Bronchospasm

Bronchospasm is a sudden, reversible narrowing of the lower airways due to contraction of bronchial smooth muscle, often accompanied by mucosal edema and mucus hypersecretion. It presents across diverse settings from asthma and allergic reactions to exercise, infection, and anesthesia. Early recognition and rapid treatment restore airflow, relieve symptoms, and prevent progression to respiratory failure.

This article introduces foundational concepts, clarifies terminology, and outlines the clinical scope of bronchospasm. Subsequent sections will expand on mechanisms, evaluation, and evidence-based management.

Introduction

Bronchospasm is a hallmark event in obstructive airway disease and a frequent cause of acute dyspnea and wheeze in both outpatient and emergency settings. It reflects hyperreactivity of airway smooth muscle to a variety of triggers that amplify cholinergic tone, inflammatory mediator release, or both. Although typically reversible with bronchodilators and anti-inflammatory therapy, severe episodes can threaten ventilation and gas exchange.

The condition spans all ages and care environments, from exercise-induced bronchoconstriction in athletes to perioperative bronchospasm during airway manipulation. Understanding its pathophysiology, precipitants, and clinical patterns enables timely intervention and targeted prevention strategies.

Definition and Overview

Meaning of Bronchospasm

Bronchospasm is defined as an abrupt increase in airway resistance caused by contraction of bronchial smooth muscle, often accompanied by airway wall edema and variable mucus plugging. The process is characteristically reversible either spontaneously or with pharmacologic therapy.

Pathophysiological Concept

• Airway smooth muscle contraction: Hyperreactive muscle constricts in response to stimuli such as allergens, cold air, pollutants, or mechanical irritation.
• Inflammatory milieu: Mediators including histamine, leukotrienes, and prostaglandins augment bronchoconstriction and edema.
• Neural control: Enhanced vagal tone and reduced beta-adrenergic responsiveness contribute to airway narrowing.

Epidemiology and Clinical Relevance

• Occurs across phenotypes of asthma, COPD with bronchial hyperreactivity, and allergic disorders.
• Common in exercise-induced bronchoconstriction, viral bronchitis, and perioperative airway events.
• Drug related forms are linked to beta-blockers, NSAIDs, and aerosol irritants.

Pathophysiology

Normal Airway Physiology

Under normal conditions, the bronchial tree maintains a balance between smooth muscle tone and airway patency to ensure efficient airflow and gas exchange. Airway smooth muscle, arranged in circular layers, regulates airway caliber by contracting or relaxing in response to neural and chemical signals. Parasympathetic cholinergic fibers release acetylcholine, which binds to muscarinic receptors to cause mild constriction, while sympathetic beta-2 adrenergic activation induces relaxation through cyclic AMP pathways.

In healthy individuals, this dynamic balance preserves airway resistance at minimal levels, allowing unrestricted ventilation. The airway epithelium also releases relaxing factors such as nitric oxide and prostaglandins that prevent excessive contraction, ensuring stable ventilation-perfusion relationships.

Mechanism of Bronchoconstriction

• Airway Smooth Muscle Hyperreactivity: In bronchospasm, smooth muscle fibers exhibit exaggerated responsiveness to a wide range of stimuli. This hyperreactivity is a characteristic feature of asthma and other reactive airway conditions, leading to rapid constriction even with minimal provocation.
• Inflammatory Mediators and Cellular Involvement: Mast cells, eosinophils, and basophils release histamine, leukotrienes, and prostaglandins during allergic or inflammatory responses. These substances increase intracellular calcium levels in smooth muscle, promoting contraction and mucosal edema.
• Neural and Humoral Pathways: Excess vagal stimulation and diminished beta-adrenergic receptor sensitivity result in loss of bronchodilatory control. Reflex bronchoconstriction may also occur following airway irritation, infection, or chemical exposure.

Consequences of Bronchospasm

• Increased Airway Resistance: Narrowing of the bronchi and bronchioles raises resistance to airflow, especially during expiration, causing air trapping and hyperinflation.
• Altered Ventilation-Perfusion Ratio: Uneven airway narrowing leads to ventilation-perfusion mismatch, where some alveoli are under-ventilated relative to blood flow.
• Impaired Gas Exchange: Resulting hypoxia and carbon dioxide retention (hypercapnia) contribute to dyspnea, wheezing, and fatigue in prolonged episodes.

