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CCRN — Adult Critical Care
CCRN Renal & Electrolyte Practice Questions
Renal and electrolyte content threads through the entire CCRN because kidney function and electrolyte balance touch every critically ill patient — and because electrolyte emergencies (especially potassium and sodium) are time-critical, ECG-relevant, and full of correction-rate traps. The exam tests AKI recognition and causes, the electrolyte derangements you act on immediately, and the basics of renal replacement therapy.
This guide reviews AKI, the high-yield electrolyte emergencies, and CRRT concepts with practice questions and rationales. Educational review only: replacement protocols, correction rates, and medication doses follow your institution's policies and current guidelines — verify before applying.
AKI and potassium
Acute kidney injury is classified by cause: prerenal (hypoperfusion — hypovolemia, low output, often reversible if perfusion is restored early), intrinsic (the kidney itself — acute tubular necrosis from ischemia or nephrotoxins, including contrast and certain drugs), and postrenal (obstruction — relieve it). The exam expects you to recognize the pattern (oliguria, rising creatinine and BUN, the BUN:creatinine ratio clues), identify and remove nephrotoxins, optimize perfusion, and dose-adjust renally cleared medications. Indications for renal replacement are often memorized as AEIOU: acidosis, electrolyte disturbance (refractory hyperkalemia), intoxications, fluid overload, and uremia (symptoms like encephalopathy or pericarditis).
Hyperkalemia is the electrolyte emergency: suspect it in AKI/CKD, missed dialysis, crush injury, tumor lysis, and massive transfusion. The ECG progression is the tested signature — peaked T waves → flattened P waves and PR prolongation → widening QRS → sine wave and arrest. Management per protocol: calcium to stabilize the myocardium first (it doesn't lower potassium but buys time), then shifting agents (insulin with glucose, beta-agonists, and addressing acidosis), and finally removal (diuresis if the kidney works, binders, or dialysis). The order — stabilize, shift, remove — is a reliable exam point.
Sodium, other electrolytes, and CRRT
Sodium and correction-rate traps: hyponatremia (assess volume status and acuity — acute symptomatic hyponatremia with seizures is treated more aggressively, but chronic hyponatremia must be corrected slowly to avoid osmotic demyelination syndrome) and hypernatremia (correct slowly to avoid cerebral edema). The recurring CCRN theme is that how fast you correct sodium can injure the brain — overcorrecting chronic hyponatremia and over-rapidly lowering chronic hypernatremia are the classic harms. Other high-yield electrolytes: hypocalcemia (Chvostek/Trousseau signs, QT prolongation, common after massive transfusion with citrate), hypomagnesemia (often coexists with refractory hypokalemia — replace magnesium to fix the potassium, and watch for torsades), and phosphate/calcium shifts in tumor lysis.
Continuous renal replacement therapy (CRRT) is favored for hemodynamically unstable patients because it removes fluid and solutes slowly and continuously, avoiding the abrupt shifts of intermittent hemodialysis. Nursing priorities the CCRN tests: monitor fluid balance and hemodynamics closely, manage anticoagulation of the circuit (citrate or heparin per protocol, watching for citrate-related ionized-calcium changes), watch for circuit clotting and access problems, replace electrolytes the therapy removes, and recognize complications (hypotension, hypothermia, electrolyte derangement). The throughline: the kidney's failures become the nurse's monitoring list, and correction rates are as important as the corrections themselves.
Practice questions with answers & rationales
Q1. A patient with missed dialysis shows peaked T waves and a widening QRS with a potassium of 7.1. What is your first intervention and why?
Answer: Give calcium per protocol first — it stabilizes the cardiac membrane within minutes and protects against lethal arrhythmia, even though it doesn't lower the potassium. Then shift potassium into cells (insulin with glucose, beta-agonist, treat acidosis) and arrange removal (dialysis is definitive in a dialysis-dependent patient). The tested sequence is stabilize → shift → remove, and recognizing the ECG progression as a membrane emergency drives the urgency.
