In-Patient Potassium Correction Protocol
Hypokalemia Management
Severity Classification and Initial Assessment
Classify hypokalemia severity immediately: mild (3.0-3.5 mEq/L), moderate (2.5-2.9 mEq/L), or severe (≤2.5 mEq/L), as this determines urgency and route of replacement. 1
- Obtain ECG immediately for all patients with K+ <3.0 mEq/L or symptomatic hypokalemia, looking specifically for ST depression, T wave flattening, prominent U waves, or arrhythmias 1
- Check magnesium level concurrently—hypomagnesemia is present in ~40% of hypokalemic patients and makes hypokalemia refractory to correction; target Mg >0.6 mmol/L (>1.5 mg/dL) 1, 2
- Verify adequate renal function (urine output ≥0.5 mL/kg/hour) before initiating potassium replacement 1
- Rule out pseudohypokalemia from hemolysis or improper sampling technique if clinically inconsistent 3
Indications for IV Potassium Replacement
Administer IV potassium for: K+ ≤2.5 mEq/L, ECG abnormalities, active cardiac arrhythmias, severe neuromuscular symptoms (paralysis, respiratory impairment), or non-functioning GI tract. 1, 3
- Cardiac monitoring is mandatory during IV potassium administration for severe hypokalemia due to arrhythmia risk 1
- Maximum peripheral IV concentration: ≤40 mEq/L; maximum rate: 10 mEq/hour 1
- Central line preferred for concentrations >40 mEq/L or rates >10 mEq/hour to minimize phlebitis 1
- Recheck potassium within 1-2 hours after IV correction to assess response and avoid overcorrection 1
Oral Potassium Replacement Protocol
For K+ >2.5 mEq/L without ECG changes or severe symptoms, use oral potassium chloride 20-60 mEq/day divided into 2-3 doses with meals. 1, 4
- Never exceed 20 mEq per single dose to minimize GI irritation 4
- Administer with meals and full glass of water; never on empty stomach 4
- For patients with difficulty swallowing: break tablets in half or prepare aqueous suspension per FDA instructions 4
- Target serum potassium 4.0-5.0 mEq/L, as both hypokalemia and hyperkalemia increase mortality, especially in cardiac patients 1
Critical Concurrent Interventions
Correct magnesium deficiency FIRST—this is the single most common reason for treatment failure in refractory hypokalemia. 1, 2
- Use organic magnesium salts (aspartate, citrate, lactate) rather than oxide/hydroxide for superior bioavailability 1
- Typical oral magnesium dosing: 200-400 mg elemental magnesium daily, divided into 2-3 doses 1
- Stop or reduce potassium-wasting diuretics if K+ <3.0 mEq/L 1
- Avoid NSAIDs entirely—they worsen renal function and interfere with potassium homeostasis 1
Medication-Specific Adjustments
For persistent diuretic-induced hypokalemia, add potassium-sparing diuretics rather than chronic oral supplementation—they provide more stable levels without peaks and troughs. 1
- Spironolactone 25-100 mg daily (first-line) 1
- Amiloride 5-10 mg daily (alternative) 1
- Triamterene 50-100 mg daily (alternative) 1
- Check K+ and creatinine within 5-7 days after initiating potassium-sparing diuretic, then every 5-7 days until stable 1
- Contraindicated if eGFR <45 mL/min or baseline K+ >5.0 mEq/L 1
For patients on ACE inhibitors/ARBs alone or with aldosterone antagonists: routine potassium supplementation is frequently unnecessary and potentially deleterious. 1
- These medications reduce renal potassium losses 1
- If supplementation needed, use only 10 mEq daily initially with monitoring within 48-72 hours 1
- Reduce or discontinue potassium supplements when initiating aldosterone antagonists to avoid hyperkalemia 1
Special Clinical Scenarios
Diabetic Ketoacidosis (DKA): Add 20-30 mEq potassium (2/3 KCl and 1/3 KPO4) to each liter of IV fluid once K+ <5.5 mEq/L with adequate urine output established 1
- If K+ <3.3 mEq/L, delay insulin therapy until potassium restored to prevent life-threatening arrhythmias 1
- Monitor potassium every 2-4 hours during active DKA treatment 1
- Typical total body potassium deficit in DKA: 3-5 mEq/kg body weight despite initially normal/elevated levels 1
Digoxin Therapy: Maintain K+ strictly 4.0-5.0 mEq/L—even modest hypokalemia dramatically increases digoxin toxicity risk 1
- Question digoxin orders in patients with severe hypokalemia until corrected 1
- Correct hypokalemia before administering digoxin 1
Heart Failure: Target K+ 4.0-5.0 mEq/L—both hypokalemia and hyperkalemia increase mortality in this population 1
- Consider aldosterone antagonists for mortality benefit while preventing hypokalemia 1
- Avoid most antiarrhythmic agents in hypokalemia (only amiodarone and dofetilide shown safe) 1
Monitoring Protocol
Recheck potassium and renal function within 3-7 days after starting supplementation, every 1-2 weeks until stable, at 3 months, then every 6 months. 1
- More frequent monitoring required for: renal impairment (Cr >1.6 mg/dL), heart failure, diabetes, concurrent RAAS inhibitors, or history of recurrent potassium abnormalities 1
- When adding potassium-sparing diuretics: check every 5-7 days until values stabilize 1
- Hold supplementation if K+ >5.5 mEq/L 1
Common Pitfalls to Avoid
- Never supplement potassium without checking and correcting magnesium first—this is the most common reason for treatment failure 1, 2
- Never combine potassium supplements with potassium-sparing diuretics without specialist consultation 1
