Eduovisual
Renal & Urinary
Hyperkalemia: ECG changes and emergency management
— Mild: K⁺ 5.5–5.9 mEq/L; moderate: 6.0–6.4; severe: ≥6.5 or any level with ECG changes or neuromuscular symptoms
— True hyperkalemia must be distinguished from pseudohyperkalemia (hemolyzed specimen, fist clenching during draw, marked leukocytosis >100k or thrombocytosis >1M, prolonged tourniquet)
— CKD/ESRD patients with missed dialysis sessions ("missed Monday HD" classic stem)
— Patients on RAAS blockers (ACEi, ARB, ARNI), spironolactone/eplerenone, trimethoprim, pentamidine, calcineurin inhibitors, NSAIDs, heparin, β-blockers, digoxin toxicity
— Crush injury, rhabdomyolysis, tumor lysis syndrome, massive hemolysis, GI bleed in CKD, burns
— Adrenal insufficiency (think hyperkalemia + hyponatremia + hypotension)
— Type 4 RTA (diabetics with hyporeninemic hypoaldosteronism)
— Hyperkalemia is the most common life-threatening electrolyte abnormality and a leading cause of preventable arrest in dialysis units
— CCS clock burns fast: identification → ECG → stabilization → shift → elimination, in that order
— Outpatient management decisions (which RAAS-blocker to continue, when to add patiromer, dietary K⁺ counseling) are equally tested
— Transcellular shifts (acidosis, insulin deficiency, β-blockade, succinylcholine in burns/denervation, digoxin) vs. impaired excretion (AKI/CKD, low aldosterone, drugs) vs. excess intake (rare unless impaired excretion)
Board pearl: A potassium of 6.8 in an asymptomatic patient with a normal ECG and a hemolyzed sample warrants a repeat, non-tourniquet venous sample before committing to aggressive therapy — but never delay treatment if any ECG change is present. The cost of treating pseudohyperkalemia is low; the cost of missing real hyperkalemia is cardiac arrest.
— Neuromuscular: ascending weakness, paresthesias, areflexia, flaccid paralysis sparing cranial nerves and diaphragm until very late
— Cardiac: palpitations, presyncope, syncope, sudden cardiac arrest (VF, asystole, PEA with wide-complex bradycardia)
— GI: nausea, vomiting, ileus (less reliable)
— Many patients are asymptomatic until the ECG goes haywire — do not let a "well-appearing" patient lull you
— Dialysis schedule: When was last HD? Missed sessions? Access functioning? Recent change in dry weight?
— Medications: ACEi/ARB/ARNI, spironolactone/eplerenone/finerenone, K⁺ supplements, salt substitutes (KCl), TMP-SMX, NSAIDs, β-blockers, digoxin, heparin, tacrolimus/cyclosporine
— Recent events: trauma/crush, prolonged immobilization, seizure, strenuous exercise, chemotherapy initiation (TLS), transfusion of old PRBCs
— Comorbidities: CKD stage, diabetes (insulin lapses, DKA), Addison's, CHF (often on multiple RAAS agents)
— Diet: banana/orange/potato/tomato/avocado loads, "low-sodium" salt substitutes containing KCl, coconut water
— "Patient with ESRD on MWF dialysis presents Monday morning…"
— "Diabetic on lisinopril and spironolactone started on TMP-SMX for cellulitis…"
— "Crush injury extricated after 6 hours of entrapment…"
— "Cancer patient 48 hours after induction chemo with rising creatinine…"
Step 3 management: When the stem hands you a CKD patient on lisinopril + spironolactone now started on Bactrim for a UTI, the test wants you to stop the offending agent(s) and check a K⁺ even before symptoms appear. Anticipatory monitoring (BMP within 5–7 days of TMP-SMX initiation in this population) is the safety-net order Step 3 rewards.
