Intraoperative Bronchospasm - Recognition and Management

Quick Answer

Immediate Recognition:

• Rising peak airway pressure (>30 cmH₂O with plateau pressure unchanged suggests bronchospasm)
• Expiratory wheeze (may be absent in severe bronchospasm = "silent chest")
• Decreased tidal volume delivery
• Prolonged expiratory phase
• Decreasing SpO2, rising EtCO2

Immediate Management (ABCD Approach):

A - Airway/Breathing:

1. Increase FiO2 to 100%
2. Deepen anaesthesia (propofol 1-2 mg/kg or volatile agent)
3. Switch to manual ventilation - assess compliance, listen for wheeze
4. Salbutamol 100 mcg (1 puff) IV or MDI via ETT adapter (5-10 puffs = 500-1000 mcg)
5. Consider IV salbutamol 10-20 mcg bolus if inhaled therapy ineffective

B - Pharmacological Escalation:

1. Magnesium sulfate 2g IV over 10-20 minutes (smooth muscle relaxant)
2. Ketamine 0.5-1 mg/kg IV (bronchodilator properties)
3. Hydrocortisone 200mg IV (anti-inflammatory, delayed effect 4-6 hours)
4. Epinephrine 10-20 mcg IV boluses (if severe/refractory)

C - Mechanical Ventilation Strategy:

1. Increase expiratory time (I:E ratio 1:3 to 1:5)
2. Decrease respiratory rate (8-10 breaths/min)
3. Permissive hypercapnia (allow PaCO2 50-70 mmHg if necessary)
4. Increase inspiratory flow rate (50-70 L/min)
5. Consider pressure-controlled ventilation

D - Differential Diagnosis & Definitive:

1. Exclude anaphylaxis, pulmonary edema, pneumothorax, aspiration, equipment malfunction
2. If life-threatening: IV epinephrine infusion 0.05-0.5 mcg/kg/min
3. Consider volatile agent bronchodilation (sevoflurane/isoflurane)
4. Emergency ICU admission if refractory

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Indigenous Health Considerations

Intraoperative bronchospasm management presents unique challenges for Aboriginal, Torres Strait Islander, and Māori patients, who experience disproportionate rates of respiratory disease and asthma-related complications. For Aboriginal and Torres Strait Islander peoples, asthma prevalence is 18% compared to 11% in non-Indigenous Australians, with significantly higher hospitalisation rates for acute exacerbations. Remote Indigenous communities face additional barriers including limited access to specialist respiratory care, poor asthma control due to medication adherence challenges, and higher rates of smoking-related chronic bronchitis that complicates perioperative airway management.

Cultural safety considerations are essential when managing acute bronchospasm crises. Indigenous patients may present with advanced disease due to delayed diagnosis and reduced access to preventive care. Communication during crisis situations requires sensitivity to historical medical mistrust—many Aboriginal patients have experienced institutional racism in healthcare settings. Aboriginal Liaison Officers and Health Workers should be involved early in perioperative management to facilitate culturally safe communication about asthma history, trigger identification, and treatment preferences. For patients with limited English proficiency, medical interpreters must be engaged to ensure accurate history-taking regarding previous intubations, ICU admissions, and medication compliance.

Māori health considerations in Aotearoa New Zealand demonstrate similar disparities, with Māori experiencing 1.5-2 times higher asthma hospitalisation rates than non-Māori populations. Higher smoking rates (32% vs 13% in non-Māori) contribute to chronic airway inflammation and bronchial hyperreactivity, increasing intraoperative bronchospasm risk during both elective and emergency procedures. Whānau-centred care principles require involving extended family in pre-operative planning, including discussions about asthma severity, previous critical incidents, and emergency management preferences. Māori Health Workers provide essential cultural brokerage during crisis situations.

Remote and rural health considerations disproportionately affect Indigenous populations accessing surgery at regional centres. RFDS transfer protocols must include bronchodilator therapy and resuscitation equipment for patients with known severe asthma/COPD travelling long distances for elective procedures. Regional hospitals serving Indigenous communities require robust difficult airway and bronchospasm management protocols, including immediate access to magnesium sulfate, ketamine, and advanced ventilation modes. Healthcare providers must recognise that Indigenous patients may have limited exposure to Western medical environments, requiring additional reassurance and clear explanation of bronchospasm management procedures, medication effects, and monitoring strategies. Culturally safe documentation of asthma history, trigger avoidance strategies, and communication preferences should be standard in all perioperative assessments for Indigenous patients.

