Hyper K, The EBM Way: Protect, Push, and Purge

As we all know hyperkalemia is a life threatening condition. But how can something so basic be shrouded in such confusion? So many choices and everyone has their own recipe to fix it. Along with all the treatment choices, come pitfalls and side effects. Thus, we need to know what is the best way to treat this without giving our patients further problems! Enter “The Algorithm”. I hold before you an approach (evidenced based of course) for treating this life threatening condition. Remember, as always this is only one option and not THE ONLY option for treatment. If your hospital has a guideline or best practice then best stick to that. Otherwise, feel free to enter into a deep forest overgrown with evidence and lush with literature about the treatment of hyperkalemia.


Hyperkalemia can be tricky. We all learn the basic ECG patterns for hyperK as it goes through stages on its way to a “sine wave” and eventual flat line. However, experience teaches that hyperK comes in many forms. The most devious is the severe symptomatic bradycardia. All too often a patient will come in for bradycardia and hypotension, then get started on the path to a pacer, only to find out their K was 10! Don’t let this happen to you! Remember the mantra:

O WATA GOO SIAM… wait no not that one this one:

Bad Brady? Give Gluconate”(Ca+2that is)

Let me repeat that “Bad Brady? Give Gluconate”( Ca+2 that is). That’s right for BAD BRADYcardia GIVE calcium GLUCONATE. Or maybe better:


Whatever it takes for you to remember, check that K when you see symptomatic bradycardia and if you don’t have time for it to result give a trial of calcium gluconate before you put in that pacer!



While we are on the topic of electricity, how good is the ECG for detecting hyperK? It depends what you are calling “ECG Changes”. Studies looking at this topic have shown that hyperK can present without any ECG findings. One study found peaked T-waves in only 34% of ECG’s and potassium levels >6.5 mEq/L1. There are also case reports of patients with potassium levels >10 mEq/L and ECG’s non-diagnostic for hyperkalemia2.  In another study it was not until the serum K > 8 that they found 100% concordance between hyperkalemia and ECG change3. So what are some predictors of hyperkalemia in the ECG? This study3suggests the best predictors by Risk Ratio (RR) for hyperkalemia are QRS prolongation (RR 4.74), junctional rhythm (RR 7.46), and bradycardia less than 50 bpm (RR 12.29) (See Table 1). Importantly, these were the ECG changes that were predictive of adverse events in hyperkalemia. Interestingly peaked T-waves in this study had an RR of 0.77[a]3.


Table 1. ECG changes associated with Hyerkalemia3

ECG Finding Risk Ratio, 95% Confidence interval
Bradycardia (HR<50) 12.3, 95% CI [6.69-22.57]
Junctional rhythm 7.46, 95% CI [5.28-11.13]
QRS prolongation >111 4.74, 95% CI [2.01- 11.15]
Peaked T-waves 0.77, 95% CI [0.35-1.70]



We all have that picture in our mind of who gets hyperkalemia but I want to talk about one group in particular that can be at a special risk. Patients with cardiac devices (pacemakers/AICDs) in addition to the typical cardiovascular collapse can have additional problems. Hyperkalemia can precipitate pacemaker problems specifically widening of the QRS, failure to capture, and delay of the interval from the pacemaker stimulus to the onset of depolarization 4.



OK, So now on to the good stuff! The treatment can be divided essentially into 3 phases, which I have dubbed: PROTECT, PUSH, PURGE (mostly because I enjoy  the alliteration[b]).

Hyper K algorithm

PDF VERSION: Hyper K algorithm-2


The first commandment of treating hyperkalemia is to PROTECT(and don’t covet) this myocardium! Calcium is the mainstay of treatment to protect the cardiac cells from the electrical disaster that is hyperkalemia. Calcium gluconate is typically the first line treatment given the fact that there is less elemental calcium than its partner calcium chloride. This becomes both its advantage and hindrance. The gluconate will not likely sclerose the veins given its concentration. Furthermore, it wont cause tissue necrosis (the opposite of helping) or thrombophlebitis unlike the chloride form. However, it may need to be repeated since it contains a third less the calcium than the chloride form. Strangely enough even in the year 2018, the optimal dose of calcium gluconate isn’t known5, however usually recommended is 10mL or 1g IV. There used to be some lore that the gluconate would require liver activation however both animal and human studies have shown that this is not the case even in liver failure5. Therefore, this is unlikely an issue. Due to the potential for harm, the chloride form is only recommended in the case of cardiac arrest or in the presences of a central line.  Calcium may be re-dosed twice based upon expert consensus5, 6.


