Hyperkalemia

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Hyperkalemia 

Hyperkalemia is defined as:Serum potassium > 5.0 mEq/L(this value is different in different guidelines i.e >5.2mEq/L,>5.5mEq/L)

Severity Classification(even this is not universal)

Severity

Potassium Level

Mild

5.1 – 5.5 mEq/L

Moderate

5.6 – 6.4 mEq/L

Severe

≥ 6.5 mEq/L or ECG changes

Clinical severity correlates more with rate of rise rather than absolute level.


Normal Potassium Physiology

Distribution

  • Total body potassium ≈ 3500 mEq
  • 98% intracellular
  • 2% extracellular

Regulation of Potassium Balance

1. Renal Excretion (Major Mechanism)

Occurs in:

  • Distal convoluted tubule
  • Collecting duct (principal cells)

Controlled by:

  • Aldosterone
  • Distal sodium delivery
  • Tubular flow rate

2. Cellular Shift

Potassium moves between intracellular and extracellular compartments via:

Factor

Effect

Insulin

Drives K inside cells

β2 stimulation

Drives K inside

Acidosis

Moves K outside

Hyperosmolality

Moves K outside

Exercise

Transient increase

Etiology of Hyperkalemia

A. Decreased Renal Excretion

Renal Causes

  • Acute kidney injury/Chronic kidney disease
  • Tubular disorders
  • Obstructive uropathy(Aldosterone resistance)

Endocrine Causes

  • Hypoaldosteronism
  • Addison disease
  • Type 4 RTA(hyperkalemia plus NAGMA)

Drug-Induced Hyperkalemia

Drug Class

Examples

Mechanism

RAAS inhibitors

ACE inhibitors, ARBs

↓ Aldosterone

Potassium-sparing diuretics

Spironolactone, Amiloride

↓ K excretion

NSAIDs

Various

↓ Renin

Heparin

UFH, LMWH

↓ Aldosterone synthesis

Trimethoprim

Co-trimoxazole

ENaC blockade

Calcineurin inhibitors

Cyclosporine, Tacrolimus

Tubular toxicity

Beta blockers

Non-selective

↓ Cellular uptake

B. Transcellular Shift Causes

  • Metabolic acidosis
  • DKA
  • Tumor lysis syndrome
  • Rhabdomyolysis
  • Hemolysis
  • Burns
  • Hyperosmolar states

C. Excess Potassium Load

  • Potassium supplements
  • Blood transfusion (stored blood)
  • Salt substitutes
  • Parenteral nutrition

D. Pseudohyperkalemia

False elevation due to sample error.

  • Hemolyzed sample
  • Leukocytosis(>50,000–100,000/μL)-reason Leukemic WBCs are often fragile.
  • Thrombocytosis(500,000–1,000,000/μL)-occurs due to

When blood clots in a serum tube:

  1. Platelets aggregate
  2. Platelets degranulate
  3. Potassium released into serum

This mainly affects: Serum potassium Not plasma potassium.

Therefore:Serum K⁺ > Plasma K⁺ by >0.4 mEq/L strongly suggests thrombocytosis-related pseudohyperkalemia.

  • Prolonged tourniquet use or fist clenching
  • Delayed sample processing.

How to confirm pseudohyperkalemia

Obtain:

  1. ABG/VBG whole blood potassium (rapid analysis)
  2. Plasma potassium (heparinized tube)
  3. Repeat sample avoiding trauma

Clinical Manifestations

Most patients are asymptomatic (even with severe hyperkalemia).

Neuromuscular Symptoms

  • Muscle weakness
  • Flaccid paralysis
  • Ascending paralysis
  • Reduced reflexes

Cardiac Manifestations (Most Dangerous)

Arrhythmias include:

  • Ventricular tachycardia
  • Ventricular fibrillation
  • Bradycardia(Rx-Epinephrine-treats both the hyperkalemia and the bradycardia)
  • Asystole

ECG Changes in Hyperkalemia 

Potassium Level

ECG Finding

5.5–6.5

Tall peaked T waves

6.5–7.5

P wave flattening, PR prolongation

7.5–8.5

QRS widening

>8.5

Sine wave pattern → arrest

ECG severity does not always correlate with potassium level.


Urinary Indices

Transtubular Potassium Gradient (TTKG)

The Transtubular Potassium Gradient (TTKG) is a calculated index used to estimate:

  • How effectively the cortical collecting duct is secreting potassium
  • Whether the kidney is responding appropriately to hyperkalemia
  • Helps differentiate renal vs extrarenal causes . But Not commonly used in routine ICU practice today.(its outdated)

TTKG

Interpretation

<5

Impaired renal excretion—Hypoaldosteronism

Type 4 RTA,Adrenal insufficiency,RAAS inhibitor use,Advanced CKD

>7

Appropriate renal response

Management

  • Treat the cause.
  • Stop nephrotoxic Drug 
  • Decrease potassium intake(decrease in diet).
  • Remove Potassium from the Body(Diuretics,dialysis,Sodium Zirconium Cyclosilicate) because rest all methods are temporary.

Cardiac Membrane Stabilization 

Indication-

  • ECG changes
  • K ≥ 6.5 mEq/L(Some guidelines consider K ≥6.0 mEq/L clinically significant regardless of symptoms.)

