Chapter 25 · Fluid, electrolyte and acid–base balance · Topic 145

Electrolyte balance

A&P IIphysiologyRead the notes

1Why this matters

Mr. Reyes, 66, has kidney failure and has missed two dialysis sessions. He feels weak, and his ECG shows tall, peaked T waves. His plasma potassium is 6.8 mmol/L. His kidneys are the main exit for potassium, and the extra now sitting outside his cells has pushed the resting potential of his heart cells toward threshold. The first drug he gets is calcium, which will not lower his potassium at all. To see why that makes sense, you need to know how your body keeps each electrolyte in balance.

2What this builds on

3Quick check before you start

1. What does aldosterone do in the principal cells of the collecting duct?

  1. Increases sodium reabsorption and potassium secretion
  2. Inserts aquaporins so water is reabsorbed
  3. Increases calcium reabsorption and phosphate excretion
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Aldosterone makes principal cells build more sodium channels, potassium channels and sodium–potassium pumps, so they reabsorb more sodium and secrete more potassium. Aquaporins are ADH's job; calcium and phosphate are PTH's.

  • Correct: Increases sodium reabsorption and potassium secretion:
  • Inserts aquaporins so water is reabsorbed:
  • Increases calcium reabsorption and phosphate excretion:

2. Potassium is about 140 mmol/L inside a cell and 4 mmol/L outside. If plasma potassium rises to 8 mmol/L, what happens to the resting membrane potential?

  1. It becomes more negative
  2. It becomes less negative
  3. It does not change
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A smaller concentration gradient means less potassium leaks out, so potassium's equilibrium potential and the resting potential move toward zero: less negative, closer to threshold.

  • It becomes more negative:
  • Correct: It becomes less negative:
  • It does not change:

3. Which hormone raises blood calcium by acting on bone, the kidneys and, through calcitriol, the intestine?

  1. Calcitonin
  2. Aldosterone
  3. Parathyroid hormone
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Parathyroid hormone releases calcium from bone, makes the kidneys keep calcium and excrete phosphate, and switches on calcitriol, which raises calcium absorption from food.

  • Calcitonin:
  • Aldosterone:
  • Correct: Parathyroid hormone:

4How it works, step by step

  1. A potato-and-banana meal adds potassium to the ECF, which holds only about 2% of your body's potassium.Plasma potassium starts to rise.
  2. Insulin released for the meal stimulates sodium–potassium pumps.Potassium moves into cells within minutes, so the rise in plasma potassium stays small.
  3. The small rise in plasma potassium acts directly on the zona glomerulosa of the adrenal cortex.Aldosterone release increases.
  4. Aldosterone makes principal cells build more sodium channels, potassium channels and sodium–potassium pumps.Principal cells secrete more potassium into the urine.
  5. Over the next hours the kidneys excrete the extra potassium.Output matches intake, plasma potassium returns to normal, and aldosterone release falls: negative feedback.

5Core concepts

Mass balanceHomeostasis

6A common mistake

The wrong idea: A low plasma sodium means the body has too little sodium, so the fix is to give salt.

What actually happens: Plasma sodium is a concentration, and it mostly reflects water. Hyponatremia almost always means too much water for the sodium present. Many patients with it, such as those with heart failure, have more total sodium than normal, along with even more extra water. Giving salt to them adds volume and worsens edema; the fix depends on the cause, often limiting water.

7Check yourself

Anything you miss goes into your review queue.

1. A marathon runner collapses, confused, after drinking at every station. She sweated about 2 L and drank about 4 L. Her plasma sodium is 124 mmol/L. What best explains her low sodium?

  1. She lost more sodium in sweat than she took in
  2. Her aldosterone release failed during the race
  3. She kept more water than she lost
  4. Her kidneys excreted too much sodium
Show the answer

She gained about 2 L of water, and exercise and nausea kept her ADH high, so her kidneys could not pass it. The same sodium is diluted in more water. Hyponatremia is almost always too much water for the sodium present.

