Asthma

Heterogenous chronic inflammatory disease of the small airways, characterised by ↑ sputum production and airway reactivity. Diagnosis requires a combination of:

Respiratory symptoms
- Wheeze
- Dyspnoea
- Chest tightness
- Cough
Variable, reversible, expiratory airflow limitation

Status asthmaticus has variable definitions, but essentially describes acute severe asthma that has not responded to initial doses of nebulised bronchodilators.

Epidemiology and Risk Factors

In Australia:

10% have chronic asthma
~50% of these have uncontrolled disease and form the highest risk group for critical care.
Significant ↓ in intensive care admissions with improved community management
Namely:
- Guidelines
- ↑ inhaled steroid use
- Asthma action plans
  Risk factors:
Atopy
↓ Exposure to childhood infections may ↑ risk of asthma, hayfever, and eczema.
Family history

Pathophysiology

Underlying pathology involves both:

Airway inflammation
- Bronchial wall hyperplasia and oedema
Sputum production
- May lead to obstruction and plugging of small airways
  Usually offset by hyperinflation.
  This leads to a combination of ↑ airway resistance and dynamic hyperinflation, with consequentially:
↑ Work of breathing
Lung compliance and the mechanical efficiency of respiratory muscles both ↓ at high lung volumes.
- Physical exhaustion
  Maintenance of elevated work of breathing may lead to tiring and respiratory failure.
V/Q mismatch
Further ↑ work of breathing.
Impaired cardiac function
- RV preload may be ↑ by the very negative intrathoracic pressures produced during vigorous inspiration
- RV afterload worsened by combination of:
  - Pulmonary vascular compression by hyperinflated lungs
  - Hypoxia
  - Acidosis
- LV preload may be ↓↓ by impaired RV function
- LV afterload significantly ↑ by negative intrathoracic pressures

Aetiology

Often triggered by exposure to an environmental or physiological precipitant, including:

Note that if the primary cause of asthma is suspected to be anaphylaxis, then adrenaline is the first-line bronchodilator and standard anaphylaxis management should be followed.

Environmental
- Cold air
- Allergens
  Common ones include:
  - Pollen
  - Rye-grass
  - Dust mites
  - Animal
- Drugs
  - NSAIDs
  - Beta-blockers
Physiological
- Excercise
- Stress
- URTI

Clinical Manifestations

Diagnostic Approach and DDx

Key differentials include:

Hyperventilation
COAD
Vocal cord dysfunction

Investigations

Bloods:

ABG/VBG
- VBG determines the lower limit of pH and the upper limit of PaCO₂
- Respiratory alkalosis predominates in early disease due to hypoxia
- As the disease worsens and V/Q mismatch ↑, an ↑ MV produces the same blood gas composition
- Respiratory acidosis emerges in late disease when the patient tires and is unable to maintain the required MV
- A lactic acidosis secondary to beta agonists may also be present

Radiology:

CXR
No role in confirmed asthma, but may be helpful to exclude other differentials.

Management

Underestimation of severity and consequent undertreatment are major contributors to asthma mortality.

Principles of severe asthma management are:

Aggressive and early use of bronchodilators
Early use of NIV
Avoid invasive ventilation if safe to do so

Resuscitation:

Patient response over the first 2 hours of treatment are an important guide to the ongoing trajectory.

