Calcium chloride

[EMTinCT]

Cool.

 

[EMTinCT]

So to recap, kidney failure leads to elevated K+, which can cause cardiac dysrhythmias. One treatment is CaCl where we think the Ca+ ions are pushing K+ into the cell by making the ECM more positive.

Amiright?

 

[chaz90]

I think that would be a fair summary.

 

[Gurby]

Most common use of CaCl out on the field as a medic. Thanks guys

Melting the ice on the steps outside base in winter.

 

[EMTinCT]

I think that would be a fair summary.

Yeah but it is correct? I was talking to gramma about it over dinner and she, not being the least bit versed in science, told me to have some more of her "fake salt" KCl crud.

 

[Brandon O]

So to recap, kidney failure leads to elevated K+, which can cause cardiac dysrhythmias. One treatment is CaCl where we think the Ca+ ions are pushing K+ into the cell by making the ECM more positive.

Amiright?

Nah, it's not to shift the K (that's albuterol, insulin/dextrose, etc). Calcium stabilizes the membrane to help prevent arrhythmia.

It's actually hard to find a useful explanation of how it works, since it's a bit counterintuitive if you're just adding up charges. After much digging here's what I came up with last year:

The dilemma is that too much extracellular potassium causes a loss of membrane potential (brings it closer to zero). How? The resting potential is mainly produced by the constant outward leak of intracellular potassium, causing an ongoing relative loss of intracellular cations (compared to intracellular negatively-charged proteins, which stay put). This creates the difference in charge across the membrane, which is only a very local effect. I had this idea that there's an overall imbalance in charges between the intra- and extra-cellular spaces, due to the different numbers of ions, but that's not right. It's a local effect and it's mostly due to the continuous potassium efflux. The Na-K exchanger contributes just a little bit (by pushing in more K than the Na it pumps out). Na influx has a minimal effect, because the membrane isn't very permeable to sodium, compared to high K permeability. So in hyperkalemia, you have more potassium outside, so there's less of a chemical gradient for K efflux, so there's less K movement, so there's less membrane potential. So maybe the potential goes from -90 to -80. That's closer to the threshold potential of -75, so it's easier to depolarize, and you get more irritability. Giving calcium extracellularly makes Ca bind around the voltage sensor and pore of all the voltage-gated channels, including Ca and Na channels (which are responsible for depolarization of pacemaker and ventricular cells, respectively). When it does this, it increases their activation threshold, so they won't open (depolarize) until you reach a higher (less negative) voltage. It desensitizes them. The activation potential therefore moves away from the abnormally-increased resting potential, giving you more breathing room between the two, and hence less excitability. The binding mechanism is not really well understood, but that seems to be the current theory, and I suppose it makes sense, since cations binding around the voltage sensors seem like they'd make it "think" there's a higher (more positive) extracellular voltage, and you'd therefore need a higher (less negative) intracellular voltage to hit the same difference.

 

[EMTinCT]

Giving calcium extracellularly makes Ca bind around the voltage sensor and pore of all the voltage-gated channels, including Ca and Na channels (which are responsible for depolarization of pacemaker and ventricular cells, respectively).

Where is the voltage sensor? I suspect it's on the outer membrane. What do you mean by, "and pore of all the voltage-gated channels"? Do mean that Ca2+ physical binds to Na+ voltage gated channels? What about the leak sodium channels?

 

[Brandon O]

Where is the voltage sensor? I suspect it's on the outer membrane.

That seems to be the understanding.

What do you mean by, "and pore of all the voltage-gated channels"? Do mean that Ca2+ physical binds to Na+ voltage gated channels?

Yep. I don't think there's a great grasp of how this works. But it's a consistent effect. Low serum calcium potentiates membrane excitability (cf. Trousseau and Chvostek signs) and high calcium inhibits it.

What about the leak sodium channels?

Hm. Good question. I'd guess no. Or at least it's fairly immaterial.

 

[EMTinCT]

That seems to be the understanding.



Yep. I don't think there's a great grasp of how this works. But it's a consistent effect. Low serum calcium potentiates membrane excitability (cf. Trousseau and Chvostek signs) and high calcium inhibits it.



Hm. Good question. I'd guess no. Or at least it's fairly immaterial.

Very interesting. Ca2+ is like putting your finger in the hole in the dam.

Not too long ago someone swore to me it was the Cl- ions but this someone couldn't come up with a mechanism. This someone's profession start with the letter 'c' and ends with 'ardiologist'.

 

[Brandon O]

Very interesting. Ca2+ is like putting your finger in the hole in the dam.

Not too long ago someone swore to me it was the Cl- ions but this someone couldn't come up with a mechanism. This someone's profession start with the letter 'c' and ends with 'ardiologist'.

Yeah, I had to do some real looking to come up with the physiology. This is one of the questions where most people stop chasing the "why" train pretty early.

 

[EMTinCT]

Yeah, I had to do some real looking to come up with the physiology. This is one of the questions where most people stop chasing the "why" train pretty early.

I noticed the lack of "why". My brain demands why/how. Thanks for geeking out.

 

[RRTMedic]

These people. There are other causes of HyperK, but we see these renal patients quite a bit. What are some reasons they become hyperkalemic, when do we often give them calcium, and why are we giving calcium? What are some other potential treatments for HyperK?

As for the ODs, in 6 years I've seen one BB overdose, and never a CCB overdose. I also do not have an iStat, and honestly probably wouldn't catch a presenting hypocalcemia patient in the field- at least not with enough certainty to want to give them any calcium. I won't likely be keeping a BP cuff inflated on their arm for 5 minutes looking for Trousseau's sign, and from what I remember, Chvotek's sign isn't all that sensitive.

Calcium Chloride (better than bicarb) -> Sodium Bicarb -> D50/Insulin -> Albuterol 25 mg/hr