Digoxin and Potassium.

  1. 0
    I'm trying to understand the rationale behind their relationship... I understand you must keep a close eye on the potassium because low potassium can increase Dig Toxicity.

    Initially my curiosity began with wanting to understand WHY we give K+ (during dig tox when K+ lvls are low)

    If....

    potassium slow down the heart??? Dig also slows the HR .... Hmmm?

    But to my understanding Dig binds to ion pumps where potassium would normally bind .... So if we have excess Dig .... Its taking up those spots potassium would normally occupy as it is!... And just to add the madness we have low potassium so now there's even fewer potassiums to bind to the pumps?

    So....this is why we would give:
    Atropine (fix bradycardia... Atropine is an anticholinergic) so it suppresses the PSN system.

    Potassium (obvious reasons)

    Digibind (antidote)

    Lidocaine.... Treat cardiac irritability?


    Does the above sound right?

    What else can you add? Textbook versus Practice?

    Currently on break from school ......

    but I'm enjoying understanding some of the stuff I learned....
    ICU here I come!


    Typing from "smart" phone... Forgive all typos and grammatical errors.
  2. 9 Comments so far...

  3. 0
    Yep..u got it..dig and K+ compete for the same receptor sites
  4. 5
    Potassium does't "slow down the heart" unless the level is very high. The gradient (difference) between intracellular K+ (high number) and extracellular K+ (low number) influences the cell membrane's ability to depolarize. A big gradient (low K+) makes the membrane depolarize more easily. Depolarization leads to contraction.

    We care about this because cardiac cells have the unique ability to 1) depolarize on their own, without a nerve to goose them into action (unlike, say, skeletal muscle, that will just lie there unless a nerve tells it to do something), and 2) spread their depolarizing cell-to-cell to all their neighbors (also unlike, say, skeletal muscle). What this means is that if a cell wall is already a little cranky from hypoxia or anything else and the serum K+ around it is low, it can depolarize whenever the heck it feels like, spreading a wave of depolarization throughout the ventricle. Because this happens outside of the control usually exerted by the cardiac conduction system, it results in funny-looking premature tracings on the EKG, called "PVCs," premature ventricular contractions.

    We care about THAT because if a depolarization wave hits a cell in a particular phase of its repolarization, the result can be a chaotic rapid heartbeat that pumps no blood. This is why we watch K+ levels particularly in anyone with any sort of cardiac crankiness or reason to have cardiac crankiness, like MI, ischemia, or surgery.

    Digoxin and slows the heart rate (from the SA node) and increases contractility in a failing heart by affecting calcium in the cells (and it does that by affecting the sodium pump in the cell membrane), and decreases AV conduction, a good idea in atrial fibrillation when you don't want to whip the ventricles into a frenzy (a lot of AF folks have ventricles that won't like going too fast).
  5. 0
    ^^^^nice^^^
  6. 1
    Guess my initial comment didn't post? Must've been a glitch.

    That was nice... I second that! Thank you so much.
    Esme12 likes this.
  7. 0
    Quote from GrnTea
    Potassium does't "slow down the heart" unless the level is very high. The gradient (difference) between intracellular K+ (high number) and extracellular K+ (low number) influences the cell membrane's ability to depolarize. A big gradient (low K+) makes the membrane depolarize more easily. Depolarization leads to contraction.

    We care about this because cardiac cells have the unique ability to 1) depolarize on their own, without a nerve to goose them into action (unlike, say, skeletal muscle, that will just lie there unless a nerve tells it to do something), and 2) spread their depolarizing cell-to-cell to all their neighbors (also unlike, say, skeletal muscle). What this means is that if a cell wall is already a little cranky from hypoxia or anything else and the serum K+ around it is low, it can depolarize whenever the heck it feels like, spreading a wave of depolarization throughout the ventricle. Because this happens outside of the control usually exerted by the cardiac conduction system, it results in funny-looking premature tracings on the EKG, called "PVCs," premature ventricular contractions.

    We care about THAT because if a depolarization wave hits a cell in a particular phase of its repolarization, the result can be a chaotic rapid heartbeat that pumps no blood. This is why we watch K+ levels particularly in anyone with any sort of cardiac crankiness or reason to have cardiac crankiness, like MI, ischemia, or surgery.

    Digoxin and slows the heart rate (from the SA node) and increases contractility in a failing heart by affecting calcium in the cells (and it does that by affecting the sodium pump in the cell membrane), and decreases AV conduction, a good idea in atrial fibrillation when you don't want to whip the ventricles into a frenzy (a lot of AF folks have ventricles that won't like going too fast).
    Nice explanation of digoxin and potassium!
  8. 1
    GrnTea, I'm studying for the PCCN exam, and this was very helpful....
    turnforthenurseRN likes this.
  9. 1
    Thanks.
    ::sigh:: Just don't ask me how much a liter of water weighs in pounds. ::still blushing::
    Esme12 likes this.
  10. 0
    Quote from GrnTea
    Thanks.
    ::sigh:: Just don't ask me how much a liter of water weighs in pounds. ::still blushing::
    ....I have done that as well.....it makes us human!!!!
  11. 1
    It's okay - I was right with you trying to help explain it.... And even when I was typing I thought, this IS what she means, right? Honest.
    GrnTea likes this.


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