.0 mmol/L)

2. Lactic acidosis (Type B)

   • β₂-agonists stimulate glycolysis
   • Lactate levels 4-8 mmol/L common
   • Does NOT indicate tissue hypoperfusion
   • Resolves with cessation of salbutamol

3. Tachyarrhythmias

   • Sinus tachycardia (common, usually benign)
   • Atrial fibrillation
   • Ventricular ectopy (more concerning)
   • May require dose reduction

4. Tremor - Usually not clinically significant in sedated patient

5. Hyperglycaemia - Monitor blood glucose

---

Hot Case Scenarios

Hot Case 1: Ventilated Asthmatic with High Airway Pressures

Setting: ICU bed space with ventilated patient

Stem: A 32-year-old female with a history of severe asthma was intubated 6 hours ago in the Emergency Department for status asthmaticus. She is receiving continuous salbutamol nebulisers, IV hydrocortisone, and IV magnesium. She is sedated with propofol and fentanyl.

The nursing staff are concerned because the ventilator is alarming with high peak pressures.

Candidate Instructions: You have 20 minutes to assess this patient and discuss your findings and management with the examiners.

---

Expected Approach:

A - Airway:

• ETT 7.5 mm, well-secured, at 22 cm at teeth
• Check for kinking, obstruction
• Listen for leak around cuff

B - Breathing:

• Ventilator settings: VC, VT 450 mL, RR 12, PEEP 5, FiO₂ 0.4
• Peak pressure: 55 cmH₂O, Plateau pressure: 28 cmH₂O
• Auscultation: Bilateral wheeze, reduced air entry throughout
• SpO₂ 94%

Key observations:

• High peak pressure (55) but acceptable plateau pressure (28) = high resistance
• The plateau is the critical parameter for barotrauma risk
• Peak-plateau gap indicates airway resistance (bronchospasm)

C - Circulation:

• HR 120 sinus, BP 95/60 mmHg
• Lactate 5.2 mmol/L
• K⁺ 2.9 mmol/L
• Peripheral perfusion satisfactory

D - Disability:

• Sedated on propofol 200 mg/hr, fentanyl 100 mcg/hr
• RASS -4

E - Exposure:

• Temperature 37.2°C
• CXR: Hyperinflated, no pneumothorax

Additional Assessment:

• Perform end-expiratory hold: Auto-PEEP 15 cmH₂O (elevated)
• Check expiratory flow waveform: Flow not returning to zero

---

Discussion Points:

Examiner: "What is your assessment of this patient?"

Candidate: "This is a 32-year-old woman with life-threatening asthma requiring mechanical ventilation. Currently, she has evidence of ongoing severe bronchospasm with:

• High peak inspiratory pressure (55 cmH₂O) but acceptable plateau pressure (28 cmH₂O) - indicating high airway resistance rather than poor compliance
• Significant auto-PEEP of 15 cmH₂O indicating dynamic hyperinflation
• Incomplete expiration on flow waveform

She has complications of therapy including:

• Hypokalaemia (2.9 mmol/L) from beta-agonist therapy
• Lactic acidosis (5.2 mmol/L) - likely Type B from salbutamol, not tissue hypoxia given adequate perfusion

My priorities are:

1. Correct the hypokalaemia urgently
2. Optimise ventilation to reduce auto-PEEP
3. Continue and escalate bronchodilator therapy"

Examiner: "How would you optimise the ventilator settings?"

Candidate: "I would reduce minute ventilation to allow more time for expiration:

• Reduce respiratory rate from 12 to 8-10/min
• Maintain or reduce tidal volume (6-8 mL/kg IBW)
• Increase inspiratory flow rate to 80-100 L/min
• Accept an I:E ratio of 1:3 to 1:5
• Consider reducing PEEP to 0-3 cmH₂O

I would accept permissive hypercapnia - aiming for pH >7.15-7.20 rather than normalising PaCO₂.

I would repeat the end-expiratory hold manoeuvre to confirm improvement in auto-PEEP."

Examiner: "The patient suddenly becomes hypotensive with BP 65/40 mmHg. What do you do?"

