CMSRN Study Guide: High-Yield Topics on Fluid and Electrolytes for the Med-Surg Certification Exam

CMSRN Study Guide: High-Yield Topics on Fluid and Electrolytes for the Med-Surg Certification Exam

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Fluid and electrolyte questions show up across the CMSRN exam because they connect to almost every patient problem. Fluids affect perfusion and blood pressure. Electrolytes control the heart, muscles, nerves, and acid–base balance. If you can read the numbers, match them to the bedside picture, and act safely, you will answer most test items right. This guide focuses on what is most testable, why it matters, and how to decide fast.

Why fluids and electrolytes are high-yield

  • They drive symptoms. Confusion, weakness, arrhythmias, and hypotension often trace back to sodium, potassium, or fluid shifts.
  • They cross with other topics. Renal failure, heart failure, GI losses, endocrine problems, and sepsis all change fluids and electrolytes.
  • They require safe action. The exam tests if you know when to act now (e.g., hyperkalemia with EKG changes) and how to give treatments safely.

Core physiology and quick math you must know

  • Where the water goes: Isotonic fluids stay in the vasculature. Hypotonic fluids move water into cells. Hypertonic fluids pull water out of cells. This matters for edema, brain swelling, and shock.
  • Osmolality (approx): 2 × Na + glucose/18 + BUN/2.8. Use it to spot true water deficits and hypertonic states.
  • Anion gap: Na − (Cl + HCO3). Normal ~8–12. A high gap means unmeasured acids (DKA, lactic acidosis, toxins).
  • Corrected calcium (if albumin low): Corrected Ca = measured Ca + 0.8 × (4 − albumin). Low albumin can hide true hypocalcemia.
  • Corrected sodium in hyperglycemia: Add ~1.6 mEq/L Na for each 100 mg/dL glucose over 100. High glucose drags water out of cells and dilutes Na.

Assessing volume status at the bedside

  • Volume deficit (hypovolemia): Tachycardia, low BP, cool extremities, dry mucosa, low urine output, rising BUN/Cr ratio (>20:1). Why: less circulating volume reduces perfusion.
  • Volume excess (hypervolemia): Edema, crackles, S3, elevated JVP, weight gain, dilutional hyponatremia. Why: excess total body water and sodium raise hydrostatic pressure.
  • Intake and output trends: A rising weight is often your best early sign of fluid retention.

IV fluids: what to choose and why

  • Isotonic (0.9% NS, Lactated Ringer’s): Good for hypotension and volume loss. They expand plasma volume. LR contains lactate (buffers acidosis), small K and Ca. Use LR in sepsis and trauma. Use NS if hyperkalemic or when mixing with some IV meds.
  • Hypotonic (0.45% NS, D5W): Move water into cells. Use for hypernatremia from pure water loss. Do not use with cerebral edema or active hypovolemia; it can worsen swelling or drop BP.
  • Hypertonic (3% NS, 7% NS): Pull water out of cells. Use for severe symptomatic hyponatremia or raised ICP. Give via central line when possible. Monitor sodium closely to avoid rapid shifts.
  • Maintenance fluids (adults): Roughly 25–30 mL/kg/day water with some Na, K, and glucose. A quick hourly estimate: 4–2–1 rule (4 mL/kg/hr for first 10 kg, then 2 mL/kg/hr for next 10, then 1 mL/kg/hr for the rest). Adjust for illness and organ function.

Hyponatremia: recognize type and correct safely

  • Why it matters: Water shifts into brain cells. Risk: seizures, herniation if acute drop; osmotic demyelination if corrected too fast.
  • Key split:
    • Hypovolemic (GI loss, diuretics): low total water and sodium, but Na lost more than water. Treat with isotonic fluids; sodium will rise as volume is restored.
    • Euvolemic (SIADH, hypothyroid): normal volume, excess water. Treat with fluid restriction; consider salt tabs, loop diuretics, or hypertonic saline if severe symptoms.
    • Hypervolemic (HF, cirrhosis, CKD): excess water and sodium, but water predominates. Treat with sodium/water restriction, diuretics; consider dialysis in renal failure.
  • Safe correction rate: Aim to raise Na by 4–6 mEq/L in first 6 hours if severe symptoms, but no more than ~8 mEq/L in 24 hours and 16 mEq/L in 48 hours. Why: slow correction prevents demyelination.
  • Hypertonic saline pearls: Use 3% NS for seizures or severe neuro signs. Give small boluses (e.g., 100 mL) and recheck Na.
  • Example: Post-op patient on hypotonic fluids becomes confused, Na 118. Likely SIADH. Stop hypotonic fluids, restrict water, consider 3% NS if neuro deficits.

Hypernatremia: go slow and replace water

  • Why it matters: Brain cells adapt to high osmolality. Rapid correction can cause cerebral edema and seizures.
  • Causes: Water loss (fever, diarrhea, DI) or sodium gain (hypertonic saline, tube feeds without enough water).
  • Treatment: Replace free water with D5W or 0.45% NS. Correct no faster than ~10–12 mEq/L in 24 hours, especially if chronic. If hypovolemic, start with isotonic fluid to stabilize BP, then switch to hypotonic.
  • Example: Elderly patient with fever, poor intake, Na 158, dry mucosa. Start NS for perfusion, then give D5W to replace water deficit slowly.

