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Question and answer links
- W1: Which ECG finding is classically associated with early hyperkalemia, while recognizing that the sequence is not reliable · Answer
- W2: Which bedside finding points toward too much fluid (hypervolemia) rather than too little? · Answer
- W3: Which treatment actually removes potassium from the body, rather than stabilizing the heart or pushing potassium tempora · Answer
- Q4: It is 18:43. The first potassium is 8.1 on a hemolyzed sample; the clean repeat was just drawn from the right arm and wi · Answer
- Q5: Mr. Hartman has taken lisinopril for 8 years with monthly pre-dialysis potassium values of 4.8–5.3 mEq/L. Which change i · Answer
- Q6: Nephrology asks you to state the indication for urgent dialysis. Which single finding, on its own, is an urgent dialysis · Answer
- Q7: He is 4 kg above dry weight with a JVP at the jaw, crackles halfway up both lungs, BP 178/96, and pulmonary edema on the · Answer
- Q8: It is 18:50. The QRS has narrowed to 122 ms after calcium. The repeat potassium is still pending (the hemolyzed value wa · Answer
- Q9: If you were thinking "the potassium emergency is over — tonight's run can wait for his regular Friday session," and you · Answer
- Q10: On Thursday a hospitalist orders a peripheral IV for an antibiotic "just in case the shin flares." Mr. Hartman has a wor · Answer
Session S1 · 2026-10-22 · in-session · 37 min Anchor: Fluids, electrolytes and acid-base — hyperkalemia emergency in a dialysis patient · Integrates: ESRD and dialysis basics, AKI complications and AEIOU, drug contributors (TMP-SMX, ACEi), pseudohyperkalemia, vascular-access protection, bedside volume exam One-line hook: Dialysis patients turn up in every ED and urgent care in Iowa, and the one who missed a session arrives carrying the single electrolyte that can stop a heart — and the first potassium you see may be the wrong number.
Learning Objectives
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10
- Pair a potassium value with the ECG and decide whether to give IV calcium before the repeat sample comes back.
- Distinguish pseudohyperkalemia (hemolysis, fist clenching, tight tourniquet, very high platelet or white cell counts) from true hyperkalemia, and explain why compatible conduction changes in this high-risk presentation require urgent treatment rather than waiting to dismiss the potassium as hemolysis.
- Read a dialysis patient's BMP in a fixed order and name which AEIOU indications for urgent dialysis are present.
- Sequence the emergency treatment — stabilize, shift, remove — and state why the removal step in an essentially anuric patient is dialysis, not a loop diuretic.
- Protect the fistula arm and identify and stop the drug contributors (trimethoprim stopped in the ED; the ACE inhibitor held for the dialysis team's decision). Counselling on dietary potassium, salt substitutes and a missed treatment is discussed before discharge, not tested.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2 · W3
W1The ECG cascade
Which ECG finding is classically associated with early hyperkalemia, while recognizing that the sequence is not reliable in an individual patient?
Sine-wave pattern with the QRS merging into the T wave
Loss of P waves with a slow, wide-complex rhythm
Tall, narrow-based ("tented") T waves
Widening of the QRS complex
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Extra potassium outside the cell narrows the gap between the resting and threshold potential of heart muscle, and the first thing that shows is faster, steeper repolarization — tall, peaked T waves with a narrow base. As the level climbs, conduction slows: the P wave flattens and disappears, the PR interval stretches, the QRS widens, and the last stop is a sine wave and then asystole or ventricular fibrillation . This is the classic teaching sequence, not a reliable progression in an individual patient: dangerous conduction changes may appear without earlier peaked T waves, and a normal ECG does not exclude severe hyperkalemia. Why not the others: A is the terminal pattern, not the first; B (absent P waves) is a late conduction change; D (wide QRS) follows the T-wave change and means the patient is already in danger. Course reading: Evidence for this case
W2Reading the volume exam
Which bedside finding points toward too much fluid (hypervolemia) rather than too little?
