When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EmergentICU

Hyperkalemia

K⁺ > 5.5 mEq/L. ECG changes dictate urgency, not the number. Calcium stabilizes the membrane. Insulin + glucose shifts K⁺ intracellularly. Kayexalate and patiromer remove K⁺. Dialysis for refractory cases.

🔍 Overview

ECG Progression

Get an ECG before anything else. ECG changes = emergent regardless of the number. A patient with K⁺ 6.0 and peaked T's is sicker than a patient with K⁺ 7.0 and a normal ECG.

K⁺ Level	ECG Finding	Urgency
5.5–6.0	Peaked T waves (tall, narrow, symmetric -earliest sign)	Urgent -start treatment
6.0–6.5	Prolonged PR interval, flattened P waves	Emergent
6.5–7.0	Widened QRS (> 120 ms)	Critical -calcium NOW
7.0–8.0	Sine wave pattern (QRS merges with T wave)	Pre-arrest. Calcium + emergent dialysis.
> 8.0	VF, asystole, PEA	Cardiac arrest. Treat during resuscitation.

Common Causes

Renal failure (AKI, CKD G4–G5) -most common, impaired K⁺ excretion
Medications -ACEi/ARBs, spironolactone, trimethoprim, NSAIDs, heparin, succinylcholine
Cellular shift -acidosis, rhabdomyolysis, tumor lysis, DKA, massive transfusion
Adrenal insufficiency -cortisol + aldosterone deficiency → impaired renal K⁺ excretion
Pseudohyperkalemia -hemolyzed sample (most common lab artifact), high WBC/plt count, tourniquet too tight

Rule out pseudohyperkalemia first: if the patient has no ECG changes, no risk factors, and the K⁺ is unexpectedly elevated → recheck on a non-hemolyzed, free-flowing sample before treating.

Pseudohyperkalemia -Deep Dive

Pseudohyperkalemia is a falsely elevated serum K⁺ due to K⁺ release from cells during or after blood collection -not a true reflection of in vivo potassium levels. Recognizing it prevents unnecessary (and potentially dangerous) treatment of a lab artifact.

Mechanisms

Hemolysis during phlebotomy -the most common cause. Traumatic draw, small-gauge needle, vigorous shaking of the tube, or pneumatic tube transport causes RBC lysis and K⁺ release. The lab usually flags the specimen as hemolyzed (hemolysis index elevated).
Prolonged tourniquet time -fist clenching with a tight tourniquet causes local ischemia and K⁺ leakage from forearm muscles. Can raise K⁺ by 0.5–1.5 mEq/L.
Thrombocytosis (plt > 500K) -during clot formation in a serum (red-top) tube, platelets degranulate and release intracellular K⁺. The higher the platelet count, the greater the artifact. A plasma (green-top/heparin) sample bypasses clotting and gives the true K⁺.
Leukocytosis (WBC > 70–100K) -seen in leukemia/lymphoma. Fragile WBCs lyse in vitro, releasing K⁺. Again, a plasma sample is more accurate.
In vitro hemolysis from specimen handling -delayed processing, refrigeration of whole blood, or prolonged storage allows ongoing K⁺ leak from cells.
Familial pseudohyperkalemia -rare inherited RBC membrane defect causing K⁺ leak at room temperature but not at 37°C.

How to Differentiate: Real vs. Pseudo

Feature	Pseudohyperkalemia	True Hyperkalemia
ECG changes	Normal -no peaked T's, no QRS widening	Peaked T waves, PR prolongation, wide QRS, sine wave
Hemolysis index	Elevated (lab flags specimen as hemolyzed)	Normal (non-hemolyzed sample)
Serum vs. plasma K⁺	Serum K⁺ significantly higher than plasma K⁺ (difference > 0.3–0.4 mEq/L)	Serum and plasma K⁺ are concordant
Clinical context	No risk factors (normal renal function, no culprit drugs, no acidosis)	AKI/CKD, K⁺-sparing drugs, acidosis, rhabdomyolysis, etc.
Symptoms	Patient is asymptomatic, feels well	May have weakness, palpitations, paresthesias
Repeat sample	Normal K⁺ on a free-flowing, non-hemolyzed redraw	Persistently elevated on repeat
Plt/WBC count	Often markedly elevated (thrombocytosis or leukocytosis)	Usually normal or irrelevant

