How Breathing and Gas Exchange Work

Clinical Orientation

A patient with Guillain-Barré syndrome tells the nurse, "I feel like I can't take a deep breath." Her vital capacity is dropping. In the next room, a patient with pulmonary fibrosis has an SpO2 of 84% on room air. Both have respiratory problems — but completely different mechanisms. One involves the bellows (ventilation), the other involves the membrane (gas exchange). This chapter answers: What mechanism links breathing and gas exchange to bedside findings, tests, red flags, and nursing priorities?

What Is Normal?

Conducting airways: The trachea, bronchi, and bronchioles down to the terminal bronchioles. These structures move air but do NOT participate in gas exchange — they are "anatomic dead space" (~150 mL in adults). Their jobs: warm, humidify, and filter air. Lined with ciliated epithelium and mucus-producing cells that trap particles and move them upward (mucociliary escalator).

Alveoli: The 300 million tiny air sacs where gas exchange occurs. Extremely thin walls (0.2-0.5 μm) — a single layer of type I alveolar cells, a fused basement membrane, and capillary endothelium. This is the alveolar-capillary membrane. Type II alveolar cells produce surfactant, which reduces surface tension and prevents alveolar collapse. Macrophages patrol the alveoli, ingesting debris and pathogens.

Pleura: Two layers (visceral on lung surface, parietal on chest wall) with a thin layer of pleural fluid between them. The pleura couples lung movement to chest wall movement — when the chest expands, the lungs expand. Negative intrapleural pressure (~ −5 cm H2O at rest) keeps the lungs inflated.

Diaphragm and respiratory muscles: The diaphragm is the primary muscle of inspiration — it contracts, flattens, and creates negative intrathoracic pressure, drawing air in. Quiet expiration is passive (elastic recoil). Forced expiration uses abdominal and intercostal muscles.

What Goes Wrong?

Four categories of respiratory failure:

1. Airway obstruction: Increased resistance to airflow. Asthma (bronchospasm), COPD (airway narrowing/collapse), foreign body, secretions, tumor.
2. Restrictive disease: Decreased lung compliance (stiff lungs). Pulmonary fibrosis, ARDS, chest wall deformity (kyphoscoliosis), obesity, neuromuscular weakness.
3. Alveolar filling/collapse: Something occupies alveolar space — pus (pneumonia), fluid (pulmonary edema), blood (hemorrhage), or the alveoli collapse (atelectasis).
4. Vascular disease: Impaired pulmonary blood flow. Pulmonary embolism, pulmonary hypertension.

Each produces different patterns of hypoxia, work of breathing, and response to oxygen therapy.

What the Nurse May See

• Increased work of breathing: Use of accessory muscles (sternocleidomastoid, scalenes), nasal flaring, tripod position, inability to speak in full sentences.
• Abnormal breath sounds: Wheezes (narrowed airways), crackles (fluid in alveoli), rhonchi (secretions in large airways), stridor (upper airway obstruction — emergency), absent/diminished (no air movement — emergency).
• Signs of hypoxemia: Tachycardia, tachypnea, confusion, cyanosis (late), low SpO2.
• Signs of hypercapnia: Somnolence, confusion, asterixis, warm flushed skin, bounding pulses.

Tests and Monitoring

• Pulse oximetry (SpO2): Measures oxygen saturation. Does NOT measure ventilation (CO2). A sedated patient can have SpO2 100% on O2 and PaCO2 80.
• ABG: The gold standard — pH, PaCO2, PaO2, HCO3, SaO2.
• Capnography (ETCO2): Continuous CO2 monitoring — best for confirming endotracheal tube placement and monitoring ventilation trends.
• Pulmonary function tests (PFTs): Spirometry — FEV1 (volume exhaled in first second), FVC (total forced vital capacity), FEV1/FVC ratio. Distinguishes obstructive (↓ ratio) from restrictive (↓ FVC, normal ratio).
• Chest X-ray, CT: Visualize infiltrates, effusions, masses, pneumothorax.

Red Flags