Asthma

• The fundamental lesion is paroxysmal, reversible airway obstruction
• The aetiology of said obstruction is polyfactorial:
1. Bronchial smooth muscle contraction & hypertrophy
2. Excessive mucous production and airway plugging
3. Infiltration of inflammatory cells
4. Mucosal oedema
5. Chronic small airway inflammation


• In part this arises due to the parasympathetic nervous system, acting via the vagus nerve and muscarinic acetylcholine receptors
• Altered bronchial smooth muscle tone leads to bronchoconstriction (1)
• Hypersecretion of mucus by goblet cells occurs, leading to airway plugging (2)
• There is mast cell and basophil infiltration and degranulation (3), leading to mucosal inflammation and mucosal oedema (4 & 5) with subsequent small airway narrowing

• Airway hyper-responsiveness
• Classic triggers include cold air, exercise, dust, cigarette smoke, viral URTI or drugs (β-blocker, NSAID)


• Increased resistance to air flow, particularly expiratory flow
• Causes an increased work of breathing
• Leads to V/Q mismatch

• Recurrent episodes of dyspnoea, cough, chest tightness and wheeze
• Typically worse in the morning due to diurnal variation
• ±presence of a specific trigger factor


• Exacerbations of asthma may also come with tachypnoea, widespread polyphonic wheeze and tachycardia
• Precise signs vary according to the severity of the 'attack'

• Is as per the BTS guidelines (link above)
• In brief, expect patients to be on an inhaled corticosteroid ± an inhaled long-acting β₂-agonist ± a leukotriene receptor antagonist depending on their level of control
• Most patients will also carry a 'reliever' inhaler i.e. short-acting β₂-agonist

• Anaphylaxis
• Upper airway obstruction e.g. croup, foreign body, other upper airway infections
• Lower airway disease e.g. pneumonia, bronchiolitis
• Pneumothorax
• Acute cardiac failure

• The BTS classify acute exacerbations, depending on their severity, as:
• Moderate acute
• Acute severe
• Life-threatening
• Near-fatal
• The precise criteria are available in the BTS guidelines
• Anecdotally, one is typically called for assistance when patients are traversing the cut-offs between acute severe and life-threatening territory, hence detailing the criteria for the latter below

• Near-fatal asthma is indicated by a high P_aCO₂ or the need for mechanical ventilation (with high pressures)

• If the clinical scenario isn't improving after the above then
1. The evidence base and/or efficacy of next-line treatments becomes more dubious
2. Critical care involvement becomes more likely

• Aminophylline
• If not already on long-term oral theophylline, a 5mg/kg (max. 500mg) loading dose IV then the infusion
• If already on maintenance therapy, skip straight to a 300 - 500μg/kg/hr infusion
• Aim for an aminophylline level of 10 - 20μg/L 4-6hrs following the start of the infusion


• Salbutamol
• IV infusion of initially 5μg/min but titrated to between 3 - 20μg/min according to effect
• Avoid unless absolutely necessary due to side-effects


• Ketamine
• Either 10 - 20mg bolus or an infusion of 1-3mg/kg/hr


• Others
• Ongoing magnesium infusion
• Adrenaline
• Nebulised (5ml of 1:1,000)
• IV (1 - 20μg/min)
• Volatile anaesthetic agent e.g. sevoflurane, isoflurane

• The predominant pathophysiological feature in status asthmaticus is gas trapping, which occurs due to:
• Increased resistance to expiratory gas flow
• Rapid respiratory rate
• Change in pulmonary elastic recoil
• Asynchronous respiratory muscle activity with flattening of the diaphragm and predominantly intercostal breathing


• Gas trapping leads to dynamic hyperinflation and generation of intrinsic positive end-expiratory pressure (PEEPi)
• There is consequent:
• Impaired gas exchange with V/Q mismatch causing hypoxaemia, then eventually hypercapnoea
• Increased work of breathing and respiratory muscle fatigue
• Risk of barotrauma & pneumothorax


• There are also cardiovascular effects, namely an impaired cardiac output owing to:
• Dehydration from reduced intake and high respiratory losses
• Impaired right heart filling due to high intrathoracic pressures from PEEPi
• Gas trapping compresses the pulmonary capillaries, increasing PVR
• Reduced diastolic LV filling due to:
• RV distension, shifting the interventricular septum
• Direct pressure on the heart by hyperinflated lungs
• Acidosis from hypercarbia
• Hypokalaemia from medical therapies


• Post intubation there is likely to be a raised P_aCO₂ but a low ETCO₂
• This is due to increased alveolar pressure and therefore large volumes of dead space
• In effect, the whole lung becomes equivalent to a West Zone 1

• I&V may be required; although it secures the airway and (a degree of) control of ventilation it does not address the underlying pathology
• The goals of mechanical ventilation are therefore to:
1. Correct hypoxaemia
2. Reduce dynamic hyperinflation
3. Allow time for medical therapy to work


