Questions: Fluid Compartments, Electrolyte Balance, and Acid-Base Regulation
3 questions to test your understanding
Score: 0 / 3
Question 1 Multiple Choice
A patient with severe COPD retains CO2 due to impaired ventilation, causing respiratory acidosis. After several days, what renal compensation would you expect?
AIncreased bicarbonate excretion to lower blood pH toward normal
BIncreased bicarbonate reabsorption and new HCO3⁻ generation to raise blood pH toward normal
CIncreased respiratory rate to blow off the retained CO2
DDecreased aldosterone secretion to reduce sodium retention
Respiratory acidosis (elevated pCO2, low pH) triggers renal compensation: the kidneys increase H⁺ excretion and bicarbonate reabsorption/generation over hours to days, raising serum HCO3⁻ and partially restoring pH. This is metabolic compensation for respiratory acidosis. Increased respiratory rate would be a respiratory (not renal) response and is already impaired in COPD. The other options move pH in the wrong direction or address the wrong mechanism.
Question 2 True / False
Drinking large volumes of plain water is the safest and most effective way to treat severe dehydration.
TTrue
FFalse
Answer: False
Plain water is hypotonic (0 mOsm). Ingesting large volumes rapidly dilutes plasma sodium, potentially causing hyponatremia — low serum Na⁺ — which produces cerebral edema, confusion, and seizures. For severe dehydration, isotonic solutions (normal saline or lactated Ringer's) are preferred because they replace volume without shifting osmolarity, keeping fluid in the extracellular compartment where it is needed. Oral rehydration solutions for mild dehydration also include electrolytes for this reason.
Question 3 Short Answer
Explain why hyperkalemia (elevated serum K⁺) is a cardiac emergency.
Think about your answer, then reveal below.
Model answer: The resting membrane potential of cardiac myocytes is set primarily by the K⁺ equilibrium potential (Nernst equation). When extracellular K⁺ rises, the gradient driving K⁺ out of cells decreases, depolarizing the resting membrane potential. This makes cells hyperexcitable, slows conduction through the AV node, widens the QRS complex, and can cause ventricular fibrillation or asystole. Because the heart has no tolerance for disrupted conduction timing, even moderate hyperkalemia (K⁺ > 6.5 mEq/L) is life-threatening.
The Nernst/Goldman equations that govern resting membrane potential are the mechanistic link between K⁺ levels and cardiac arrhythmia risk. This question tests whether students can connect electrolyte physiology to the action potential concepts from neuroscience prerequisites.