The Key Move

If you suspect pseudohyperkalemia: Redraw blood from a free-flowing venipuncture (no tourniquet or < 1 min), into a green-top (lithium heparin) tube for plasma potassium. This avoids both clotting artifact (thrombocytosis) and most hemolysis artifact. If the plasma K⁺ is normal while the original serum K⁺ was elevated → pseudohyperkalemia confirmed.

Never assume pseudohyperkalemia if the patient has ECG changes. Even if the sample appears hemolyzed, if the ECG shows peaked T waves or QRS widening, treat as true hyperkalemia while redrawing. The cost of treating a false positive (calcium, insulin) is far less than the cost of missing real hyperkalemia (cardiac arrest).

🚨 Management

Treatment Ladder

Three categories of treatment -use them in order: (1) Stabilize the membrane, (2) Shift K⁺ into cells, (3) Remove K⁺ from the body. Only #3 actually lowers total body potassium.

Step	Drug (Brand)	Dose	Onset	Duration	Mechanism
1. STABILIZE	Calcium gluconate FIRST IF ECG CHANGES	1–2 g (10–20 mL of 10%) IV over 2–3 min	1–3 min	30–60 min	Stabilizes cardiac membrane. Does NOT lower K⁺. Repeat in 5 min if ECG unchanged. Use calcium chloride (1g) via central line for more rapid effect.
2a. SHIFT	Insulin + Glucose 1ST LINE SHIFT	Regular insulin 10 units IV + D50 25g (1 amp) IV	15–30 min	4–6 hrs	Insulin drives K⁺ into cells via Na⁺/K⁺-ATPase. Must give dextrose or the patient becomes hypoglycemic (10–75% incidence) AHA Hyperkalemia Guidelines, 2023. Check glucose at 1h and 2h. Give D10 drip if glucose < 250 before insulin.
2b. SHIFT	Sodium bicarbonate	50–100 mEq (1–2 amps) IV over 5 min	15–30 min	2 hrs	Drives K⁺ into cells via H⁺/K⁺ exchange. Most effective if acidotic (pH < 7.2). Minimal effect if pH normal. Avoid in volume overload (sodium load).
2c. SHIFT	Albuterol (nebulized)	10–20 mg nebulized (4–8× standard asthma dose)	15–30 min	2–4 hrs	β₂-mediated K⁺ shift into cells. Drops K⁺ by 0.5–1.0 mEq/L. Watch for tachycardia. Often forgotten -add it to insulin/glucose.
3a. REMOVE	Furosemide (Lasix) IF RENAL FUNCTION OK	40–80 mg IV	30–60 min	6 hrs	Enhances renal K⁺ excretion. Only works if kidneys functional. Give with NS if volume depleted.
3b. REMOVE	Patiromer (Veltassa) CHRONIC	8.4 g PO daily	4–7 hrs	Ongoing	K⁺ binder. NOT for acute emergencies (too slow). Best for chronic hyperK management to allow continuation of ACEi/ARB/MRA. OPAL-HK, 2015
3c. REMOVE	Sodium zirconium cyclosilicate (Lokelma) CHRONIC/SUBACUTE	10 g PO TID × 48h (acute) → 5–10 g daily	1–2 hrs	Ongoing	Faster than patiromer. Can be used in acute setting (onset 1–2h). Well-tolerated. HARMONIZE, 2014
3d. REMOVE	Hemodialysis REFRACTORY / SEVERE	Emergent HD	Immediate	Definitive	Most effective K⁺ removal. Drops K⁺ by 1–2 mEq/L per session. Indicated: refractory to medical therapy, anuric patient, K⁺ > 6.5 with ECG changes + CKD/ESKD.