— Bradycardia (sinus brady, junctional escape, AV block) is the classic finding
— Hypotension if hemodynamically unstable or if adrenal insufficiency is the driver
— Tachypnea may reflect compensatory response to metabolic acidosis (a common co-traveler)
— Symmetric flaccid weakness, often starting in lower extremities and ascending — mimics Guillain-Barré
— Diminished or absent deep tendon reflexes
— Preserved mental status (a key distinction from CNS causes of weakness)
— Irregular rhythm, bradycardia, occasionally a regularized "sine wave" pulse in extremis
— Look for signs of pericardial effusion in ESRD (uremic pericarditis can coexist)
— Hypovolemic (vomiting, AI, diuretic-induced K⁺ retention paradox): flat JVP, dry mucosa, orthostasis → IV fluids help
— Euvolemic/hypervolemic (ESRD, oliguric AKI, CHF): elevated JVP, edema, rales → loop diuretic if making urine; dialysis if anuric
— Examine AV fistula for thrill/bruit in ESRD patient — patency matters for emergent HD
— Hyperpigmentation of palmar creases/buccal mucosa → primary adrenal insufficiency
— Crush marks, compartment tenseness, tea-colored urine → rhabdomyolysis
— Petechiae/bruising in TLS or hematologic malignancy
Key distinction: Hyperkalemic ascending paralysis vs. Guillain-Barré — both present with symmetric ascending weakness and areflexia, but hyperkalemia patients have a history of CKD or RAAS blockade, a markedly abnormal ECG, and immediate reversal with calcium and K⁺-lowering therapy. GBS will have CSF albuminocytologic dissociation and normal electrolytes. Always check a K⁺ before lumbar puncture in any new ascending weakness.
— STAT 12-lead ECG — this is the single most important test; do not wait for repeat K⁺
— BMP (K⁺, Cr, BUN, glucose, HCO₃⁻, anion gap)
— VBG or ABG for pH and rapid K⁺ (point-of-care)
— Ca²⁺, Mg²⁺, Phos (TLS pattern: ↑K, ↑Phos, ↑uric acid, ↓Ca)
— CK if rhabdo suspected; LDH, uric acid if TLS; haptoglobin/retic if hemolysis
— Digoxin level if on digoxin
— Cortisol/ACTH if AI suspected
— UA, urine K⁺, urine osm if cause unclear (TTKG is now de-emphasized)
— K⁺ 5.5–6.5: peaked, narrow-based T waves (best seen in precordial leads), shortened QT
— K⁺ 6.5–7.5: PR prolongation, flattening/loss of P waves, first-degree AV block
— K⁺ 7.0–8.0: QRS widening, bundle branch block patterns, fascicular blocks
— K⁺ >8.0: sine-wave pattern (merged QRS-T), VF, asystole, PEA
— Brugada-like pattern, bradyarrhythmias, idioventricular rhythm also seen
— ECG changes correlate poorly with absolute K⁺ level — rate of rise matters more
— Chronic ESRD patients tolerate higher levels with fewer ECG changes than acute hyperkalemia
— A normal ECG does not rule out dangerous hyperkalemia; treat the number plus the clinical picture
— Hypocalcemia, hypothermia, and digoxin toxicity all worsen the cardiac effects
CCS pearl: In an unstable rhythm, the order matters: obtain ECG → give IV calcium first → then insulin/dextrose and albuterol → then elimination (loop, K⁺-binder, or dialysis). Do not "wait for confirmatory labs" when the ECG already confirms toxicity. Repeat ECG every 15–30 minutes during active treatment.
— Repeat venous sample without tourniquet, no fist clenching, processed promptly
— Plasma K⁺ (heparinized tube) is more accurate than serum K⁺ when leukocytosis >100k or platelets >1M (serum K⁺ is falsely elevated due to release during clotting)
— Point-of-care iSTAT/VBG K⁺ returns in minutes and is reliable for emergent decisions
— Renal vs. extrarenal: spot urine K⁺ <20 mEq/L suggests impaired renal excretion; >40 suggests transcellular shift or excess intake with intact kidneys
— Aldosterone/renin ratio for hypoaldosteronism workup (outpatient)
— Plasma cortisol + cosyntropin stimulation if AI suspected
— CK, urine myoglobin for rhabdomyolysis
— Uric acid, LDH, phosphate for tumor lysis syndrome (Cairo-Bishop criteria)
— Digoxin level — toxicity causes hyperkalemia by Na/K-ATPase inhibition; level >2 ng/mL with symptoms warrants digoxin immune Fab
— Renal ultrasound in new AKI to evaluate for obstruction
— Bedside echo if hemodynamically unstable to evaluate for pericardial effusion, RV strain, contractility
— CT for crush/compartment syndrome workup
— Hyperkalemic periodic paralysis (autosomal dominant, SCN4A mutation): episodic weakness triggered by rest after exercise, cold, K⁺-rich meals
— Pseudohypoaldosteronism (Gordon syndrome): hypertension + hyperkalemia + metabolic acidosis with normal renal function
Board pearl: In digoxin toxicity, avoid IV calcium — the dogma of "stone heart" is largely debunked, but the definitive therapy is digoxin-specific Fab fragments, and serum K⁺ will correct as digoxin is bound and Na/K-ATPase resumes function. Giving calcium here is not the right answer on the test.
