Saturday, 22 November 2008

What are the symptoms of hypokalemia?

(That's 'hypokalaemia' if you're outside of North America!)

Physiologically, hypokalaemia's dominant effect is the hyperpolarisation of cells. Remember that there is an electrochemical gradient across our cells: the complicated arrangement of the various ions on either side of our cells ends up making the interior of the cells negative, relative to their outsides. Sometimes this is referred to as the resting membrane potential, and this fact is exploited by excitable cells like neurones and muscle cells - the right signal causes rapid changes in the membrane potential, setting off a chain reaction that culminates in something useful (like the muscle contracting).

With less positively charged potassium ions on the outside of the cell (the definition of hypokalaemia), potassium ions from within the cell leave to replace them, causing the inside of the cell to become even more negatively charged than before. The result is that the cells become 'hyperpolarised' - less likely to fire off action potentials.

From this fact, most of the symptoms can be deduced:

  • Cardiac arrhythmias can be induced by hypokalaemia. Also, certain ECG changes are typical: increased PR interval (slowed atrio-venticular conduction) and flattened or inverted T-waves (delayed repolarisation) are seen.
  • Skeletal muscle weakness may exist, and occasionally be profound (anybody unlucky enough to see a hypokalaemic kwashiorkor child will attest to this). It usually involves the peripheral muscles, sparing the facial and respiratory muscles. At the final end of the continuum, rhabdomyolysis (destruction of skeletal muscle) may ensue.
  • Smooth muscle weakness usually manifests clinically as constipation and paralytic ileus.
  • Glucose intolerance is also sometimes found, and it is due to the fact that hypokalaemia impairs insulin release: the pancreas' beta cells also need to depolarise before the agree to give up their insulin.
  • Polyuria and dehydration is the main symptom complex not directly caused by hyperpolarisation of cells. Potassium is the 'rate limiting' element to the thick ascending loop of Henle's Na+/K+/2Cl- pump (the others are usually present in abundance). A lack of potassium means that the pump can't absorb all the sodium it needs to, and since sodium carries water with it, you get both polyuria and dehydration.
  • Metabolic alkalosis requires some expaining too, since it also isn't directly due to hyperpolarisation. At the distal parts of the kidney's nephrons, it is helpful to think of sodium being reabsorbed in exchange for either potassium or hydrogen. The situation is a little more complicated than this, but that doesn't matter. The point is that if potassium is low, more hydrogen must be booted out the cells to get enough sodium in. The result of this is, of course, a metabolic alkalosis (which is fortunately usually quite mild).

EDIT: I forgot the last point off the original version of this post!

5 comments:

  1. Jeremy, that last sentence does not match up with the heading 'metabolic alkalosis'.

    I like your explanations very much. It matches the way I've been trying to learn: Understand the underlying mechanism and then relate it to each symptom. I can't memorise laundry lists. Thanks.

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  2. Sorry! It's not very clear, is it? Let me try to break it down into stages:

    1. The body REALLY wants to reabsorb sodium, but unfortunately it is so designed that it must push 'out' something in return (from the body into the renal tubules, for excretion) at the distal convoluted tubule. It has a choice in this regard: the exchanged ion must either be potassium OR hydrogen.

    2. Less potassium being available for excretion means that the body must excrete proportionately more hydrogen ions if it is to reabsorb enough sodium.

    3. Since the body is now excreting more hydrogen ions, it develops a mild metabolic alkalosis.

    Does this make more sense? Perhaps I should draw a picture of the process in another post - do you think that would help?

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  3. By the way, the process also works in reverse too. If you already have a metabolic alkalosis for whatever reason (e.g. vomiting), then the body is forced to excrete more potassium at the distal convoluted tubule.

    In either case, the result is a hypokalaemic metabolic alkalosis, and the above explains why the two facets so frequently go together.

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  4. Yes, that explanation is very helpful. What I understand is that sodium is reabsorbed via a channel which expects either potassium or hydrogen to be released into the lumen. If there is a low supply of potassium, the potassium is retained in the body and the Hydrogen is released into the lumen.

    This leads to lower levels of hydrogen in the body. Lower H+ means metabolic alkalosis.

    Your final sentence is "The result of this is, of course, a metabolic acidosis (which is fortunately usually quite mild)." Did you mean to say "metabolic alkalosis"?

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  5. Oops - yes, you're absolutely right. "Metabolic alkalosis" is what it should read. I'll change it now - thanks.

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