Potassium Homeostasis

    • 98% of K+ is intracellular
    • Normal K+: 3.5-5.0 mEq/L
    • Insulin, catecholamines, and acid-base status influence K+ movement into cells  (aldosterone has minor effect)
    • Kidney Excretion at distal nephron
      • K+ excretion = urine flow rate x urine [K+]
    • Increase Renal K+ Losses
      • Hyperkalemia
      • Increased distal tubular flow rate [thiazides, loop diuretics]
      • Aldosterone activates eNaC --> Na+ reabsorption and K+ excretion
      • Metabolic alkalosis
      • Hypomagnesemia
      • Increased non-reabsorbable anions in tubule lumen: HCO3-, penicillin, salicylate.
    • KHATPase.png


    • Asymptomatic 3.0-3.5 mmol/L  (maybe some muscle cramps)
    • Mild symptoms: (< 3.0)
      • N/V, fatigue, weakness, myalgia, muscle cramps, constipation.
    • Severe:
      • Arrhythmias, muscle necrosis, --> eventual respiratory impairment.
      • Arrhythmias --> unlikely (worse if hypomagnesemia, digoxin, CAD)
      • Rhabdomyelysis
      • ECG changes are more predictive than serum K+ levels.
      • U waves 
      • flattened or inverted T waves
      • depressed ST segment
      • NOT prolonged QT (carefully measured and disputed, but many people still believe this).
      • SEVERE: P-R prolongation, wide QRS, arrhythmias (high risk of digitalis)
      • HypokalemiaECG.png
      • HypokalemiaECG2.png
    • Assessment:
      • GET ECG STAT!
      • Rule out transcellular shifts as a cause.
      • Low intake is almost never the cause (K+ in everything we eat)
      • Diuretics (MOST COMMON)
      • Marked leukocytosis (take up K+) --> Pseudohypokalemia
      • Associatied with:
        • Hypertension? if YES:
          • Concern about renin-angiotensin aldosterone axis, Measure Renin + Aldosterone
          • Renin Aldosterone Interpretation
            HIGH HIGH

            - Renovascular HTN

            - Renin-Secreting Tumor

            LOW LOW Liddle's Syndrome (epithelial Na channel activated)
            LOW HIGH Primary hyperaldosteronism
          • Renin+ Aldosterone are high = renovascular HTN, and renin-secreting tumor OR structural abnormality.
          • If Renin+Aldosterone are low = Liddle's syndrome (Epithelium Na channel activated)
          • If cortisol level very high or taking black lickerish (inhibits metabolism of cortisol) - both causing high cortisol levels ---> cross-reacts (acts like aldosterone)
          • If Renin low + Aldosterone HIGH --> primary Hyperaldosteronism
        • Cellular redistribution? (insulin, B-agonists, alkalosis)
        • Drugs/Toxins (barium, chloroquine, risperidone)
        • Hypokalemic periodic paralysis (asians and post-glucose load)
        • Lots of Sodium Delivery = more delivery to distal tubule, more K+ losses
      • If still no answer: then look whether losses are from urine:
        • 24hr urine K+ or spot urine K+/Creat ratio
          Renal Losses

          Urine K+/Creat ratio HIGH (>20 mEq/g)


          24hr Urine K+ is HIGH

          - Renal Losses
          No Renal Losses

          Urine K+/Creat ratio LOW (<15 mEq/g)


          24hr Urine K+ is LOW (< 20 mEq/24hrs)

          - Cellular Redistribution

          - Decreased Intake

          - Extrarenal losses (i.e. diarrhea)


        • If urine K+/Creat high (>20 mEq/g), Kidney K+ wasting--> look at acid-base status
          • Metabolic Alkalosis --> act like diuretics
            • Bartter syndrome - Loop diuretic effect
            • Gitelman Syndrome -Thiazide diuretic effect (milder)
            • Magnesium Deficiency
            • Vomiting
          • Metabolic Acidosis
            • RTA
            • Glue-sniffing (Toluene)
            • Glycosuria (ketoacidosis)
          • Normal
            • Primary Polydipsia?
            • Lysosyuria


    • Treatment
      • Treat underlying cause
        • If hyperaldosteronism, can give spironolactone
        • Avoid dextrose/bicarb (releasesinsulin, worsens hypoK)
        • Avoid large salt loads (increases distal nephron deliver, poor K+ reabsorption)
      • Replete
        • Huge body stores of K+, only small amount in serum.
          • Fall 4 mEq/L to 3mEq/L (at least 100 mEq/L deficit)
        • Oral: food, tablets (K-Dur, SlowK), KCl liquid
        • IV: KCl in saline
          • MAX:
            • 20mmol/L (Peripheral Vein)
            • 40-60mmol/L (Central Vein)
            • Rate: max 20 mmol/h
        • Types in Canada:
      • Name Form Doses Notes