Candidate: "This is most likely due to worsening auto-PEEP causing reduced venous return, OR a tension pneumothorax. My immediate action would be:

1. Disconnect the patient from the ventilator for 20-30 seconds

   • Allow complete passive exhalation
   • Observe for blood pressure recovery

2. If blood pressure recovers → confirms auto-PEEP

   • Reconnect with more conservative settings
   • Further reduce respiratory rate

3. If blood pressure does NOT recover:

   • Perform bilateral needle decompression (2nd ICS MCL)
   • Give push-dose adrenaline 10-20 mcg IV
   • Arrange urgent portable CXR"

---

Hot Case 2: Deteriorating Asthmatic Pre-Intubation

Setting: ICU resuscitation bay

Stem: A 45-year-old Indigenous man from a remote community has been transferred by RFDS for severe asthma. He has been receiving continuous nebulised salbutamol, IV hydrocortisone, and IV magnesium for the past 4 hours but is deteriorating.

He is sitting upright, using accessory muscles, and can only speak single words.

Candidate Instructions: You have 20 minutes to assess this patient and discuss your management with the examiners.

---

Expected Approach:

Initial Assessment:

• Patient in extremis, tripod position, profoundly dyspnoeic
• Speaking in single words only
• Accessory muscle use (SCM, intercostals prominent)
• Diaphoretic, appears exhausted

Observations:

• RR 35, HR 135 sinus, BP 140/90 mmHg
• SpO₂ 88% on 15 L Hudson mask
• Temperature 37.5°C

Examination:

• Minimal wheeze (silent chest) - ominous
• Poor air entry bilaterally
• Alert but becoming drowsy

ABG:

• pH 7.22, PaCO₂ 65 mmHg, PaO₂ 55 mmHg, HCO₃ 26 mmol/L, lactate 4.5 mmol/L

Assessment: "This patient has near-fatal asthma with:

• Life-threatening features: silent chest, SpO₂ <92%, drowsiness
• Rising PaCO₂ (65 mmHg) - respiratory failure
• Respiratory acidosis (pH 7.22)
• He requires urgent intubation"

---

Discussion Points:

Examiner: "Describe how you would intubate this patient."

Candidate: "Intubation in status asthmaticus is high-risk. I would:

Preparation:

• Senior airway operator (myself or most experienced available)
• Standard difficult airway equipment
• Vasopressor ready (push-dose adrenaline 10-20 mcg)
• IV fluids running
• Plan for post-intubation hypotension

Preoxygenation:

• Attempt preoxygenation if patient tolerates (may not)
• Consider high-flow nasal oxygen during intubation

Induction:

• Ketamine 1.5-2 mg/kg IV - preferred for bronchodilator properties and haemodynamic stability
• Rocuronium 1.2 mg/kg IV - rapid paralysis

Intubation:

• Direct or video laryngoscopy
• Size 7.5-8.0 ETT
• Confirm with capnography

Post-intubation:

• Conservative initial ventilator settings: RR 8, VT 6-8 mL/kg, high flow
• Anticipate hypotension - be ready to disconnect circuit
• Deep sedation to prevent dyssynchrony"

Examiner: "What cultural considerations are important for this patient?"

Candidate: "As an Indigenous man from a remote community, important considerations include:

1. Involve family - Aboriginal families often make decisions collectively; involve family in discussions about prognosis and treatment

2. Aboriginal Health Worker/Liaison Officer - Contact the ALO to facilitate communication and cultural support

3. Communication - He may speak English as a second or third language; use interpreter services if needed; speak clearly and check understanding

4. Cultural safety - Acknowledge cultural practices; some communities have specific beliefs about illness and healing

5. Remote community context - He may have limited access to regular healthcare and medications; assess barriers to preventer therapy adherence

6. Follow-up planning - Ensure culturally appropriate discharge planning with community health services; involve Aboriginal Medical Service if available

7. Sorry business - If prognosis is poor, understand that large numbers of family may need to visit; accommodate this"

Examiner: "What specific challenges might have led to this presentation?"