- Avoid routine triple combination of ACE inhibitor + ARB + aldosterone antagonist due to excessive hyperkalemia risk 1
- Never administer >20 mEq potassium as single oral dose—divide throughout the day 4
- Separate potassium administration from other oral medications by at least 3 hours for certain formulations 1
Hyperkalemia Management
Severity Classification and Immediate Assessment
Classify hyperkalemia as mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L)—but ECG changes indicate urgent treatment regardless of absolute potassium level. 5
- Obtain ECG immediately for all patients with K+ >6.0 mEq/L, looking for peaked T waves, flattened P waves, prolonged PR interval, widened QRS 5
- Verify result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique 5
- ECG changes are highly variable and less sensitive than laboratory values—do not rely solely on ECG 5
Emergency Treatment for Severe Hyperkalemia (K+ ≥6.5 mEq/L or ECG Changes)
Administer IV calcium FIRST to stabilize cardiac membranes within 1-3 minutes—calcium does NOT lower potassium, only temporizes for 30-60 minutes. 5
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 5
- Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (more potent, requires central line) 5
- Monitor ECG continuously during and for 5-10 minutes after administration 5
- If no ECG improvement within 5-10 minutes, repeat dose 5
- Never administer calcium through same IV line as sodium bicarbonate—precipitation will occur 5
Simultaneously initiate intracellular potassium shift with all three agents for maximum effect: 5
Insulin 10 units regular IV + 25g dextrose (D50W 50 mL) 5
Albuterol 20 mg nebulized in 4 mL 5
Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, HCO3 <22 mEq/L) 5
Definitive Potassium Removal
Choose method based on renal function and clinical urgency: 5
Loop diuretics (furosemide 40-80 mg IV): For adequate kidney function; increases renal potassium excretion 5
Hemodialysis: Most effective and reliable method for severe hyperkalemia, especially with renal failure, oliguria, or unresponsive to medical management 5
Newer potassium binders (preferred for subacute/chronic management):
Avoid sodium polystyrene sulfonate (Kayexalate): Delayed onset, limited efficacy, risk of bowel necrosis 5
Medication Management During Acute Episode
Temporarily discontinue or reduce contributing medications when K+ >6.5 mEq/L: 5
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) 5
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 5
- NSAIDs and COX-2 inhibitors 5
- Trimethoprim, heparin, beta-blockers 5
- Potassium supplements and salt substitutes 5
Chronic Hyperkalemia Management (K+ 5.0-6.5 mEq/L)
For patients on RAAS inhibitors with cardiovascular disease or proteinuric CKD: maintain RAAS inhibitor therapy using potassium binders rather than discontinuing these life-saving medications. 5
- Initiate patiromer or SZC while continuing RAAS inhibitor unless alternative treatable cause identified 5
- RAAS inhibitors provide mortality benefit in heart failure and slow CKD progression 5
- Discontinuing RAAS inhibitors leads to worse cardiovascular and renal outcomes 5
Dietary modifications: 5
- Limit bioavailable potassium from processed foods 5
- Avoid salt substitutes containing potassium 5
- Avoid herbal supplements that raise K+ (alfalfa, dandelion, horsetail, nettle) 5
- Evidence linking dietary potassium to serum levels is limited—potassium-rich diet has cardiovascular benefits 5
Monitoring Protocol for Chronic Hyperkalemia
Check potassium within 1 week of starting or escalating RAAS inhibitors, especially in high-risk patients (CKD, heart failure, diabetes). 5
- After initiating potassium binder: recheck at 1 week, then 1-2 weeks, 3 months, then every 6 months 5
- Individualize frequency based on eGFR, comorbidities, and medication regimen 5
- Monitor closely for hypokalemia when using potassium binders—hypokalemia may be more dangerous than hyperkalemia 5
Special Population: CKD Patients
Patients with advanced CKD (stage 4-5) tolerate higher potassium levels due to compensatory mechanisms, but target 4.0-5.0 mEq/L minimizes mortality risk. 5
- Optimal range broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 vs. 3.5-5.0 mEq/L for stage 1-2 5
- Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression 5
- For dialysis patients: target predialysis K+ 4.0-5.5 mEq/L 5
Critical Pitfalls to Avoid
- Never delay treatment while waiting for repeat labs if ECG changes present—ECG changes indicate urgent need regardless of exact potassium value 5
- Never give insulin without glucose—hypoglycemia can be life-threatening 5
- Never use sodium bicarbonate without metabolic acidosis—ineffective and wastes time 5
- Remember calcium, insulin, and beta-agonists are temporizing only—they do NOT remove potassium from body 5
- Do not rely solely on ECG findings—highly variable and less sensitive than laboratory tests 5
- Never permanently discontinue RAAS inhibitors in cardiovascular disease/proteinuric CKD—use potassium binders instead 5
Post-Dialysis Hyperkalemia Management
Potassium can rebound within 4-6 hours post-dialysis as intracellular potassium redistributes—monitor patients with severe initial hyperkalemia (>6.5 mEq/L) every 2-4 hours initially. 5