A fall in systolic pressure of more than 20 mmHg on standing
A jugular venous pressure above 8 cm at 45 degrees
Dry mucous membranes with slow skin turgor at the forearm
A weight that is 3 kg below the last clinic visit
Show answer and explanation · Link to this question
Correct answer: B
Learning point: The jugular vein is a window on the pressure in the right side of the heart. When the circulation is overfilled, that pressure rises and the vein stays full high up the neck. Pair it with the lungs (crackles), the legs (pitting edema), the blood pressure (often high) and the weight trend, and the exam gives one answer. One liter of retained fluid weighs about one kilogram, which is why the dialysis unit weighs patients before and after every run. Why not the others: A is orthostatic hypotension — a sign of volume depletion; C is dryness, the opposite finding; D is weight loss, which in a dialysis patient usually means fluid came off. Course reading: Evidence for this case
W3Shift versus remove
Which treatment actually removes potassium from the body, rather than stabilizing the heart or pushing potassium temporarily into cells?
Regular insulin 10 units IV with 25 g of dextrose
Nebulized albuterol 10–20 mg
Calcium gluconate 1 g IV over 2–3 minutes
Hemodialysis
Show answer and explanation · Link to this question
Correct answer: D
Learning point: Hyperkalemia treatment has three jobs that run in parallel . Stabilize — calcium protects the heart muscle membrane but changes the potassium not at all. Shift — insulin (with glucose so the patient does not go low) and a beta-agonist drive potassium into cells for a few hours; the total amount in the body is unchanged and it will come back out. Remove — a loop diuretic if the kidneys make urine, a gut binder, or dialysis. Only the third group lowers total-body potassium, and in a patient with no kidney function, dialysis is the only one that works fast. Why not the others: A and B are shift therapies — temporary by design; C is membrane stabilization and does nothing to the potassium level. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q4 · Q5
Setting: Community hospital emergency department, Wednesday, 18:05. Two days after an ice storm.
Mr. Dale Hartman is 58. He has had type 2 diabetes for 22 years, and the diabetes took his kidneys. Two and a half years ago he reached end-stage renal disease (ESRD) — kidney function too low to keep a person alive without something to replace it — and he has been on in-center hemodialysis ever since: three times a week, Monday-Wednesday-Friday, his blood runs through a filter that pulls out waste, potassium, acid and water, then returns. His access is a left upper-arm arteriovenous fistula — a surgeon joined an artery to a vein so the vein grew big and tough enough to be needled three times a week. It was created six months before he started dialysis so it had time to mature. He makes "maybe a cup" of urine a day — essentially anuric, and far too little for any diuretic to matter.
Sunday night's ice storm closed the roads. The unit cancelled Monday's shift. Tuesday the unit reopened but his transport van did not run, and he figured he would "just go Wednesday." By Wednesday morning his ankles were swollen over his shoes, he could not lie flat, he had no appetite, he was nauseated and had a metallic taste in his mouth, and he skipped his 13:00 chair time because he felt too weak to walk to the car. His wife drove him in at 18:00 when he started gasping on the stairs. His last dialysis was Friday — five days ago.
Last Thursday — six days ago — an urgent care treated a cellulitis (a skin infection) of his right shin with trimethoprim-sulfamethoxazole DS (160 mg/800 mg), one tablet twice a day for seven days — the standard dose, not adjusted for kidney failure. He started it Friday morning, before his last dialysis run, and has taken it every day since: this morning's tablet was his eleventh, day 6 of 7, and the bottle with the last three is in his jacket. The redness is fading.
At home, his wife stocked the pantry before the storm — including a "lite" salt substitute she had read was better for blood pressure. He has been shaking it on his food for about two weeks. He takes no NSAIDs and no over-the-counter supplements.
Vitals: BP 178/96 (right arm) · Pulse 54, regular · Respirations 26/min · Temp 36.8 °C · Weight 86.0 kg (his dry weight — the weight at which he carries no extra fluid — is 82.0 kg) · SpO₂ 89% on room air, 94% on 4 L by nasal cannula. Volume-exam framework: quick-start guide, Part 6.