Potassium disorders: cardiac first, then cause

  • Hypokalemia (K < 3.5):
    • Why it matters: Risk of arrhythmias and muscle weakness. Low Mg makes it harder to correct.
    • Causes: Diuretics, GI loss, insulin/alkalosis shifts.
    • EKG: Flattened T waves, U waves, ST depression.
    • Treatment: Replace K and fix Mg. Use oral K if mild. IV if symptomatic or K < 3.0. Peripheral rate ≤10 mEq/hr; central up to 20 mEq/hr with monitoring. Use NS as a carrier. Never IV push potassium.
    • Rule of thumb: 10 mEq KCl may raise serum K by ~0.1 mEq/L; responses vary with deficits and renal function.
  • Hyperkalemia (K ≥ 5.5):
    • Why it matters: Can cause fatal arrhythmias.
    • EKG: Peaked T waves, widened QRS, sine wave in extremes. If EKG changes, treat now.
    • Stabilize membrane: IV calcium gluconate. It buys time by protecting myocardium; it does not lower K.
    • Shift K into cells: Regular insulin with dextrose, albuterol, sodium bicarbonate if acidotic. These work within minutes.
    • Remove K: Loop diuretics if kidneys work, cation exchange resins (sodium zirconium cyclosilicate or polystyrene), or hemodialysis for severe/renal failure.
    • Stop sources: Hold ACE/ARB, spironolactone, K supplements.

Magnesium: the stealth partner

  • Hypomagnesemia: Causes weakness, tremor, seizures, and refractory hypokalemia/hypocalcemia. Why: Mg is needed for Na-K-ATPase and PTH release.
  • Treatment: Replace Mg first or alongside K. Typical IV: 1–2 g Mg sulfate slowly; more if severe or with torsades. Reduce dose in renal failure.
  • Hypermagnesemia: Think renal failure or excess Mg antacids. Signs: decreased reflexes, hypotension, bradycardia. Treat with IV calcium for symptoms, fluids/diuretics, dialysis if needed.

Calcium: think neuromuscular and QT interval

  • Hypocalcemia:
    • Causes: Post-thyroidectomy hypoparathyroidism, pancreatitis, citrate from transfusions, severe hypomagnesemia.
    • Signs: Numbness, cramps, tetany, Chvostek/Trousseau, seizures. EKG: prolonged QT.
    • Treatment: IV calcium gluconate for symptoms; correct Mg; oral Ca/vitamin D for chronic deficits.
  • Hypercalcemia:
    • Causes: Hyperparathyroidism, malignancy. EKG: short QT. Symptoms: stones, bones, groans, psychiatric overtones.
    • Treatment: Isotonic saline to expand volume and promote calciuresis; loop diuretics after rehydration; calcitonin short term; bisphosphonates for malignancy-related.

Phosphate and chloride: small ions, big consequences

  • Hypophosphatemia: Weakness, rhabdomyolysis, respiratory failure. Often from refeeding syndrome or alcohol use. Replace carefully; check for concurrent low K and Mg.
  • Hyperphosphatemia: CKD. Can cause hypocalcemia and soft tissue calcifications. Use phosphate binders and diet control.
  • Chloride: High chloride from large volumes of NS can cause non–anion gap (hyperchloremic) metabolic acidosis. Balanced fluids (like LR) lower this risk. This is why fluid choice matters.

Acid–base: quick pattern recognition

  • Metabolic acidosis:
    • High anion gap: DKA, lactic acidosis, toxins (methanol, ethylene glycol), renal failure. Treat the cause and support perfusion/oxygenation.
    • Normal gap (hyperchloremic): Diarrhea, renal tubular acidosis, large NS infusions. Treat the driver; consider balanced fluids.
  • Metabolic alkalosis: Vomiting, diuretics. Often chloride-responsive. Give chloride (NS) and potassium; stop losses.
  • Respiratory acidosis/alkalosis: Think ventilation. COPD or oversedation for acidosis; pain, anxiety, pregnancy, sepsis for alkalosis. Fix the ventilation first.
  • Mixed disorders are common: Example: septic patient with lactic acidosis and respiratory alkalosis from tachypnea. Look at pH, PaCO2, HCO3, and anion gap together.

Medications that move electrolytes

  • Diuretics:
    • Loop (furosemide): Lose Na, K, Mg, Ca. Good for fluid overload. Watch for hypokalemia and contraction alkalosis.
    • Thiazides: Lose Na, K, Mg. Retain Ca. Can cause hyponatremia.
    • K-sparing (spironolactone): Retain K. Watch for hyperkalemia, especially in CKD or with ACE/ARB.
  • ACE inhibitors/ARBs: Can raise K and lower GFR. Hold in acute kidney injury or severe hyperkalemia.
  • Insulin: Drives K into cells. Useful for hyperkalemia; can worsen hypokalemia.
  • Beta-agonists (albuterol): Shift K into cells; adjunct for hyperkalemia.
  • Antacids/laxatives with Mg or phosphate: Can cause hypermagnesemia or hyperphosphatemia in CKD.

