Applied Physiology: Oxygen, Carbon Dioxide and Perfusion
Core concepts
Respiratory physiology questions hinge on the oxygen cascade and CO2 carriage. Know that oxygen content = (1.34 × Hb × SaO2) + (0.003 × PaO2); haemoglobin carries almost all oxygen, so anaemia and desaturation hurt far more than a modest PaO2 fall. Understand the oxyhaemoglobin dissociation curve: right shift (↑CO2, ↑H+, ↑temperature, ↑2,3-DPG) releases oxygen; left shift (alkalosis, hypothermia, fetal Hb, stored blood) holds it. CO2 travels mainly as bicarbonate (~70%), with ~20–25% carbamino compounds and ~5–10% dissolved; this explains why end-tidal CO2 underestimates PaCO2 in states with increased dead space.
Cardiovascular physiology: Starling curve, preload-dependence, and the Fick principle (VO2 = CO × arteriovenous oxygen difference). Understand autoregulation of cerebral and renal blood flow, and that mean arterial pressure drives organ perfusion more than systolic pressure.
Traps
- Confusing shunt (perfusion without ventilation, does not correct with oxygen) with dead space (ventilation without perfusion).
- Forgetting that functional residual capacity falls under anaesthesia and with obesity, reducing safe apnea time.
- Assuming pulse oximetry reflects ventilation - it reflects oxygenation only.
- Overlooking that CO2 accumulates when minute ventilation falls even if SpO2 is normal.
Rule of thumb
For any physiology stem, ask: is this an oxygenation problem (shunt, diffusion, Hb) or a ventilation problem (dead space, hypoventilation)? The answer usually falls out of that single distinction.
Worked example
A patient with a large pulmonary embolism has rising EtCO2–PaCO2 gradient. That is increased dead space, not shunt - oxygen therapy will not fix the gradient; ventilation/perfusion mismatch from obstructed perfusion is the mechanism.