Respiratory System Pathophysiology

Respiratory Tract Structure

• Upper Tract: nose, pharynx, larynx - filters, warms, humidifies air
• Lower Tract: trachea → bronchi → bronchioles → alveoli
• Right lung: 3 lobes (upper, middle, lower)
• Left lung: 2 lobes (upper, lower) with cardiac notch
• Alveoli: tiny air sacs where gas exchange occurs, 70 m² surface area

Lung Volumes & Capacities

• Tidal Volume (TV): 500 mL (normal breath)
• Inspiratory Reserve (IRV): 3100 mL (max after normal inspiration)
• Expiratory Reserve (ERV): 1200 mL (max after normal expiration)
• Residual Volume (RV): 1200 mL (remains after max expiration)
• Vital Capacity: TV + IRV + ERV = 4800 mL
• Total Lung Capacity: VC + RV = 6000 mL

Gas Exchange Mechanics

• Ventilation: movement of air in/out of lungs
• Diffusion: passive movement across alveolar-capillary membrane
• Perfusion: blood flow through pulmonary circulation
• V/Q Ratio: balance of ventilation and perfusion (ideal: 1)

Oxygen Transport

• Dissolved in plasma: 3 mL O2/L blood (1.5%)
• Bound to hemoglobin: Hb + O2 → HbO2 (98.5%)
• Each Hb molecule: carries 4 O2 molecules
• Oxygen-Hemoglobin Curve: sigmoid shape reflects cooperative binding

Oxygen Content Calculation

CaO2 = (Hb × 1.34 × SaO2) + (0.003 × PaO2)

• Hb: hemoglobin (g/dL)
• SaO2: arterial oxygen saturation (%)
• PaO2: partial pressure of O2 in arterial blood (mmHg, normal 80-100)

Carbon Dioxide Transport

• Dissolved in plasma: 5-10% (PaCO2 = 35-45 mmHg)
• Bound to hemoglobin: 5-10% (carbaminohemoglobin)
• As bicarbonate: 85% (main transport form)
• Chloride shift: HCO3- exits RBCs in exchange for Cl-

COPD (Chronic Obstructive Pulmonary Disease)

Asthma

• Reversible airway obstruction (unlike emphysema)
• Pathophysiology: IgE-mediated or non-IgE inflammation, bronchoconstriction, edema, mucus plugging
• Acute attack: severe bronchoconstriction, ↑↑ work of breathing, pulsus paradoxus, respiratory failure risk
• Triggers: allergens, infections, cold air, exercise, stress

ARDS (Acute Respiratory Distress Syndrome)

• Non-cardiogenic pulmonary edema from inflammatory response
• Causes: sepsis, aspiration, trauma, pneumonia, pancreatitis
• Pathophysiology: ↑ vascular permeability, fluid accumulation, hyaline membrane formation
• Result: severe hypoxemia, V/Q mismatch, shunting, very low compliance

Pneumonia

• Infection of lung parenchyma (bacterial, viral, fungal)
• Causes: aspiration or inhalation of pathogen
• Pathophysiology: inflammatory response → consolidation, V/Q mismatch, hypoxemia
• Common pathogens: S. pneumoniae, H. influenzae, viruses (RSV, influenza)

Pulmonary Embolism (PE)

• Clot lodges in pulmonary arteries → obstruction of blood flow
• Causes: DVT, atrial fibrillation, immobility, malignancy
• Pathophysiology: V/Q mismatch, PaO2 ↓, alveolar collapse, RV strain
• Severity: determined by size/location of clot and cardiopulmonary reserve

Type I (Hypoxemic Failure)

• Criteria: PaO2 <60 mmHg on supplemental O2
• Gas: Normal or low PaCO2
• Causes: pneumonia, ARDS, pulmonary edema, diffusion impairment
• Problem: oxygenation, not ventilation

Type II (Hypercapnic Failure)

• Criteria: PaCO2 >50 mmHg
• Gas: ± low PaO2
• Causes: COPD, asthma, neuromuscular disease, hypoventilation
• Problem: inadequate ventilation

Respiratory Symptoms

• Dyspnea: subjective sensation of breathing discomfort (not same as hypoxemia)
• Orthopnea: dyspnea when lying flat (need extra pillows)
• PND: paroxysmal nocturnal dyspnea (sudden awakening)
• Cough: protective reflex, can be acute/chronic, productive/dry
• Hemoptysis: blood in sputum (infection, malignancy, PE, TB)

Physical Examination

• Breath Sounds: vesicular (normal), bronchial (abnormal), diminished (COPD, obesity)
• Crackles: fine (asthma, fibrosis), coarse (pneumonia, edema)
• Wheezes: high-pitched, narrowed airways (asthma, COPD)
• Stridor: loud, high-pitched, upper airway obstruction
• Use of accessory muscles: suggests ↑ work of breathing

Diagnostic Tests

• ABG: pH, PaO2, PaCO2, HCO3-, SaO2, A-a gradient
• Pulse Oximetry: non-invasive SaO2 measurement
• Chest X-ray: infiltrates, hyperinflation, pneumothorax, pleural effusion
• PFTs: spirometry (FEV1, FVC, FEV1/FVC ratio), lung volumes, DLCO
• CT Scan: detailed anatomy, interstitial disease, PE diagnosis

COPD Management

• Smoking Cessation: most important intervention
• Medications: bronchodilators, corticosteroids, oxygen therapy
• Rehabilitation: exercise training, pursed-lip breathing, education
• Advanced: lung volume reduction, lung transplant

Asthma Management (Step-wise)

• Mild Intermittent: SABA as needed
• Mild-Moderate: low-dose ICS or ICS/LABA
• Moderate-Severe: medium-high dose ICS/LABA ± other agents
• Acute Exacerbation: frequent SABA, systemic corticosteroids, oxygen

Hypoxemia Treatment

• Supplemental Oxygen: goal PaO2 >60, SaO2 >88-92%
• Treat underlying cause: antibiotics for infection, diuretics for edema
• Improve ventilation: bronchodilators, mechanical support if needed

Mechanical Ventilation

• Non-invasive: CPAP, BiPAP (maintains airway pressure)
• Invasive: endotracheal intubation with mechanical ventilation
• Indications: hypoxemia, altered mental status, severe work of breathing

1. Compare and contrast Type I and Type II respiratory failure in terms of pathophysiology, causes, and expected ABG findings.

2. Explain why a patient with emphysema develops a "barrel chest" and uses pursed-lip breathing.

3. A patient with acute asthma attack has PaO2 of 65 mmHg on room air. Explain the pathophysiological mechanism of hypoxemia.

4. Describe the difference between ventilation-perfusion mismatch and true shunting in terms of response to supplemental oxygen.

5. Why does a patient with COPD often have polycythemia?