Candidate: "Several factors may contribute:

1. Access to healthcare - Remote communities have limited access to specialist care, emergency services, and medications

2. Preventer therapy adherence - May be challenging due to cost, supply issues, or health literacy

3. Delayed presentation - Distance from hospital, limited transport, competing priorities

4. Environmental triggers - Dust, smoke from cultural burning, overcrowded housing

5. Comorbidities - Higher rates of smoking, obesity, and other chronic diseases in Indigenous populations

6. Social determinants - Poverty, housing quality, and other social factors affecting health

These factors contribute to the 1.7× higher asthma hospitalisation rates in Aboriginal and Torres Strait Islander peoples. Addressing them requires a whole-of-system approach including community-based programs, Aboriginal Medical Services, and culturally appropriate education."

---

Viva Scenarios

Viva 1: Pathophysiology of Dynamic Hyperinflation

Examiner: "Can you explain the pathophysiology of dynamic hyperinflation in severe asthma?"

Candidate: "Dynamic hyperinflation occurs when there is insufficient time for complete exhalation between breaths, leading to progressive air trapping and increased end-expiratory lung volume above functional residual capacity.

In severe asthma, three factors increase airway resistance:

1. Bronchospasm - smooth muscle contraction
2. Mucosal inflammation and oedema
3. Mucus plugging

This markedly increases the expiratory time constant (tau = resistance × compliance). Normally, it takes 3 time constants to exhale 95% of tidal volume. In severe asthma, the time constant is so prolonged that standard respiratory rates don't allow complete exhalation."

Examiner: "What are the consequences of dynamic hyperinflation?"

Candidate: "There are several important consequences:

Respiratory:

• Increased work of breathing - the patient breathes on the flat portion of the compliance curve
• Respiratory muscle fatigue
• V/Q mismatch

Haemodynamic:

• The positive alveolar pressure at end-expiration (auto-PEEP) increases intrathoracic pressure
• This reduces venous return to the right heart
• It also increases right ventricular afterload by compressing pulmonary vessels
• The net effect is reduced cardiac output and hypotension
• This is why patients may arrest at or shortly after intubation

Barotrauma:

• Alveolar overdistension increases risk of pneumothorax and pneumomediastinum

Clinical signs:

• Pulsus paradoxus - exaggerated BP variation with respiration due to swing in pleural pressure"

Examiner: "How do you measure auto-PEEP at the bedside?"

Candidate: "I would measure auto-PEEP using the end-expiratory hold manoeuvre:

1. Ensure the patient is deeply sedated or paralysed - no spontaneous respiratory effort
2. Press the 'expiratory hold' button on the ventilator
3. Wait 2-3 seconds for pressure equilibration throughout the respiratory system
4. Read the pressure displayed - this is the total PEEP

Auto-PEEP = Total PEEP - Set (external) PEEP

For example, if set PEEP is 5 cmH₂O and total PEEP is 18 cmH₂O, auto-PEEP is 13 cmH₂O.

I would also look at the flow-time waveform - if the expiratory flow doesn't return to zero before the next breath, this indicates incomplete exhalation and air trapping."

Examiner: "How would you manage a patient with significant auto-PEEP?"

Candidate: "My approach would focus on reducing minute ventilation to allow more time for exhalation:

1. Reduce respiratory rate - often to 8-10/min or even lower
2. Keep tidal volume low - 6-8 mL/kg ideal body weight
3. Increase inspiratory flow - 80-100 L/min to shorten inspiratory time
4. Adjust I:E ratio - aim for 1:3 to 1:5
5. Minimise set PEEP - usually 0-5 cmH₂O
6. Accept permissive hypercapnia - pH down to 7.15-7.20

I would monitor the effect of these changes by repeating the end-expiratory hold and observing the flow waveform. The goal is to see flow returning to zero before the next breath."

---

Viva 2: Escalation Therapy Decision-Making

Examiner: "A patient with status asthmaticus is not responding to standard therapy. What escalation options would you consider and in what order?"

Candidate: "After optimising standard therapy (continuous nebulised salbutamol, ipratropium, IV steroids, IV magnesium), I would consider escalation in approximately this order:

First-line escalation:

1. IV salbutamol - 200 mcg loading then 5-20 mcg/min infusion. This bypasses the poor drug delivery in severely obstructed airways.

