Here are comprehensive one-paragraph answers for each question:

The cornerstone of bronchial asthma pharmacotherapy is a stepwise approach combining relievers and controllers. Short-acting beta-2 agonists (SABAs) such as salbutamol (albuterol) are the primary bronchodilators for acute relief, acting on airway smooth muscle to reverse bronchoconstriction rapidly. Inhaled corticosteroids (ICS) — budesonide, fluticasone, beclomethasone — are the most effective long-term controllers, reducing airway inflammation, hyperresponsiveness, and exacerbation frequency. According to current guidelines (GINA/CTS), daily ICS + PRN SABA remains first-line for mild persistent asthma, while for patients with poor adherence, PRN budesonide/formoterol (a combined ICS/LABA) is an alternative in those ≥12 years. Long-acting beta-2 agonists (LABAs) such as formoterol and salmeterol are added as step-up therapy but never used as monotherapy. In intensive/acute settings (status asthmaticus), management includes: repeated or continuous nebulized SABAs, systemic corticosteroids (IV methylprednisolone or oral prednisolone), IV or nebulized ipratropium bromide (anticholinergic), supplemental oxygen to maintain SpO₂ ≥92%, IV or inhaled magnesium sulfate (bronchodilator via calcium antagonism), and, in refractory cases, IV aminophylline (theophylline) or subcutaneous epinephrine. Mechanical ventilation (NIV or intubation) is reserved for impending respiratory failure.

Cardiac asthma is a manifestation of acute left ventricular failure causing cardiogenic pulmonary edema, where elevated pulmonary venous pressure drives fluid into alveoli and triggers reflex bronchoconstriction — it must be distinguished from bronchial asthma (aided by BNP/NT-proBNP measurement, echocardiography). Treatment targets rapid reduction of preload, afterload, and pulmonary congestion: the patient is placed in a sitting/semi-Fowler position; IV loop diuretics (furosemide 40–80 mg IV) reduce preload and have a direct vasodilatory effect; nitrates (nitroglycerin sublingual or IV) are powerful venodilators that rapidly decrease preload and are the agents of choice when systolic BP is adequate (>100 mmHg); morphine sulfate (2–5 mg IV) reduces anxiety, sympathetic tone, and preload (though its use is increasingly debated); oxygen therapy (high-flow via mask, or NIV — CPAP/BiPAP) reverses hypoxemia and reduces the work of breathing; if pulmonary edema is refractory, inotropes (dobutamine, dopamine) are added for cardiogenic shock; ACE inhibitors reduce afterload acutely. In hypertensive emergencies precipitating pulmonary edema, IV nitroprusside or nitroglycerin is preferred. The key principle is treating the underlying cause (e.g., revascularization for ACS, rate control for arrhythmias).

The emergency algorithm for cardiac asthma (cardiogenic pulmonary edema) proceeds in a structured sequence: (1) Positioning — seat the patient upright with legs dependent to reduce venous return; (2) Oxygen — high-flow O₂ via face mask (6–8 L/min) targeting SpO₂ >95%; if inadequate, initiate CPAP (5–10 cmH₂O) or BiPAP, which reduces preload, improves oxygenation, and avoids intubation in most cases; (3) IV access + monitoring — ECG, pulse oximetry, BP, BNP if available; (4) Nitroglycerin (NTG) — 0.4–0.8 mg sublingual immediately, then IV NTG infusion (10–200 mcg/min) titrated to BP (contraindicated if systolic BP <90 mmHg or if phosphodiesterase inhibitors were taken); (5) Furosemide IV — 40–80 mg IV bolus (promotes rapid venodilation before diuresis begins); (6) Morphine — 2–4 mg IV slowly (reduces sympathetic drive and preload; use cautiously, avoid in hypotension/COPD); (7) Identify and treat precipitants — ACS (urgent reperfusion), hypertensive crisis (IV antihypertensives), arrhythmia (rate/rhythm control), infection; (8) Inotropes/vasopressors — dobutamine if low-output state with hypotension; (9) Intubation — if the patient deteriorates despite NIV (refractory hypoxemia, exhaustion, loss of consciousness).

COPD management (GOLD Guidelines) is stratified by symptom burden (mMRC/CAT score) and exacerbation history. The mainstay of stable COPD treatment is inhaled bronchodilators: long-acting muscarinic antagonists (LAMAs) such as tiotropium and long-acting beta-2 agonists (LABAs) such as indacaterol are preferred over SABAs for regular use, and LAMA+LABA dual therapy is recommended for patients with persistent dyspnea; triple therapy (LAMA + LABA + ICS) is reserved for those with frequent exacerbations (≥2/year) or eosinophil count ≥300 cells/µL. Phosphodiesterase-4 inhibitors (roflumilast) reduce exacerbations in severe COPD with chronic bronchitis phenotype. Smoking cessation remains the single most effective intervention to slow FEV₁ decline. Pulmonary rehabilitation (exercise training + education) is strongly recommended for all symptomatic patients and improves exercise capacity and quality of life. Long-term oxygen therapy (LTOT, >15 hours/day) is indicated when PaO₂ ≤55 mmHg (or ≤60 mmHg with cor pulmonale/polycythemia) and is the only pharmacological intervention proven to improve survival. Acute COPD exacerbations are treated with short-acting bronchodilators (salbutamol + ipratropium), systemic corticosteroids (prednisolone 40 mg/day × 5 days), antibiotics if purulent sputum/infection is present, controlled oxygen (target SpO₂ 88–92%), and NIV (BiPAP) for hypercapnic respiratory failure (pH <7.35, PaCO₂ >45 mmHg).