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Clinical Overview

Definition and Classification

Intraoperative bronchospasm is defined as acute, reversible narrowing of the bronchial airways resulting from smooth muscle contraction, mucosal edema, and increased secretions, occurring during the perioperative period under general anaesthesia. [1,2] It represents a common anaesthetic emergency with potentially life-threatening consequences if not promptly recognised and managed.

Classification by Severity: [3,4]

Epidemiology

Incidence: Intraoperative bronchospasm occurs in 0.2-2.0% of general anaesthetics, with higher rates in specific populations: [5,6]

• Asthmatic patients: 4-10% incidence
• Active smokers: 3-5% incidence
• COPD patients: 5-8% incidence
• Paediatric patients with URI: 5-10% incidence

Risk Factors: [7,8]

Patient Factors:

• Active asthma (especially poorly controlled)
• Recent asthma exacerbation (<4 weeks)
• Current smoking or recent smoking cessation (<8 weeks)
• COPD with chronic bronchitis phenotype
• Recent upper respiratory tract infection
• Obesity (decreased functional reserve)
• History of intubation for asthma

Surgical/Anaesthetic Factors:

• Airway instrumentation (intubation, suctioning)
• Light anaesthesia depth
• Histamine-releasing drugs (atracurium, mivacurium, morphine)
• β-blocker use (systemic or topical)
• Latex allergy
• Aspiration risk procedures

Pathophysiology

Mechanism of Bronchoconstriction: [9,10]

The pathophysiology involves multiple pathways:

1. Cholinergic Pathway:

   • Vagal stimulation from airway instrumentation
   • Acetylcholine release at muscarinic M3 receptors
   • Smooth muscle contraction
   • Mucus gland secretion

2. Inflammatory Pathway:

   • Mast cell degranulation (IgE-mediated or direct)
   • Release of histamine, leukotrienes, prostaglandins
   • Bronchial smooth muscle contraction
   • Vascular permeability and edema

3. Irritant Pathway:

   • Direct stimulation of irritant receptors
   • Reflex bronchoconstriction
   • Common with airway manipulation, secretions

4. Pharmacological Triggers:

   • Histamine release from specific drugs
   • β-blockade (loss of β2-mediated bronchodilation)
   • Prostaglandin release

Physiological Consequences: [11,12]

• Increased airway resistance: Predominantly expiratory
• Air trapping: Incomplete expiration, "stacking"
• Dynamic hyperinflation: Intrinsic PEEP development
• V/Q mismatch: Increased dead space, hypoxemia
• Hemodynamic compromise: Reduced venous return, hypotension
• Respiratory muscle fatigue: Especially if prolonged

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Recognition and Diagnosis

Clinical Signs

Early Recognition Indicators: [13,14]

Ventilator Alarms and Waveforms:

1. Rising peak inspiratory pressure (PIP):

   • Normal: <20 cmH₂O
   • Mild bronchospasm: 20-30 cmH₂O
   • Moderate: 30-40 cmH₂O
   • Severe: >40 cmH₂O

2. Unchanged plateau pressure (Pplat):

   • PIP rises, Pplat stable suggests airway resistance (bronchospasm)
   • Both rise suggests compliance problem (pneumothorax, edema)
   • Formula: Resistance = (PIP - Pplat) / Flow

3. Expiratory flow pattern:

   • Prolonged expiratory phase
   • Incomplete return to baseline
   • "Scooped" expiratory limb on flow-time curve

4. EtCO2 changes:

   • Increasing baseline (hypercapnia)
   • "Shark fin" or prolonged upstroke (delayed emptying)
   • Decreasing amplitude (poor tidal delivery)

Auscultation Findings: [15,16]

• Wheezing: High-pitched sound during expiration
  • Expiratory > inspiratory indicates lower airway obstruction
  • Silent chest: No audible wheeze despite severe obstruction (ominous sign)
• Prolonged expiration: Audible extended expiratory phase
• Reduced breath sounds: Poor air entry