The second commandment of the algorithm; thou shalt PUSH thine K into thine cells. By pushing the K back into the cells you are merely hiding the K from the now excited myocardium. Remember, this is only a temporary fix. Potassium is pushed into the cell using a beta-2 agonist such as albuterol. Catecholamines work on the sodium-potassium ATP-ase pump. There is nothing special about albuterol (sorry albuterol), any catecholamine will do. However, albuterol is probably the safest and the easiest to administer. Epinephrine could do the same but would have too many side effects so its not really used. The does of albuterol is big however 10-20mg nebulized. These doses can cause a decrease of serum K+ by 0.6 mEq/L within 30 min and 1.0 mEq/L 1 h after administration for 10mg and 20 mg, respectively5. Tell your patient to expect a few jitters with this and consider that up to 40% of patients on oral beta-blocker therapy may be resistant to this therapy. However, predicting who gets this is impossible. The second drug to accomplish this PUSH is insulin given with glucose to prevent hypoglycemia. Insulin can decrease K+ by 0.6–1.2 mEq/L 5, with an onset of action about 15 min, peak around 30-60 min, and last about 4 hours6.  Insulin/glucose combined with albuterol appear to have a synergistic effect5. The last treatment is controversial. The use of 8.4% Bicarbonate has long been held as the go to treatment. Recently, however, the thrill is gone. There is insufficient data showing benefit for bicarb. Several studies reported that sodium bicarbonate did not lower serum potassium significantly or promptly. In one (poorly done) study 1 mEq (1 amp) of bicarb decreased serum K only by 0.15 mEq/L 5. No study has found immediate reductions in serum K+ and the effects may be not be observed until 4-6 hours later5–7. Sodium bicarbonate may expose patients to a large fluid load, hypernatremia, and metabolic acidosis. Therefore, sodium bicarbonate should no longer be the first line therapy for hyperkalemia6. Bicarb may be useful when patients are acidotic or hypovolemic requiring a fluid load given its large amount of sodium6, 7. Table 2 is a summary of the PUSH therapies.

Table 2. Therapies to PUSH K intracellularly.

Calcium (either) 10 ml Immediate 30 min N/A
Albuterol 10mg 25-30 min 1 hr 0.6
Albuterol 20mg 30 min 2 hr 1.0
Insulin 10-20 mg 15 min 4 hr 0.6-1.2
Bicarbonate 4-6 hrs 4-6hrs 0.15?


Obviously, giving doses of insulin can result in a decrease in blood glucose and even life threatening hypoglycemia. Therefore glucose is given in conjunction with insulin. The question is how much insulin and how much glucose? No one knows the answer to this question. Many different schemas have been suggested. Altering the insulin dose has been suggested; from ultra short acting insulin to infusions of insulin. Additionally, altering the amount of glucose; using a continuous infusion vs. bolus has also been suggested. There is no consensus between expert panels on the dose or route of insulin or glucose. Frequent monitoring for hypoglycemia is definitely recommended. One poorly done before and after study suggested 5 units of insulin in ESRD patients (see my post on that study here). One conservative dosing regimen is given below in table 3.  


TABLE 3. Insulin/Glucose Dosing options

Insulin Options Glucose Dose Glucose Re-Dose Lab Monitoring
Regular 5 U

(Consider in ESRD)

25g D50

(1 amp)

None BS q 1 hr x3

BMP 1 hr post insulin

Regular 10 U 25g D50

(1 amp)

25g D50 @ 1 hr post insulin BS q 30 min x 6

BMP 2hr post insulin

Regular 10 U

(Consider if glucose <100 mg/dL)

D10W gtt @

200 ml/h infusion

None BS q 1hr x3

BMP 2hr post insulin

ESRD = End Stage Renal Disease, BMP = Basic Metabolic Panel, glucose mg/dL


This phase will depend on whether or not the patient has working kidneys. In the case that the kidneys are not working, there is a post obstructive uropathy, or there is oliguria; hemodialysis (HD) is the answer (or CRRT). This means placing a call to your friendly neighborhood nephrologist and dialysis nurse and getting them to come out. HD is also the gold standard treatment. Although there are no definitive studies on the timing or dose of HD. Recommendations for initiation can include: persistent ECG changes, poor response to treatments, and severe AKI. Kayexalate (Sodium PolyStyrene/SPS), once the mainstay of treatment, has fallen out of favor. Multiple consensus panels have endorsed not using it 6, 7.  One such panel recommended “that all other treatment options be exhausted prior to using this [SPS] potentially harmful therapy with little evidence of efficacy”6. Subsequently, the FDA has added a warning for colonic necrosis to the Kayexalate labeling when co-administered with sorbitol8. If, on the other hand, the kidneys are working then loop diuretics may be used at a dose of 20 mg (naive and CKD stage <3) or 40 mg (not naive or CKD stage ≥3).


On the horizon are new potassium binding medications. One expert consensus panel[c]recommended using Patiromir in the acute setting7despite ZERO studies performed in the ED.  Patiromer is an FDA approved new potassium binder that exchanges calcium for potassium for treatment of chronic hyperkalemia.  Side effects include binding oral medications, constipation, and hypomagnesaemia.  Furthermore, its effect is not reached until about 7 hours. Another possibility is the yet unapproved Sodium zirconium cyclosilicate (ZS-9). In a study of 45 patients with serum potassium concentrations of at least 6 mEq/l, 10 g of ZS-9 reduced the serum K by 0.4 mEq/l at 1 hour, by 0.6 mEq/l at 2 hours, and by 0.7 mEq/l at 4 hours9.


