Potassium
·
Normal value of K: 3.5 – 5 mmol/L
·
Standard western diet contains ~
70 mmol/day
·
Shifts from ICF to ECF in
response to:
o Insulin deficiency
o b-blockers
o Acidosis
o Cell necrosis
·
Excreted in the distal tubule (K
and H swapped for Na) under the influence of aldosterone. High HCO3
excretion also ® K loss (eg alkalosis)
·
Investigations:
o H+
o HCO3-: usually  when K ¯ and visa-versa except when there is acidosis (eg renal tubular necrosis, diarrhoea)
o Creatinine
o Urinary K: > 20 mmol/L Þ renal K loss
o Na: ¯ in hyperkalaemia, consider renal tubule disorder, ¯mineralocorticoid
o Glucose
o ECG (if widened QRS complexes give Ca).
·
Key differentials: Diabetic
ketoacidosis, renal failure
· Low:
o Redistribution: alkalosis, b-agonists
o Loss: GI, renal, thiazide or loop diuretics
o ¯Intake
(starvation, surgery)
·
High:
o Redistribution: acidosis
o Massive cell lysis
o ¯Excretion:
DRUGS (eg ACE inhibitors), renal failure, hypoaldosteronism
·
Causes:
o Usually ¯ renal excretion
o Shift from ICF (eg acidosis, massive cell lysis)
o Low aldosterone: ACE inhibitors
(instead use spironolactone), ¯renin (renal disease, NSAIDs, diabetes), poor adrenal function (eg
Addison‟s)
o Renal unresponsive to aldosterone: interstitial nephritis, K sparing
diuretics
o Renal failure: hyperkalaemia once GFR < 25 ml/min
·
Signs: myocardial depression,
peaked T wave, flat P wave, wide QRS, VF, diarrhoea, abdominal pain, muscle
excitability
·
Treatment:
o If severe (> 6.5 mmol/L) consider:
§ Glucose 50 g + soluble insulin 10 U over 15 mins
§ IV calcium gluconate – stabilises myocytes but doesn‟t change K
§ b2 agonist
(salbutamol)
§ Dialysis if extreme
o If moderate (5.5 – 6.5 mmol/L): Calcium resonium 15 g po (calcium
binding resins), Ârenal loss through diuretics, mineralocorticoids
·
Causes:
o GI losses (ECF volume contraction):
§ Vomiting, NG suction ® alkalosis ® ÂHCO3 in urine and Âaldosterone ® renal
loss of K
§ Diarrhoea: ® K loss and metabolic acidosis
o Urinary losses:
§ Diuretics: thiazides or loop
§ Alkalosis (also shift to ICF if significant alkalosis)
§ ECF normal or high: high aldosterone or hypermineralocorticoid (eg
Cushing‟s)
o K shift into cells: metabolic alkalosis, insulin, b-adrenergics
o ¯Intake
(starvation, surgery)
·
Symptoms:
o Muscle weakness, cramps
o GI: constipation, ileus
o Polyuria, nocturia
o Urine – if  volume then diuretics or osmotic diuresis, if not consider aldosterone
action
·
Signs: arrhythmias, PR prolonged,
inverted T waves, U waves, VF, GI ileus, muscle weakness, hypotonicity, digoxin
toxicity, alkalosis
·
Treatment: May have large total
body deficit (eg DKA). Replacement KCl
up to 40 mmol/hour
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