At triage a 20-gauge IV was placed in the left forearm — the fistula arm — and the first blood sample was drawn back through it, with a tourniquet on while he pumped his fist to "bring up a vein." An ECG was recorded at 18:12.
Exam: Sitting bolt upright, speaking in short sentences. Jugular venous pressure visible at the angle of the jaw with the head of the bed at 45 degrees. Crackles halfway up both lung fields. Heart sounds regular and slow; no rub. 2+ pitting edema to the knees. Left upper arm: fistula with a strong thrill (the buzz you feel) and a continuous bruit (the whoosh you hear). Right shin: fading erythema, no warmth. Alert and oriented; mild symmetric leg weakness, painless, with no muscle tenderness in the thighs, calves or shoulders; no asterixis (the flapping tremor of the outstretched hands seen in uremia).
ECG 18:12: Rate 54. P waves flattened and hard to find. PR 240 ms where it can be measured. QRS 148 ms. Tall, peaked T waves in V2–V5.
18:35 — the lab calls: "Critical potassium 8.1 mEq/L. Specimen hemolyzed; potassium may be falsely elevated." A repeat is drawn from the right antecubital vein at 18:42 — no fist pumping, tourniquet off as soon as the needle is in. The result will take about 25 minutes.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Lisinopril | 10 mg | PO | Daily (8 years) | Hypertension |
| Amlodipine | 10 mg | PO | Daily | Hypertension |
| Insulin glargine | 12 units | SC | Nightly | Type 2 diabetes |
| Sevelamer carbonate | 800 mg | PO | Three times daily with meals | High phosphate (a phosphate binder, not a potassium binder) |
| Atorvastatin | 40 mg | PO | Nightly | Hyperlipidemia |
| Aspirin | 81 mg | PO | Daily | Cardiovascular prevention |
| Trimethoprim-sulfamethoxazole DS (160/800 mg) | 1 tablet | PO | Twice daily × 7 days — day 6 of 7, still taking | Right-shin cellulitis (urgent care; standard dose) |
| Epoetin alfa | per unit protocol | IV | With dialysis | Anemia of kidney disease |
Pause — commit before the reveal
Q4Treat the number or treat the ECG?
It is 18:43. The first potassium is 8.1 on a hemolyzed sample; the clean repeat was just drawn from the right arm and will not be back for about 25 minutes. The ECG shows flattened P waves, PR 240 ms, QRS 148 ms and peaked T waves. What do you do now?
Wait for the repeat — hemolysis falsely raises potassium, and treating a false value risks hypercalcemia
Give calcium gluconate IV now, start the shift therapies, and let the repeat confirm the level
Give insulin and dextrose now but hold the calcium until the repeat proves the potassium is real
Give furosemide 80 mg IV and page nephrology; the potassium will come down with the fluid
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Hemolysis adds potassium to the tube after the blood has left the body; it cannot change what the heart has been bathing in. A QRS of 148 ms with vanishing P waves is the heart telling you its potassium is dangerously high, whatever the tube says. A convincing ECG is treated the moment you see it — calcium gluconate 10%, 10 mL (1 g) over 2–3 minutes, repeated in 5 minutes if the QRS has not narrowed — and the repeat sample is sent at the same time, not instead. Calcium works in minutes and lasts only 30–60 minutes, so the shift and removal steps start right behind it: stabilize, shift, remove, in parallel, is the sequence every emergency guideline teaches . Why not the others: A confuses "the number may be inflated" with "the patient may be safe" — the ECG has already answered that; C has the sequence backwards: calcium is the one treatment that protects the heart now and is the step you least want to delay; D is the loop-diuretic reflex in a man who is essentially anuric — it removes nothing, and nephrology should already have been paged. Course reading: Evidence for this case
Q5What pushed the potassium up this week?
Mr. Hartman has taken lisinopril for 8 years with monthly pre-dialysis potassium values of 4.8–5.3 mEq/L. Which change in the last two weeks best explains a potassium that is now dangerous, on top of the five days without dialysis?