  • She lost more sodium in sweat than she took in: She did lose some sodium in sweat, but sweat is more dilute than plasma. That loss alone would raise, not lower, her plasma sodium concentration.
  • Her aldosterone release failed during the race: Nothing suggests aldosterone failed, and losing aldosterone takes days to lower sodium. Her problem developed over hours from drinking.
  • Correct: She kept more water than she lost: Correct. A net gain of water dilutes her plasma sodium.
  • Her kidneys excreted too much sodium: Her kidneys were keeping, not wasting, what they could; with ADH high they could not excrete the extra water.

2. A woman has had a plasma sodium of 112 mmol/L for a week. Her doctors raise it by no more than about 8 mmol/L in the first day. Why so slowly?

  1. Her kidneys cannot excrete water any faster than that
  2. Faster correction would cause hypernatremia
  3. Her brain cells have adapted, and fast correction can damage them
  4. Salt given by vein takes several days to reach the plasma
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Over about two days, brain cells in dilute plasma shed potassium and small organic solutes, so they stop swelling. If plasma sodium then rises quickly, water rushes out of these adapted cells and they are damaged, especially the myelin in the pons: osmotic demyelination. Slow correction gives them time to regain solute.

  • Her kidneys cannot excrete water any faster than that: Healthy kidneys can excrete water much faster than this. The limit protects the brain, not the kidneys.
  • Faster correction would cause hypernatremia: Raising sodium from 112 by 8 a day would take days to reach even the low normal range. Overshooting to above 145 is not the concern.
  • Correct: Her brain cells have adapted, and fast correction can damage them: Correct. Adapted brain cells shrink too fast when the plasma is concentrated quickly.
  • Salt given by vein takes several days to reach the plasma: IV salt enters the plasma at once. The limit on speed is chosen by the doctors, not set by delivery.

3. A man's cells hold 3,500 mmol of potassium, and his 14 L of ECF has a potassium of 4.0 mmol/L. Crushed muscle releases 2% of his cell potassium into the ECF. Before any is excreted, what is his plasma potassium?

  1. About 4.1 mmol/L
  2. About 6.5 mmol/L
  3. About 9.0 mmol/L
  4. About 74 mmol/L
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2% of 3,500 mmol = 70 mmol. Spread through 14 L: 70 ÷ 14 = 5.0 mmol/L added. 4.0 + 5.0 = 9.0 mmol/L, which is life-threatening.

  • About 4.1 mmol/L: This treats the release as a tiny change. Because the ECF holds so little potassium, 70 mmol is more than it held to begin with.
  • About 6.5 mmol/L: 6.5 is the result for a 1% release (35 mmol ÷ 14 L = 2.5 added). The question says 2%.
  • Correct: About 9.0 mmol/L: Correct. 70 mmol ÷ 14 L = 5.0 mmol/L added to 4.0.
  • About 74 mmol/L: 74 adds the 70 mmol to the concentration without dividing by the volume.

4. Mr. Reyes, whose potassium is 6.8 mmol/L with peaked T waves, first receives calcium gluconate by vein. His potassium is unchanged 10 minutes later. Why was calcium given first?

  1. It raises heart cells' threshold, protecting the heart for a while
  2. It binds potassium in the plasma so it cannot act on cells
  3. It stimulates the kidneys to secrete potassium
  4. It moves potassium into cells, like insulin does
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Hyperkalemia moves the resting potential of heart cells toward threshold. Raising extracellular calcium raises the threshold, restoring the gap between rest and threshold. It buys 30 to 60 minutes while insulin and glucose shift potassium into cells and dialysis removes it. It does not lower potassium.

  • Correct: It raises heart cells' threshold, protecting the heart for a while: Correct. Calcium stabilizes the heart's membranes without changing potassium.
  • It binds potassium in the plasma so it cannot act on cells: Calcium and potassium are both cations and do not bind each other; his potassium is unchanged.
  • It stimulates the kidneys to secrete potassium: Calcium does not drive potassium secretion, and his kidneys have failed anyway.
  • It moves potassium into cells, like insulin does: Calcium does not shift potassium into cells. That is what insulin, glucose and beta-2 agonists do.

5. During a panic attack, a student breathes fast and deep. Her fingers and lips tingle and her hands cramp. Her total calcium is normal. What explains her symptoms?