Drug

Dose

Onset

Duration

Key Notes

IV Calcium Gluconate (10%)

30 mL(3 gm)IV over 10min

1–3 min

30–60 min
  • Does NOT lower K
  • Re-dosing once or twice if needed

IV Calcium Chloride (10%)

10 mL(1gm)IV over 10 min

1–3 min

30–60 min

Via central line

Feature

10% Calcium Gluconate (10 mL)

10% Calcium Chloride (10 mL)

Salt Content

1 g

1 g

Elemental Calcium

~93 mg

~273 mg

Calcium (mEq)

~4.65 mEq

~13.6 mEq

Shift Potassium into Cells

Indications:

  • K ≥6.5
  • ECG changes
  • Rapidly rising potassium
  • Dialysis delay

Therapy

Dose

Onset

Duration

↓K Expected

*Regular Insulin + Dextrose

10 units IV + 25 g glucose over 2–5 min

15–30 min

4–6 hrs

↓ 0.6–1.2 mEq/L

Nebulized Salbutamol

10–20 mg

30 min

2–4 hrs

↓ 0.5–1 mEq/L

IV hypertonic Sodium Bicarbonate

If pH is normal, bicarbonate has minimal potassium-lowering effect.Hypertonic sodium bicarbonate boluses fail to lower potassium reliably because the potassium-lowering effect of alkalinization is offset by osmotic potassium efflux (“solvent drag”) caused by the hypertonicity of the solution.

Isotonic Bicarbonate
  • Prepared by:150 mEq NaHCO₃ Added to 1 L D5W Result:≈150 mEq/L bicarbonate.
  • it works  only on patients with metabolic acidosis.
  • can not be used on patients with volume overload.

*Hypoglycemia can occur several hours after insulin administration, especially in CKD patients.

*Studies have shown that 5 units can achieve nearly the same potassium reduction as 10 units, while significantly reducing the risk of hypoglycemia.

  • Glucose 250–300 mg/dL—Some clinicians omit the initial dextrose dose.
  • Glucose >300 mg/dL—initial dextrose is generally unnecessary.

DKA and Hyperkalemia

Hyperkalemia in DKA occurs despite total body potassium depletion.

Treatment:

  • IV fluids
  • Continuous insulin infusion

Do not give additional hyperkalemia insulin boluses if standard DKA insulin therapy has already started.

*Monitoring Glucose: 30 min, 1 h, 2 h, 4 h, and 6 h.Potassium: repeat at 1–2 h


Remove Potassium from Body 

Therapy

Key Notes

**Diuretics (Furosemide) k/a kaliuresis
  • Onset—1–2 hrs
  • Use only If urine output present.
  • IV furosemide(80-250 mg) or bumetanide(2-5 mg IV).
  • +/- Thiazide (500-1,000 mg IV chlorothiazide, or 5-10 mg metolazone)
  • +/- Acetazolamide (250-1,000 mg IV/PO).
  • +/- Fludrocortisone 0.2 mg PO

Sodium Polystyrene Sulfonate(SPS)
  • Onset—2–6 hr
  • Risk: bowel necrosis

Patiromer

Onset—4–7 hrs

CKD less effective,

Not for emergencies

Sodium Zirconium Cyclosilicate
  • Onset—1–2 hrs
  • Dose-10 gm PO TDS for 2-3 days
  • Do not give in NPO patient.
  • Contraindications-severe constipation, bowel obstruction.
  • Side effect—it has high sodium which causes volume overload
  • Safer than SPS

Hemodialysis

Indicated in refractory causes

**Monitoring Potassium Removal Through the Kidneys (Kaliuresis)

  • Consider fludrocortisone if the patient starts making a good amount of urine but the blood potassium level is not decreasing as expected. This suggests that the kidneys are producing urine but are not excreting enough potassium.
  • If there is little or no urine output despite diuretic therapy, urinary potassium removal has failed. In this situation, dialysis is usually required to remove excess potassium.

If the Patient Is Producing Urine

  • Large urine losses should generally be replaced with IV fluids to avoid dehydration and worsening kidney function.

Choice of Replacement Fluid

Serum Bicarbonate (HCO₃⁻)

Recommended Fluid

< 22 mEq/L (metabolic acidosis present)

Isotonic sodium bicarbonate

≥ 22 mEq/L

Ringer’s Lactate(it does not cause Hyperkalemia)

Monitoring During Treatment

  • Check electrolytes frequently, especially:
    • Potassium (K⁺)
    • Magnesium (Mg²⁺)
    • Calcium (Ca²⁺)
    • Phosphate (PO₄³⁻)
  • Replace any electrolyte deficiencies promptly, particularly magnesium, as low magnesium can make potassium correction more difficult.

 References

1. Harrison’s Principles of Internal Medicine (22nd Edition)

Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 22nd ed. New York: McGraw-Hill Education; 2024.


2. ISCCM Protocol Book (3rd Edition)

Mehta Y, Divatia JV, Zirpe KG, Govil D, editors. ISCCM Manual of Clinical Practice Recommendations and Protocols. 3rd ed. New Delhi: Jaypee Brothers Medical Publishers; 2023.


3. EMCrit – Hyperkalemia (Internet Book of Critical Care)

Farkas J. Hyperkalemia. In: Internet Book of Critical Care (IBCC) [Internet]. EMCrit Project; updated Jul 4, 2024 [cited 2026 Jul 7]. Available from: EMCrit Hyperkalemia (IBCC)


4.Washington Manual of Critical care


5.Isccm Text Book of Critical Care(2026)

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