>> Update: For a new take on kayexalate, see Mak Moayedi's Lecture
Hey folks. As I get ready for ACEP, I just wanted to get a quick podcast put up. One of the listeners requested an episode on the treatment of hyperkalemia in the ED.
There was a fantastic article published in Critical Care Medicine on the topic by a Dr. Weisberg. I go through my management and discuss some of the pearls from the article.
Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51.
Additional References added Feb 2012
ECG is insensitive and non-specific for severe hyperkalemia issues; essentially is crap (Clin J Am Soc Nephrol 3: 324-330, 2008). ECG peaked T waves, that resolved after K normalized were noted in only 1 of the 14 hyperkalemic patients who went on to have arrhythmia or cardiac arrest. Only half of them had any T-wave changes.
Calcium Gluconate doesn't require Hepatic Metabolization before it is active
[cite source='pubmed']2360741[/cite]Hyperkalemia and the ECG
Slow A-Fib
from Steve Smith's Blog
Learning Points:
1. When a patient is bradycardic, especially if irregular, one must always think of hyperK and one must get a 12-lead ECG.
2. One must recognize this pattern as hyperK
3. Calcium's effect is almost miraculous
4. Slow atrial fibrillation implies an sick AV node, or one affected by electrolytes, ischemia, or medications/drugs. Otherwise, the ventricular response should be fast.
Furosemide Dosing
Lasix Naive: 1 mg/kg
Prior Use: 1.5 mg/kg
Updates
- Fantastic EMPharm Review with my bud, Bryan Hayes
- Lactated Ringers is Safe and Probably Recommended
- This recent article showed a 100% preceding of bad events by altered ecg
- RCT of 7-day course of kayex1
- Risk of Hospitalization for Serious Adverse Gastrointestinal Events Associated With Sodium Polystyrene Sulfonate Use in Patients of Advanced Age. JAMA Intern Med. 2019 Jun 10. doi: 10.1001/jamainternmed.2019.
0631.
and now to the podcast…
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The Trueginator wrote me with this ACEP Abstract:
Beneficial Effect of Calcium Treatment for Hyperkalemia Is Mediated by Calcium-Dependent Conduction, Not “Membrane Stabilization”
Abstract seems to indicate we should be saying, “cardiac protection” instead of “membrane stabilization.”
As a pharmacist, it is the medication of choice, being a membrane stabilizing agent, but pushing it to fast can lead: cardiotoxicity, hypotension, local thrombophlebitis, tingling sensation, calcium taste, flushing, nausea, vomiting, sweating and
irritation and potential for extravasation (especially if it is a peripheral stick)
Mark,
I believe he was referring to Calcium Gluconate.
thanks for reviewing hyperK, as this comes up virtually every shift. I disagree that the ECG should not be the initial intervention when potassium is reported as high. The Weisberg paper supports the assertion that “the first cardiac manifestation of hyperkalemia may be ventricular fibrillation” with a single reference, a study by Dodge from 1953. The Dodge study is amazing. These guys gave a huge slug of oral potassium to a bunch of different types of subjects and watched the ECG. They remark on the ECG changes across all these subjects in excruciating detail for many pages, and then, at the end of the paper, they mention that, by the way, an hour after they gave their 15 grams of KCl, one study subject XXXXX DIED. “The fatality occurred in a 47 year old white man who complained of exertional dyspnea for nine years and intermittent claudication for three years. There was no history of angina pectoris, chest pain, or congestive heart failure. His cardiac examination was entirely normal with the exception of the electrocardiogram which showed a normal QRS loop but an abnormally directed T vector, producing inverted T waves in Leads I and Va to Vg. One hour… Read more »
I think this excerpt sums it up best These classic ECG changes, which have been well described in the literature, are not always present.3–5 The relation between ECG changes and serum potassium will vary between people. It is therefore important to realise that the ECG is not always a reliable test for mild to moderate hyperkalaemia.4 Even in severe hyperkalaemia, only minimal changes may be seen on the ECG.5 (from Emerg Med J 2002;19:74-77) 3. Yu AS. Atypical electrocardiographic changes in severe hyperkalaemia. Am J Cardiol1996;77:906–8. 4. Wrenn KD, Slovis CM, Slovis BS. The ability of physicians to predict hyperkalaemia from the ECG. Ann Emerg Med1991;20:1229–32. 5. Martinez-Vea A, Bardaji A, Garcia C. Severe hyperkalaemia with minimal electrocardiographic manifestations: a report of seven cases. J Electrocardiol1999;32:45–9. I believe (I hope) in the podcast I made clear that we should be sure the elevated potassium is not spurious before treating with calcium. But once you are assured of that, I maintain that high Ks (as to what is a high K, it probably depends on the scenario) should probably receive calcium. I was taught the same as you and I believed that a normal EKG in the setting of very high… Read more »
you CENSORED me? sheesh.
my only concern with CaCl2 vs. CaGlu is extravasation. a rare but serious complication, and if there is no chance the patient will benefit…
I understand that the ECG does not correlate well with the level, but the point is which predicts a patient-oriented outcome, the level or ECG?