Hemodynamic Signs: [17,18]

• Tachycardia (sympathetic response)
• Hypertension initially, hypotension if severe
• Arrhythmias (hypoxia-related)
• Jugular venous distension (air trapping)

Differential Diagnosis

Critical Distinctions: [19,20]

Diagnostic Algorithm: [21,22]

1. Immediate assessment: Look, listen, feel
2. Manual ventilation: Assess compliance
3. Auscultate chest: Wheeze location, symmetry
4. Check EtCO2 waveform: Characteristic patterns
5. Visualise airway: Laryngoscopy to exclude upper airway obstruction
6. Suction ETT: Exclude secretions/plug
7. CXR if unclear: Exclude pneumothorax, edema

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Acute Management

Immediate Response (First 3 Minutes)

STEP 1: Deepen Anaesthesia and Increase Oxygen [23,24]

1. FiO2 100% (immediate)
2. Propofol 1-2 mg/kg bolus OR increase volatile agent concentration
   • Anaesthetic depth often inadequate
   • Propofol has mild bronchodilator properties
3. Muscle relaxation: Ensure adequate paralysis (check TOF)
   • Fighting ventilator worsens bronchospasm
   • Give additional NMBA if needed

STEP 2: Inhaled Beta-Agonist Therapy [25,26]

Salbutamol (Albuterol) Administration:

Via ETT (most common):

• MDI with ETT adapter: 5-10 puffs (500-1000 mcg)
  • Wait 30 seconds between puffs
  • Synchronize with inspiration
  • Disconnect ventilator briefly for each puff
• Nebuliser via T-piece: 2.5-5 mg in 3 mL saline
  • Takes 10-15 minutes
  • May require manual ventilation coordination

IV Administration (if inhaled ineffective):

• 10-20 mcg IV bolus over 1 minute
• Follow with 5-20 mcg/min infusion
• Monitor for tachycardia, arrhythmias, hypokalemia
• Titrate to effect

STEP 3: Manual Ventilation Assessment [27,28]

Switch to Manual (Bag) Ventilation:

1. Disconnect ventilator
2. Connect Mapleson C circuit or self-inflating bag
3. Assess compliance:
   • Feel for resistance during inspiration
   • Listen for wheeze during expiration
   • Assess expiratory time
4. Ventilation strategy:
   • Slow rate (8-10 breaths/min)
   • Prolonged expiration (2-3 seconds)
   • Small tidal volumes (6-8 mL/kg)

Pharmacological Management

Magnesium Sulfate: [29,30,31]

Mechanism:

• Smooth muscle relaxation (calcium channel antagonist)
• Inhibits mast cell degranulation
• Reduces acetylcholine release at neuromuscular junction

Dosing:

• 2g IV over 10-20 minutes (adults)
• 40-50 mg/kg IV (paediatrics)
• May repeat once if partial response

Monitoring:

• Deep tendon reflexes (should remain present)
• Blood pressure (hypotension possible)
• Heart rate (bradycardia at high doses)
• Serum magnesium (target 2-3 mmol/L)

Evidence:

• Meta-analysis shows benefit in refractory asthma [31]
• Peak effect 15-30 minutes
• Safe in pregnancy

Corticosteroids: [32,33]

Agents and Dosing:

• Hydrocortisone 200mg IV (fast onset of action)
• Methylprednisolone 40-80mg IV
• Dexamethasone 8-12mg IV (longer duration)

Onset and Duration:

• Clinical effect: 4-6 hours
• Peak anti-inflammatory effect: 12-24 hours
• Duration: 24-48 hours

Rationale:

• Reduce airway inflammation
• Upregulate β2-receptor expression
• Prevent late-phase reaction

Ketamine: [34,35]

Mechanism:

• Stimulates catecholamine release (β2 effect)
• Direct smooth muscle relaxation
• Antagonises NMDA receptors involved in bronchoconstriction
• Preserves airway reflexes (unlike other agents)

Dosing:

• 0.5-1 mg/kg IV bolus
• Follow with 0.5-2 mg/kg/hr infusion

Indications:

• Severe/refractory bronchospasm
• When other agents failing
• Haemodynamically unstable patient (preserves BP)

Side Effects:

• Emergence reactions (treat with benzodiazepine)
• Increased secretions (requires suctioning)
• Tachycardia, hypertension

Epinephrine (Adrenaline): [36,37]

Indications:

• Life-threatening bronchospasm
• Cardiovascular collapse
• Failure of other agents

Dosing:

• 10-20 mcg IV boluses (titrate carefully)
• 0.05-0.5 mcg/kg/min infusion (refractory cases)

Precautions:

• Monitor ECG continuously
• Risk of arrhythmias, severe hypertension
• Have vasodilators available (phentolamine, nitroglycerine)

Ventilation Strategies

Mechanical Ventilation Adjustments: [38,39,40]

Key Principles:

1. Prolong expiratory time (prevent air trapping)
2. Reduce respiratory rate (allow complete expiration)
3. Permissive hypercapnia (accept elevated PaCO2)
4. Minimise intrinsic PEEP (reduce air trapping)

Recommended Settings:

Permissive Hypercapnia: [41,42]

Rationale:

• Accept elevated PaCO2 to minimise airway pressures
• Reduce risk of barotrauma
• Prevent dynamic hyperinflation

Targets:

• PaCO2 50-70 mmHg acceptable (pH >7.20)
• pH >7.20 (prevent severe acidaemia)
• Monitor for haemodynamic effects

Pressure-Controlled Ventilation: [43,44]

Advantages:

• Constant pressure delivery (limits barotrauma)
• Decelerating flow pattern (better distribution)
• Tidal volume varies with compliance

Settings:

• Inspiratory pressure 20-25 cmH₂O initially
• Adjust to achieve 4-6 mL/kg tidal volume
• I:E ratio 1:4 or longer expiration

Refractory Bronchospasm

Definition: Failure to respond to first-line therapy within 30 minutes with ongoing:

• Peak pressures >40 cmH₂O
• Inability to ventilate adequately
• Progressive desaturation
• Haemodynamic compromise

Advanced Interventions: [45,46,47]

1. Inhalational Anaesthetic Agents:

   • Sevoflurane: Potent bronchodilator, rapid onset
   • Isoflurane: Good bronchodilation, longer experience
   • Contraindication: Malignant hyperthermia risk, difficult to use in closed circuit
   • Technique: High concentration (2-3 MAC), closed circuit or draw-over

2. Heliox (Helium-Oxygen Mixture): [48,49]

   • 80:20 or 70:30 helium:oxygen
   • Lower density reduces turbulent flow
   • Improves ventilation in severe obstruction
   • Requires special equipment (heliox-compatible ventilator)
   • May limit FiO2 delivery (max 30-40% with 70:30)

3. Bronchoscopy:

   • Rigid bronchoscopy preferred (ventilation possible)
   • Remove mucus plugs, blood clots
   • Direct instillation of bronchodilators
   • Assess for foreign body, tumour

4. ECMO/ECPR: [50,51]

   • For life-threatening, refractory cases
   • V-V ECMO for isolated respiratory failure
   • V-A ECMO if cardiac failure
   • Transfer to ICU/tertiary centre

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Special Populations and Considerations

Asthmatic Patients

Pre-operative Optimisation: [52,53]

Assessment:

• Recent exacerbation history
• Current medications and compliance
• Prior intubations/ICU admissions
• Current peak flow/spirometry if available

Optimisation Targets:

• No exacerbation in preceding 4 weeks
• Peak flow >80% predicted or personal best
• Stable maintenance medications
• Consider pre-operative steroids if suboptimal

Perioperative Management:

• Continue inhaled corticosteroids
• Consider pre-operative nebulised β2-agonist
• Avoid histamine-releasing agents if possible
• Use propofol for induction (bronchodilator properties)
• Consider TIVA (reduces airway reactivity)
• Extubate deep if appropriate

Chronic Obstructive Pulmonary Disease

Unique Features: [54,55]

• Fixed + variable obstruction: Less responsive to bronchodilators
• Air trapping: More pronounced than asthma
• Bullae: Risk of pneumothorax with high pressures
• Cor pulmonale: RV dysfunction, fluid sensitive