The TMP-SMX course — trimethoprim blocks potassium secretion in the collecting duct
The amlodipine — calcium-channel blockers block potassium secretion in the collecting duct
The sevelamer — the binder exchanges phosphate for potassium in the gut
The atorvastatin — statin muscle injury released potassium from muscle cells
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Trimethoprim inhibits distal-nephron ENaC and can impair renal potassium secretion; lisinopril and the potassium-chloride salt substitute add risk. With very little residual kidney function, the size of trimethoprim's renal contribution is uncertain. The missed dialysis sessions and potassium load are the dominant established explanations. Stop the avoidable contributors and arrange definitive potassium removal. Why not the others: B — amlodipine has no meaningful effect on potassium handling; C — sevelamer binds phosphate, not potassium, and does not release potassium; D — statin rhabdomyolysis can raise potassium, but his weakness is symmetric and painless — the hyperkalemia pattern — he has no muscle tenderness, and the shin infection is resolving; the CK in Part 2 will confirm it. Course reading: Evidence for this case
What the team did at 18:45. Calcium went through a new right-arm peripheral IV. TMP-SMX was stopped; the infection treatment and antibiotic choice will be reviewed with the dialysis team. The left-arm IV was removed with careful hemostasis, and the wrist band and handoff identify the functioning fistula: avoid routine IVs, blood draws and blood-pressure cuffs on that arm. The reason is protection from vessel injury, infection and thrombosis; forearm veins do not all drain through an upper-arm fistula or share its pressure. Preserve veins in both arms for future access, avoid unnecessary punctures and PICCs, and consult the access team when alternative access is difficult (KDOQI 2019, 6.10).
Part 2 — Data
Answers for this section: Q6 · Q7
19:05 — the repeat potassium, drawn at 18:42 from the right arm, is back. The full panel, with his monthly pre-dialysis labs from three weeks ago for comparison:
| Test | Result (18:42 sample) | 3 weeks ago (pre-dialysis) | Reference range |
|---|---|---|---|
| Sodium | 136 mEq/L | 138 | 136–145 mEq/L |
| Potassium | 7.3 mEq/L (not hemolyzed) | 5.1 | 3.5–5.0 mEq/L |
| Chloride | 100 mEq/L | 102 | 98–107 mEq/L |
| Bicarbonate | 15 mEq/L | 22 | 22–28 mEq/L |
| Anion gap (calculated) | 21 mEq/L | 14 | 8–12 mEq/L |
| BUN | 110 mg/dL | 58 | 7–20 mg/dL |
| Creatinine | 11.2 mg/dL | 8.9 | 0.7–1.3 mg/dL |
| eGFR | not reported — not valid on dialysis | — | — |
| Glucose | 168 mg/dL | 152 | 70–99 mg/dL |
| Calcium | 8.2 mg/dL | 8.6 | 8.5–10.5 mg/dL |
| Phosphorus | 7.4 mg/dL | 5.2 | 2.5–4.5 mg/dL |
| Magnesium | 2.3 mg/dL | 2.1 | 1.7–2.2 mg/dL |
| Albumin | 3.6 g/dL | 3.7 | 3.5–5.0 g/dL |
| Creatine kinase (CK) | 96 U/L | — | 30–200 U/L |
| Venous blood gas | pH 7.24 · pCO₂ 36 mmHg | — | pH 7.32–7.42 · pCO₂ 41–51 mmHg (venous) |
| Hemoglobin | 10.4 g/dL | 10.6 | 13.5–17.5 g/dL |
| White cells | 8.9 ×10⁹/L | 7.8 | 4.0–11.0 ×10⁹/L |
| Platelets | 230 ×10⁹/L | 244 | 150–400 ×10⁹/L |
Urinalysis: not obtained — he could not produce a sample, and in a patient who is essentially anuric it would not change a decision tonight.