Kayexalate (sodium polystyrene sulfonate) -avoid if possible. Slow onset (hours), questionable efficacy SPS Efficacy Review, 2013, and risk of intestinal necrosis (especially with sorbitol). Patiromer and Lokelma have replaced it. If you must use it: 15–30 g PO or 30–50 g PR, never with sorbitol.

🔄 Updated Practice: Old teaching: sodium polystyrene sulfonate (Kayexalate) for hyperkalemia. This is OUTDATED -kayexalate works slowly (hours to days), has unreliable efficacy, and risks intestinal necrosis (especially with sorbitol). Newer potassium binders -patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) -are faster, safer, and better tolerated. Use these instead for non-emergent K⁺ lowering.

📋 Clinical Example -Hyperkalemia Emergency Management

Patient: 68F with CKD Stage IV on lisinopril (Zestril) + spironolactone (Aldactone), K⁺ 7.1, ECG shows peaked T waves and widened QRS.

Immediate (seconds to minutes -stabilize the heart):

Calcium gluconate 1g IV over 2–3 min → repeat ECG. Does NOT lower K⁺ -stabilizes cardiac membrane. Effect lasts 30–60 min. Repeat if ECG still abnormal.

Shift K⁺ intracellularly (minutes to hours):

Regular insulin 10 units IV + D50 1 amp (25g glucose) -onset 15–30 min, lowers K⁺ by 0.5–1.0. Check glucose q1h × 4h (hypoglycemia risk peaks at 2–4h, give D10 infusion if needed).
Albuterol (ProAir) 10–20mg nebulized -onset 15–30 min, lowers K⁺ by 0.5–1.0. Additive with insulin.
Sodium bicarbonate 50 mEq IV -only if concurrent metabolic acidosis. Limited K⁺-lowering effect alone.

Remove K⁺ from body (hours):

Furosemide (Lasix) 40–80mg IV -if any residual kidney function.
Patiromer (Veltassa) 8.4g PO or sodium zirconium (Lokelma) 10g PO -newer K⁺ binders. Onset hours. Better tolerated than kayexalate.
Hemodialysis -definitive treatment for severe/refractory hyperkalemia or anuric patients.

Fix the cause: Hold lisinopril + spironolactone. Recheck K⁺ in 2h.

Stop the Source

Hold offending medications: ACEi/ARB, spironolactone, trimethoprim, NSAIDs, K⁺-sparing diuretics
Stop all IV potassium (check infusions, TPN, LR has 4 mEq/L K⁺)
Low-K⁺ diet if chronic
Treat underlying

🧪 Workup

Workup
ECG -first test
Repeat K⁺ -rule out hemolysis
BMP
Med review -ACEi, ARB, spironolactone, TMP-SMX
CK -rhabdomyolysis
LDH, UA, PO₄ -TLS

💊 Medications

Medications
Drug Dose Route Notes
Ca gluconate 1g IV/5min IV Stabilize. Does NOT lower K⁺.
Insulin 10U+D50 IV Best shifter. Check glucose 1h.
Albuterol 10-20mg neb Neb Additive with insulin
Patiromer (Veltassa) 8.4g daily PO GI elimination (preferred). Onset 4–7h.
SZC (Lokelma) 10g PO × 3 doses PO GI elimination. Faster onset (~1h). Preferred in acute setting.
Kayexalate (SPS) 15-30g PO GI elimination (outdated -prefer patiromer or Lokelma. Risk of intestinal necrosis.)

📋 On Rounds

Pimp Questions

Does calcium gluconate lower potassium?

No. Calcium stabilizes the cardiac membrane by raising the threshold potential -it makes the heart less susceptible to arrhythmia. It does NOT move K⁺ at all. It buys you time (30–60 min) while insulin/glucose and other therapies take effect. That's why you always follow calcium with insulin/glucose.

Why do you need to check glucose after giving insulin for hyperkalemia?