Etiology and Risk Factors

Allergic and Immunologic Triggers

Allergic mechanisms represent one of the most common causes of bronchospasm. Exposure to environmental allergens such as pollen, animal dander, or dust mites stimulates IgE-mediated mast cell degranulation, releasing histamine and leukotrienes that cause airway constriction. Individuals with atopy or allergic asthma are particularly prone to recurrent episodes following antigen exposure.

Environmental and Occupational Exposures

Inhalation of irritants such as smoke, industrial dust, volatile chemicals, and cold air can induce reflex bronchoconstriction. Occupational bronchospasm is commonly seen among workers exposed to isocyanates, cleaning agents, or metal fumes. Chronic exposure may lead to airway remodeling and persistent hyperreactivity.

Infectious Causes

Respiratory infections, especially viral illnesses like influenza, parainfluenza, and respiratory syncytial virus, can precipitate bronchospasm through airway inflammation and edema. Bacterial infections such as bronchitis and pneumonia may also contribute to transient airway narrowing during the acute phase.

Drug-Induced Bronchospasm

• Beta-blockers: Non-selective agents such as propranolol block beta-2 receptors, inhibiting bronchodilation and precipitating constriction in susceptible individuals.
• NSAIDs: In some asthmatic patients, inhibition of cyclooxygenase pathways enhances leukotriene production, triggering airway narrowing (aspirin-exacerbated respiratory disease).
• Contrast Media and Anesthetic Agents: Certain radiologic dyes and volatile anesthetics can provoke bronchospasm through direct airway irritation or hypersensitivity reactions.

Exercise-Induced Bronchospasm

Physical exertion, particularly in cold or dry environments, can cause transient airway narrowing due to hyperventilation-induced cooling and drying of the bronchial mucosa. This form is common among athletes and individuals with underlying asthma and typically appears within minutes of exercise onset or cessation.

Anesthesia-Related and Intubation-Induced Bronchospasm

During anesthesia, airway manipulation, endotracheal intubation, or exposure to irritant gases can elicit bronchospasm, especially in patients with reactive airway disease. The risk is heightened by inadequate anesthesia depth or pre-existing respiratory conditions. Prompt recognition and bronchodilator administration are essential intraoperatively to prevent hypoxia.

Other Risk Factors

• Cold air and pollutants: Exposure to cold, dry air or environmental pollutants may provoke airway irritation and spasm.
• Tobacco smoke: Both active and passive smoking increase airway inflammation and hyperreactivity, enhancing susceptibility to bronchospasm.
• Genetic predisposition: Family history of asthma or allergic diseases increases the likelihood of developing bronchial hyperreactivity.

Clinical Features

Respiratory Symptoms

Bronchospasm typically manifests with acute or recurrent respiratory symptoms that reflect airway narrowing and increased resistance to airflow. The severity of symptoms can vary from mild intermittent episodes to life-threatening obstruction, depending on the underlying cause and extent of bronchial involvement.

• Wheezing: A high-pitched whistling sound most prominent during expiration, caused by turbulent airflow through constricted bronchi. It may be diffuse or localized depending on the distribution of bronchospasm.
• Chest tightness: A subjective sensation of pressure or constriction in the chest resulting from increased intrathoracic pressure and hyperinflation.
• Shortness of breath (Dyspnea): A feeling of breathlessness or labored breathing, often aggravated by exertion or exposure to triggering agents.
• Cough: Usually dry or minimally productive, it may occur at night or early morning and worsen after exposure to irritants or allergens.

Physical Examination Findings

• Prolonged expiratory phase: Due to delayed emptying of air from the constricted airways, resulting in audible wheezing during expiration.
• Use of accessory muscles: Contraction of neck and intercostal muscles indicates increased work of breathing, particularly in severe cases.
• Reduced air entry: Diminished breath sounds on auscultation, reflecting airflow limitation and localized or diffuse bronchoconstriction.
• Hyperresonant percussion note: Indicates air trapping and lung hyperinflation, often seen in prolonged or severe episodes.