Chest radiograph (portable, 18:30): Enlarged cardiac silhouette. Bilateral perihilar haziness in a bat-wing pattern (fluid spreading out from the center of each lung), Kerley B lines (short horizontal lines at the lung edges — fluid in the lung lymphatics) at both bases, small bilateral pleural effusions. Read: pulmonary edema.
Point-of-care glucose: 168 mg/dL at 18:50, before insulin.
Acid-base check: The anion gap is 21 mEq/L before albumin adjustment. Winter's formula predicts an arterial PCO₂ near 30.5 ± 2 mmHg. A venous PCO₂ cannot be converted reliably for an individual by subtracting a fixed number; the VBG supports acidemia but does not securely exclude an additional respiratory disorder.
Q6Which number buys him dialysis tonight?
Nephrology asks you to state the indication for urgent dialysis. Which single finding, on its own, is an urgent dialysis indication for Mr. Hartman?
BUN 110 mg/dL
Creatinine 11.2 mg/dL
Bicarbonate 15 mEq/L with a venous pH of 7.24
Potassium 7.3 mEq/L with a QRS of 148 ms
Show answer and explanation · Link to this question
Correct answer: D
Learning point: The AEIOU mnemonic names the reasons to dialyze tonight rather than tomorrow: Acidosis that is severe and refractory, Electrolytes — refractory hyperkalemia, especially with ECG changes, Intoxication with a dialyzable drug, Overload — pulmonary edema that diuretics cannot fix, and Uremia with symptoms (pericarditis, confusion, bleeding, intractable nausea). Potassium 7.3 with a wide QRS is the E, and in a man with no kidney function it is unlikely to be controlled durably by shifting treatment alone — medical therapy only hides it for a few hours. He also has the O (pulmonary edema, no meaningful urine to diurese) and early U (anorexia, nausea, metallic taste). The A is present but moderate (pH 7.24, appropriately compensated) and will correct with the run; on its own it would not force dialysis tonight. Why not the others: A and B are markers of kidney failure, not indications — his BUN and creatinine are high every day he is on dialysis, and no single value of either triggers an urgent run; C is real acidosis, but it is neither severe (pH is not below 7.1–7.2) nor refractory, and bicarbonate alone would not be the reason to call the dialysis nurse in. Course reading: Evidence for this case
Pause — commit before the reveal
Q7The fluid decision
He is 4 kg above dry weight with a JVP at the jaw, crackles halfway up both lungs, BP 178/96, and pulmonary edema on the film. He is essentially anuric — about a cup of urine a day. Which plan is right for his volume status?
Normal saline 1 L bolus — his heart rate is 54 and the ECG changes may reflect poor perfusion
Furosemide 80 mg IV push, repeated at 1 hour if urine output stays low
No fluids and no diuretic; sit him up, give oxygen, and let the dialysis run take the fluid off
Furosemide 160 mg IV plus metolazone 5 mg PO to overcome diuretic resistance
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The combined weight gain, high JVP, crackles, edema and chest film support severe congestion. With only a small residual urine volume, diuretics cannot be relied on for prompt adequate removal. Urgent dialysis provides definitive potassium and volume treatment. Some patients with residual kidney function still respond to loops; this is not a rule that every low-output dialysis patient has zero response at every dose. Support breathing and avoid unnecessary IV volume while arranging treatment. Why not the others: A adds volume despite clear congestion. B and D delay dependable removal by relying on diuretics in a patient with very little residual output. Treat the hyperkalemic ECG and arrange urgent dialysis in parallel. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q8 · Q9 · Q10
Dose context for this fictional US course. The initial 1 g calcium gluconate dose with ECG-guided repeat dosing follows the 2021 emergency-medicine consensus, section 2, Step 2 and section 1.6.1. The 5-unit regular-insulin/25-g glucose regimen appears in the KDIGO conference report, Figure 3. These are protocol options, not universal doses: UKKA 2026 specifies calcium gluconate 3 g over 10 minutes and insulin 10 units with 25 g glucose. Follow the institution's protocol, repeat the ECG and potassium, and use the full glucose-monitoring schedule.