Hypoglycemia occurs in 10–75% of patients treated with insulin for hyperkalemia (higher than most realize). The D50 wears off before the insulin does. Check glucose at 1 hour and 2 hours minimum. Many institutions now use D10 infusion running alongside insulin instead of a single D50 bolus to prevent delayed hypoglycemia.

What's the dose of nebulized albuterol for hyperkalemia?

10–20 mg -that's 4 to 8 times the standard 2.5 mg asthma dose. This is the most commonly underdosed hyperkalemia treatment. At high doses, β₂-mediated Na⁺/K⁺-ATPase activation shifts K⁺ into cells, dropping serum K⁺ by 0.5–1.0 mEq/L. Side effect: tachycardia. Use cautiously with cardiac patients.

What is the onset and duration of each hyperkalemia treatment, and why does the order matter?

(1) Calcium (membrane stabilization): onset 1-3 min, duration 30-60 min. Give first if ECG changes -protects the heart immediately but does NOT lower K⁺. (2) Insulin 10 units + D50 (shift): onset 15-30 min, duration 4-6h. Most reliable K⁺ shifter -lowers K⁺ by 0.5-1.2 mEq/L. Always give D50 concurrently (even if glucose is high -insulin-induced hypoglycemia is the #1 complication)

Clinical Examples

📋 Case 1, Hyperkalemia with ECG Changes from RAAS Inhibitors

Key findings: K⁺ 7.1, ECG: peaked T waves, widened QRS. Cr 4.2 (baseline 3.5), pH 7.32. No hemolysis on repeat sample.

Management:

Calcium gluconate 1g IV over 5 min (membrane stabilization, onset 1-3 min), QRS narrows immediately

Insulin 10U IV + D50 (shift K⁺ intracellularly, onset 15-30 min)

Albuterol 10 mg continuous neb (additive shift, lowers K⁺ 0.5-1.0 mEq/L)

Hold lisinopril + spironolactone; nephrology consult for RAAS inhibitor safety reassessment

Teaching point: The combination of ACEi + MRA in CKD is the most common cause of dangerous hyperkalemia. Always recheck K⁺ and Cr within 1 week of starting or uptitrating RAAS inhibitors.

📋 Case 2, Pseudohyperkalemia vs True Hyperkalemia

Patient: 45 y/o F with CML (WBC 180K), routine labs show K⁺ 6.8. Asymptomatic, normal ECG, no prior renal disease.

Key findings: Cr 0.9 (normal), bicarb 24, glucose 105. Sample noted as "slightly hemolyzed." Repeat K⁺ from free-flowing venipuncture without tourniquet: 4.4.

Management:

Recognize pseudohyperkalemia, hemolyzed sample is the #1 cause of spurious K⁺ elevation

Extreme leukocytosis (CML) causes in-vitro K⁺ release from fragile WBCs during clotting

Send plasma K⁺ (heparinized tube, no clotting) for accurate result in leukocytosis

Do NOT treat unless confirmed on repeat and/or ECG changes present

Teaching point: Always recheck before treating. Hemolyzed samples, prolonged tourniquet use, fist clenching, and extreme leukocytosis/thrombocytosis all cause pseudohyperkalemia. Treating a false K⁺ risks iatrogenic hypokalemia.

📋 Case 3, Hyperkalemia from Tumor Lysis Syndrome

Patient: 58 y/o M with newly diagnosed Burkitt lymphoma, K⁺ 7.8 with sine-wave pattern on ECG 12h after starting chemotherapy.

Key findings: K⁺ 7.8, phosphate 8.2, uric acid 14.5, Ca²⁺ 6.8, LDH 4,200, Cr 3.6. Classic tumor lysis syndrome (TLS).

Management:

Calcium gluconate 1g IV x2 (sine wave = near-arrest, may need repeat dose)

Emergent dialysis, K⁺ 7.8 with sine wave is refractory-level hyperkalemia

Rasburicase 0.2 mg/kg IV for uric acid (avoid allopurinol in established TLS)

Aggressive IVF for renal protection; avoid calcium-containing solutions (risk of calcium-phosphate precipitation)

Teaching point: TLS causes hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Sine-wave pattern on ECG is a pre-arrest rhythm, this patient needs emergent dialysis, not just medical management.