Management Modifications:

• Lower tidal volumes (4-6 mL/kg)
• Longer expiratory times (I:E 1:4 to 1:5)
• Lower PEEP (risk of air trapping)
• Avoid N₂O (expands bullae)
• Consider regional techniques if appropriate

Paediatric Patients

Unique Considerations: [56,57]

• Higher incidence: 5-10% with recent URI
• Small airway diameter: More susceptible to obstruction
• Faster desaturation: Reduced functional reserve
• Respiratory muscle fatigue: Develops rapidly

Management:

• Weight-based dosing critical:
  • Salbutamol 100-200 mcg inhaled
  • Magnesium 40-50 mg/kg IV
  • Hydrocortisone 4 mg/kg IV
• Higher respiratory rates acceptable: Allow for metabolism
• Early escalation: Children decompensate faster

Pregnancy

Physiological Changes: [58,59]

• Reduced FRC: 20% reduction by third trimester
• Increased oxygen consumption: 20-30% increase
• Airway edema: Upper and lower airway
• Gastroesophageal reflux: Aspiration risk

Management:

• Left lateral tilt: After 20 weeks gestation
• Aspiration prophylaxis: Sodium citrate, metoclopramide, ranitidine
• Early intubation: Difficult airway risk
• Foetal monitoring: When viable (>24 weeks)
• Medication safety: Salbutamol, magnesium, steroids all safe

Indigenous Health Considerations

Note: This section provides expanded detail on cultural safety for ANZCA exam preparation, building upon the Quick Answer section above.

Aboriginal and Torres Strait Islander Health: [60,61,62]

Respiratory Disease Burden:

• Asthma prevalence 18% (vs 11% non-Indigenous)
• Hospitalisation rates 2.5x higher for asthma
• COPD mortality 3x higher than non-Indigenous
• Smoking rates 37% in remote communities

Perioperative Implications:

• Higher baseline airway reactivity
• Greater likelihood of poorly controlled disease
• Increased risk of intraoperative bronchospasm
• Potential for delayed presentation with complications

Cultural Safety in Crisis Management:

1. Communication During Bronchospasm:

   • Clear explanation of what's happening (with ALO/health worker)
   • Reassurance about effectiveness of treatment
   • Family communication (often collective decision-making)
   • Use of plain language, avoid medical jargon

2. Medication Considerations:

   • Check understanding of inhaler technique pre-operatively
   • Many Aboriginal patients use traditional remedies alongside Western medicine—non-judgmental inquiry
   • Ensure access to puffers post-operatively in rural/remote settings

3. Remote Health Service Context:

   • Regional hospitals may lack ICU backup
   • Early recognition of when to transfer
   • RFDS retrieval with bronchodilator capability
   • Telemedicine consultation with respiratory specialists

Māori Health (Aotearoa New Zealand): [63,64,65]

Respiratory Health Disparities:

• Asthma hospitalisation 1.5-2x higher than non-Māori
• Smoking prevalence 32% (vs 13% non-Māori)
• Higher COPD prevalence and severity

Te Tiriti o Waitangi Obligations:

• Partnership: Māori involvement in care decisions
• Protection: Equitable outcomes (manage bronchospasm as aggressively as for any patient)
• Participation: Māori Health Workers as part of team

Whānau-Centred Bronchospasm Management:

1. Pre-Operative Planning:

   • Involve whānau in asthma history taking
   • Discuss previous experiences with airway management
   • Plan for communication during crisis

2. During Crisis:

   • Clear, calm communication
   • Karakia may be requested—facilitate access
   • Whānau may wish to remain present—negotiate appropriately
   • Māori Health Worker liaison

3. Post-Crisis:

   • Explanation of events to whānau
   • Discussion of ongoing asthma management
   • Cultural support if prolonged ICU admission required

Research and Evidence Base: [66,67,68]

Indigenous Respiratory Research Gaps:

• Limited research on Indigenous-specific bronchospasm management
• Need for culturally adapted asthma programs
• Importance of community-based participatory research

ANZCA Training Implications:

• Cultural safety training mandatory for all trainees
• Understanding of health disparities and their impact on anaesthetic risk
• Recognition that "standard" management requires cultural adaptation