One last item to tackle is the “Stone Heart” condition. The “stone heart” theory ascribes calcium as the precipitating condition in which the heart is unable to contract. This occurs when a patient with hyperkalemia is given calcium while currently taking digoxin. The thought is that this may be due to the failure of diastole from calcium binding to troponin and the heart freezes like a stone. This has been “romanticized” into lore. Besides how can one deny a sexy name like “Stone Heart”, it rings of truth! Thus far however, not animal studies, case reports, nor retrospective reviews have found an association of mortality with administration of calcium for hyperkalemia in occult digoxin toxicities 10–12.  The romance may be gone. It was a good run “Stone Heart”. I’ll miss you most of all.


How bad is Hyperkalemia? That question can be seen in the graph below from a study by  Einhorn in archives of internal medicine 2009. This study looked at 66,259 Hyperkalemia events (not patients) in a VA population. They found a 2.4% incidence of death WITHIN ONE DAY (yes one day!). The found that in the patient with no chronic kidney disease a serum K between 5.5 and 6.0 had an OR of death within 24 hours of 10 and above 6.0 had an OR of death of almost 32! Those are huge numbers. In actual cases the group with no CKD had an inpatient mortality of 3.2% for K 5.5 to 6.0 meq/L and 8.6% for those with K greater than 6! For the CKD group (as a whole) it was 1.8% for K between 5.5 and 6.0 and 4.8% for those with a k >6.0. Those numbers while about half of these with chronic kidney disease still represents a very high mortality! Thus Hyperkalemia should be taken very seriously and both treated and admitted unless they are very reliable or have good follow up. Screen Shot 2019-03-19 at 10.29.59 PM



  1. Freeman K, Feldman JA, Mitchell P et al. Effects of presentation and electrocardiogram on time to treatment of hyperkalemia. Acad Emerg Med 2008; 15, 239-249.
  2. Szerlip HM, Weiss J, Singer I. Profound hyperkalemia without electrocardiographic manifestations. Am J Kidney Dis 1986; 7, 461-465.
  3. Durfey N, Lehnhof B, Bergeson A et al. Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events. West J Emerg Med 2017; 18, 963-971.
  4. Barold SS, Herweg B. The effect of hyperkalaemia on cardiac rhythm devices. Europace 2014; 16, 467-476.
  5. Long B, Warix JR, Koyfman A. Controversies in Management of Hyperkalemia. J Emerg Med 2018; 55, 192-205.
  6. Rossignol P, Legrand M, Kosiborod M et al. Emergency management of severe hyperkalemia: Guideline for best practice and opportunities for the future. Pharmacol Res 2016; 113, 585-591.
  7. Rafique Z, Weir MR, Onuigbo M et al. Expert Panel Recommendations for the Identification and Management of Hyperkalemia and Role of Patiromer in Patients with Chronic Kidney Disease and Heart Failure. J Manag Care Spec Pharm 2017; 23, S10-S19.
  8. Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective. J Am Soc Nephrol 2010; 21, 733-735.
  9. Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: something old, something new. Kidney Int 2016; 89, 546-554.
  10. Hack JB, Woody JH, Lewis DE, Brewer K, Meggs WJ. The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model. J Toxicol Clin Toxicol 2004; 42, 337-342.
  11. Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med 2011; 40, 41-46.
  12. Van Deusen SK, Birkhahn RH, Gaeta TJ. Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity. J Toxicol Clin Toxicol 2003; 41, 373-376.


[a]For those of you keeping score you might say with an RR of 0.77 peaked T-waves are PROTECTIVE of adverse events of hyperkalemia but this is probably because we are used to looking for peaked T-waves so physicians were more likely to recognize these and treat earlier rather then it being protective of adverse events in hyperK

[b]I always get confused between alliteration, consonance and assonance. So FYI, the difference is in where the rhyme occurs. Alliteration it’s the beginning (e.g. Larry likes Laurie), consonance it’s the end (frog on a log), and assonance its the middle (e.g. rock in a box was locked)

[c]This panel discussion was funded by Relypsa and facilitated by Magellan Rx Management. Relypsa is the manufacturer of Veltassa (patiromer). Rafique is a principal investigator for Relypsa and serves as a consultant for Instrumentation Laboratory, Magellan Health, Relypsa, and ZS-Pharma. Butler serves as consultant for Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, CardioCell, Janssen, Merck, Novartis, Relypsa, and ZS-Pharma. Lopes and Farnum are employed by Magellan Rx Management. Rafique designed the management protocol for this panel discussion and contributed to the writing and editing of this report document. The other authors report no conflicting interests.


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