Hyperkalemia and Acid-Base Questions in CRNA Interviews

What does hyperkalemia do to the cardiac action potential?

Electrolyte questions separate candidates who memorize lab ranges from candidates who can explain ion shifts across a cell membrane. “Peaked T waves, give calcium” is the bedside version. The interview version explains why the T wave peaks and why calcium buys time while leaving the potassium level unchanged. It happens in two stages:

• Early: high extracellular potassium shrinks the gradient across the membrane, so the resting potential becomes less negative and sits closer to threshold. Cells are briefly more excitable. High extracellular K+ also increases potassium channel (IKr) conductance, so phase 3 repolarization speeds up and the T wave becomes tall and narrow.
• Late: a resting potential that stays depolarized inactivates fast sodium channels. Phase 0 slows, conduction slows, the P wave flattens, the QRS widens, and QRS and T eventually merge into a sine wave before arrest.

How do you treat hyperkalemia in the right order?

Say it as three verbs: stabilize, shift, eliminate.

Stabilize the membrane

Calcium chloride 1 g (central line preferred) or calcium gluconate 3 g, given over 5–10 minutes, pushed in arrest. Calcium restores conduction while potassium is still high. Repeat if the ECG does not improve.

Shift potassium into cells

10 units regular insulin IV with 25 g dextrose, plus nebulized albuterol 10–20 mg. Both stimulate the Na+/K+-ATPase pump. Check glucose hourly; consider 5 units of insulin in renal failure. Sodium bicarbonate helps only when the patient is acidemic. If intubated, keep CO2 from rising.

Eliminate it from the body

Loop diuretic if the kidneys make urine, a gut binder such as sodium zirconium cyclosilicate (Lokelma), or dialysis. Stop ACE inhibitors, ARBs, and potassium-sparing drugs. Recheck a BMP every 2 hours.

How do you work through metabolic acidosis?

Low pH with low bicarbonate means metabolic acidosis. Calculate the anion gap next: Na+ − (Cl− + HCO3−).

As hydrogen ions rise outside the cell, they move in and potassium moves out. That shift is larger in normal-gap (mineral) acidosis than in lactic or ketoacidosis. Severe acidemia also blunts the vascular response to catecholamines, which is why pressors seem to stop working.

• High gap: lactic acidosis, ketoacidosis, toxic ingestion, renal failure.
• Normal gap: bicarbonate loss from diarrhea, renal tubular acidosis, or large volumes of 0.9% saline.

Which acid-base traps show up in interviews?

Intubating severe metabolic acidosis

That patient survives on Kussmaul breathing, a huge minute ventilation that blows off CO2. Set a routine rate after intubation and CO2 climbs, pH can drop below 7.0, and the patient can arrest. Match the pre-intubation minute ventilation, check an early ABG, and treat the cause.

Normal potassium in DKA

Acidemia pushes potassium out of cells, so the serum level can look normal while total-body potassium is severely depleted. Insulin drives it back in and can unmask profound hypokalemia. Confirm potassium is at least 3.3 mEq/L before starting insulin. Current DKA consensus reserves bicarbonate for pH below 7.0. Refractory acidosis or a dialyzable toxin points to dialysis.

How do you do drip math under pressure?

Two identities cover almost every question: concentration × volume = total drug, and dose rate ÷ concentration = infusion rate.

Code-dose epinephrine: a 10 mL prefilled syringe at 0.1 mg/mL holds 1 mg. Norepinephrine 4 mg in 250 mL is 16 mcg/mL, so 8 mcg/min is 0.5 mL/min, or 30 mL/hr.

How do you practice the hyperkalemia follow-up?

A first rep sounds like this: potassium is 6.8 with a widening QRS, and you give insulin, dextrose, and Kayexalate. The follow-up asks why the patient fibrillates five minutes later.

A repaired answer sounds like this: sodium channels are already inactivating and nothing I gave works fast enough, so calcium comes first to stabilize conduction. Then insulin with dextrose and albuterol to shift, then diuresis, Lokelma, or dialysis to remove. I reassess QRS width on the monitor and a repeat potassium.

Practice the two-stage explanation (faster repolarization and peaked T waves, then sodium channel inactivation and a sine wave) in three timed 45-second reps. Then run a hyperkalemia case in the MoxPrep practice bank and see whether your first rep puts calcium first.

Why does calcium come before insulin in hyperkalemia?

Calcium protects conduction within minutes while potassium is still high. Insulin and albuterol take 15 to 30 minutes to lower the level, which is too slow when the QRS is already widening.

Why check potassium before starting insulin in DKA?

Acidosis hides a total-body potassium deficit. Insulin drives potassium back into cells, so starting it below 3.3 mEq/L can cause dangerous hypokalemia and arrhythmias.