Systemic Manifestations

• Tachypnea and tachycardia: Compensatory responses to hypoxia and elevated respiratory effort.
• Anxiety or agitation: Common in acute bronchospasm due to hypoxemia and the subjective sensation of suffocation.
• Cyanosis: Bluish discoloration of lips or nail beds in severe obstruction, reflecting inadequate oxygenation.
• Fatigue and confusion: Late signs of respiratory muscle exhaustion or impending respiratory failure.

Diagnosis

Clinical Evaluation

The diagnosis of bronchospasm is primarily clinical, based on characteristic symptoms, physical findings, and response to bronchodilator therapy. A detailed history should identify potential triggers, timing, frequency, and associated systemic features. Distinguishing acute bronchospasm from other causes of dyspnea is essential for prompt and appropriate treatment.

• History taking: Focus on recent allergen exposure, infection, medication use, physical exertion, or anesthesia.
• Symptom pattern: Episodic nature and reversibility after bronchodilator use support the diagnosis.
• Family or personal history: Presence of asthma, atopy, or chronic respiratory disease provides important diagnostic clues.

Investigations

• Spirometry and Pulmonary Function Tests: Demonstrate reversible airway obstruction characterized by reduced FEV₁ and FEV₁/FVC ratio, with significant improvement after bronchodilator administration.
• Peak Expiratory Flow Rate (PEFR): Provides rapid assessment of airflow limitation and helps monitor response to therapy in acute or chronic cases.
• Arterial Blood Gas (ABG) Analysis: Reveals hypoxemia in moderate cases and hypercapnia in severe bronchospasm, indicating respiratory muscle fatigue.
• Chest X-ray: Usually normal but may show hyperinflated lungs or exclude differential diagnoses such as pneumonia, pneumothorax, or foreign body aspiration.
• Allergy Testing: Skin prick tests or serum IgE measurements may identify specific allergens responsible for recurrent episodes.
• CT or Bronchoscopy: Reserved for atypical cases to evaluate structural abnormalities or obstruction not explained by routine studies.

Differential Diagnosis

Several respiratory and cardiovascular conditions can mimic bronchospasm. Differentiating these based on history, clinical presentation, and diagnostic findings ensures appropriate treatment.

Condition	Distinguishing Features
Asthma	Recurrent, reversible airway obstruction often triggered by allergens or exercise; may be associated with atopy.
Chronic Obstructive Pulmonary Disease (COPD)	Progressive, partially reversible obstruction in smokers; less variability in symptoms and airflow limitation.
Foreign Body Aspiration	Sudden onset of unilateral wheeze or localized decreased breath sounds, often in children.
Anaphylaxis	Accompanied by urticaria, hypotension, and angioedema; rapid onset after allergen exposure.
Pulmonary Embolism	Dyspnea with pleuritic chest pain and hypoxia; imaging or D-dimer testing confirms diagnosis.

Complications

Although bronchospasm is often transient and reversible, prolonged or severe episodes can lead to a range of complications affecting pulmonary function and systemic physiology. These complications arise due to sustained hypoxia, increased work of breathing, and secondary effects on the cardiovascular system.

Acute Respiratory Distress

Severe bronchospasm may precipitate acute respiratory distress, characterized by marked dyspnea, tachypnea, and hypoxemia. Persistent airway obstruction leads to dynamic hyperinflation, reduced tidal volume, and ventilation-perfusion mismatch. Without prompt intervention, oxygenation deteriorates rapidly, progressing toward respiratory failure.

Status Asthmaticus

When bronchospasm fails to respond to standard bronchodilator and corticosteroid therapy, it may evolve into status asthmaticus—a life-threatening condition marked by severe, persistent airway obstruction. Patients often present with silent chest, severe hypoxia, hypercapnia, and altered mental status. This condition requires urgent intensive care management with continuous bronchodilators, systemic steroids, and ventilatory support.