📣 Sample Presentation

One-Liner

"Mr. Russo is a 74-year-old with CKD4 on lisinopril and spironolactone presenting with weakness. K⁺ 7.1. ECG shows peaked T waves and widened QRS."

Key Points to Cover on Rounds

K⁺ 7.1 with ECG changes -emergent management initiated. Calcium gluconate 1g IV (membrane stabilization) → QRS narrowed within 3 min. Insulin 10 units IV + D50 (shift). Albuterol 10 mg continuous neb (shift). Kayexalate 30g PO (elimination). Repeat K⁺ at 1h: 6.2, at 2h: 5.8, ECG normalized. Offending agents: lisinopril and spironolactone held. Nephrology consulted -not meeting urgent dialysis criteria. Plan: serial K⁺ q4h, renally dose medications, nephrology to reassess RAAS inhibitor safety.

Monitoring
ECG after each intervention
K⁺ at 1h and 2h
Glucose at 1h post-insulin
Continuous telemetry if >6.5
UOP

⚡ Summary

Summary

ECG Changes
Peaked T waves → flattened P → widened QRS → sine wave → VF/asystole. ECG changes ≠ K⁺ level (treat ECG, not number).

Stabilize
Calcium gluconate 1g IV (onset 1-3 min, duration 30-60 min). Protects myocardium. Does NOT lower K⁺.

Shift K⁺
Insulin 10 units + D50 (best shifter, onset 15-30 min). Albuterol 10-20 mg neb (additive). Bicarb only if pH < 7.2.

Eliminate K⁺
Patiromer/Lokelma (gut, hours -avoid kayexalate). Furosemide (renal, if UOP). Dialysis (definitive, immediate clearance during session).

Common Causes
RAAS inhibitors (ACEi/ARB + spironolactone), CKD, rhabdomyolysis, tumor lysis, acidosis, tissue necrosis, hemolysis.

Pseudo-hyperK
Hemolyzed sample (#1 cause), prolonged tourniquet, fist clenching, extreme leukocytosis/thrombocytosis. Recheck before treating.

📄 One Pager

Nephrology / Emergency · One Pager

Hyperkalemia

ECG changes → calcium gluconate first (stabilize). Then shift (insulin + D50 + albuterol). Then eliminate (patiromer/Lokelma, diuretics, dialysis).

🧪 ECG Progression

Peaked T → flattened P → widened QRS → sine wave → VF/asystole. Treat ECG changes, not the K⁺ number. ECG changes can occur at any level.

💊 Common Causes

RAAS inhibitors (ACEi + spironolactone), CKD, rhabdomyolysis, tumor lysis, acidosis, hemolysis, tissue necrosis. Always check for pseudo-hyperK (hemolyzed sample).

💊 Key Drugs

Calcium gluconate1g IV over 5 min
Regular insulin10 units IV + D50
Albuterol10-20 mg continuous neb
Kayexalate15-30g PO

⚠️ Pitfalls

Insulin without D50 (hypoglycemia)
Not checking ECG
Not holding offending meds (ACEi, spironolactone, TMP-SMX)
Treating hemolyzed sample

RoundsRx · Nephrology / Emergency AHA Hyperkalemia 2020 · KDIGO

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Drug	Dose	Route	Notes
Ca gluconate	1g IV/5min	IV	Stabilize. Does NOT lower K⁺.
Insulin	10U+D50	IV	Best shifter. Check glucose 1h.
Albuterol	10-20mg neb	Neb	Additive with insulin
Patiromer (Veltassa)	8.4g daily	PO	GI elimination (preferred). Onset 4–7h.
SZC (Lokelma)	10g PO × 3 doses	PO	GI elimination. Faster onset (~1h). Preferred in acute setting.
Kayexalate (SPS)	15-30g	PO	GI elimination (outdated -prefer patiromer or Lokelma. Risk of intestinal necrosis.)