Severe Bronchospasm Jeopardy Template

Causes of Bronchospasm/ Clinical Assessment

Physiology of Bronchospasm

Management of Bronchospasm

Ventilation in Bronchospasm

100

A 25-year-old female with a history of childhood asthma presents to ED with a 3 day history of cough and sore throat.

What additional history would you ask to help guide management?

What would you look for on physical examination? And what investigations might you order?

History:

Recent infections (URTI, flu-like symptoms)?
Medication use (e.g. puffers, steroids)?
Allergies or triggers?
History of intubation or hospitalisations/ICU stay due to asthma?
Smoking history?

Physical Exam:

Wheezing, SOB, cough
Work of breathing: tachypnoea, sP02, use of accessory muscles, nasal flaring, paradoxical breathing?
Signs of respiratory failure or impending exhaustion?

Investigations:

ABG, bloods
Chest XR
Viral PCR
Peak expiratory flow

100

Describe what bronchospasm is in simple terms? (if you were explaining to a patient).

Bronchospasm is when the muscles around your airways tighten up, causing the airways to narrow. This makes it harder for air to move in and out of your lungs, which can lead to symptoms like wheezing, shortness of breath, coughing, and chest tightness.

100

What first line pharmacotherapy are used in acute bronchospasm in the ICU setting?

Beta2-agonists (Salbutamol, terbutaline)

Anticholinergics (Ipratropium)

Corticosteroids (Prednisolone)

100

What is the target oxygen saturation in someone with COPD?

Generally between 88-92%

For most other patients, a target SpO2 of >92% is sufficient

200

What are differential causes of bronchospasm?

Asthma exacerbation

Acute viral infection (Influenza, RSV)

COPD exacerbation

Anaphylaxis

Foreign body aspiration

Bronchiectasis or chronic bronchitis

Inhalation of irritants/smoke

Drugs: NSAIDs, beta-blockers, ACE inhibitors

200

Describe the physiology of bronchospasm.

Bronchial smooth muscle constriction via vagal and inflammatory mediators.
Airway inflammation and increased mucus production.
Bronchial hyperresponsiveness and exaggerated reactions to stimuli.
V/Q mismatch leading to hypoxemia and hypercapnia.

200

What is the mechanism of action of first line pharmacotherapy (beta2-agonist, anticholinergic, and corticosteroid) in reversing bronchospasm?

1. β2-agonists (e.g. Salbutamol)

β2-agonists are bronchodilators that work by stimulating β2-adrenergic receptors on the smooth muscle cells of the bronchial tree. This activation leads to an increase in cyclic AMP within the cells, which causes smooth muscle relaxation and bronchodilation.
β2-agonists are commonly administered via nebulization or metered-dose inhalers (MDIs) for rapid relief of bronchoconstriction. In severe cases, continuous nebulization or intravenous β2-agonists may be used.

2. Anticholinergics (e.g. Ipratropium)

Anticholinergics work by blocking muscarinic receptors (mainly M3 receptors) in the smooth muscle of the airways, which inhibits the parasympathetic nerve response. This reduces bronchoconstriction and mucus production.
Ipratropium is often given in conjunction with β2-agonists, especially in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) or when there is significant mucus production. It can be given by nebulization and can enhance the bronchodilator effect of β2-agonists.

3. Corticosteroids (e.g. Prednisolone)

Corticosteroids are anti-inflammatory agents that work by reducing airway inflammation and preventing further bronchoconstriction. They decrease the production of inflammatory mediators (like leukotrienes and prostaglandins) and suppress immune cell activity in the lungs (e.g., eosinophils, mast cells).
Systemic corticosteroids are often initiated early in severe exacerbations of asthma or COPD to reduce inflammation and prevent the recurrence of bronchospasm. They take several hours to show effects but are crucial for longer-term control.

200

What are the advantages vs disadvantages of NIV in bronchospasm?

Advantages:

- Helps overcome PEEPi from gas trapping -> reduces inspiratory WOB

- Increases TV and minute ventilation

- Can decrease expiratory work by opposing dynamic airway compression and allowing more expiration with less gas trapping and hyperinflation

- Reduce V/Q mismatch

Disadvantages:

- Claustrophobia/agitation

- Gastric distension

- Dyssynchrony

- Increased expiratory work and hyperinflation

300

What are markers of imminent respiratory arrest?