Q2. Differentiate prerenal AKI from acute tubular necrosis, and why does it matter?
Answer: Prerenal AKI is hypoperfusion with intact tubules — the kidney avidly reabsorbs sodium and water, and it's often rapidly reversible if perfusion is restored (volume, cardiac output). ATN is intrinsic tubular damage (ischemic or nephrotoxic) that doesn't reverse simply by restoring perfusion. It matters because prerenal injury responds to perfusion optimization while ATN requires supportive care and time, removal of nephrotoxins, and possibly renal replacement — and over-aggressive diuresis in a prerenal patient worsens the perfusion deficit.
Q3. Why must chronic hyponatremia be corrected slowly, and what is the feared complication of overcorrection?
Answer: The brain adapts to chronic hyponatremia by extruding osmoles; correcting sodium too quickly pulls water out of brain cells abruptly, causing osmotic demyelination syndrome (central pontine myelinolysis) with potentially devastating, permanent neurologic injury. So chronic hyponatremia is corrected within conservative limits per protocol. (Acute symptomatic hyponatremia — seizures — warrants more aggressive initial correction, but still with careful limits.) Correction rate is the safety issue the exam emphasizes.
Q4. Your patient's potassium stays low despite repeated replacement. What electrolyte should you check and why?
Answer: Magnesium — hypomagnesemia causes renal potassium wasting and makes hypokalemia refractory to replacement; you often cannot correct the potassium until the magnesium is repleted. Hypomagnesemia also predisposes to torsades de pointes and other arrhythmias. Checking and replacing magnesium is the classic answer to 'why won't this potassium come up,' and it's a frequent CCRN discriminator.
Q5. List common indications for initiating renal replacement therapy.
Answer: The AEIOU memory aid: severe Acidosis refractory to treatment, Electrolyte disturbances (notably refractory hyperkalemia), Intoxications with dialyzable substances, fluid Overload unresponsive to diuretics, and Uremia with symptoms (encephalopathy, pericarditis, bleeding). The decision integrates trajectory and the whole clinical picture, not a single number — but recognizing these indications is the testable knowledge.
Q6. Why is CRRT preferred over intermittent hemodialysis in a hemodynamically unstable patient?
Answer: CRRT removes fluid and solutes slowly and continuously, avoiding the rapid fluid and osmotic shifts of intermittent hemodialysis that can cause hypotension in an unstable patient. The trade-off is the need for continuous anticoagulation of the circuit and intensive nursing monitoring (fluid balance, electrolytes, circuit clotting, temperature, access). Matching the modality to hemodynamic stability is the concept the exam tests.
Q7. A patient on citrate-anticoagulated CRRT develops perioral tingling and a prolonged QT. What's the likely cause?
Answer: Citrate chelates calcium, so citrate anticoagulation can lower ionized calcium — producing hypocalcemia signs (perioral/peripheral tingling, Chvostek/Trousseau, QT prolongation, and potentially tetany or arrhythmia). Management per protocol involves monitoring ionized calcium and supplementing calcium while adjusting the citrate. Recognizing the citrate–calcium relationship is a specific but well-tested CRRT nursing point.
Common mistakes to avoid
- Giving potassium-shifting drugs before membrane-stabilizing calcium in severe hyperkalemia — stabilize, then shift, then remove.
- Treating ATN like prerenal AKI (or over-diuresing a prerenal patient) by ignoring the cause.
- Correcting chronic hyponatremia too quickly and risking osmotic demyelination — or lowering hypernatremia too fast and causing cerebral edema.
- Replacing potassium repeatedly without checking and correcting magnesium.
- Not recognizing standard renal-replacement indications (AEIOU) when they're present.
- Overlooking citrate-related hypocalcemia in CRRT, or treating CRRT like intermittent dialysis in an unstable patient.