A
- Intubation and invasive ventilation
  - Required in rare instances
  - Associated with significant morbidity and mortality
    - Dynamic hyperinflation
    - Precipitation of worse bronchospasm
  - Usually requires significant permissive hypercapnoea, and therefore sedation and paralysis for patient tolerance
  - Decision to intubate is made clinically, evidence in favour of:
    - Significant respiratory distress (not necessarily tachypnoea)
    - Severe hypoxia
    - Deteriorating conscious state
  - Initial ventilator settings:
    - Volume control
    - ZEEP
      Recommendations for set PEEP are variable. 0-5cmH₂O is probably okay, provided set PEEP < iPEEP.
    - V_T 5-7mL/kg
    - RR 8-12
    - Short inspiratory time/High inspiratory flow rate
      Aim expiratory time >4s. Pip will be ↑ but alveolar pressures will be significantly ↓ due to the airway obstruction. Once ventilation is established, Pplat should be assessed with an inspiratory hold and should be maintained at <25cmH₂O.
  - Haemodynamic deterioration following intubation is often due to dynamic hyperinflation
    The ventilator should be disconnected and prolonged (60s) expiration allowed to occur to reduce cardiac compression, before continuing ventilation at a lower rate.
B
- Oxygen
  Target SpO₂ 94-98%. Excessive supplementation likely harmful.
- Bronchodilators
  - Inhaled
    - Short-acting beta-agonists
      - Salbutamol
        5-10mg nebulised Q2H, or continuously if clinical concern dictates.
      - Adrenaline
        For patients non-responsive to nebulised salbutamol. 5mg nebulised Q2H.
    - Anticholinergic
      - Ipratropium bromide
        500ug nebulised Q4H.
  - Intravenous
    - Beta-agonists
      Consider if no response to inhaled beta-agonists.
      - Salbutamol
        5-10ug/min or 100-250ug bolus in extremis.
      - Adrenaline 10ug bolus, with infusion at 1-10ug/min.
    - Corticosteroids
    - Magnesium
      Controversial, but probably beneficial in adults and unlikely to be harmful.
      - 5-10mmol IV over ~20 minutes
  - Anaesthetic agents
    - Ketamine
      Direct and indirect (via ↑ sympathetic tone) bronchodilation. Useful as an induction agent for endotracheal intubation or as a component of post-intubation sedation, but not independently of this.
    - Volatile
      Many inhaled anaesthetic agents (sevoflurane, isoflurane, enflurane, halothane) are effective direct bronchodilators, with use limited by requiring an intubated patient and a ventilator capable of administering them.
- Non-Invasive Ventilation
  PEEP ↓ inspiratory threshold work and may split open small airways, whilst Psup ↓ inspiratory work and ↑ V_T and MV.
  - Indicated for:
    - Moderate-severe dyspnoea or ↑ work of breathing
    - Respiratory acidosis
  - Commence with:
    - CPAP 5cmH₂O
      ↑ If difficulty initiating inspiration.
    - Psup 8-10cmH₂O
      ↑ If low Vt/ RR.
  - Target V_T ~7mL/kg, RR ~25
- VV ECMO
  May be required if oxygenation is unable to be managed effectively following intubation.

To initiate gas flow into the lungs, the patient must generate enough inspiratory force such that Palv < Patm.

If iPEEP is high, then a very negative intrapleural pressure must be generated before Palv is less than Patm and inspiration commences. Application of external PEEP reduces this gradient, and therefore reduces the amount of work performed before inspiration commences (inspiratory threshold work).

Note that this differs from the controlled ventilation settings, because NIV assumes spontaneous breathing. Inspiratory threshold work is irrelevant in fully controlled ventilation.

Specific therapy:

Pharmacological
Community management of asthma is a cornerstone of preventing severe exacerbations. Agents used include:
- Inhaled “preventers”
  Usually one (or combination therapy) of:
  - Long-acting beta-agonists
    e.g. Salmeterol.
  - Inhaled corticosteroids
    e.g. Fluticasone.
- Leukotriene antagonists
Physical
- Asthma management plan

Disposition:

Intensive care admission is recommended for:
- Severe asthma
- Respiratory arrest
- Altered mental state
- Dysrhythmias
- Myocardial ischaemia

Marginal and Ineffective Therapies

Aminophylline
Inferior bronchodilator relative to others available, with a narrow therapeutic range and poor side effect profile.
Heliox
70% helium/30% oxygen mixture improves work of breathing and effect of inhaled bronchodilators. This is limited by availability of heliox and the low delivered FiO₂.

Anaesthetic Considerations

Complications

Death
B
- Dynamic hyperinflation
  Airway obstruction leads to incomplete exhalation in a normal expiratory time. If expiratory time is not prolonged (due to the next breath being taken), then there is progressive accumulation of gas in the lungs and a rise in lung volume. This may precipitate:
  - Hypotension and cardiovascular collapse
    Progressive impairment to VR due to ↑ intrathoracic pressure.
  - Barotrauma
    - Pneumothorax
      - Unilateral pneumothorax will result in preferential ventilation of the uninjured lung, ↑ the risk of a second (bilateral) pneumothorax
        Respiratory rate should be further ↓ following diagnosis of a PTx to reduce this risk.
      - Catheters should be inserted by blunt dissection to minimise risk of lung injury.
E
- Critical Illness Myopathy
  ## Prognosis
Mortality 10-20% among those requiring invasive ventilation