Respiratory Failure

In extreme cases, respiratory muscle fatigue and rising carbon dioxide levels result in type II respiratory failure. Signs include confusion, lethargy, and cyanosis, reflecting hypercapnic encephalopathy. Arterial blood gas analysis typically shows elevated PaCO₂ with respiratory acidosis. Mechanical ventilation may be required to stabilize gas exchange and relieve respiratory muscle load.

Air Trapping and Dynamic Hyperinflation

Incomplete expiration during bronchospasm traps air within the lungs, leading to progressive hyperinflation. This increases intrathoracic pressure, reduces venous return, and can impair cardiac output. The resulting “auto-PEEP” phenomenon contributes to hemodynamic instability and worsens respiratory distress, especially in mechanically ventilated patients.

Secondary Complications

• Hypoxemia-induced cardiac stress: Prolonged oxygen deprivation can precipitate arrhythmias, ischemia, or cardiac arrest in susceptible individuals.
• Pneumothorax: Forceful coughing or barotrauma during ventilation may rupture alveoli, leading to pneumothorax or subcutaneous emphysema.
• Metabolic derangements: Lactic acidosis from muscle overuse and hypoxia can further compromise respiratory and cardiac performance.

Treatment and Management

Immediate Management

Prompt recognition and rapid intervention are essential in reversing bronchospasm and restoring airway patency. Initial management focuses on relieving airway constriction, correcting hypoxia, and addressing underlying triggers.

• Airway, Breathing, Circulation (ABC): Assess airway patency, oxygen saturation, and vital signs. Initiate oxygen therapy via face mask or nasal cannula to maintain SpO₂ above 94%.
• Short-Acting Beta-2 Agonists (SABA): Inhaled bronchodilators such as salbutamol or albuterol are first-line agents that relax bronchial smooth muscle. Nebulized delivery ensures rapid relief in acute episodes.
• Anticholinergic Agents: Ipratropium bromide can be added to beta-agonists to enhance bronchodilation through inhibition of vagal-mediated constriction.
• Systemic Corticosteroids: Intravenous or oral steroids such as hydrocortisone or prednisolone reduce airway inflammation and prevent recurrence. Their effect is delayed but crucial for sustained recovery.
• Intravenous Magnesium Sulfate: Used in severe bronchospasm resistant to initial therapy; it relaxes smooth muscle by inhibiting calcium influx and inflammatory mediator release.
• Adrenaline (Epinephrine): Indicated in anaphylaxis-related bronchospasm; administered intramuscularly to counteract allergic airway constriction and circulatory collapse.

Long-Term Management

Long-term management aims to control inflammation, reduce airway hyperreactivity, and prevent recurrent episodes. Regular monitoring and patient education are key components of effective maintenance therapy.

• Inhaled Corticosteroids (ICS): Cornerstone of long-term control, reducing airway inflammation and hyperresponsiveness.
• Long-Acting Beta-2 Agonists (LABA): Used in combination with ICS for patients with frequent episodes or nocturnal symptoms.
• Leukotriene Receptor Antagonists: Agents such as montelukast or zafirlukast reduce leukotriene-mediated bronchoconstriction and inflammation.
• Allergen and Trigger Avoidance: Identifying and avoiding specific triggers such as dust mites, smoke, or occupational irritants prevents relapse.
• Vaccination: Annual influenza and pneumococcal vaccines help prevent infections that can exacerbate bronchospasm.

Supportive Care

• Hydration: Adequate fluid intake thins mucus secretions, improving clearance and airflow.
• Humidified Oxygen: Maintains mucosal moisture and comfort during oxygen therapy.
• Chest Physiotherapy: Beneficial in cases with retained secretions or mucus plugging, promoting expectoration.
• Continuous Monitoring: Frequent reassessment of respiratory rate, oxygen saturation, and peak expiratory flow ensures timely adjustment of therapy.

Refractory and Severe Cases

Patients unresponsive to standard therapy require escalation of care in an intensive care setting. Mechanical ventilation with controlled parameters may be necessary to support gas exchange and reduce work of breathing. Non-invasive ventilation can be considered in moderate cases to avoid intubation. Sedation and muscle relaxation may be used cautiously under expert supervision to prevent dynamic hyperinflation and ventilator-associated injury.

