Bronchoconstriction - Causes, Symptoms, Diagnosis, and Treatment

Introduction:

Bronchoconstriction can be defined as the contraction of the bronchial muscles causing the bronchial lumen to narrow and obstruct air movement to and from the lungs. The bronchial wall consists of smooth muscles innervated by the autonomic nervous system. Muscle tonicity is regulated to match the body's requirement for air. Bronchoconstriction can often be confused with the word bronchospasm (muscles that cover the lungs' airway become tight), which refers to spontaneous activation of the parasympathetic nervous system that gives rise to bronchial constriction, known as bronchospasm.

What Is the Pathophysiology of Bronchoconstriction?

Various triggering factors such as infection, irritants, pollution, exercise, exposure to cold air, or psychogenic factors may be involved. Mast cells present in the lungs and inflammatory cells recruited as a result of the initial reaction produce a multitude of mediators such as histamine, tumor necrotizing factor (TNF) alpha, prostaglandins (PGs), leukotrienes (LTs), platelet-activating factors (PAF), interleukins (IL) which constrict bronchial smooth muscle, cause mucosal edema or swelling, hyperemia (increased blood flow), and viscid secretions, all resulting in reversible airway obstruction. The inflammation perpetuates itself from cell-to-cell communication and the recruitment of more and more inflammatory cells. Bronchial smooth muscle hypertrophy occurs over time, and damage to bronchial epithelium accentuates the hyperreactivity. Vagal discharge to the bronchial muscle is enhanced reflexively. Airway remodeling progressively worsens the disease.

Where Can One See Bronchoconstriction?

Bronchoconstriction can be characteristically seen in cases of:

• Asthma: Asthma is a chronic inflammatory disorder that is characterized by hyperresponsiveness of the tracheobronchial smooth muscle to various stimuli, resulting in narrowed airways. Increased secretion, along with mucosal edema and mucus plugging, makes it difficult for the air to flow unobstructed through the airways and to breathe.

• Emphysema: Emphysema (damage to lung's air sac) is a condition in which there is destruction and enlargement of the lung parenchyma distal to the terminal part. The most significant risk factor for emphysema is cigarette smoking. Smoking stimulates inflammatory cells, causing elastolysis and emphysema. A characteristic feature of emphysema is a barrel chest. Typically, the anteroposterior to transverse ratio is 5:7 or 1:2, but in the case of emphysema, it becomes 1:1 due to hyperinflation

• Infection: Viral infections.

• Stress: Psychological stress.

• Others: Other health issues.

What Are the Causes of Bronchoconstriction?

The exact cause is unknown. However, there are various triggering agents which may cause bronchi to constrict, such as:

• Allergens.

• Smoke.

• Cold air.

• Dry air.

• Environmental pollutants.

• Chemicals.

• Respiratory infections.

• Pulmonary diseases.

• Stress.

• Exercise.

What Are the Signs and Symptoms of Bronchoconstriction?

The signs and symptoms of bronchoconstriction are:

• Cough, specifically in the early morning.

• Wheeze (a high-pitched whistling noise that occurs while breathing).

• Shortness of breath.

• Chest tightness.

• Chest pain.

• Fatigue.

What Is the Management of Bronchoconstriction?

Bronchoconstriction can be managed with the help of drugs that relaxes the muscles around the airways. These drugs are most effective against acute asthma attacks.They can be of three types:

Beta 2- Agonists: The adrenergic drugs cause bronchodilation through beta two receptor stimulation, which causes increased cAMP (cyclic adenosine monophosphate) formation in the bronchial muscle cells, thereby causing bronchodilation. In addition, high levels of cAMP in mast cells and other inflammatory cells reduce mediator release. The beta-two adrenergic receptors are primarily found on the alveolar cells and have less or no effects on other organs. These drugs are the drug of choice in reversible airway obstruction but should be used cautiously in hypertensive and cardiac patients. They are the fastest-acting bronchodilators when inhaled. In addition, they increase mucus clearance by increasing ciliary action.

It can be further classified into the following:

• Short-Acting Beta Agonists (SABA): Itis the best drug for relieving asthma attacks. They are also used to prevent exercise-induced asthma. Most drugs, especially inhaled ones, act within minutes, and the action lasts for two to four hours. It is, therefore, used to abort and terminate asthma attacks, but it is not suitable for round-the-clock prophylaxis. Inhalation routes mainly give them through metered dose inhalers or nebulizers. It can be given orally or parenterally. Examples- Salbutamol and Terbutaline.

• Long-Acting Beta Agonists (LABA): They are used to prevent asthma attacks and are effective for 12 hours, so it is administered twice daily. Therefore, they can be used for rapid reversal of bronchoconstriction and shed round-the-clock bronchodilation on a regular morning evening. For example- Salmeterol and Formoterol.

• Ultra Long-Acting Beta-Agonists: They are effective for up to 24 hours, so only a single dose per day is given, for example- Indacaterol.

• Anticholinergics: Anticholinergics are another group of bronchodilators that can provide quick relief from an asthma attack. They act by blocking the muscarinic receptors. They are long-acting muscarinic antagonists that cause bronchodilation and decrease mucus production like Ipratropium bromide and Tiotropium. They are the quaternary derivatives of atropine. Common adverse effects include nasal dryness, irritation, dry mouth, bleeding, and trouble breathing.

• Methylxanthines: They are also bronchodilators; the most common example is Theophylline. It is a narrow therapeutic index drug requiring therapeutic drug monitoring. It is rarely used in chronic obstructive pulmonary disease (COPD). The adverse effects include headache, nausea, and vomiting.

• Leukotriene Antagonists: They are synthesized by the inflammatory cells in the airways, like Montelukast and Zafirlukast. These are leukotriene receptor antagonists, which inhibit leukotriene release. It is a major inflammatory mediator causing swelling. They are indicated for the prophylactic therapy of mild to moderate asthma as an alternative to inhaled corticosteroids. They are well-absorbed drugs. Both drugs are safe and produce mild side effects like headaches and rashes.

• Mast Cell Stabilizers: Like Sodium cromoglycate, which is administered in an aerosol form by a metered dose inhaler. It is a synthetic chromone derivative that inhibits the degranulation of mast cells by triggering stimuli. Mast cells release mediators like histamine, leukotrienes, and other inflammatory cells. It does not act as a bronchodilator, so it is ineffective if given during an asthma attack. It is not orally absorbed.

Conclusion:

Bronchoconstriction is a defense mechanism of the body against toxic irritants harmful to the body. The irritants activate the sensory nerves, and the action potentials are conducted through the vagus nerve to the brainstem, which immediately causes reflex bronchoconstriction, accompanied by hypersecretion of mucus, cough, and dyspnea (shortness of breath). Severe bronchoconstriction may be fatal and can lead to death. Therefore, early intervention and management are recommended in these cases.