18:45 Calcium gluconate 10%, 10 mL (1 g) IV over 3 minutes through the new right-forearm IV, on the monitor . TMP-SMX stopped; lisinopril held. 18:50 QRS 148 → 122 ms; faint P waves reappear; rate 60.
Pause — commit before the reveal
Q8After the calcium, before the machine
It is 18:50. The QRS has narrowed to 122 ms after calcium. The repeat potassium is still pending (the hemolyzed value was 8.1); glucose 168; no meaningful urine output; nephrology says dialysis can start in about 75 minutes. What is the right plan for the next 75 minutes?
Nothing further until dialysis — the calcium corrected the ECG; recheck the potassium after the run
Insulin with dextrose, nebulized albuterol, an oral binder as a bridge, and scheduled glucose checks
Sodium bicarbonate as the main potassium therapy, with calcium repeated every 10 minutes until the run
Furosemide 160 mg IV so that potassium starts leaving in the urine while the machine is set up
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Calcium bought 30–60 minutes of membrane protection and changed the potassium by nothing. Dialysis is not an event that happens when you say the word — a nurse has to drive in, a machine has to be primed and tested, the access has to be cannulated — so the gap is covered by the shift therapies that every emergency-department bundle agrees on : insulin with dextrose (onset about 15 minutes, drops potassium 0.6–1.0 mEq/L for a few hours) and high-dose nebulized albuterol — 10–20 mg, far above a bronchodilator dose, which lowers potassium a further 0.5–1.0 mEq/L in dialysis patients ; the two effects are additive . A binder started now has begun working by the time the run ends, which matters because potassium rebounds when the shift wears off and after dialysis. Check glucose before insulin and at 30, 60, 90, 120, 180, 240, 300 and 360 minutes afterward; delayed hypoglycemia in kidney failure requires the full monitoring schedule (UKKA 2026, Guideline 17.2). And recheck the ECG and potassium: the one-hour value tells you whether the shift took. Why not the others: A mistakes a narrower QRS for a lower potassium — calcium hides the danger for an hour and then it is back; C leans on bicarbonate, which is not a reliable stand-alone potassium treatment (its effect depends on the acid-base picture and it adds sodium and fluid to a man already in pulmonary edema), and repeating calcium every 10 minutes is not the protocol; D is the loop-diuretic reflex again — no meaningful urine, no removal. Course reading: Evidence for this case
18:50 Regular insulin 5 units IV push with dextrose 50%, 50 mL (25 g) IV . The usual dose is 10 units; in kidney failure, insulin lingers and the liver makes less glucose, so hypoglycemia is common and late — many protocols use 5 units, and either way obtain glucose before treatment and at 30, 60, 90, 120, 180, 240, 300 and 360 minutes afterward (UKKA 2026, Guideline 17.2); monitor longer or more often if hypoglycemia occurs. 18:55 Albuterol 10 mg by nebulizer over 15 minutes (a bronchodilator dose is 2.5 mg; the potassium effect needs 10–20 mg, and it adds to the insulin effect) .
19:05 The repeat potassium returns: 7.3, not hemolyzed. The emergency was real.
19:10 Sodium zirconium cyclosilicate 10 g by mouth — a potassium binder, a powder that traps potassium in the gut so it leaves in the stool. It starts to work within about an hour . Tonight it is a bridge, not the destination; it does not replace dialysis in a patient who needs it.
19:15 Nephrology at the bedside; the on-call dialysis nurse is driving in through the ice. 19:50 Potassium 6.4; glucose 142 mg/dL. The ED charge nurse, watching the board fill with storm admissions, asks whether — with the potassium down almost a full point — the emergency run could be cancelled and he could go back to his regular Friday chair.
Q9Evidence update
Concordance-style practice. There is no expert panel behind this key, the teaching explanation; "Unchanged" means the finding does not move the hypothesis, not "I'm not sure."