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Differential Diagnosis in Detail

Anaphylaxis vs. Bronchospasm

Differentiating Features: [69,70]

Management Implications:

• Anaphylaxis: Immediate epinephrine 50-100 mcg IV/IM
• Bronchospasm: Beta-agonists first, escalate as needed

Aspiration

Recognition: [71,72]

• Risk factors: Full stomach, GERD, emergency surgery, pregnancy
• Clinical: Sudden desaturation, decreased compliance
• Signs: Gastric contents visible in airway, acidic pH of secretions
• CXR: Patchy infiltrates (often right lower lobe)

Management:

• Head-down position
• Suction immediately
• Saline lavage (limit to 50-100 mL to avoid spreading)
• Consider bronchoscopy for particulate matter
• Steroids not proven beneficial acutely
• Antibiotics if evidence of infection develops

Pneumothorax

Distinguishing Features: [73,74]

• Sudden onset (not progressive like bronchospasm)
• Unilateral findings
• ↑ Pplat (compliance problem, not resistance)
• Tracheal deviation (tension)
• Absent breath sounds one side

Confirmation:

• CXR (upright if possible)
• Ultrasound (absent lung sliding)
• Clinical suspicion → immediate needle decompression if tension

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Prevention

Pre-Operative Assessment

Risk Stratification: [75,76]

High-Risk Patients:

• Emergency surgery within 4 weeks of asthma exacerbation
• Recent hospitalisation for asthma/COPD
• Current smoking
• Poor medication compliance
• Prior intubation for respiratory failure

Optimisation Strategies:

1. Smoking cessation: Ideally 8 weeks pre-operatively (minimum 4 weeks)
2. Corticosteroid optimisation:
   • Ensure on maintenance inhaled steroids
   • Consider course of oral steroids if poorly controlled
3. Pre-operative bronchodilator: Nebulised β2-agonist morning of surgery
4. Delay elective surgery: If acute exacerbation or recent URI

Perioperative Techniques

Induction Strategies: [77,78]

1. Propofol induction:

   • Bronchodilator properties
   • Suppresses airway reflexes
   • Preferred over thiopentone

2. Ketamine induction:

   • Excellent for high-risk asthmatics
   • Bronchodilation + haemodynamic stability
   • Consider 1-2 mg/kg + midazolam

3. Avoid histamine-releasing agents:

   • Atracurium, mivacurium
   • Morphine (use fentanyl instead)

4. Deep extubation:

   • Extubate at adequate depth (reduces stimulation)
   • Lidocaine 1-1.5 mg/kg IV 3 minutes pre-extubation
   • Ensure full reversal of muscle relaxation

Airway Management: [79,80]

• Regional techniques when appropriate (avoid airway instrumentation)
• LMA vs. ETT: LMA may reduce stimulation, but seal less reliable
• If intubation necessary:
  • Adequate depth before laryngoscopy
  • Lidocaine spray to cords
  • Gentle technique, minimise attempts

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ANZCA Exam Focus

Written Examination (SAQ)

High-Yield Topics:

1. Ventilator waveform interpretation

   • Distinguishing bronchospasm from pneumothorax (PIP vs Pplat)
   • "Shark fin" EtCO2 pattern
   • Flow-time and pressure-time curves

2. Pharmacological management

   • Salbutamol dosing (inhaled vs IV)
   • Magnesium sulfate mechanism and dosing
   • Corticosteroid onset timing
   • Ketamine as rescue therapy

3. Mechanical ventilation strategy

   • Permissive hypercapnia rationale
   • I:E ratio adjustment
   • Pressure vs volume control

4. Differential diagnosis

   • Bronchospasm vs anaphylaxis vs pneumothorax
   • Clinical features distinguishing each
   • Management priorities

Common SAQ Scenarios:

Scenario 1: "During maintenance of anaesthesia for laparoscopic cholecystectomy, you notice rising peak airway pressures. Describe your assessment and management. (20 marks)"

Scenario 2: "A 45-year-old asthmatic patient undergoing hernia repair develops intraoperative bronchospasm. Outline your pharmacological management. (15 marks)"

Viva Voce Examinations

Expected Viva Themes:

Theme 1: Recognition

• "You're anaesthetising a patient when the ventilator alarm sounds for high airway pressure. What do you do?"
  • Key points: Manual ventilation, auscultation, waveform analysis

Theme 2: Management

• "How would you manage severe intraoperative bronchospasm unresponsive to initial therapy?"
  • Key points: Magnesium, ketamine, ventilation strategy, epinephrine

Theme 3: Prevention

• "What strategies would you use to prevent bronchospasm in a patient with severe asthma?"
  • Key points: Optimisation, propofol, avoid histamine releasers, deep extubation

Theme 4: Differential

• "A patient develops high airway pressures and desaturation. How do you differentiate bronchospasm from other causes?"
  • Key points: PIP vs Pplat, auscultation, other clinical signs

Viva Scenario Example

Examiner: "You are anaesthetising a patient with asthma for elective surgery. Peak airway pressures begin to rise. What is your immediate assessment?"

Candidate Response Framework:

1. Immediate Actions:

   • "I would switch to manual ventilation to assess compliance"
   • "Increase FiO2 to 100%"
   • "Deepen anaesthesia with propofol"

2. Assessment:

   • "Auscultate for wheeze and symmetry"
   • "Check PIP vs plateau pressure - if only PIP rises, suggests bronchospasm"
   • "Look at EtCO2 waveform for shark fin pattern"
   • "Suction ETT to exclude mucus plug"

3. Initial Treatment:

   • "Salbutamol 5-10 puffs via ETT"
   • "Magnesium sulfate 2g IV"
   • "Hydrocortisone 200mg IV"

4. Ventilation Strategy:

   • "Increase expiratory time (I:E 1:4)"
   • "Reduce respiratory rate to 8-10/min"
   • "Permissive hypercapnia if necessary"

Examiner Follow-up: "The patient is not responding. What next?"

Candidate: "I would escalate to IV salbutamol 10-20 mcg bolus followed by infusion, consider ketamine 0.5-1 mg/kg for its bronchodilator properties, and if life-threatening, IV epinephrine 10-20 mcg titrated carefully."

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Short Answer Questions

SAQ 1: Ventilator Waveform Interpretation

Question: (20 marks) During general anaesthesia for laparoscopic surgery, you notice the following ventilator alarms:

• Peak inspiratory pressure: 42 cmH₂O (previously 18 cmH₂O)
• Plateau pressure: 20 cmH₂O (unchanged)
• SpO2: 94% and falling

a) What is the most likely diagnosis? Justify your answer. (5 marks)

b) Describe your immediate management. (10 marks)

c) How would you distinguish this from a pneumothorax? (5 marks)

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Model Answer:

a) Diagnosis: Intraoperative Bronchospasm (5 marks)

Justification:

• PIP rises (42 cmH₂O) while Pplat unchanged (20 cmH₂O) = increased airway resistance (bronchospasm)
• Difference (PIP-Pplat) = 22 cmH₂O indicates high resistance
• Desaturation due to V/Q mismatch, air trapping
• Formula: Resistance = (PIP - Pplat) / Flow

If both PIP and Pplat elevated → compliance problem (pneumothorax, edema)

b) Immediate Management (10 marks):

Immediate (First 2 minutes):

1. Increase FiO2 to 100% (1 mark)
2. Deepen anaesthesia: Propofol 1-2 mg/kg or increase volatile (1 mark)
3. Switch to manual ventilation to assess compliance and listen for wheeze (2 marks)
4. Ensure adequate paralysis - check TOF, give additional NMBA if needed (1 mark)

Pharmacological (Next 5 minutes): 5. Salbutamol 5-10 puffs (500-1000 mcg) via MDI + ETT adapter (2 marks) 6. Magnesium sulfate 2g IV over 10-20 minutes (1 mark) 7. Hydrocortisone 200mg IV (delayed effect but essential) (1 mark)

c) Distinguishing from Pneumothorax (5 marks):

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SAQ 2: Pharmacological Management of Severe Bronchospasm

Question: (15 marks) A 35-year-old patient with severe asthma develops intraoperative bronchospasm that is not responding to inhaled salbutamol. The patient is becoming increasingly difficult to ventilate with SpO2 88% on 100% oxygen.