— Is there an ECG change? → emergency, give calcium now
— Is the K⁺ ≥6.5 or rising rapidly? → emergency, treat even without ECG change
— Is the patient symptomatic (weakness, arrhythmia)? → emergency
— If yes to any → full three-step therapy: stabilize, shift, eliminate
— Stabilize myocardium (minutes): IV calcium gluconate or chloride
— Shift K⁺ intracellularly (15–60 min): insulin + dextrose, nebulized albuterol, sodium bicarbonate (if acidemic)
— Eliminate K⁺ from the body (hours): loop diuretic if making urine, K⁺-binders (patiromer, sodium zirconium cyclosilicate), hemodialysis for refractory/ESRD
— Mild (5.5–5.9), asymptomatic, no ECG changes: stop offending drugs, dietary counseling, oral K⁺-binder, recheck in 24–72h
— Moderate (6.0–6.4), no ECG changes: shift + eliminate therapies, monitor on telemetry, recheck K⁺ q2h
— Severe (≥6.5 or any ECG change or symptoms): full protocol with calcium, continuous cardiac monitoring, prepare for emergent HD
— ACEi/ARB/ARNI, K⁺-sparing diuretics, NSAIDs, TMP-SMX, K⁺ supplements, salt substitutes, heparin
— Hold β-blockers only if bradycardic; otherwise they can stay
— Slow onset (hours), unclear efficacy, risk of intestinal necrosis especially with sorbitol and in post-op patients
— Largely supplanted by patiromer and sodium zirconium cyclosilicate (SZC) in modern guidelines
Step 3 management: A K⁺ of 6.0 with no ECG changes in a stable CKD patient does not require IV calcium. Calcium is for membrane stabilization when arrhythmia risk is real — peaked T's, widened QRS, or symptomatic patient. Over-treating mild hyperkalemia is a wrong-answer trap.
— Calcium gluconate 1–2 g (10–20 mL of 10%) IV over 2–3 min — peripheral line OK
— Calcium chloride 1 g IV — central line preferred (3× more elemental Ca, more vesicant)
— Onset 1–3 min, duration 30–60 min; redose if ECG changes persist after 5 min
— Does not lower K⁺ — only stabilizes the myocardium
— Use cautiously in digoxin toxicity (give Fab instead)
— Regular insulin 10 units IV + dextrose 25 g IV (50 mL of D50) — give dextrose first or simultaneously unless glucose >250
— Drops K⁺ by 0.5–1.2 mEq/L within 15–30 min, lasts 4–6 h
— Monitor glucose q1h × 6h — hypoglycemia occurs in up to 20%, often delayed at 1–3 h
— In CKD/ESRD, consider 5 units insulin + D10 infusion to reduce hypoglycemia risk
— Albuterol 10–20 mg nebulized (4–8× standard asthma dose), lowers K⁺ by 0.5–1.0 mEq/L in 30 min
— Additive to insulin; ~40% of patients are non-responders, so don't rely on it alone
— Caution in tachyarrhythmia, ACS
— Useful primarily in metabolic acidosis (HCO₃⁻ <22); not first-line in isolation
— 50–150 mEq IV; effect modest and slow
— Furosemide 40–80 mg IV if urine output is preserved; doubles in CKD
— Useful adjunct, ineffective in anuric patients
— Patiromer 8.4 g PO daily — onset ~7 h; chronic and subacute use
— Sodium zirconium cyclosilicate (SZC) 10 g PO TID for 48 h, then daily — onset ~1 h, can be used acutely
— SPS (Kayexalate) — avoid when possible due to bowel necrosis risk
Board pearl: Calcium does not lower K⁺. A common distractor: post-calcium patient with stable ECG but persistent K⁺ of 6.8 — the next step is insulin + dextrose, not more calcium.
