How to correct hyperkalemia (elevated potassium levels) or hypokalemia (low potassium levels)?

How to Correct Potassium Levels

Hyperkalemia Management

For hyperkalemia, immediately stabilize the cardiac membrane with intravenous calcium, then shift potassium into cells with insulin/glucose and beta-agonists, and finally eliminate potassium from the body using diuretics, potassium binders, or hemodialysis depending on severity and renal function. 1

Severity Classification

• Mild hyperkalemia: 5.0-5.9 mEq/L 1
• Moderate hyperkalemia: 6.0-6.4 mEq/L 1
• Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 1
• ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of potassium level 1

Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes is preferred for rapid increase in ionized calcium 1
• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes is an alternative 1
• Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2
• Critical point: Calcium does NOT lower serum potassium—it only protects against arrhythmias 1
• Administer through central line when possible, as peripheral extravasation can cause severe tissue injury 1
• Monitor heart rate during administration and stop if symptomatic bradycardia occurs 1

Step 2: Shift Potassium Into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1

  • Can be repeated every 4-6 hours if hyperkalemia persists 2
  • Monitor glucose closely to avoid hypoglycemia, especially in patients with low baseline glucose, no diabetes, female sex, or altered renal function 2
  • Verify potassium is not below 3.3 mEq/L before administering 2

• Nebulized albuterol: 10-20 mg over 15 minutes 1

  • Can reduce serum potassium by approximately 0.5-1.0 mEq/L 1
  • Effects last 2-4 hours 2

• Sodium bicarbonate: 50 mEq IV over 5 minutes 1

  • Only use in patients with concurrent metabolic acidosis (pH < 7.35, bicarbonate < 22 mEq/L) 1, 2
  • Effects take 30-60 minutes to manifest 2

Step 3: Eliminate Potassium From Body (Definitive Treatment)

• Loop diuretics (furosemide): 40-80 mg IV 1

  • Only effective in patients with adequate renal function 1
  • Can be used in patients with GFR ≥50 mL/min/1.73m² 3

• Newer potassium binders (preferred): 1, 2

  • Patiromer or sodium zirconium cyclosilicate (SZC/ZS-9)
  • Safer alternatives to traditional resins 1
  • Allow continuation of beneficial RAAS inhibitor therapy 2, 3

• Sodium polystyrene sulfonate (Kayexalate): 15-50 g orally or rectally 1

  • Avoid chronic use due to risk of bowel necrosis 2, 3
  • Reserved for subacute treatment only 4

• Hemodialysis: Most effective method for severe hyperkalemia, especially in renal failure 1

  • Indicated for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 2

Management of Patients on RAAS Inhibitors

• For K+ 5.0-6.5 mEq/L: Initiate potassium-lowering agent and maintain RAAS inhibitor therapy 1, 2
• For K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent 1, 2
• Once K+ controlled (<5.0 mEq/L), consider reintroducing RAAS inhibitors at lower doses with close monitoring 3

Critical Monitoring

• Check potassium levels every 2-4 hours after initial treatment 2
• Reassess 7-10 days after starting or increasing RAAS inhibitor doses 2
• Exclude pseudo-hyperkalemia from hemolysis or improper sampling before aggressive treatment 1, 2

Key Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Do not use sodium bicarbonate without metabolic acidosis 2
• Remember that calcium, insulin, and beta-agonists only temporize—they do not remove potassium 2
• Temporary measures provide only transient effects (1-4 hours), and rebound hyperkalemia can occur after 2 hours 1

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Hypokalemia Management

For hypokalemia, oral potassium chloride replacement is preferred except in life-threatening situations (ventricular arrhythmias, digitalis toxicity, paralysis), when intravenous replacement is indicated. 5, 4, 6

Assessment and Causes

• Hypokalemia is defined as serum potassium <3.5 mEq/L 4
• Common causes include diuretic use, gastrointestinal losses, inadequate intake, or transcellular shifts 4
• Measure spot urine potassium and creatinine to differentiate renal from extrarenal losses 7
• Evaluate acid-base status as part of initial diagnostic workup 7

Oral Replacement (Preferred Route)

• Potassium chloride tablets or liquid are the treatment of choice 8, 5
• Reserved for patients who cannot tolerate liquid preparations or have compliance issues 8
• Used for treatment of hypokalemia with or without metabolic alkalosis, digitalis intoxication, and hypokalemic familial periodic paralysis 8
• Serum potassium is an inaccurate marker of total-body deficit—mild hypokalemia may reflect significant depletion 5

Intravenous Replacement (For Urgent Situations)

• Indications for IV replacement: 5, 4, 6

  • Ventricular arrhythmias
  • Digitalis intoxication
  • Paralysis
  • No functioning bowel
  • Cardiac ischemia
  • ECG changes or neurologic symptoms

• Administration guidelines: 8

  • 300-500 mL/hr of 10% dextrose solution containing 10-20 units crystalline insulin per 1,000 mL
  • Monitor for arrhythmias and electrolyte changes closely 8
  • Risk of hyperkalemia in patients with impaired renal function 6

Speed and Extent of Replacement

• Dictated by clinical picture with frequent reassessment of serum potassium 5
• Goal is to correct deficit without provoking hyperkalemia 5
• In patients with potassium wasting (increased renal clearance), addition of potassium-sparing diuretics may be helpful 5

Additional Considerations

• Correct associated fluid and electrolyte disorders (hypokalemia rarely occurs in isolation) 6
• Identify and eliminate causes of potassium loss 6
• Consider dietary supplementation with potassium-containing foods for mild cases 8
• Patients on digitalis require careful monitoring—too rapid correction can produce digitalis toxicity 8
• Chronic mild hypokalemia can accelerate CKD progression, exacerbate hypertension, and increase mortality 5