a) Outline your step-wise pharmacological escalation. (10 marks)

b) What mechanical ventilation strategy would you employ? (5 marks)

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Model Answer:

a) Pharmacological Escalation (10 marks):

Step 1: Optimise Inhaled Therapy (2 marks)

• Ensure adequate delivery: 10 puffs salbutamol via ETT with 30-second intervals
• Consider nebulised salbutamol 5mg if MDI ineffective
• Verify ETT position and patency (suction if secretions)

Step 2: Intravenous Bronchodilators (2 marks)

• Salbutamol IV 10-20 mcg bolus over 1 minute
• Follow with 5-20 mcg/min infusion titrated to effect
• Monitor for tachycardia, arrhythmias, hypokalemia

Step 3: Magnesium Sulfate (2 marks)

• 2g IV over 10-20 minutes
• Mechanism: Smooth muscle relaxation, calcium channel blockade
• Monitor deep tendon reflexes and blood pressure
• Peak effect 15-30 minutes

Step 4: Ketamine (2 marks)

• 0.5-1 mg/kg IV bolus
• Mechanism: Catecholamine release, direct smooth muscle relaxation
• Preserves airway reflexes and haemodynamics
• May follow with 0.5-2 mg/kg/hr infusion

Step 5: Epinephrine (Life-Threatening) (2 marks)

• 10-20 mcg IV boluses carefully titrated
• Or infusion 0.05-0.5 mcg/kg/min
• Continuous ECG monitoring mandatory
• Reserved for cardiovascular collapse or refractory bronchospasm

b) Mechanical Ventilation Strategy (5 marks):

Key Principles:

1. Prolong expiratory time to prevent air trapping
   • I:E ratio 1:4 to 1:5
2. Reduce respiratory rate
   • 8-10 breaths/min (allow complete expiration)
3. Permissive hypercapnia
   • Accept PaCO2 50-70 mmHg if necessary
   • Maintain pH >7.20
4. Increase inspiratory flow
   • 60-80 L/min (shorter inspiratory time)
5. Pressure-controlled ventilation
   • Limits peak pressures
   • Decelerating flow pattern

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SAQ 3: Prevention and Optimisation

Question: (15 marks) You are assessing a 42-year-old patient with severe asthma for elective laparoscopic cholecystectomy. The patient had an asthma exacerbation 2 weeks ago requiring oral steroids.

a) What are the key considerations regarding timing of surgery? (5 marks)

b) Describe your anaesthetic technique to minimise bronchospasm risk. (10 marks)

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Model Answer:

a) Timing Considerations (5 marks):

1. Delay Elective Surgery (3 marks):

   • Ideally wait 4-6 weeks after asthma exacerbation
   • Risk of intraoperative bronchospasm significantly higher within 4 weeks
   • Patient had steroids 2 weeks ago (recent exacerbation)
   • Recommendation: Postpone surgery if possible

2. If Surgery Essential (2 marks):

   • Optimise asthma control before proceeding
   • Ensure peak flow >80% predicted
   • Pre-operative pulmonary function tests if available
   • High-risk case requiring senior anaesthetist

b) Anaesthetic Technique (10 marks):

Pre-Operative (2 marks):

1. Continue regular inhaled corticosteroids (do not withhold)
2. Nebulised salbutamol 5mg morning of surgery
3. Consider oral steroids if suboptimal control (prednisolone 40mg)

Induction (3 marks): 4. Propofol 2-3 mg/kg for induction (bronchodilator properties) 5. Avoid histamine-releasing agents:

• No atracurium or mivacurium
• Use rocuronium or vecuronium instead

6. Fentanyl rather than morphine (less histamine release)

Maintenance (3 marks): 7. Consider TIVA with propofol/remifentanil (reduced airway reactivity vs volatile) 8. If volatile: Sevoflurane or isoflurane (bronchodilator properties) 9. Ensure adequate depth before airway manipulation

Extubation (2 marks): 10. Deep extubation if appropriate (reduces stimulation) 11. Lidocaine 1-1.5 mg/kg IV 3 minutes pre-extubation 12. Ensure complete reversal of neuromuscular blockade

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