Physiology and Pathophysiology: Oxygen Delivery, Ventilation, and Homeostasis
Oxygen transport
Oxygen delivery is cardiac output multiplied by arterial oxygen content. Arterial content depends mainly on hemoglobin and saturation; dissolved oxygen is tiny. The oxyhemoglobin curve shifts right with acidosis, hypercapnia, fever, and elevated 2,3-DPG, reducing affinity and improving tissue unloading, but reducing arterial saturation at a given PaO2. Pulse oximetry estimates saturation, not content, and cannot detect anemia or hyperoxia.
V/Q mismatch
Shunt is perfusion without ventilation; it does not improve much with supplemental oxygen because shunted blood never sees alveolar gas. Dead space is ventilation without perfusion; it responds to changes in tidal volume and can worsen with hypotension or pulmonary embolism. A normal alveolar-arterial gradient rises with age. Hypoxemia from shunt responds poorly to FiO2, whereas hypoxemia from hypoventilation or diffusion limitation usually improves. Mixed venous oxygen saturation reflects the balance of oxygen delivery and consumption; a low value suggests inadequate delivery or increased demand.
Acid-base and fluids
Use the anion gap and delta gap to classify metabolic acidosis. Hypotonic fluids expand intracellular water; isotonic crystalloid remains mostly extracellular. Colloid and crystalloid questions usually test the same principle: volume status and ongoing losses drive choice more than formula alone.
Worked example: A patient with cardiac output 5 L/min, hemoglobin 10 g/dL, SaO2 100%, and PaO2 100 mm Hg has CaO2 ≈ (1.34 × 10 × 1.0) + (0.003 × 100) = 13.7 mL/dL. DO2 = 5 × 13.7 × 10 = 685 mL/min. Rule of thumb: DO2 = CO × CaO2 × 10; a falling mixed venous saturation is an early warning of supply-demand imbalance.
Trap: do not expect a large FiO2 response in a true shunt, and do not confuse SpO2 with oxygen content.