High potassium in the blood. Potassium is expressed by the chemical symbol "K". It stands for Kalium which is the Medieval Latin word for potash, a mineral used for hundreds of years as a fertiliser, and a natural potassium salt formed millions of years ago when ancient seas dried up. Burning plant matter in iron cauldrons (pots) yields high concentrations of potassium which in English, is termed potash.
Literally, Hyperkalaemia means high(hyper)-Potassium (Kal)-of the blood (aemia).
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In our bodies potassium is abundant inside our cells. It is a positively charged ion (electrolyte) termed K+.
In blood and other extra cellular fluid, it's concentration is very low relative to the high intracellular concentration. The principle of diffusion predicts that it will leak out of our cells to balance (equilibrate) with extracellular fluid.
In converse to K+, sodium (Na+) is abundant outside cells and does the same as potassium, in that it attempts to ooze into cells.
Normal blood potassium ranges from 3.5-5 mmol/L. Should potassium rise beyond 5.5 then it is called Hyperkalaemia. This is life threatening, and exerts its effects on muscle action, particularly cardiac muscle.
Elevated potassium leads to cardiac arrest. ... Badness!
Given potassium is normally abundant inside cells, it stands to reason that when cells are damaged, destroyed and die, their potassium leaches out and increases levels in the extracellular (interstitial fluid and blood) fluid.
Under normal circumstances, your kidneys remove excess K out of your blood and some of it is transported back into cells (influx).
Causes of Hyperkalaemia
Too much in, cell destruction or not enough excretion are the main causes.
Too much.
When we eat foods rich in potassium, it is rapidly absorbed via our gut and enters the blood stream. It is then either transported to cells where insulin is responsible for facilitating its movement into the cell as glucose is transported into cells for energy production.
In condition of tissue damage (burns, crush injuries and a muscle breakdown called Rhabdomyolysis), damaged cells leak massive amounts of K into the blood. The bigger the trauma, the bigger the potassium rise.
Not enough excretion.
If your kidneys fail, you can't excrete potassium. It accumulates. Remember it is continually leaking into your blood, so your kidneys need to be continually functioning to regulate potassium levels in blood. In renal injury or failure, accumulation is swift.
Diagnosis and suspicion
Muscle weakness especially after strenuous exercise (??rhabdomyolysis)
Lethargy,
Reduced urine production
ECG abnormalities eg tall tented T waves and s widening QRS complex=badness.
Serum K (blood test) is the fastest way to definitively assess Hyperkalaemia and is part of a routine test called U&Es (Urea and Electrolytes).
Treatment
Driving kidneys to excrete is the simplest strategy. By giving IV Normal saline, and or adding a diuretic, the patients kidneys can excrete more potassium. The common choice is a loop diuretic like Frusemide (Lasix). Naturally these are not appropriate if the cause was renal impairment.
Insulin and glucose infusions
Insulin acts like a swipe key that open channels (gates) in the cell membranes to let glucose into cells. When this occurs, potassium molecules are moved into the cell with glucose. Therefore an effective treatment for critically high potassium levels is an insulin infusion (with glucose).
- 10-20 units IV Actrapid insulin and 25-50g IV glucose.
- Starts working in 20mins
- Will reduce potassium by 0.5- 1mmol/L
Salbutamol.
Yep you read right. Salbutamol or Ventolin either IV or Nebulised (10-20mg) causes potassium to influx very effectively. This is the preferred option in renal disease patients when diuretics are useless and mucking around with glucose and insulin is a risky gig.
Salbutamol is as quick as the insulin, 20-30 mins and strips about 1mmol/L.
Resonium
Speaking of renal patients. A slow but relatively effective treatment for Hyperkalaemia is using oral or rectal Resonium resin. This old school treatment binds with potassium in the bowel and facilitates its removal in faeces.
It relies on gastric motility, so it is slow to onset, but gets the job done in the non acute patient. It is given as a 30-45g dose usually mixed with a laxitive (to really get things moving) - sorbitol is a favourite.
When things are Critical!!
If the patient has dangerous potassium levels (>8.5) then dialysis is the game changer.
Capable of stripping K+ at a rate of 1-2mmol/L over a two hour treatment, this intensive treatment is a proven lifesaver.
So there we have it. A very basic overview of hyperkalaemia . I hope you enjoyed my latest #KYJ.