If you were thinking "the potassium emergency is over — tonight's run can wait for his regular Friday session," and you then learn that his potassium has fallen from 7.3 to 6.4 an hour after insulin with dextrose and nebulized albuterol, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Insulin and albuterol move potassium into cells; they remove none of it. A fall of about one point in the first hour is exactly what the shift is expected to do, and it wears off over the next few hours, so the number says nothing about the total-body excess. Nothing that made tonight's run necessary has changed: no meaningful urine, 4 kg over dry weight with pulmonary edema, BUN 110 and bicarbonate 15. Why not the others: A and B — the fall adds no new reason against waiting; every reason he needs the run tonight was present before this number; D and E read a shifted potassium as a removed one. Course reading: Evidence for this case
20:00 The dialysis nurse arrives; fistula cannulated. 20:10 Hemodialysis begins — a 4-hour run on cardiac monitoring.
The run. 21:10 (one hour in): potassium 5.6, QRS 98 ms, P waves back. 21:50: glucose 76 mg/dL — he drinks 4 oz of juice; 22:50 glucose 118. 00:10, end of run: potassium 4.4, weight 83.4 kg (2.6 kg removed — nephrology chose not to chase the full 4 kg in one run; pulling too much too fast drops the blood pressure and cramps, so an extra run is scheduled for Thursday). BP 148/84, breathing comfortably on room air. He lies flat for the first time in two days. He is admitted to telemetry. 02:10: potassium 5.0 — the expected rebound as potassium comes back out of cells and out of tissue stores, which is why the post-dialysis value is never the last one you check. Thursday 07:00: potassium 5.3, nausea gone, eating breakfast.
Q10The band on the wrist
On Thursday a hospitalist orders a peripheral IV for an antibiotic "just in case the shin flares." Mr. Hartman has a working left upper-arm fistula. Which instruction belongs on his chart and wristband?
A PICC line is preferred, because it spares peripheral veins and can be used for weeks
Blood pressure cuffs on the fistula arm are acceptable as long as the thrill is checked afterward
No IVs, blood draws or blood pressure cuffs on the left arm; place the IV in the right arm
Place IVs in the left hand, below the fistula, where the veins are not part of the access
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Protect his functioning fistula and preserve vessels for future access. KDOQI 2019 uses an individualized ESKD Life-Plan rather than a universal fistula-first hierarchy. A mature fistula has important advantages for this patient, but another patient may appropriately receive a graft, catheter, peritoneal dialysis or transplant. Use the right arm for necessary routine peripheral access here; avoid a PICC without nephrology/access-team review. Routine fistula cannulation belongs to trained dialysis personnel. Why not the others: A risks sacrificing veins needed for future access; B applies pressure to the access arm; D still places an unnecessary IV in the fistula arm. These are vein-preservation decisions, not a claim that every ipsilateral vein is part of one high-pressure circuit. Course reading: Evidence for this case
The conversations before discharge — the part of the case that prevents the next one.
- The lisinopril. Held in hospital while the potassium settled. Whether it resumes is the dialysis team's call at his next session, not the ED's and not the patient's. In a man who is essentially anuric the drug is not protecting kidney function; its job is blood pressure, which other classes can do. The precipitants this week were trimethoprim, the salt substitute and five missed days — not a drug he had tolerated for eight years. "Stop it forever" and "never mention it" are both wrong; "hold, hand off, let the team decide" is right.
- Potassium in the diet, and the salt-substitute trap. Most "salt substitutes" and "lite" salts swap sodium for potassium chloride, and so do many reduced-sodium broths and seasoning blends; coconut water carries about as much potassium as a large banana. The "lite" salt from the pantry goes in the trash, and his wife — who bought it to help — hears why. A dialysis dietitian goes over higher- and lower-potassium foods and cooking methods before he leaves.
- Interdialytic weight gain. Every kilogram he gains between runs is a liter of fluid the next run has to pull off; the long gap after a weekend, or after a missed session, is when the gain and the potassium both run highest. Dry weight 82 kg goes on his discharge sheet, with the fluid and salt limits the unit uses.
