Respiratory disorders encompass a diverse range of conditions affecting the airways, lung parenchyma, pulmonary vasculature, pleura, and respiratory muscles. They rank among the most common reasons for healthcare visits and are the third leading cause of death globally. Understanding pulmonary physiology — ventilation, gas exchange, perfusion, and mechanics — is essential for diagnosis and management.
Obstructive Lung Diseases
Asthma
Asthma is a chronic inflammatory disorder of the airways characterized by reversible airflow obstruction, airway hyperresponsiveness, and respiratory symptoms (wheezing, dyspnea, chest tightness, cough) that vary over time and in intensity.
Pathophysiology. Airway inflammation driven by type 2 immune responses (eosinophils, mast cells, IgE) leads to bronchoconstriction, mucus hypersecretion, and airway remodeling in chronic disease. Triggers include allergens, viral infections, exercise, cold air, and irritants.
Classification and treatment. Asthma is classified as intermittent or persistent (mild, moderate, severe) based on symptom frequency and lung function. Stepwise therapy includes as-needed short-acting beta-agonists (SABA) for all patients, inhaled corticosteroids (ICS) as controller therapy, and add-on therapies (long-acting beta-agonists [LABA], leukotriene receptor antagonists, tiotropium, biologic therapies [omalizumab, mepolizumab, benralizumab, dupilumab]) for uncontrolled disease. The GINA guidelines now recommend as-needed ICS-formoterol as preferred reliever therapy for mild asthma.
Chronic Obstructive Pulmonary Disease
COPD is a preventable and treatable disease characterized by persistent airflow limitation resulting from airway and parenchymal damage caused by exposure to noxious particles or gases, primarily cigarette smoke. It encompasses emphysema (alveolar destruction) and chronic bronchitis (airway inflammation and mucus hypersecretion).
Pathophysiology. Inhaled toxins induce chronic inflammation, protease-antiprotease imbalance, oxidative stress, and apoptosis. Alpha-1 antitrypsin deficiency accounts for 1–3% of COPD cases. The resulting small airway disease and parenchymal destruction reduce elastic recoil and cause expiratory airflow limitation.
Diagnosis. Spirometry confirms the diagnosis: post-bronchodilator FEV1/FVC <0.70. The GOLD system classifies severity by FEV1 percent predicted (GOLD 1–4). Symptoms are assessed with the CAT or mMRC questionnaire. Exacerbation history guides treatment.
Treatment. Smoking cessation is the most effective intervention. Pharmacotherapy includes bronchodilators (LABA, long-acting muscarinic antagonists [LAMA]), ICS (for patients with eosinophilic inflammation or frequent exacerbations), and combination LABA/LAMA/ICS. Pulmonary rehabilitation improves exercise capacity and quality of life. Long-term oxygen therapy improves survival in patients with chronic hypoxemia. Lung volume reduction surgery and transplantation are options for advanced disease.
Interstitial Lung Disease
Interstitial lung diseases (ILDs) are a heterogeneous group of disorders characterized by inflammation and fibrosis of the lung interstitium. The most common is idiopathic pulmonary fibrosis (IPF), a progressive fibrotic disease with a median survival of 3–5 years.
Pathophysiology. In IPF, recurrent alveolar epithelial injury triggers aberrant wound healing, fibroblast proliferation, and excessive extracellular matrix deposition driven by transforming growth factor-beta (TGF-β). The characteristic radiologic and histologic pattern is usual interstitial pneumonia (UIP) with honeycombing, traction bronchiectasis, and subpleural fibrosis.
Diagnosis. High-resolution CT (HRCT) shows UIP pattern (reticulation, honeycombing, traction bronchiectasis). In uncertain cases, surgical lung biopsy or cryobiopsy is performed. Multidisciplinary discussion among pulmonologists, radiologists, and pathologists is essential for accurate diagnosis.
Treatment. Antifibrotic therapy (pirfenidone, nintedanib) slows disease progression. Lung transplantation is the only curative option. Acute exacerbations of IPF are treated with high-dose corticosteroids. Many ILDs (hypersensitivity pneumonitis, connective tissue disease-associated ILD, sarcoidosis) benefit from immunosuppression.
Pulmonary Vascular Disease
Pulmonary Embolism
PE results from thrombus (usually from deep veins of the lower extremities) traveling to the pulmonary circulation. Massive PE causes obstructive shock. Diagnosis is established by CT pulmonary angiography or ventilation-perfusion (V/Q) scanning. Risk stratification (PESI or sPESI score, right ventricular dysfunction on echocardiography, troponin and BNP levels) guides management. Anticoagulation is the mainstay of treatment; thrombolysis is reserved for hemodynamically unstable patients.
Pulmonary Hypertension
PH is defined by mean pulmonary artery pressure >20 mmHg at rest. Group 1: pulmonary arterial hypertension (PAH) — idiopathic, heritable, drug-induced, connective tissue disease-associated. Group 2: PH due to left heart disease (most common). Group 3: PH due to lung disease. Group 4: chronic thromboembolic PH (CTEPH). Group 5: miscellaneous. PAH-specific therapies include prostacyclin analogs, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and soluble guanylate cyclase stimulators.
Pleural Disease
Pleural effusion. Accumulation of fluid in the pleural space. Transudative effusions result from increased hydrostatic pressure (heart failure) or decreased oncotic pressure (cirrhosis, nephrotic syndrome). Exudative effusions result from increased capillary permeability (pneumonia, malignancy, TB). Light’s criteria distinguish transudate from exudate. Treatment addresses the underlying cause; therapeutic thoracentesis relieves dyspnea.
Pneumothorax. Air in the pleural space. Primary spontaneous pneumothorax occurs in young, tall, thin individuals. Secondary spontaneous pneumothorax occurs in patients with underlying lung disease (COPD, cystic fibrosis, ILD). Tension pneumothorax is a life-threatening emergency requiring immediate needle decompression. Management includes observation (small, stable), needle aspiration, chest tube drainage, and pleurodesis for recurrent cases.
Respiratory Failure
Respiratory failure occurs when the respiratory system fails to maintain adequate gas exchange. Type 1 (hypoxemic) respiratory failure: PaO2 <60 mmHg with normal or low PaCO2, caused by V/Q mismatch or shunt (pneumonia, ARDS, PE). Type 2 (hypercapnic) respiratory failure: PaCO2 >50 mmHg, caused by hypoventilation (COPD exacerbation, neuromuscular disease, opioid overdose). Acute respiratory distress syndrome (ARDS) is severe type 1 respiratory failure with bilateral infiltrates and non-cardiogenic pulmonary edema. Management includes oxygen therapy, non-invasive positive pressure ventilation, and mechanical ventilation with lung-protective strategies (low tidal volumes, plateau pressure <30 cm H₂O).
Summary
Respiratory disorders range from common conditions (asthma, COPD, sleep apnea) to rare diseases (IPF, PAH). Accurate diagnosis requires integration of history, pulmonary function testing, imaging, and sometimes biopsy. Asthma and COPD — the two most common obstructive lung diseases — are managed with inhaled therapies targeting bronchodilation and inflammation. Pulmonary embolism requires prompt diagnosis and anticoagulation. Interstitial lung diseases demand expert multidisciplinary evaluation. Across all respiratory disorders, smoking cessation, vaccination, and pulmonary rehabilitation improve outcomes.