Podcast #107 - Emergent Management of Hyperkalemia

We see changes in potassium levels all of the time in patients.  However, what works and what does not?  What is the evidence behind the management?  Are there special pearls?  These questions and much more are addressed in this podcast with Michelle Perkins.

Intro—Why Worry?

• Why is potassium important?
  • It is important to have some understanding of what potassium (K+) does in the body to understand how to treat the imbalance
  • The resting electrical potential of cell membranes depends to a large extent on the ration of extracellular to intracellular K+
  • The potassium equilibrium across the membrane is regulated mostly by insulin and catecholamines
  • It doesn’t take much to mess this up. Just a small change in extracellular K+ can have a major impact on cell membrane stability
• So why worry?
  • These patients die if you don’t treat quickly and appropriately
•  So who do you suspect this in?
  • Common etiologies for hyperK include intrinsic kidney issues—excretion issues. 
  • The other major category is endogenous –increased K+ generated by cell death—all the lyses: hemolysis, rhabdo, tumor lysis, tissue lysis due to burns or trauma.
•  So you may have some clue from history. Often you don’t. So how do these folks present?
  • Completely asymptomatic—this isn’t uncommon
  • Super vague symptoms—generalized weakness, palpitations, even parasthesias or paralysis
  • PEA arrest---not uncommon, either
• What do you see objectively?
  • Major red flag on exam is what you see on the monitor and EKG
  • The dogma is that EKG changes (where we got the image for our post) follow a progression from early electrophysiologic changes to later ones
    • Peaked T-waves
    • Weird wide QRS morphology
    • Lost P-waves
    • ”Slow V-tach”—meaning V-tach morphology, but slow
    • ”Sine wave” morphology—the QRS has gotten so weird and wide that it’s morphing with the T-wave
    • V-fib
    • Asystole
• Don’t count on this dogma!
  • The sensitivity of EKG changes isn’t great—sometimes you can see virtually no changes at all—You can go from normal EKG to vfib arrest. The electrophysiologic changes are related more to the rate of change than to the absolute number.

 
Emergent Treatment

• So who do you treat emergently?
  • If the K is >6.5 regardless of EKG OR if the K is >5 WITH EKG treatment, treat emergently!
  • If the K is >5, but < 6.5 with no EKG changes, then the treatment isn’t as emergent
•  What does emergent tx look like?
  • If the patient is having abnormalities on their EKG, their myocytes’ membranes have been destabilized—job one is to stabilize the membranes!
  • Calcium—calcium restores the normal membrane potential of the myocytes. If you’re concerned about the EKG changes or the clinical picture, give it. You’re not going to hurt the patient (more on this later), and it’s potentially life-saving.
  • The effect is nearly instantaneous
• How do you give it?
  • Historically, Calcium gluconate was recommended, as it’s less likely to cause tissue damage if there’s an IV infiltrate
  • BUT, calcium chloride has more available elemental calcium, and if a patient is crashing, then extravascation is the least of their worries.
  • Give what you have available. If you’re giving Ca Gluconate, understand that you might need more (think 3 amps, rather than one)
• What about stone heart?
  • Historically, if hyperK is felt to be due to dig toxicity, it’s been thought that sudden death due to “stone heart” was a concern with calcium administration
  • This was based on some case studies of sudden deaths when Calcium was administered in hyperK in the face of dig toxicity, as well as some theoretical biochemical pathways that lead to myocyte standstill
  • This has been debunked.
  • The treatment of hyperkalemia caused by dig toxicity is digibind. But if you’re seeing EKG changes consistent with hyperkalemia and you think dig is involved, just give the calcium.
• What is the role of hypertonic saline?
  • Hypertonic saline (meaning 3% NS) has a role in the acute management of hyperkalemia ONLY in the setting of concurrent hyponatremia. Again, its role is one of membrane stabilization, working synergistically with the calcium, and doesn’t affect K+ levels.

 
Treating the Underlying Problem

• So, you’re taking care of the immediate life-threating issues, but you’re not taking care of the underlying issue. How do you decrease the potassium?

Shift the potassium from extracellular to intracellular

• Insulin!
• As mentioned before, insulin is a major regulator of potassium equilibrium across the cell membranes.
  • Drives the extracellular potassium intracellularly
  • You generally administer 10 units of IV insulin, given with D50 (2 amps) to prevent hypoglycemia.
  • This will typically drive down the K+ by 0.6 meq within 10-15 minutes.
  • Can repeat ad lib

What else can we use to drive down the extracellular potassium?

• Albuterol
  • As noted before, catecholamines play a role in potassium hemostasis across cell membranes
  • Beta-agonists such as albuterol can mimic catecholamine effects on myocytes, causing potassium to be driven intracellularly
  • The dose is generally higher than used with bronchospasm, generally 10-20 mg nebulized,
  • This works synergistically with insulin/glucose—can lower another 0.6 meq/dose
  • Can’t give alone! If you give it without insulin, can actually raise potassium

 Potassium elimination

• Also need to work on getting rid of the potassium from the system
• Diuretics
  • Eliminates potassium via the kidneys
  • They still work even with bad kidneys
  • Only work if a patient is hypervolemic
  • Takes some time for elimination
• Sodium bicarb
  • Used as a drip, used to alkalize the urine, increasing potassium excretion
  • Again, not a quick fix
• Kayexalate
  • No. No No No.
  • Potassium binder, theorized to work by binding potassium in the intestine
  • It’s variable in its efficacy, which is questionable at best
  • Has been shown to cause intestinal necrosis
• Veltassa and Z5-9
  • ​Also potassiumbinders, Veltassa approved here, and Z5-9 approved in Europe and rejected here
  • These are for use in chronic hyperkalemia, and have no use in emergent treatment of hyperkalemia

Hyperkalemic cardiac arrest

• So what happens if they arrest or you suspect that their arrest is due to hyperkalemia?
• Follow ACLS guidelines
  • Calcium, calcium, calcium and watch the QRS morphology on the monitor—titrate to morphology
  • Epi, which you’ll be using in the PEA algorithm anyway—shifts potassium into the cells via the catecholamine pathway that we discussed previously with albuterol
  • Insulin and glucose, repeat ad lib
  • Continue the code until ROSC or normal K+
  • Remember if you get ROSC, the calcium effect isn’t going to last for long—need to be aggressive in working on lowering the potassium.

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