- Missed-treatment plan. Call the unit the same day — units reschedule and have a weather plan; do not "wait for the next regular day." While waiting: lowest-potassium eating, fluid limit, no salt substitute. Go to the ED, not the unit, for shortness of breath, weakness, palpitations or chest pain.
- Uremic symptoms. Loss of appetite, nausea, metallic taste, itching, confusion, chest pain that is worse lying down (pericarditis), unusual bleeding or bruising. Any of them after a missed run is a same-day call.
- The urgent care prescription. A note goes to the urgent care: TMP-SMX in a dialysis patient needs a reduced dose and a potassium check — or a different antibiotic. His course was stopped on day 6 with the cellulitis resolving and was not restarted. His dialysis unit's name and phone number go on his wallet card so the next prescriber can call.
Resolution and Teaching Points
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10
Mr. Hartman had an extra dialysis run Thursday afternoon and left Friday at 82.4 kg with a potassium of 4.9, back on his Monday-Wednesday-Friday chair, lisinopril on hold pending the unit's review, a new wallet card, and a wristband he says he will keep wearing "so nobody sticks the wrong arm." The urgent care updated its protocol for antibiotics in dialysis patients. He has not missed a Monday since.
Clinical Pearl — Treat the ECG, not the tube A hemolyzed sample inflates the number; it cannot widen a QRS. The ECG can have other causes of widening, but specimen hemolysis itself cannot produce a conduction abnormality. A convincing ECG gets calcium before the repeat comes back, and the repeat is sent at the same time, never instead.
Clinical Pearl — Three ways the tube lies, and one way the ECG does Pseudohyperkalemia means the tube holds more potassium than the patient: hemolysis during a hard draw, fist pumping against a tourniquet, or very high platelet or white counts leaking potassium after the draw. None of them reaches the heart. The reverse warning matters as much: a normal ECG does not exclude dangerous hyperkalemia — roughly half of patients above 6.5 show no ECG change . His hemolyzed 8.1 was inflated; the real 7.3 was still an emergency.
Clinical Pearl — Three jobs, in parallel Stabilize (calcium — protects the membrane, changes the potassium not at all, lasts under an hour). Shift (insulin with dextrose, nebulized albuterol — temporary, hours). Remove (loop diuretic if there is urine, binder, dialysis). In an essentially anuric patient, removal means dialysis, and every temporizing step exists to cover the time it takes to start.
Clinical Pearl — Read the BMP in order, every time Na → K → Cl → HCO₃ → anion gap → BUN/creatinine → glucose, then Ca, Mg, PO₄. The order makes you see the emergency (K 7.3) before the distraction (creatinine 11.2), compute the gap instead of eyeballing it, and remember that no eGFR equation applies to a dialysis patient.
Clinical Pearl — Find the hits Trimethoprim can impair residual renal potassium excretion. Do not infer a proven colonic ENaC mechanism or quantify its contribution in this nearly anuric patient.
Clinical Pearl — The fistula arm is a protected zone Avoid routine IVs, blood draws and blood-pressure cuffs on the functioning access arm to reduce vessel injury, infection and thrombosis. Preserve veins in both arms and avoid unnecessary PICCs; difficult-access decisions require the access team. Access choice follows the patient’s KDOQI life-plan rather than an absolute fistula-first rule for every patient.
Pitfall — The loop-diuretic reflex Pulmonary edema plus hyperkalemia calls for dependable removal. With minimal residual urine output, diuretics cannot be relied on for adequate urgent removal; arrange dialysis. Some residual-function patients still respond to loops, so do not teach that every low-output dialysis patient has zero response at every dose.
Pitfall — "The ECG is better, so the potassium is better" Calcium narrows the QRS and lowers the potassium by zero. Insulin lowers it for a few hours and then it rebounds. The one-hour recheck, the glucose checks, and the post-dialysis recheck are where the case is actually won or lost.
Concept Links
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-22, aki-24, ckd-17, ckd-23, ckd-25, lytes-01, lytes-03, lytes-12, lytes-13, lytes-14.