Anatomy, Physiology and Pathophysiology
This domain tests structure-function links and the compensatory mechanisms that explain why a patient looks the way they do. Expect to interpret an arterial blood gas, calculate cardiac output or a drug-independent physiological value, and explain a sign from its mechanism rather than from memory.
Core rules
- Cardiac output = heart rate x stroke volume. Mean arterial pressure = diastolic + one third of the pulse pressure; BP = CO x systemic vascular resistance.
- Total body water is about 60% of body weight, two thirds intracellular. Isotonic loss shows as tachycardia, low urine output and delayed capillary refill before hypotension appears.
- Read an ABG in order: pH first (acidaemia or alkalaemia), then PaCO2 (respiratory), then HCO3 (metabolic). Compensation rarely returns pH fully to normal.
- Anion gap = Na - (Cl + HCO3), normal roughly 8-12 mmol/L. A raised gap means unmeasured anions: ketones, lactate, uraemia, toxins.
- Nephron logic: bulk reabsorption in the proximal tubule, fine tuning in the distal tubule and collecting duct via aldosterone (sodium) and ADH (water).
- Respiratory drive is set by CO2 and pH in the CSF, not by oxygen - which is why oxygen can blunt ventilation in a chronic CO2 retainer.
Worked example
ABG: pH 7.28, PaCO2 30 mmHg, HCO3 14 mmol/L, Na 140, Cl 100. Reasoning: pH is low, so acidosis. HCO3 is low, so the primary problem is metabolic. PaCO2 is low, so the lungs are compensating. Expected CO2 by Winter's formula = 1.5 x 14 + 8, giving 27-31, so compensation is appropriate. Anion gap = 140 - 114 = 26, so this is a high anion gap metabolic acidosis - ketoacidosis, lactic acidosis, renal failure or toxin. Treatment targets the cause, not the number on the printout.
Traps
Calling a normal pH 'no disorder' when two opposing processes cancel out; ignoring potassium shifts as pH changes; assuming oedema is always low albumin; forgetting that a raised anion gap needs a cause, not bicarbonate.