— ESRD/anuric AKI with hyperkalemia — dialysis is definitive; pharmacologic shift is only a bridge
— Refractory hyperkalemia despite medical therapy
— Severe hyperkalemia with hemodynamic instability or arrhythmia
— Concurrent AEIOU indications: Acidosis, Electrolytes, Ingestions (lithium, salicylate, methanol/ethylene glycol, metformin), Overload, Uremia
— Call nephrology stat, place temporary HD catheter (vascath) in IJ or femoral if no access
— Avoid subclavian catheters in ESRD patients — preserves future fistula sites
— Standard run: 3–4 h with low-K⁺ dialysate (1–2 mEq/L); removes ~25–50 mEq/h
— Rebound hyperkalemia is common 1–6 h post-HD as intracellular K⁺ re-equilibrates — recheck K⁺ at 1 h and 6 h post-run
— Continue insulin/dextrose redosing q4–6h
— Continuous cardiac monitoring, repeat calcium if ECG worsens
— SZC or patiromer can be started orally if patient can tolerate
— In crush injury / rhabdomyolysis: aggressive IV fluids (NS or LR — yes, LR's 4 mEq/L K⁺ is fine and may reduce AKI), avoid bicarbonate unless severe acidemia, dialyze if AKI with refractory hyperkalemia
— In TLS: rasburicase for uric acid, aggressive hydration, dialysis if needed
— In digoxin toxicity: digoxin immune Fab is the procedure of choice; dialysis does not remove digoxin (high Vd, protein-bound)
— Much less efficient for acute hyperkalemia; rarely first-line in the ED
— SZC 10 g × 1 can drop K⁺ within an hour as a bridge
CCS pearl: In an ESRD patient with K⁺ 7.2 and peaked T waves, the orders are (1) calcium gluconate IV, (2) insulin + D50, (3) albuterol neb, (4) cardiac monitor, (5) consult nephrology for emergent HD, (6) place temporary vascath if no access — all clicked in the first simulated 15 minutes. Do not advance the clock without these.
— Higher baseline risk: age-related GFR decline, polypharmacy (ACEi + spironolactone + NSAID is the classic "triple whammy"), reduced thirst, sarcopenia masking weakness
— Insulin dosing: consider 5 units regular insulin instead of 10 in patients with eGFR <30 or weight <60 kg — hypoglycemia risk is markedly elevated and often delayed
— Monitor glucose q1h × 6h minimum
— Falls risk from hyperkalemic weakness — assess gait before discharge
— Reconcile every medication; salt substitutes (Morton Lite Salt, NoSalt) are commonly missed sources
— RAAS blockade is still first-line for proteinuric CKD and HF — do not reflexively discontinue forever
— For K⁺ 5.1–5.5: dietary counseling, patiromer or SZC to enable RAAS continuation (PEARL-HF, AMBER trials)
— For K⁺ >5.5 despite binders: dose reduce RAAS, add loop diuretic, treat metabolic acidosis with oral bicarbonate to target HCO₃⁻ ≥22
— Interdialytic K⁺ rise of 1.0–1.5 mEq/L is normal; >2.0 suggests dietary or missed-session issue
— Education: avoid bananas, oranges, potatoes, tomatoes, melons, nuts, chocolate, salt substitutes
— Low-K⁺ dialysate (1 mEq/L) increases sudden cardiac death risk if predialysis K⁺ is not very high — most patients dialyze against 2 mEq/L
— Cirrhotics on spironolactone for ascites are at risk; hyperkalemia often forces spironolactone hold and shift toward midodrine/albumin/paracentesis
— Hepatorenal syndrome compounds excretion deficit
— Avoid lactulose-induced dehydration causing prerenal AKI and secondary hyperkalemia
Key distinction: In CKD, the answer is rarely "stop ACEi forever." The Step 3 answer is add a K⁺-binder + dietary counseling + recheck, preserving RAAS for its renal and cardiovascular benefit. Permanent discontinuation increases mortality in HFrEF and accelerates CKD progression.
— Hyperkalemia is uncommon in healthy pregnancy due to physiologic aldosterone elevation and increased GFR
— Causes: preeclampsia with AKI, drug-induced (heparin, methyldopa rarely), adrenal crisis, congenital adrenal hyperplasia flare
— ACEi/ARB are contraindicated in pregnancy regardless of K⁺ status (fetal renal dysgenesis, oligohydramnios)
— Treatment principles unchanged: calcium gluconate, insulin/dextrose, albuterol are all safe in pregnancy; avoid SPS (constipation, bowel ischemia); patiromer/SZC are category-uncategorized — use only if benefit outweighs risk
— Magnesium sulfate (often co-administered for preeclampsia) does not directly worsen hyperkalemia but can compound weakness
— Neonates: physiologic K⁺ up to 6.0 acceptable; consider CAH (21-hydroxylase deficiency) — salt-wasting crisis with hyperkalemia, hyponatremia, hypotension, ambiguous genitalia in females
— Treatment doses are weight-based:
— — Calcium gluconate 60 mg/kg (0.6 mL/kg of 10%) IV slow
— — Insulin 0.1 unit/kg + D25W 2 mL/kg
— — Albuterol nebulized 2.5 mg (<25 kg) or 5 mg (≥25 kg)
— Pediatric ESRD: HD or PD as indicated
— Episodic flaccid paralysis triggered by rest after vigorous exercise, fasting, cold, K⁺-rich meals
— Diagnosis: SCN4A mutation, provocative testing
— Treatment: oral carbohydrate, mild exercise during attack, acetazolamide or thiazide for prophylaxis (counterintuitive — induces mild hypokalemia)
— Hyperkalemia + hyponatremia + hypotension + hyperpigmentation
— Treat with hydrocortisone 100 mg IV + aggressive NS + standard hyperkalemia therapy; cortisol replacement is the definitive fix
Board pearl: A neonate with vomiting, hyponatremia, hyperkalemia, hypotension, and ambiguous genitalia is 21-hydroxylase deficiency CAH until proven otherwise — give IV hydrocortisone, NS, dextrose, and treat hyperkalemia per protocol.