Second-line options: 2. Ketamine - either for induction if intubation needed, or as infusion for sedation with bronchodilatory properties. Good safety profile.

3. Aminophylline - 5 mg/kg loading then 0.5-0.7 mg/kg/hr infusion. Limited evidence but sometimes helps. Need to monitor levels.

4. Heliox - if available, can reduce work of breathing and improve drug delivery. Limited by inability to give high FiO₂.

Rescue therapies: 5. Volatile anaesthetic agents - sevoflurane or isoflurane if available. Requires specialised equipment.

6. ECMO - for refractory hypercapnic respiratory failure. Should be considered early as asthma has excellent ECMO outcomes (83% survival)."

Examiner: "What is the evidence for IV magnesium in acute severe asthma?"

Candidate: "The key evidence comes from the 3Mg Trial (PMID: 23725650), a UK-based factorial RCT of 1,109 patients.

Key findings:

• IV magnesium sulfate 2 g over 20 minutes
• Improved lung function (PEF and FEV₁) compared to placebo
• Did not significantly reduce hospital admissions overall
• BUT showed benefit in patients with more severe exacerbations

Cochrane review (PMID: 24115140):

• Concluded IV magnesium reduces hospital admissions in severe acute asthma
• Safe with few side effects

Mechanism:

• Calcium antagonist - inhibits calcium-mediated smooth muscle contraction
• Inhibits mast cell degranulation
• May potentiate beta-agonist effects

Current practice:

• Recommended in life-threatening asthma and those not responding to initial therapy
• Dose: 2 g IV over 20 minutes, can repeat once
• Watch for hypotension if given too quickly"

Examiner: "When would you consider ECMO and what outcomes would you quote?"

Candidate: "I would consider ECMO in the following scenarios:

Indications:

• Refractory hypercapnic respiratory failure with severe acidosis (pH <7.15) despite optimal ventilation
• Unable to ventilate safely - plateau pressures or auto-PEEP remain dangerously high
• Haemodynamic instability from severe auto-PEEP
• Cardiac arrest or peri-arrest from respiratory failure

Contraindications to consider:

• Relative: prolonged arrest with hypoxic brain injury, severe comorbidities, advanced age

Outcomes: The ELSO registry data (PMID: 24713915) shows approximately 83% survival for asthma patients on ECMO. This is one of the highest survival rates of any ECMO indication.

Reasons for good outcomes:

1. Asthma is a reversible disease - once bronchospasm and inflammation resolve, lung function can return to normal
2. Typically younger patients with fewer comorbidities
3. No parenchymal lung destruction (unlike ARDS)
4. Often rapid weaning from ECMO (days rather than weeks)

Practical considerations in Australia:

• Contact ECMO retrieval service early (before patient arrests)
• VV-ECMO usually sufficient unless cardiac arrest
• Can cannulate peripherally in most cases
• Melbourne, Sydney, Brisbane, Adelaide, Perth have ECMO services"

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Z context)? Back: Higher asthma prevalence and hospitalisation rates. Involve whānau (extended family) in care discussions. Utilise Māori Health Workers for cultural support. Respect tikanga (cultural protocols), especially in end-of-life care.

Card 44

Front: What is the typical duration of corticosteroid therapy after an asthma exacerbation? Back: 5-7 days. No taper required for short courses. Continue same dose throughout (e.g., prednisolone 50 mg daily).

Card 45

Front: What should you do if a ventilated asthmatic has rising peak pressures but stable plateau pressures? Back: Stable plateau pressure means alveolar pressure is safe. Rising peak pressure indicates worsening AIRWAY RESISTANCE (bronchospasm or mucus plug). Actions: increase bronchodilators, consider suction/bronchoscopy for mucus, check ETT position/patency.

---

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Cross-References

Prerequisites

• Respiratory Physiology
• Mechanical Ventilation Modes
• Ventilator Waveforms

Related Topics

• ARDS
• Non-Invasive Ventilation
• VV-ECMO
• Difficult Airway Management
• Anaphylactic Shock

Complications

• ICU-Acquired Weakness
• Pneumothorax

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Last updated: January 2026 Citation Count: 52 PubMed PMIDs Lines: 1,687