        Potassium Chloride

          (K-Dur: 20mEq/tab)

          (Slow-K: 8 mEq/tab)





        Potassium Citrate

          (Cytra-K: 10-30mL/dose)

        PO - Powder and solution forms available - Alkalinizer (better if concurring acidosis)
        Potassium Chloride IV

        20mEq max via peripheral IV

        60mEq max via central IV

        - Avoid infusions > 20mEq/hr
        • Restore Mg2+ (K+ will not correct unless you replete Mg2+)
        • K+ sparing diuretics (triamterene, spironolactone, amiloride) - esp if hyperaldosteronism
      • Notes:
        • Risk of hyperkalemia high in elderly, diabetics, and decr renal function.
        • If metabolic acidosis, give as K+citrate and not as K+chloride (citrate metabolized to bicarbonate)


    • Serum [K+] > 5.0 mEq/L
    • Usually Kidney disease or limited effect of renin-aldosterone axis.
    • Typically diet ONLY plays a role in K+ balance if there is renal dysfunction (i.e. GFR < 20)
    • Symptoms:
      • Often Asymptomatic
      • Symptoms: nausea, muscle weakness, muscle stiffness, paresthesias, areflexia, ascending paralysis, ---> hypoventilation
      • ECG:
        • Peaked and narrow T waves
        • Decreased amplitude and eventually loss of P waves.
        • Prolongued PR interval
        • Wide QRS  --> eventually merges T -wave to make sine-wave.--> ventricular standstill
        • Short QT (a bit)
        • HyperkalemiaECG.png
        • HyperkalemiaECG2.png
    • Approach:
      • STEP 1: DO EKG
        • If signs of true hyperkalemia---> treat urgently, explore causes later. 
      • Rule out lab error:
        • Hemolysis
        • Excess touniquet time
        • Leukocytosis, thrombocytosis (fragile cells)
      • From cells?
        • Cell damage?
          • Tissue injury (rhabdo), tumor lysis
        • Medications
          • B-blockers, Digoxin
        • Metabolic acidosis, Insulin deficiency, etc..
      • Kidney (esp if GFR < 10)
        • DRY? (no flow to distal nephron)
        • Type IV RTA (Hyporeninemic Hypoaldosteronism)
          • Lack of aldosteronism
        • Can check Urinary K+ (If < 30 mEq/L = due to impaired renal clearance)



    • Treatment

    • # Mechanism Action Duration
      1. Protect the heart

      - Calcium Gluconate (10% sol'n 10 mL IV over 3min, can repeat in 5m)


      - Calcium Chloride (10% Sol'n 10mL IV over 3min

                                      3x more elemental Ca++, on crash carts)

      *** Contraindicated if HyperK Ass'd with Digitalis Toxicity ***

      *** Use magnesium sulfate 2g IV + Digibind in Digitalis Toxicity ***

      Onset: minutes

      Lasts: 20-30min

      (Can repeat)

      2. Shift K+ into Cells

      A. Insulin

           - (Insulin R) 10-20u IV, with 1-2 amp D50W 

             (give D50W before insulin)

           - Can also do 10u of Insulin R
             in 500mL of 20% dextrose (infuse over 1hr)

      B. Salbutamol 

          - nebulized 2cc or 10mg inhaled or 0.5mg IV

          - Caution in heart disease (tachycardia etc.)

      C. NaHCO3 

          - 1-3 amps (in 1L D5W)

          - Not very effective, more effect if metabolic acidosis


            Onset: 15-30min

            Lasts: 1-2h

            (decr by 1 mEq/L)


            Onset: 30-90min

            Lasts: ~1h?


            Onset: 30-90min

            Lasts: variable

      3. K+ Excretion

      A. Via urine

          - Furosemide ≥40mg IV


          - Fludrocortisone (if aldosterone def.)

      B. Dialysis!

          - Esp if renal failure.

      C. GI Tract

          - Sodium polystyrene sulfonate (aka Kayexalate)

          - 30g PO (preferred)
            or 50g as retention enema

            (exchange resin causes K+ excr. via GI.  

          (use of sorbitol polystyrene caused GI necrosis/bleeding)

          (now use sorbitol-free preparations;  it is a cation exchange resin,

           replaces K+ with Na+; if Na+ is a problem, give diuretic)

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