— Sudden cardiac death via VF, asystole, PEA — leading cause of mortality
— High-grade AV block, bradyasystolic arrest, idioventricular rhythm
— Sine-wave morphology is pre-arrest; do not delay calcium
— Hyperkalemia-induced Brugada phenocopy can be confused with primary Brugada syndrome
— Flaccid paralysis, respiratory muscle weakness in severe cases (less common than digital/limb weakness)
— Persistent weakness even after correction if rhabdomyolysis underlies it
— Hypoglycemia from insulin (10–20%, often delayed 1–3 h, more common in CKD/ESRD, low BMI, no DM) — monitor glucose q1h × 6h
— Hypocalcemia from rapid PO₄ correction or bicarbonate infusion
— Volume overload / hypernatremia from sodium bicarbonate, especially in HF/ESRD
— Bowel necrosis from SPS (Kayexalate), particularly with sorbitol, post-op patients, opioids, ileus — boxed-warning consideration
— Tissue necrosis / extravasation from peripheral calcium chloride — use gluconate peripherally
— Hyperglycemia if dextrose given without insulin or in DM patients
— Tachyarrhythmia / tremor from high-dose albuterol; caution in CAD
— K⁺ rises again 2–6 h after shift therapy as intracellular K⁺ leaks back — redose insulin or proceed to elimination
— Post-HD rebound of 0.5–1.0 mEq/L is expected — recheck at 1 h and 6 h
— Failure to recognize adrenal crisis, TLS, or digoxin toxicity → recurrence and worse outcomes
— Not addressing dietary or medication source → ED bounce-back
Step 3 management: When admitting any hyperkalemia patient, order scheduled glucose checks q1h × 6h post insulin and repeat BMP at 2 h and 6 h post-treatment to catch rebound. These are CCS-clickable orders that affect the score.
— Severe hyperkalemia (K⁺ ≥6.5) with any ECG change
— Hemodynamic instability, ventricular arrhythmia, post-arrest
— Need for continuous insulin infusion, frequent calcium redosing, or imminent dialysis without bed-side capability
— Massive rhabdomyolysis, TLS, crush syndrome with ongoing K⁺ release
— Concurrent severe acid-base disturbance, AKI, multiorgan failure
— K⁺ 6.0–6.4 without ECG changes after initial treatment
— Post-HD with rebound concern
— Stable ESRD patient awaiting next HD slot
— Mild-moderate hyperkalemia (5.5–6.0) corrected, stable, awaiting evaluation of underlying cause
— Drug-induced hyperkalemia after offending agent stopped, K⁺ trending down
— Asymptomatic, K⁺ <5.5 after intervention, ECG normal, reliable follow-up
— Outpatient med reconciliation arranged, K⁺-binder if needed, BMP within 48–72 h
— Nephrology: ESRD, refractory hyperkalemia, need for HD access, CKD with recurrent episodes
— Cardiology: arrhythmia, digoxin toxicity, post-arrest
— Endocrinology: adrenal insufficiency, CAH, hyporeninemic hypoaldosteronism
— Oncology: TLS prevention/management
— Toxicology / poison control: digoxin, β-blocker, salt-substitute overdose
— Smaller hospitals without HD capability: stabilize with calcium + insulin/dex + albuterol + SZC, then transfer with EMS on telemetry to a center with dialysis
— Document time of last calcium dose for receiving team
CCS pearl: Even in a non-ICU CCS case, continuous cardiac telemetry is a required order until K⁺ is consistently <5.5 with normal ECG. Forgetting telemetry on a hyperkalemic patient is a documented score deduction.
