Hi everyone, it's Jessica again, and welcome to CritIC.
Ask any internist what his favorite electrolyte is, and you'll get a serious response.
Mine's potassium.
This video covers hypokalemia.
While sodium is the most abundant extracellular cation, potassium resides predominantly inside
of our cells.
Serum levels of potassium, which are the extracellular levels, vary between 3.5 and 5 mmol/l.
Intracellular potassium levels are way higher, being around 150 mmol/l.
This is important to realize in both the workup and the treatment of hypokalemia.
Let me explain why.
If we have low serum levels, this could either indicate that a lot of potassium is shifted
towards the intracellular compartment (meaning total body potassium is normal), or that both
the extracellular and the intracellular compartment are depleted (total depletion).
Note that this is a beneficial characteristic in the treatment of hypokalemia.
Remember that our kidney is great at retaining sodium, and excreting potassium.
So this means that in patients with normal renal function, it's very hard to
"overdose" your patient when supplementing, though beware of transcellular shifts.
Why are we so worked up about potassium?
Well, that's because it is an important ion involved in neuromuscular excitability.
Low levels could cause muscle weakness, paralysis and cardiac arrhythmias resulting in death.
So we always check if the patient is symptomatic and ask for an ECG immediately.
When consulted, don't forget to actually name the symptoms, like muscle cramps, muscle weakness,
tingling sensations, etc.
Symptoms or ECG abnormalities require monitoring and supplementation on a cardiac or critical
care unit.
Now, back to the workup of hypokalemia.
There is either a transcellular shift (from extracellular to intracellular compartment),
or a total depletion of potassium.
Let's talk about total depletion first.
Total depletion is either because there isn't enough potassium coming into our body (through
a bad diet, or through malabsorption), though this is pretty uncommon.
Or because you're losing potassium.
Potassium loss can either be renal or gastro-intestinal, the latter we usually call extrarenal.
Total depletion is usually through loss, so your job is to figure out if it is gastrointestinal
or renal.
Gastrointestinal loss is easy to figure out: does your patient vomit or have diarrhea?
Renal loss can be determined by measuring potassium in urine, the cutoff being 20 mmol/l
in a urine sample.
I'll get back to the causes for renal potassium loss later on in this video.
Now let's talk about the transcellular shift.
There are 4 ways in which a transcellular shift occurs.
First, hydrogen ions and potassium ions shift over the cell membrane.
Alkalosis (in which there is low extracellular hydrogen) causes a shift of hydrogen from
intracellular to extracellular to compensate.
To maintain electrolyte balance in the cell, potassium shifts into the cell, resulting
in low serum potassium levels.
So the first cause for transcellular shift in hypokalemia is alkalosis.
The second cause for transcellular shift is hypothermia.
Please note that rewarming the patient therefore results in normalization of serum potassium levels.
The third cause is the stimulation of beta-receptors, so it should be on your mind when your patient
is nebulizing with salbutamol.
And the last cause for transcellular shift is insulin!
Insulin brings potassium inside the cell.
This trick is used in the treatment for hyperkalemia, which I'll get back to in another video.
Now let's focus a bit more on renal loss of potassium, since it is very common.
Renal potassium handling is governed by the mineralocorticoid action of aldosterone and
by our potassium pumps in our renal tubules.
This means that all syndromes that result in increased mineralocorticoid activity could
result in renal potassium loss and thus hypokalemia.
Examples being hyperaldosteronism, Cushing's disease, licorice ingestion (which is very
common in my country!), etc.
These patients commonly have hypertension.
Loop and thiazide diuretics influence the handling of potassium in our tubules.
Also note that there are syndromes mimicking these effects.
These are Barter and Gitelmann respectively.
So check for diuretics.
These people are usually hypotensive.
And there is one thing you may never forget in the workup of hypokalemia.
Always check magnesium levels.
Magnesium is necessary for maintaining potassium levels by blocking the ROMK potassium channels
in the distal tubule and thus decreasing potassium secretion in the kidney.
So in combined hypokalemia and hypomagnesemia, you can supplement potassium all you want,
but you'll keep losing it through the kidney if you don't correct serum magnesium levels.
A common cause for hypomagnesemia is the use of proton pomp inhibitors.
Though I don't want to get into treatment too much as this video would be endless,
a few words on supplementation:
for asymptomatic patients with potassium levels of above 2.5,
it's preferred to supplement orally.
Intravenous administration can irritate the veins and could cause skin necrosis.
Please check your local protocol on the maximum concentration of intravenous supplementation.
It may be necessary to place a central venous catheter.
Take a few moments to look at the flowchart we created.
When consulted about hypokalemia, it's very important to check for symptoms and get an ECG immediately.
Get lab work on serum creatinin, magnesium and a venous blood gas analysis and get a
urine sample on potassium and creatinin.
Never forget to check their list of medication for possible causes like diuretics, insulin,
nebulizers, laxatives, proton pump inhibitors in case of hypomagesemia, etc.
And that's it.
Let me know if this video was helpful.
As always, share it if you liked it, or give it a thumbs up.
Take care and I'll see you in the next one.