Prevention and Patient Education

Preventing bronchospasm involves identifying and avoiding known triggers, maintaining optimal control of underlying respiratory conditions, and ensuring correct use of medications. Patient education plays a crucial role in minimizing recurrence, improving adherence to therapy, and recognizing early warning signs of airway obstruction.

Avoidance of Known Triggers

• Environmental Control: Patients should minimize exposure to allergens such as dust mites, pollen, animal dander, and molds. Regular cleaning, use of air filters, and maintaining low indoor humidity can help reduce allergen load.
• Air Quality Management: Avoidance of tobacco smoke, industrial fumes, and air pollutants is essential. Staying indoors on high-pollution days and using protective masks can decrease irritation-related bronchospasm.
• Occupational Safety: Workers exposed to chemicals or particulate matter should use protective gear and undergo regular respiratory evaluations to detect early airway hyperreactivity.

Proper Inhaler Technique and Adherence

Incorrect use of inhalers significantly reduces medication efficacy. Patients must be educated on correct inhalation technique, device maintenance, and adherence to prescribed dosages. Demonstrations using metered-dose or dry-powder inhalers during clinical visits reinforce proper usage and ensure consistent drug delivery to the airways.

• Use of spacer devices can improve deposition of inhaled medication, particularly in children and elderly patients.
• Regular follow-up appointments help monitor compliance and address technique errors early.

Smoking Cessation

Smoking exacerbates airway inflammation and reduces the effectiveness of bronchodilator and corticosteroid therapy. Complete cessation of smoking, including avoidance of passive exposure, is strongly advised. Counseling, nicotine replacement therapy, and pharmacologic aids such as bupropion or varenicline can enhance success rates in motivated individuals.

Vaccination

Respiratory infections frequently precipitate bronchospasm, especially in patients with asthma or COPD. Vaccination helps reduce this risk.

• Influenza vaccine: Annual vaccination decreases the likelihood of viral infection-induced airway constriction.
• Pneumococcal vaccine: Protects against bacterial infections that can worsen bronchial inflammation.

Pre-Exercise Bronchodilator Use

In individuals with exercise-induced bronchospasm, using a short-acting beta-2 agonist 10–15 minutes before physical activity can prevent airway narrowing. Warming up gradually and avoiding cold, dry air also help minimize bronchoconstrictive episodes during exercise. Long-term control with inhaled corticosteroids may be necessary for frequent or severe symptoms.

Patient Self-Management and Early Intervention

Educating patients to recognize early symptoms such as mild wheezing or chest tightness allows prompt use of rescue medication before severe obstruction develops. Personalized action plans detailing when to use bronchodilators, adjust maintenance therapy, or seek emergency care empower patients and improve outcomes. Pulmonary rehabilitation programs may further enhance self-care skills and lung function.

Prognosis and Outcomes

Factors Influencing Recovery

The prognosis of bronchospasm depends on its underlying cause, frequency of episodes, and timeliness of treatment. Patients with well-controlled asthma or reactive airway disease typically achieve complete recovery with appropriate management. Conversely, recurrent or severe bronchospasm associated with chronic lung conditions can lead to long-term airflow limitation and structural airway remodeling.

• Favorable factors: Early diagnosis, adherence to inhaled therapy, and effective trigger avoidance improve long-term prognosis.
• Unfavorable factors: Ongoing exposure to allergens, poor medication compliance, and coexisting disorders such as COPD or cardiovascular disease may worsen outcomes.

Prognosis in Recurrent or Chronic Cases

Chronic or recurrent bronchospasm, especially in poorly controlled asthma, can lead to persistent airway inflammation and remodeling. Over time, this results in fixed airflow obstruction resembling chronic obstructive patterns. However, with appropriate therapy—including anti-inflammatory treatment and patient education—most patients achieve near-normal lung function and symptom-free intervals.

Long-Term Effects on Pulmonary Function

Repeated episodes of bronchospasm cause structural changes such as smooth muscle hypertrophy, basement membrane thickening, and submucosal fibrosis. These alterations increase airway rigidity and reduce reversibility of obstruction. Regular pulmonary function testing helps monitor these changes and adjust treatment to preserve maximal lung capacity.