— Hemolyzed specimen — visible pink plasma, elevated LDH, suppressed haptoglobin if true hemolysis
— Fist clenching, prolonged tourniquet → release of intracellular K⁺ during draw
— Leukocytosis >100k or thrombocytosis >1M — serum K⁺ falsely high; plasma K⁺ is normal
— Familial pseudohyperkalemia (red cell membrane defect)
— Cold storage of sample
— AKI (prerenal, intrinsic, postrenal) — check BUN/Cr, urine output, ultrasound
— CKD stage 4–5 — chronic baseline issue
— Type 4 RTA / hyporeninemic hypoaldosteronism — diabetics, non-anion-gap metabolic acidosis, mild CKD
— Primary adrenal insufficiency (Addison's) — hyperK + hypoNa + hypotension + hyperpigmentation
— Aldosterone synthase deficiency, 21-hydroxylase deficiency
— ACEi, ARB, ARNI (sacubitril/valsartan), direct renin inhibitors
— Spironolactone, eplerenone, finerenone, amiloride, triamterene
— NSAIDs (reduce GFR, suppress renin)
— Calcineurin inhibitors (tacrolimus, cyclosporine)
— Heparin (suppresses aldosterone)
— TMP-SMX, pentamidine (block ENaC)
— Metabolic acidosis (non–anion-gap especially; DKA contributes mostly via insulin deficiency)
— Insulin deficiency / hyperglycemia (DKA, HHS)
— β-blocker (especially nonselective)
— Digoxin toxicity (Na/K-ATPase block)
— Succinylcholine in burn, denervation, prolonged immobility patients
— Hyperkalemic periodic paralysis
— IV KCl errors (med-safety event)
— Massive transfusion of old PRBCs
— Salt substitutes, K⁺ supplements
Key distinction: Type 4 RTA = mild hyperkalemia + non-AG metabolic acidosis in a diabetic with modest CKD; treat with fludrocortisone (rarely) or loop diuretic + dietary K⁺ restriction, not RAAS blockade.
— Rhabdomyolysis — crush injury, prolonged immobilization (think "found down"), statin/colchicine toxicity, exertional, neuroleptic malignant syndrome, serotonin syndrome
— — Labs: CK >5× normal, myoglobinuria, ↑K, ↑Phos, ↓Ca, AKI
— Tumor lysis syndrome — high tumor burden hematologic malignancies (Burkitt, ALL), post-chemo or spontaneous
— — Labs: ↑K, ↑Phos, ↑uric acid, ↓Ca, AKI (Cairo-Bishop criteria)
— — Prevention: hydration, allopurinol or rasburicase
— Massive hemolysis — transfusion reaction, TTP, G6PD crisis
— Burns, major surgery, ischemic gut
— Guillain-Barré syndrome — ascending paralysis, areflexia, but normal K⁺, CSF albuminocytologic dissociation
— Myasthenia gravis — fluctuating fatigability, ocular involvement
— Botulism — descending paralysis, autonomic features
— Tick paralysis — ascending, resolves with tick removal
— Hypokalemic periodic paralysis — opposite electrolyte!
— STEMI — peaked T waves in early phase can be confused; hyperkalemic peaked T's are typically diffuse, narrow-based, symmetric, whereas hyperacute MI T's are regional, broad-based
— Brugada syndrome — type 1 pattern can be mimicked by hyperkalemia ("Brugada phenocopy"); resolves with K⁺ correction
— Sodium channel blocker toxicity (TCA, cocaine) — wide QRS, similar appearance; check K⁺ and drug history
— Adrenal crisis — always check cortisol when hyperK + hypoNa + hypotension coexist
— CAH in neonate — see Chunk 10
Board pearl: A patient with "peaked T waves" and chest pain — always check K⁺ before catheterizing. A hyperkalemic peaked T can look like a hyperacute MI but reverses with calcium and insulin; a needless cath lab activation is a documented patient-safety event.
— Reconcile medications — eliminate or dose-reduce ACEi, ARB, ARNI, spironolactone, NSAIDs, TMP-SMX as appropriate
— For HFrEF or proteinuric CKD: do not permanently abandon RAAS unless K⁺ remains uncontrollable despite optimization
— Consider patiromer 8.4 g daily or SZC 5–10 g daily to enable RAAS continuation (DIAMOND, AMBER, PEARL-HF trials support this strategy)
— Avoid high-K⁺ foods: bananas, oranges/OJ, potatoes, tomatoes/tomato sauce, melons, avocados, spinach, nuts, beans, chocolate, coconut water
— Salt substitutes (Morton Lite Salt, NoSalt, "low-sodium soy sauce") often contain KCl — frequently missed source
— Lower-K⁺ alternatives: apples, berries, grapes, white bread, rice, pasta
— Soaking/boiling vegetables (leaching) reduces K⁺ content
— Oral sodium bicarbonate to target serum HCO₃⁻ ≥22 in CKD with metabolic acidosis reduces both K⁺ and CKD progression
— Tight glycemic control reduces hyperkalemic episodes in type 4 RTA and DKA-prone patients
— Stress importance of attending all sessions; address transportation, financial, depression barriers
— Social work referral if missed sessions are recurrent
— Patiromer: calcium-based, GI-friendly, slow onset, OK for chronic
— SZC: faster onset, sodium load may worsen HF/edema
— SPS: avoid for chronic outpatient use
Step 3 management: A HFrEF patient with K⁺ 5.4 on max-dose ARNI + spironolactone — the answer is start patiromer or SZC and continue RAAS, not stop spironolactone. RAAS preservation drives mortality benefit.