Altered mental state

Paradoxical respiration

Bradycardia

Quiet chest

Absence of pulsus paradoxus

300

Which interleukins are associated with the inflammatory cascade that contributes to bronchospasm?

IL-4 plays a central role in promoting the immune response that leads to airway inflammation and bronchoconstriction. IL-5 is involved in eosinophil recruitment and IL-13 contributes to airway hyperresponsiveness and mucus production.

300

What is the escalation of medical therapy for bronchospasm?

1st line: Salbutamol, Ipratropium, Corticosteroids

2nd line: Magnesium sulfate

3rd line: IV salbutamol; PDE inhibitors (Aminophylline)

4th line: Ketamine; Volatile anaesthetics (AnaConDa device); Neuromuscular blockade (NMBD); Adrenaline; Heliox; Omalizumab (longer term)

300

When is invasive ventilation indicated? And what are associated risks?

Indications:

Arrest

Severe hypoxia

Altered mental state, uncooperative or can't protect airway

Failure to respond to treatment

Associated risks: Gas trapping --> Hypotension -> PEA arrest, Pneumothorax (barotrauma)

400

Which muscle relaxant is the most likely to be associated with a risk of bronchospasm?

Suxamethonium

400

What is the waterfall effect in bronchospasm?

The waterfall effect in bronchospasm refers to a phenomenon where bronchoconstriction leads to a progressive and self-perpetuating cycle of worsening airway obstruction, making it increasingly difficult to reverse the bronchospasm. This effect can occur particularly in severe cases of bronchospasm, such as in asthma or chronic obstructive pulmonary disease (COPD) exacerbations.

How the Waterfall Effect Works in Bronchospasm:

Initial Bronchoconstriction: In conditions like asthma or COPD, the airways narrow due to inflammation, smooth muscle constriction, and mucus production. This leads to a reduction in airflow and impaired ventilation.
Increased Airway Resistance: The narrowing of the airways increases resistance to airflow, especially during exhalation. The patient may struggle to expel air fully from the lungs, leading to air trapping and hyperinflation of the lungs.
Increased Work of Breathing: As the airways constrict further, the patient needs to exert more effort to breathe. This causes increased work of breathing and can lead to respiratory fatigue.
Decreased Oxygenation: The difficulty in breathing efficiently results in poor oxygenation (hypoxemia) and retention of carbon dioxide (hypercapnia), which can lead to respiratory acidosis.
Further Bronchospasm: As the patient becomes more hypoxic and hypercapnic, the body releases inflammatory mediators (e.g., histamine, leukotrienes) and activates the autonomic nervous system, which causes more bronchoconstriction and exacerbates the cycle. This is the "waterfall" effect—the worsening of bronchospasm feeds into itself, making the situation more severe.
Worsening of Clinical Symptoms: The cycle of worsening obstruction, increasing inflammation, and diminished oxygenation creates a vicious cycle that can rapidly escalate into a life-threatening situation if not reversed.

400

What is AMAX4 and what does it stand for?

AMAX4 is an algorithm for critical care clinicians in anaphylaxis and asthma resuscitation.

Adrenaline 1mcg/kg IV push

Muscle relaxant

Airway - ETT with cuff for high pressures

Xtreme ventilation/Xtra bronchodilators/Xtra vasopressors/Consider pneumothorax

4 minutes to hypoxic brain injury

400

What are indications for considering VV ECMO?

VV ECMO may be indicated in severe bronchospasm when:

There is refractory hypoxemia or hypercapnia despite maximal conventional therapy.
The patient has respiratory muscle fatigue and exhaustion.
There is ARDS secondary to bronchospasm.
Mechanical ventilation fails to optimize oxygenation or ventilation.

VV ECMO is typically considered a rescue therapy when conventional methods (e.g., bronchodilators, steroids, mechanical ventilation) are insufficient, and it is used to provide time for the underlying bronchospasm to resolve while preventing further complications like ventilator-induced lung injury.