Bronchospasm is a sudden, reversible narrowing of the lower airways caused by
contraction of bronchial smooth muscle, airway wall edema, and increased mucus
production. Although commonly associated with asthma or reactive airway disease,
bronchospasm can occur in any patient under the right physiologic or environmental
triggers, including during dental procedures involving sedation.
Because sedation blunts protective reflexes and reduces a patient’s ability to compensate, bronchospasm
in the dental office represents a high-risk airway emergency that demands rapid recognition and decisive action.
Physiology of Bronchospasm
1. Airway Hyperreactivity
Airway irritant receptors (C-fibers, rapidly adapting receptors) respond to triggers such as allergens, cold air, chemical fumes, or mechanical stimulation. Activation of these receptors stimulates vagal cholinergic pathways, releasing acetylcholine that binds to M3 receptors on bronchial smooth muscle, causing constriction.
2. Smooth Muscle Constriction
Bronchial smooth muscle contracts circumferentially around the airway, reducing its diameter. Because airway resistance increases exponentially as radius decreases, even subtle narrowing can severely impede airflow.
3. Inflammatory Edema and Mucus Production
Histamine, leukotrienes, and prostaglandins increase vascular permeability and activate goblet cell mucus secretion. Edema thickens airway walls, and mucus reduces lumen diameter, especially in small bronchi.
4. Ventilation–Perfusion Mismatch
Airflow restriction limits oxygen delivery to alveoli while perfusion remains unchanged. Hypoxemia and rising CO₂ follow, progressing more rapidly under sedation because compensatory mechanisms are impaired.
Triggers of Bronchospasm in the Dental Setting:
• Airway irritation from suction devices, dental debris, or water spray
• Sedative medications that release histamine or reduce protective reflexes
• Undiagnosed or poorly controlled asthma
• Upper respiratory infections
• Allergic reactions to latex, medications, or dental materials
• Anxiety and catecholamine surges
• Cold or dry gas flow
• Airway manipulation (oral airways, nasopharyngeal airways, throat packs)
Why Sedation Increases Risk
1. Blunted Reflexes
Coughing and gagging—critical for clearing secretions—are suppressed, allowing obstruction to worsen silently.
2. Depressed Respiratory Drive
Sedatives diminish the brainstem’s responsiveness to CO₂ and hypoxia.
3. Reduced Airway Tone
Sedation promotes upper-airway collapse, increases airway resistance, and reduces functional residual capacity.
4. Delayed Recognition
Without a dedicated anesthesia provider, early signs such as increased airway pressures or subtle wheezing may be missed.
Clinical Manifestations of Bronchospasm During
Sedation
• Wheezing or prolonged exhalation
• Rising end-tidal CO₂, “shark-fin” ETCO₂ waveform
• Decreasing oxygen saturation
• Increased work of breathing (if awake)
• Difficulty ventilating or high airway resistance
• Tachycardia, agitation, or sudden hemodynamic changes• “Silent chest” in severe obstruction
Preventative Measures in the Dental
Setting
Prevention begins before the patient enters the operatory and continues throughout the
procedure.
1. Pre-Procedure Assessment
• Thorough medical history focusing on asthma, COPD, allergies, recent respiratory infections, hospitalizations, and inhaler use.
• Confirm current asthma control: frequency of rescue inhaler use, nighttime symptoms, steroid medications.
• Ensure high-risk patients have taken their routine bronchodilator on the day of the procedure.
• Identify medication allergies and latex sensitivities.
• Evaluate for signs of active respiratory infection; postpone elective sedation if present.
2. Optimization Before Sedation
• For asthma patients, consider pre-treatment with albuterol (2–4 puffs) even if asymptomatic.
• Maintain a calm environment to reduce anxiety-related bronchoconstriction.
• Use humidified oxygen when possible.
• Avoid sedatives known for histamine release in susceptible individuals.
3. Equipment & Monitoring Preparedness
• Have rescue medications immediately accessible (albuterol MDI with spacer, nebulizer setup, epinephrine, corticosteroids).
• Continuous monitoring with pulse oximetry, capnography, and, for deeper sedation, ECG and BP readings at appropriate intervals.
• Ensure suction devices are functioning and avoid unnecessary airway stimulation.
4. Staff Training
• Conduct regular simulation training on airway obstruction scenarios, including bronchospasm.
• Establish a clear emergency role assignment plan (who ventilates, who administers medications, who calls EMS).
Airway Management & Treatment of Bronchospasm in the Dental Office
Rapid response is essential. Treatment begins with stopping the procedure and following a structured escalation.
1. Immediate First Steps
• Stop the dental procedure and remove any instruments or debris.
• Administer 100% oxygen; switch to positive-pressure ventilation if needed.
• Ensure the airway is open using chin lift, jaw thrust, or placement of an oropharyngeal/nasopharyngeal airway if tolerated.
2. Assess Ventilatory Effort
• If breathing spontaneously, encourage the patient to take slow, deep breaths.
• If ventilation is inadequate, begin bag-mask ventilation with attention to expiratory time to avoid gas trapping.
3. Pharmacologic Management
First-Line: Bronchodilation
• Albuterol (salbutamol) MDI, 4–8 puffs via spacer, repeat q20 minutes as needed.
• For severe cases: Nebulized albuterol (2.5–5 mg).
Adjuncts
• Ipratropium bromide (neb 0.5 mg) may be added for enhanced bronchodilation.
• Epinephrine for severe bronchospasm, anaphylaxis, or impending respiratory arrest:
0.3–0.5 mg IM (1:1000) in adults
0.01 mg/kg IM in children
• Corticosteroids (e.g., dexamethasone, methylprednisolone) help reduce airway inflammation but have delayed onset.
If an Allergic Etiology Is Suspected
• Administer epinephrine IM immediately, even in moderate bronchospasm.
• Add antihistamines (e.g., diphenhydramine) and IV fluids.
4. Advanced Airway Measures (If Needed)
These require appropriate training and equipment:
• Bag-mask ventilation with PEEP or optimized technique
• Supraglottic airway device if mask ventilation is difficult
• Endotracheal intubation if ventilation or oxygenation cannot be maintained
o This is high-risk during bronchospasm and requires an experienced
provider
• Avoid repeated or traumatic attempts, which may worsen bronchospasm.
5. Call EMS Early
If bronchospasm does not resolve quickly, oxygen saturation continues to fall, or advanced airway intervention is required, activate emergency medical services immediately.
6. Post-Event Care
• Monitor the patient until stable and asymptomatic.
• Document the episode thoroughly.
• Recommend follow-up with a primary care or pulmonary specialist.
• Conduct an internal review to identify opportunities to improve office readiness.
Conclusion
Bronchospasm during dental sedation is a high-acuity event that demands prevention, rapid recognition, and coordinated intervention. Understanding the underlying physiology and maintaining strict safety protocols—including pre-procedure screening, continuous monitoring, immediate access to rescue medications, and properly trained personnel - are essential to preventing catastrophic airway emergencies in the dental office. With robust preparation and appropriate staffing, the risk of serious outcomes can be significantly reduced.
Bronchospasm Risks During Sedation – Quick Quiz
Test your understanding of bronchospasm risk factors, triggers, and management in the dental office.