Caused by:-<\/p>\n
- \n
- Increased intake (food, IV fluids, potassium supplements)(unlikely to be sole cause)<\/li>\n
- Tissue breakdown (e.g. tissue damage, bleeding, haemolysis, rhabdomyolysis)<\/li>\n
- K+ release from cells (e.g. in hyperglycaemia, acidosis)<\/li>\n
- Endocrine – Addison’s disease; drugs – spironolactone (aldosterone antagonist)<\/li>\n
- Impaired excretion in urine (e.g. in renal failure, and with drugs – ACE inhibitors, potassium-sparing diuretics)<\/li>\n<\/ul>\n
Clinical signs are rare. An ECG may show tall T waves, increased PR interval and widened QRS complexes. In severe cases, the P and T waves are absent. A plasma K+ of over 7 mmol\/l may lead to cardiac arrest.<\/p>\n
ECG in hyperkalaemia<\/h4>\n
![\"Cilein](\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/04\/CilienHyperkal.gif\")
<\/p>\nThis brilliant animation of the ECG in hyperkalaemia by Dr Cilein Kearns @artibiotics<\/a><\/p>\n
\nTreatment of acute hyperkalaemia<\/span><\/strong><\/h3>\n
Intravenous calcium<\/span><\/strong>\u00a0is necessary only if there is dysrhythmia or severe ECG changes
\n10% gluconate or chloride, 10mls over 5 minutes (maximum 2mls\/min)<\/p>\n- \n
- Give if ECG changes – peaked T-waves, prolonged PR<\/li>\n
- Check in 15 minutes and if still abnormal, repeat once or twice<\/li>\n
- Does not change [K+]; reduces excitability of membranes<\/li>\n<\/ul>\n
Intravenous glucose<\/span><\/strong>\u00a0(dextrose)
\n50ml 50% (25g) + 5u Actrapid over 20 minutes (i.e., maximum ratio of 5g:1 unit)<\/p>\n- \n
- Acts in 30 minutes, peak effect 90 minutes, lasts up to 6 hours<\/li>\n
- Lowers [K+] by 0.7-1.6mmol\/l<\/li>\n
- Can be followed by slow infusion of 10-50% dextrose (give insulin only if glucose high)<\/li>\n
- Monitor blood sugar after administration<\/li>\n<\/ul>\n
Salbutamol<\/span><\/strong>
\n5mg nebulised<\/p>\n- \n
- Acts in 60 minutes, peaks 90 minutes, lasts up to 6 hours<\/li>\n
- Similar to dextrose in efficacy<\/li>\n<\/ul>\n
Sodium bicarbonate<\/span><\/strong>
\n50 mmol, usually as 330mls 1.26% (isotonic) (50ml of 8.4%, but this is irritant)<\/p>\n- \n
- The least effective intervention and involves sodium load; consider if acidotic and extra sodium tolerable<\/li>\n
- Can reduce [K+] by 0.2-0.3mmol\/l<\/li>\n
- Not routine but may be useful in emergency<\/li>\n<\/ul>\n
Dialysis<\/span><\/strong>
\nOnly necessary if renal function very poor – working kidneys excrete potassium!<\/p>\n- \n
- Note that above treatments do not remove, they only redistribute [K+]<\/li>\n
- A standard haemodialysis removes 40-60mmol [K+]<\/li>\n
- Haemodialysis lowers [K+] faster than haemofiltration or peritoneal dialysis<\/li>\n<\/ul>\n
Potassium binding resins and compounds<\/span><\/strong>
\nCalcium Resonium is the original. Not useful in acute setting but may be short\/medium term option if dialysis not desirable or possible. Unpleasant to take, causes constipation, limited effectiveness. Other more effective and apparently less toxic compounds are in development.<\/p>\nDiet<\/span><\/strong>
\nMay explain acute hyperkalaemia usually only if there are other risk factors such as drugs, reduced renal function.\u00a0 In the presence of risk factors and an episode of hyperkalaemia, important for prevention.<\/p>\n
\nHypokalaemia<\/span><\/strong><\/h3>\n
A decrease in plasma K+ is commonly caused by:-<\/p>\n
- \n
- Loss of K+ from GI tract (e.g. vomiting, diarrhoea, intestinal obstruction)<\/li>\n
- Shift into cells (e.g. insulin treatment of hyperglycaemia)<\/li>\n
- Endocrine \u00e2\u20ac\u201c hyperaldosteronism, primary or secondary<\/li>\n
- Drug treatment (e.g. most diuretics)<\/li>\n<\/ul>\n
The clinical features include lethargy and muscle weakness. Tingling in fingers, paralysis and coma are present in more severe cases. In chronic hypokalaemia there may be nocturia, polyuria or polydipsia.<\/p>\n
There is commonly divergence between serum [K] and whole body stores – e.g. depletion yet normal plasma [K] in diabetic ketoacidosis; low plasma [K] despite normal total body potassium in metabolic alkalosis.<\/p>\n
Hypokalaemia is treated by giving KCl, intravenously in severe cases, and correcting any associated salt and water imbalance. Recurrence is prevented by encouraging a K+ rich diet, but K+ supplementation or a K+-sparing diuretic is advisable if the patient requires diuretics, and supplementation if receiving intravenous fluid treatment.<\/p>\n
\nFurther info<\/span><\/strong><\/h3>\n
- \n
- Diet and potassium<\/a><\/li>\n
- Hyperkalaemia<\/a>\u00a0management from Edren handbook<\/li>\n
- Fluid spaces and requirements<\/a><\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"
The usual dietary intake of K+ is about 80 mmol\/day. 85% of normal potassium excretion is in urine. Potassium balance depends on regulation of urinary excretion. Endogenous potassium is largely intracellular, hence changes in K+ distribution between ECF and ICF may greatly affect plasma K+ concentration. Hyperkalaemia Caused by:- Increased\u2026<\/p>\n
- Hyperkalaemia<\/a>\u00a0management from Edren handbook<\/li>\n
- Diet and potassium<\/a><\/li>\n