High-yield safety checks

  • Potassium IV: No IV push. Peripheral ≤10 mEq/hr; central up to 20 mEq/hr with continuous monitoring. Check urine output first. Use pumps and double-checks.
  • Hypertonic saline: Prefer central line. Recheck sodium every 2–4 hours. Stop if Na is correcting too fast.
  • Magnesium: Give slowly to avoid hypotension. Reduce dose in renal failure.
  • Calcium with phosphate: Avoid mixing in the same line without compatibility; risk of precipitation.
  • Fluids in heart failure/CKD: Start low, go slow. Use dynamic reassessment (vitals, lungs, weights, I&O).

Clinical patterns the exam loves

  • SIADH after head injury or small cell lung cancer: Low Na, low serum osmolality, urine osmolality high. Restrict fluids; hypertonic saline if severe symptoms.
  • DKA: High anion gap acidosis, high K on labs but total body K is low. Start isotonic fluids first, then insulin, and replace K as it falls.
  • Pancreatitis with hypocalcemia: Lipase binds Ca in fat necrosis; watch for tetany and prolonged QT. Replace Ca if symptomatic.
  • Tumor lysis syndrome: HyperK, hyperphosphatemia, hypocalcemia, AKI. Treat hyperkalemia urgently; manage phosphate and fluids; consider dialysis.
  • Refeeding syndrome: Sudden drop in phosphate, K, Mg after starting nutrition. Replace electrolytes first and advance feeds slowly.
  • High chloride acidosis from large NS boluses: Switch to LR or balanced fluid if persistent acidosis without other cause.

Case examples with decisions

  • Case 1: 72-year-old with vomiting, BP 88/50, dry mucosa, Na 130, BUN/Cr 35/1.0.
    • Why: Hypovolemic hyponatremia. Sodium low due to water retention from ADH in volume loss.
    • Action: Give isotonic LR or NS boluses. Sodium will rise as volume corrects. Monitor Na to avoid rapid overcorrection once ADH falls.
  • Case 2: 60-year-old with CKD, K 6.8, peaked T waves.
    • Why: Life-threatening hyperkalemia.
    • Action: Calcium gluconate now; insulin with dextrose; albuterol; arrange dialysis. Stop ACE inhibitor and spironolactone.
  • Case 3: 40-year-old marathoner, confused after race, Na 118.
    • Why: Exercise-associated hyponatremia from excess hypotonic intake + ADH.
    • Action: Small bolus 3% NS if neuro symptoms, strict monitoring, avoid hypotonic fluids.

What to watch on labs and monitoring

  • Trends matter more than a single number. Serial BMPs tell you direction and speed of change.
  • Link labs to vitals and EKG. Potassium and calcium problems announce themselves on the monitor before the chem panel comes back.
  • Urine clues: Low urine sodium and high osmolality suggest volume depletion. High urine sodium in hyponatremia suggests SIADH or renal salt wasting.

Rapid review checklist for test day

  • Isotonic for shock; hypotonic for free water; hypertonic for severe symptomatic hyponatremia or raised ICP.
  • Hyponatremia correction: usually ≤8 mEq/L per 24 hours to avoid demyelination.
  • Hypernatremia correction: go slow (≤10–12 mEq/L per 24 hours), treat water deficit after stabilizing perfusion.
  • Hypokalemia: replace K + Mg; never IV push K; max peripheral 10 mEq/hr.
  • Hyperkalemia with EKG changes: calcium first; then insulin/dextrose, albuterol; remove K (diuretic, binder, dialysis).
  • Hypocalcemia: tetany, prolonged QT; give IV calcium if symptomatic; check Mg.
  • Hypercalcemia: IV isotonic fluids, then loop; consider calcitonin and bisphosphonates.
  • Hypophosphatemia: think refeeding; replace before advancing nutrition.
  • Anion gap = Na − (Cl + HCO3); corrected Ca and corrected Na in hyperglycemia can change decisions.
  • Large NS volumes can cause hyperchloremic acidosis; consider LR.

Study strategy: how to lock this in

  • Connect signs to numbers. For each disorder, tie 3 signs, 3 causes, and 3 actions. Say them out loud.
  • Practice calculations. Do five quick anion gaps and corrected calcium problems each study session.
  • Use scenarios. Write a one-line plan for common cases: GI loss + hypovolemia, CKD + hyperkalemia, SIADH, DKA, refeeding.
  • Memorize safety limits. Potassium infusion rates. Sodium correction rates. Hypertonic saline monitoring.

Fluids and electrolytes reward a stepwise approach: identify volume status, read the labs in context, choose the right fluid or replacement, and correct at a safe pace. If you always ask “what is the risk if I go too fast?” you will choose safer answers on the exam and at the bedside.

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