— BMP within 48–72 hours of ED discharge or hospitalization for any hyperkalemic episode
— If drug-induced: BMP at 1 week and 4 weeks after dose adjustment
— Chronic CKD on RAAS + binder: BMP every 1–3 months once stable
— ESRD: routine pre-HD K⁺ checks each session
— On patiromer: K⁺, Mg²⁺ (binder reduces Mg²⁺ absorption), Ca²⁺
— On SZC: K⁺, edema (sodium load), HCO₃⁻ (may rise)
— On finerenone: K⁺ at 4 weeks, then periodically; hold if >5.5
— On digoxin: levels, K⁺, Mg²⁺, renal function
— Recognize symptoms warranting return: weakness, palpitations, syncope, missed dialysis
— Medication adherence and never double-dose RAAS or diuretics
— Read labels for salt substitutes and OTC NSAIDs (ibuprofen, naproxen)
— Hold ACEi/ARB and NSAIDs during acute illness with vomiting/diarrhea ("sick-day rules")
— Hold ACEi/ARB, diuretics, metformin, SGLT2i during vomiting, diarrhea, or oral intake <50% × 24 h — prevents AKI and hyperkalemia
— Resume after adequate intake and consult provider
— Post-arrest patients: cardiac rehab, ICD evaluation if recurrent arrhythmic substrate
— Post-rhabdo: gradual return to activity, statin re-challenge if drug-induced
— Establish/confirm nephrology follow-up for CKD/ESRD
— Primary care visit within 1–2 weeks
— Pharmacy review for polypharmacy reduction
CCS pearl: Always click "counsel patient on medications" and "schedule follow-up BMP in 48–72 hours" before ending an ED disposition for hyperkalemia. These are the longitudinal-care orders that distinguish Step 3 from Step 2.
— IV KCl administration errors are sentinel events — never give undiluted KCl IV push; concentration limits and smart pumps mandated by Joint Commission
— Look-alike/sound-alike: calcium gluconate vs. calcium chloride (different elemental Ca); insulin vials (regular vs. NPH vs. analog); high-alert designation
— Closed-loop verification at the bedside for all IV electrolyte orders
— FDA boxed warning for intestinal necrosis — avoid in post-op, ileus, opioid use, bowel obstruction
— Many institutions have largely abandoned SPS in favor of patiromer/SZC
— Emergent dialysis for life-threatening hyperkalemia in an unconscious patient → emergency exception to informed consent applies; document clearly and notify surrogate ASAP
— Patient with capacity who refuses dialysis despite K⁺ 7.5 — respect autonomy if decision-making capacity is confirmed; ensure understanding of imminent mortality; involve ethics, palliative care, social work; document conversation
— Suspected medication non-adherence due to cost/access → social work, pharmacist assist, 340B/manufacturer assistance for binders
— Elder neglect (missed dialysis in dependent adult) → adult protective services in many jurisdictions
— Pediatric CAH-related crisis → ensure proper sick-day stress dosing education to caregivers; CPS only if neglect suspected
— Hyperkalemia is a common cause of 30-day readmission in CKD/HF; ensure med reconciliation and outpatient K⁺ binder access at discharge
— Pharmacy callbacks and 48–72 h post-discharge lab draw reduce readmissions
— In advanced illness, hyperkalemic arrest is often the proximate cause of death after voluntary HD discontinuation — provide compassionate withdrawal counseling, palliative care consult, hospice referral
Step 3 management: A patient with K⁺ 7.0 on the inpatient ward with peaked T waves — verify the medication list immediately for an inadvertent KCl infusion or duplicate spironolactone order. Iatrogenic hyperkalemia is a reportable patient safety event in many systems and requires root-cause analysis.