• Minute ventilation is the most important determinant of hyperinflation
• Inspiratory flow and shape of pressure waveform are less important
• Increased expiratory times are beneficial, though the effect of increasing beyond 3 - 4s are minimal
• No rationale for using PEEPe to counter PEEPi


• Hypercarbia is generally well tolerated and permissive hypercapnoea is reasonable
• The exception is those with cerebral injury/anoxia following cardio/respiratory arrest - may require extracorporeal CO₂ removal to facilitate neuroprotection
• Measures to combat respiratory acidosis from CO₂ include reducing CO₂ production e.g. antipyretics, active cooling

• Profound hypotension is a significant risk with induction of anaesthesia and ventilation, due to:
• Vasodilatory effects of induction agents
• Pre-existing dehydration
• Loss of sympathetic drive, upon which the patient was reliant
• Loss of venous return due to high intra-thoracic pressures from PPV/pneumothorax
• Impaired LV filling from RV distension
• Tension pneumothorax
• Any normal cause of hypotension e.g. sepsis, MI


• Other complications include:
• Cardiac stunning; due to massive sympathetic activation
• Arrhythmias
• Rhabdomyolysis; due to hypoxaemia and extreme exertion
• Lactic acidosis (polyfactorial)
• Myopathy; particularly if prolonged neuromuscular blockade alongside steroids and mechanical ventilation
• CNS injury

• No demonstrable benefit from NIV in asthma of any degree of severity
• ECMO may be successful although is limited by availability and side-effect profile
• Extra-corporeal CO₂ removal may be more feasible e.g. Novalung
• Mucolytics (e.g. recombinant human DNase, NAC, hypertonic saline) are not evidenced-based and routine use is not recommended
• Bronchoscopy may help in patients with persistent shunt due to mucus plugging, though is often complicated by bronchospasm
• Antibiotic use is not routinely recommended
• Heliox use is not supported by an evidence base, has a limited F_iO₂ of 0.4 and requires re-calibration of pneumotachographs and spirometry

• Asthma precipitants
• Exercise tolerance
• Previous exacerbations and hospitalisation/ICU admission
• Medications used and frequency of reliever inhaler therapy
• Steroids: recent or long-term use
• NSAID tolerance; NSAIDs may precipitate acute exacerbations in up to 5% (paediatric) or 20% (adult) of asthma patients

• Serial PEFR measurements and comparison to predicted/individual best
• Otherwise as indicated by ASA and planned operation

• Continue bronchodilator therapy preoperatively
• Encourage cessation
• May need anxiolysis if anxiety is a trigger for acute exacerbations
• Patients with signs and symptoms suggestive of a worsening disease state should have elective surgery postponed

• Morphine
• Owing to its histamine-releasing properties, which may exacerbate things
• Fentanyl and alfentanil are suitable opioids to use
• One may wish to avoid opioids in the extremely brittle asthmatic owing to their respiratory effects


• Atracurium and mivacurium, as both cause histamine release
• Desflurane (if you can even find some) - it is an airway irritant
• NSAIDs if the patient has a known history of NSAID-induced bronchospasm
• β-blockers should be used with caution
• Anticholinesterase reversal i.e. neostigmine may trigger bronchospasm

• Propofol, ketamine, midazolam and etomidate are safe induction agents
• Laryngoscopy and intubation may exacerbate asthma, so should be done under suitable depth of anaesthesia and degree of neuromuscular blockade
• Most volatile agents are bronchodilators, of which halothane is the most potent

• Factors that may lead to bronchospasm include:
• Airway manipulation including ETT insertion
• Anaphylaxis or anaphylactoid reactions
• Aspiration
• Pre-existing infection
• Pre-operative non-compliance with asthma medication
• Drugs (see above)
• If bronchospasm occurs:

Bronchospasm is an anaesthetic emergency and I would seek senior anaesthetic support as well as making a rapid but thorough assessment of the patient

• Ask the surgeon to kindly stop, while calling for senior help and applying 100% oxygen
• ABCDE approach
• Identify and stop any obvious precipitants
• Assess ventilation and/or move to manual ventilation
• Increase depth of volatile agent
• Auscultate chest to exclude pneumothorax
• Administer salbutamol nebuliser via breathing circuit or directly down ETT
• Consider IV magnesium or IV salbutamol

• Anaesthesia may be required during an acute exacerbation
• Overzealous administration of induction agents may lead to profound cardiovascular instability (see Ventilation section)
• As such, ketamine is the preferred agent owing to the maintained sympathetic drive and putative bronchodilation
• Volatile anaesthesia and suitable neuromuscular blockade should be used, to improve chest wall compliance
• Bronchospasm may necessitate the use of high ventilatory pressures to ensure adequate tidal volumes; the risk of barotrauma and pneumothorax means a degeree of permissive hypercapnoea is acceptable
• Ventilatory strategy follows that on ICU, as per the section above

• Suitable monitoring post-operatively in recovery and on the ward
• Re-instigate usual asthma therapies as soon as possible
• Provide adequate analgesia, lest pain provoke an exacerbation