  1. Fast breathing removes calcium from the blood in exhaled air
  2. Her parathyroid glands stop releasing PTH during panic
  3. Epinephrine drives calcium into bone
  4. Alkalosis makes albumin bind more calcium
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Hyperventilation blows off CO₂, so the blood becomes alkaline. In alkalosis, albumin gives up hydrogen ions and binds more calcium, so ionized calcium falls although the total is unchanged. Low ionized calcium makes nerves and muscles overexcitable: tingling and cramps.

  • Fast breathing removes calcium from the blood in exhaled air: Calcium is not a gas and does not leave in exhaled air. Breathing changes CO₂, which changes pH.
  • Her parathyroid glands stop releasing PTH during panic: PTH takes minutes to hours to act, and panic does not switch it off. Her total calcium is normal.
  • Epinephrine drives calcium into bone: Nothing like this happens in minutes, and her total calcium has not fallen.
  • Correct: Alkalosis makes albumin bind more calcium: Correct. Only the free fraction falls, so the total calcium looks normal.

6. A severely malnourished man is admitted and fed generously. Two days later he is weak and struggling to breathe, and his phosphate is 0.9 mg/dL. What caused the fall in phosphate?

  1. The food contained too little phosphate
  2. Insulin drove phosphate into cells to make ATP and glycogen
  3. His kidneys began excreting extra phosphate in response to PTH
  4. His bones took up phosphate to mineralize new matrix
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Feeding releases insulin, which drives glucose and phosphate into cells, where phosphate is used to make ATP, glycogen and phosphorylated sugars. His stores were already low, so plasma phosphate crashes. Without it, cells cannot make enough ATP, and the diaphragm weakens.

  • The food contained too little phosphate: Food contains plenty of phosphate. The fall comes from phosphate moving into cells faster than it can be absorbed.
  • Correct: Insulin drove phosphate into cells to make ATP and glycogen: Correct. This is refeeding: an internal shift into cells.
  • His kidneys began excreting extra phosphate in response to PTH: PTH does increase phosphate excretion, but nothing here raised PTH. The fall came within two days of feeding.
  • His bones took up phosphate to mineralize new matrix: Bone mineralization is slow and would not drop phosphate this fast. The fast shift is into cells.

7. A man with heavy alcohol use has a potassium of 2.9 and a calcium of 7.6 mg/dL. Three days of potassium tablets do not raise his potassium. Which test is most likely to explain why?

  1. Plasma sodium concentration
  2. Plasma chloride
  3. Plasma magnesium
  4. Blood glucose
Show the answer

Heavy alcohol use often causes low magnesium. Magnesium normally limits potassium flow out of principal cells; without it, potassium keeps leaking into the urine. Low magnesium also blocks PTH release and action, lowering calcium. Both correct only when magnesium is replaced.

  • Plasma sodium concentration: Low sodium does not explain potassium that will not correct, or low calcium.
  • Plasma chloride: Chloride changes with vomiting and diuretics, but low chloride does not block potassium replacement or PTH.
  • Correct: Plasma magnesium: Correct. Low magnesium keeps potassium and calcium low until it is corrected.
  • Blood glucose: Glucose affects potassium shifts through insulin, but it does not explain both the resistant potassium and the low calcium.

8Summary

Each electrolyte has an external balance, intake against output, set mostly by the kidneys, and an internal balance, its split between cells, bone and ECF. Sodium balance: the amount of sodium sets ECF volume (aldosterone, ANP, pressure natriuresis), while plasma sodium concentration reflects water (ADH, thirst); hyponatremia (below 135 mmol/L) is usually too much water, hypernatremia (above 145) too little, and both are corrected slowly when chronic. Potassium balance: 98% is inside cells, insulin and epinephrine move it in, and principal cells secrete it under aldosterone; hypokalemia makes skeletal muscle harder to fire but the heart prone to arrhythmias, hyperkalemia moves them toward threshold and endangers the heart. Calcium and phosphate balance: PTH and calcitriol are the main regulators, only ionized calcium is active, and alkalosis lowers it; kidney failure raises phosphate, and refeeding can crash it. Chloride follows sodium and trades places with bicarbonate; magnesium is set by the thick ascending limb, and low magnesium keeps potassium and calcium low.

9What comes next

10Connections