Respiratory Pharmacology: Asthma Management

Topic/Respiratory Pharmacology

• Topic: Pathophysiology and management of reactive airway disease
• Objectives:
  • Review airway physiology
  • Explain the inflammatory process and how it contributes to bronchoconstriction
  • List asthma triggers
  • Describe the clinical presentation of an asthma patient
  • Explain how end tidal monitoring is beneficial in monitoring a patient suffering from an asthma attack
  • Differentiate between asthma and status asthmaticus
  • Explain best evidence-based treatment for asthma including the roles of beta 2 agonists, anticholinergics, steroids, and sympathomimetics
• NOCP:
  • Conduct respiratory system assessment and interpret findings
  • Conduct oximetry testing and interpret findings
  • Conduct end tidal carbon dioxide monitoring and interpret findings
  • Follow safe process for responsible medication administration
  • Administer medication via inhalation
  • Provide care to patients experiencing signs & symptoms involving respiratory system

Physiology of Airway Disease – Asthma

• Review of Airway Physiology:
  • Air moves through upper airways (mouth, nose) into lower airways (trachea, bronchioles, alveoli)
  • Trachea and upper bronchi have cartilage, lower airways have smooth muscle allowing for contraction and relaxation
  • Alveoli are the site of gas exchange
  • Airways are innervated by autonomic nervous system with parasympathetic & sympathetic stimulation
  • Normally parasympathetic stimulation (vagus) overrides sympathetic, resulting in a slight bronchoconstriction.
  • Exercise increases need for airflow, inhibiting vagal bronchoconstriction and increasing sympathetic bronchodilation

Inflammatory Mediators

• Mast cells release chemicals that cause inflammation.
• Mast cells are immune cells found in tissues throughout the body, near blood vessels, nerves, skin, lungs, and digestive tract.
  • Allergic reactions : Histamine, heparin released in allergic response
  • Immune defense; Act as sentinels, detecting and responding to harmful pathogens
  • Wound healing and tissue repair : Contribute to wound healing and angiogenesis
  • Regulation of blood flow : Release histamine, increasing blood flow in immune responses and healing

Clinical Significance

• Mast Cell Activation Syndrome (MCAS): Mast cells release too many chemicals leading to chronic and systemic issues.
• Anaphylaxis: Severe, potentially life-threatening reaction involving widespread mast cell activation and histamine release

Key Roles of Mast Cells in Asthma

• Release of Mediators: Mast cells release histamine, leukotrienes, prostaglandins causing inflammation, bronchoconstriction, increased mucus
• Bronchoconstriction: Histamine, other mediators constrict airway smooth muscles leading to breathing difficulty.
• Inflammatory Response: Mast cells contribute to early-phase and late-phase response, allergen exposure, inflammation, and hyperresponsiveness
• Recruitment of Other Immune Cells: Mast cells attract other immune cells (eosinophils & T cells) amplifying inflammatory response, contributing to chronic asthma

Asthma - Intrinsic vs. Extrinsic

• Extrinsic Asthma (Allergic Asthma):
  • Onset in childhood & adolescence
  • Family history common
  • Often associated with other allergic disorders
  • Attacks related to specific allergens (pollen, mold, pet dander, foods)
  • Immune response involves IgE antibodies recognizing allergens
  • Most common type of asthma (60-90%)

Asthma Symptoms

• Wheezing, coughing, chest tightness, difficulty breathing
• Attacks can vary from mild to severe episodes
• Variation in onset time
• Worse at night

Asthma and the Role of ETCO2

• Mechanism: Asthma is ventilation problem, not oxygenation
• Airway constriction: Prolonged expiration, wheezing, turbulent airflow
• Carbon dioxide buildup: Air trapped in alveoli, fatigue, inability to exhale completely
• Capnography: Reflects real-time CO2 elimination during exhalation, helping assess severity
• ETCO2 levels: Typically 35-45 mmHg; In asthma, it may fall initially as respiratory rate increases to compensate for CO2 overload but then rises with worsening respiratory failure (over 100 mmHg)

Status Asthmaticus

• Severe asthma attack unresponsive to standard treatment
• Progressive complication, life-threatening
• Inflammation and mucosal plugging increase airway hyperreactivity
• Symptoms include exhaustion, decreased alertness, hypoxia, cyanosis, absence of breath sounds
• Requires aggressive treatment

Beta 2 Agonists

• Mechanism: Beta-2 agonists stimulate beta-2 adrenergic receptors in bronchial smooth muscles relaxing them enabling better airflow.
• Actions: Bronchodilation, inhibits bronchoconstricting agent release, enhances mucociliary clearance.
• Salbutamol (albuterol): Common beta-2 agonist, quick onset of action, often preferred as rescue medication.

Corticosteroids (Dexamethasone)

• Mechanism: Decreasing inflammation.
• Actions: Enhancing surfactant levels and improving pulmonary circulation

Anticholinergics (Ipratropium Bromide)

• Mechanism: Antagonist to muscarinic acetylcholine receptors, inhibiting bronchoconstriction and secretions.
• Actions: Slower onset but longer duration of action. Often used as maintenance treatment.

Immunoglobulins (IgE)

• Role: Immune response component, antibodies responding to allergens
• Clinical relevance: When allergens bind to IgE antibodies on mast cells, it initiates a cascade of inflammation and bronchoconstriction.

Medication Administration: MDI/NEB/IM

• Specific medications: salbutamol, epinephrine, dexamethasone
• Routes MDI, NEB, & IM
• Dosage: Weight-based dosage calculations, and consideration for contraindication
• Procedure: Specific step-by-step instructions for each administration method

This quiz focuses on the pathophysiology and management of reactive airway diseases, particularly asthma. It covers airway physiology, inflammatory processes, common triggers, and the clinical presentation of asthma patients. Additionally, it reviews evidence-based treatments and the benefits of monitoring methods such as end tidal carbon dioxide measurement.