Quality of Life and Functional Outcomes

Successful management of bronchospasm significantly enhances quality of life by improving exercise tolerance, sleep quality, and psychological well-being. Comprehensive care—including pharmacologic control, trigger modification, and lifestyle adaptation—reduces hospitalizations and absenteeism, leading to better physical and social functioning.

Prognostic Summary

With proper diagnosis, individualized therapy, and consistent follow-up, bronchospasm has an excellent prognosis in the majority of cases. Early intervention during acute episodes and adherence to preventive measures remain the cornerstone of favorable outcomes. Patients who actively engage in their care demonstrate lower recurrence rates and improved long-term respiratory health.

Recent Advances and Research Directions

Novel Bronchodilator Agents

Ongoing research continues to refine pharmacologic management of bronchospasm through the development of new bronchodilators with improved efficacy, faster onset, and longer duration of action. Ultra-long-acting beta-2 agonists such as indacaterol and vilanterol provide sustained bronchodilation for up to 24 hours, improving adherence and reducing dosing frequency. New-generation muscarinic antagonists, including tiotropium and glycopyrrolate, are being evaluated for their role in chronic bronchospastic disorders beyond COPD, such as severe asthma.

Combination inhalers that integrate multiple mechanisms—such as beta-2 agonists with corticosteroids or dual bronchodilator formulations—are also demonstrating superior control in patients with overlapping airway diseases. Future advancements may include fast-acting inhaled agents with nanoparticle delivery systems for enhanced airway penetration and reduced systemic side effects.

Targeted Biologic Therapies

The emergence of biologic agents represents a major shift in the treatment of severe and refractory bronchospastic conditions. These therapies specifically target immune mediators involved in airway inflammation and hyperreactivity.

• Anti-IgE Therapy (Omalizumab): Reduces allergic airway inflammation by blocking circulating IgE, beneficial for atopic individuals with frequent bronchospasm episodes.
• Anti-IL-5 Agents (Mepolizumab, Reslizumab, Benralizumab): Decrease eosinophil proliferation and activation, mitigating airway inflammation and reducing exacerbation rates.
• Anti-IL-4 and Anti-IL-13 Pathway Inhibitors (Dupilumab): Address type-2 inflammation by modulating cytokine signaling involved in mucus production and smooth muscle responsiveness.

These biologics have significantly improved outcomes in patients who do not respond adequately to traditional inhaled therapies. Ongoing clinical trials aim to identify new targets and biomarkers to personalize therapy for patients with different endotypes of airway hyperreactivity.

Noninvasive Ventilation and Advanced Respiratory Support

Recent advances in ventilatory support have expanded treatment options for patients with severe bronchospasm unresponsive to conventional therapy. Noninvasive ventilation (NIV) using bilevel positive airway pressure (BiPAP) can reduce the work of breathing, correct hypercapnia, and prevent the need for intubation in select cases. Heliox therapy—administering a helium-oxygen gas mixture—has been shown to improve airflow in resistant bronchospasm by decreasing gas density and airway turbulence.

High-flow nasal cannula oxygen therapy (HFNC) is another emerging approach, offering heated, humidified oxygen at high flow rates to improve oxygenation and comfort. These supportive strategies are particularly valuable in acute care settings, allowing stabilization before definitive treatment or recovery.

Genetic and Molecular Insights into Airway Hyperreactivity

Genetic research has identified several polymorphisms associated with bronchial hyperresponsiveness, including variations in beta-2 adrenergic receptors, cytokine genes, and inflammatory mediators. These discoveries provide insight into why some individuals are more susceptible to severe or recurrent bronchospasm. Studies on epigenetic regulation and gene-environment interactions are further revealing how environmental exposures modify genetic predisposition to airway reactivity.

At the molecular level, advances in transcriptomic and proteomic profiling have uncovered new biomarkers of airway inflammation, enabling precision medicine approaches. Future diagnostic models may incorporate these biomarkers to predict disease severity, optimize treatment selection, and monitor therapeutic response more accurately.

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