— Peaked T → loss of P → wide QRS → sine wave → asystole/VF
— Calcium, Beta-agonist, Insulin/dextrose, Glucose, Kayexalate/binder, Diuretic, Dialysis
— ACEi/ARB/ARNI, spironolactone/eplerenone/finerenone, NSAIDs, TMP-SMX, heparin, tacrolimus, digoxin, β-blockers, succinylcholine in burn/denervation
— Insulin/dextrose: 0.5–1.2 mEq/L over 30 min
— Albuterol 10–20 mg neb: 0.5–1.0 mEq/L over 30 min
— Bicarbonate: 0.3–0.5 mEq/L (only if acidemic)
— Dialysis: 1 mEq/L per hour, ~25–50 mEq total
— Calcium does not lower K⁺
— Bicarbonate alone is not first-line; insulin + dextrose is
— Don't give calcium in digoxin toxicity (controversial but tested as "avoid")
— Recheck K⁺ q2h × several rounds — rebound is real
— Always look for pseudohyperkalemia in a well-appearing patient with normal ECG
— ACEi/ARB + diuretic + NSAID = AKI risk multiplied
— Hyperkalemia + hyponatremia + hypotension + hyperpigmentation = primary AI
— Hyperkalemia in neonate + ambiguous genitalia + salt wasting = 21-hydroxylase deficiency CAH
— ↑K, ↑PO₄, ↑uric acid, ↓Ca, AKI
— CK >5× ULN, ↑K, ↑PO₄, ↓Ca, myoglobinuria (positive urine dip for blood, no RBCs on micro)
— 1 mEq/L bath in patients with low predialysis K⁺ → ↑ SCD risk
Board pearl: When the stem asks "what is the next best step" in hyperkalemia with peaked T waves — the answer is almost always calcium gluconate IV, even before insulin or dialysis. Stabilize, then shift, then eliminate.
— "65 y/o M with ESRD on MWF HD presents Monday with weakness. ECG shows wide QRS and peaked T waves. K⁺ 7.8."
— Answer: IV calcium gluconate first; then insulin/dex + albuterol; emergent HD
— "72 y/o diabetic on lisinopril and spironolactone presented with cellulitis, started on TMP-SMX 5 days ago, now with K⁺ 6.5."
— Answer: stop offending agents; treat per severity; in HF context, consider patiromer + continue RAAS at reduced dose
— "Construction worker pinned for 8 hours, freed, CK 45,000, K⁺ 6.8."
— Answer: aggressive IV NS, calcium, insulin/dex, monitor for compartment syndrome, dialysis if AKI refractory
— "Patient with vitiligo and fatigue presents hypotensive, K⁺ 6.0, Na 128, glucose 55."
— Answer: IV hydrocortisone 100 mg, NS, dextrose, standard hyperK therapy; check cortisol/ACTH
— "Elderly woman on digoxin with worsening renal function, nausea, K⁺ 6.2, junctional bradycardia, dig level 4.5."
— Answer: digoxin immune Fab; avoid IV calcium per traditional teaching
— "Newly diagnosed Burkitt lymphoma 36 h post-induction, K⁺ 6.4, PO₄ 8, uric acid 14, Ca 6.8, Cr rising."
— Answer: hydration, rasburicase, treat hyperK, monitor for HD need
— "Asymptomatic patient with WBC 220,000 (CML) has K⁺ 6.0, normal ECG."
— Answer: plasma K⁺ in heparinized tube; do not aggressively treat
— "Female neonate day 10 with vomiting, weight loss, hypotension, K⁺ 7.0, Na 122, ambiguous genitalia."
— Answer: IV hydrocortisone, NS, dextrose, treat hyperK
— "Chest pain, ECG with peaked T waves in V2-V4, K⁺ pending."
— Answer: check K⁺ before cath; if hyperK is the cause, treat and reassess
Key distinction: Step 3 stems often reward the second-order question (long-term plan, follow-up cadence, which drug to keep) rather than just "what do you give now." Read past the acute resuscitation to find the right discharge or transition order.
Hyperkalemia is a time-critical emergency where the order of operations is rigid: get the ECG, give IV calcium to stabilize the myocardium, shift K⁺ intracellularly with insulin + dextrose (± albuterol, ± bicarbonate if acidemic), and then eliminate K⁺ with loop diuretic, oral binder, or — definitively in ESRD/refractory cases — emergent hemodialysis.
Board pearl: The single most missed wrong-answer trap is "give more calcium" when the K⁺ remains elevated — calcium buys time; only shift and elimination actually lower potassium. Master that distinction and the majority of Step 3 hyperkalemia stems become straightforward.