Potassium

Pathophysiology

• 98% of total body potassium is located inside cells - but we monitor potassium by measuring the 2% (actually we measure the intravascular potassium, which is only 0.4%!)
• Total body potassium about 50mEq / kg
• Daily requirement 50mmol

Hyperkalaemia

• Much worse-tolerated than hypokalaemia - can be life-threatening
• Aetiology
  • Trans-cellular shift - potassium release from cells - high urine K (>30mEq/L)
    • Acidosis - although a causal link has not been firmly established
    • Tumour lysis syndrome - appears within 7 days of cytotoxic chemotherapy - AKI, hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia
    • Drugs - beta blockers, digitalis, succinylcholine
    • Insulin deficiency
  • Impaired renal excretion - urine K < 30mEq/L
    • Drugs that inhibit RAAS - ACE inhibitors, ARBs, K+-sparing diuretics, NSAIDs, heparin, Bactrim
    • Renal failure - usually doesn't occur until eGFR<10, but can appear earlier in interstitial nephritis
    • Adrenal insufficiency - only seen in chronic adrenal insufficiency
  • Pseudohyperkalaemia - present ex vivo but not in vivo. Repeat the venipuncture when suspected.
    • Mostly potassium release from traumatic haemolysis during venipuncture
    • K+ release from fist muscles during clenching
    • K+ release from clot formation in the tube in patients with severe leucocytosis (>50) or thrombocytosis (1,000)
  • Excessive supplementation
    • Blood transfusion - begins to appear after 7 units
• Clinical manifestations
  • Slowed impulse transmission, which can progress to heart block and bradycardic arrest
  • ECG changes usually start at K=7
    • Tall, tapering T wave in V2 and V3
    • P wave amplitude decreases and PR interval lengthens
    • P waves disappear and QRS widens
    • VF/asystole
• Severity
• Approach
  • Hyperkalaemia is actually quite tricky to treat in some post-op patients
  • Assess and stabilise cardiac membrane
    • Calcium gluconate 10% in 10mL over 3 minutes; repeat after 5 minutes if necessary; effects last 30-60 minutes; opposes the cardiac depolarisation produced by hyperkalaemia
    • Use calcium chloride 10mL of 10% for circulatory shock
  • Treat hyperkalaemia - both trans-cellular shift and removal of K from body
    • Reduce intake
      • Stop fluids containing K+
      • Stop supplements
      • Low-potassium diet
    • Shift intracellular
      • Insulin 10 units actrapid in 50mL of 50% dextrose over 5 minutes, with close BSL monitoring, with highest risk after 60 mins. Takes 30-60 minutes. Should decrease K by 0.6mEq/L.
      • 10mg salbutamol neb over 30 mins, or 5mg if IHD history. Causes tachycardia as high doses are needed to do anything.
    • Increase excretion
      • Resonium 30g in 50mL of 20% sorbitol (oral - preferred) or 50g in 200mL of 20% sorbitol (retention enema). Onset at 2 hours, peak at 6 hours.
        • Don't use resonium in post-op patients or those with ileus - it can cause intestinal necrosis in rare case reports. It also takes 1-2 hours to work, and has minimal effect if just one dose.
      • Frusemide (only if normal renal function, otherwise talk to ICU)
      • Dialysis - very effective
  • Identify aetiology
• Management
  • Urgent repeat - do a VBG + UEC + CMP
  • ECG
    • If any ECG changes, manage as per severe hyperkalaemia

Hypokalaemia

• Aetiology
  • Trans-cellular shift - potassium movement into cells
    • Alkalosis (variable and unpredictable)
    • Hypothermia (transient)
    • Insulin
    • Inhaled beta-2 agonist bronchodilators in combination with diuretics
  • Decrease in total body potassium
    • Urine loss - diuretics, NGT (loss of volume and H+), alkalosis, magnesium depletion (impairs potassium reabsorption in renal tubules). Urine chloride levels are low with NGT and alkalosis, and high with diuretics and magnesium depletion.
    • GIT loss - diarrhoea
• Clinical manifestations
  • Mostly asymptomatic
  • Symptoms <2.5
    • ECG abnormalities - prominent U waves, flattening and inversion of T waves, prolongation of QT interval. Hypokalaemia alone is not a risk factor for severe arrhythmias, but can add to others
    • Diffuse muscle weakness
• Management
  • Eliminate or treat any condition leading to trans-cellular shifts
  • Identify and correct hypomagnesaemia
  • Estimate potassium deficits (mEq and mmol are 1:1 for potassium)
  • Replace
    • IV if potassium <3.3 or questionable GIT absorption. Reasonable to give both in many cases.
    • Check again in 12 hours if K < 3, otherwise check again 24 hours
    • Potassium chloride (best option in most)
      • 600mg PO tablets contain 8mmol potassium
        • Slow-K is modified release
        • Span-K is immediate release
      • Chlorvescent contains 14mmol potassium (not good for patients with ileus or struggling with fluid intake)
      • Can put 10mmol potassium chloride in 100mL normal saline
    • Potassium phosphate - can be used in concomitant hypophosphataemia, best choice in DKA because of phosphate depletion
    • Potassium bicarbonate - good in hypokalaemia and combined metabolic acidosis
  • Serum K can be slow to rise, as explained by the total body K/serum K curve above, and the large total estimated deficits for near-normal serum levels
  • Don't need to give calcium gluconate