The patient oriented outcomes are dysrhythmia and death. It would seem that the ECG is specific, but insensitive for these patient oriented outcomes.
I think we can agree that if the patient looks well, not-so-high K (6.0-7.0), you believe the lab is real, and no EKG changes, that if you are going to give calcium, it should be in the form of calcium gluconate.
Scott, do you have any knowledge of whats new with IV calcium along with digoxin. The old myth warns about “stone heart” but I’ve heard evidence is weak and based on very old cases in the literature.
Anyone?
A listener wrote to send me an article demonstrating that CaGluc doesn’t require hepatic breakdown to achieve its ionized form. Great job myth busting, Greg! Article is
Anesthesiology 1990;73:62.
Have gotten a few questions regarding Digoxin and Hyperkalemia. Here is the answer from one of my crit care pseudo-fellows:
On Tue, Oct 5, 2010 at 5:17 AM, Amanda Holland Yang wrote:
So, according to Levine in the journal of emergency medicine, don’t worry about the calcium… they did a chart review of all pts diagnosed by a clincian with dig toxicity. 23 had gotten calcium, and there was no increased incidence of life threatening dysrhythmias or death. The poison center and north shore had a problem with this in their follow up letter though, arguing that maybe the patients weren’t truly dig toxic, just had elevated levels.
Levine says that if someone is known to be dig toxic, obviously just give them digibind rather than calcium, but if you are treating someone for hyperkalemia and don’t know that they are on digoxin, it should not be a problem. I think this sounds reasonable.
Levine – THE EFFECTS OF INTRAVENOUS CALCIUM IN PATIENTS WITH
DIGOXIN TOXICITY Journal of Emergency Medicine
Very good!! Many clinicians rely only on EKG as an indicator, also the tx for the fast remediation is the Ca for membrane stabiliztion, specifically the gluconate salt. The myth of grab NAHCO3 although could be use as an adjunct, depending on the clinical situation, has to be dispelled. Very often, there is an overkill, then the pendulum goes to the other side, and u may see hypokalemia- so prudent use of these pharmacological interventions and understaning of mechanism of actions, onset and duration is critical.
I was treating a patient with hyperkalemia (7.2) and bradycardia. I gave 3 amps of calcium gluconate, which my nurses refused to push. They said they only had ever given one amp.
The article used for this podcast states the dose of calcium is 10ml of Ca gluconate. However, if I would normally use 10ml of CaCl, then shouldn’t I give 3 amps of calcium gluconate?
1 amp of CaCl or 3 amps of CaGluconate just as you say. Thing is CaGluconate should not be pushed. Each amp should drip in over ~10 minutes. Perhaps this is why the nurses balked?
Thanks for the quick response. I did make a mistake as I pushed it instead of dripped it in. Glad there were no adverse outcomes
The nurses balked because they said they had never given 3 amps before, only 1. What confuses me is that the table posted on hyperkalemia above states to give 10ml (1 amp) of calcium gluconate.
Pushing CaGluc just results in occasional hypotension. Even if it happens, you can fix it with some fluids and it will be short-lived. So no big deal. The comments Mark makes below actually mostly apply to calcium chloride which can cause irritation and thrombophelbitis in extravasation. CaGluc can actually be given sub-q for HF toxicity and is ok in extravasation.
The dose in the table is for immediate stabilization, but I would give at least 2-3 grams (amp) total.
so in essence, cagluc is the agent of choice? faster onset than the cloride salt, no hepatic breakdown to become pharmacodynamic, no tissue necrosis issues in peripherial sticks- should be on our rigs opposed to cacl then, if pts are presenting with hyperkalemia, and in arrest and the medic is doing their H and T and found a pt may have some high T waves (PEA arrests) in consult with Medical control,
Calcium Chloride if they are crashing because you can slam it in, but you better have a good vein. CaCl also agent of choice if you have a central line. Pretty much everyone else, CaGluc is prob. safer.
Hi Scott,
I have been listening to your program and has change my perspective in medicine. I am family medicine trained with fellowship in sports medicine. I do sports medicine in my newly open private practice and work some nights in the ER. I listen to your podcast on hyper k . Great. You made a comment about given insulin subcutaneously. Do you give insulin subq or IV in the ER in patient that has hyperglycemia after fluid and normal potassium that is not in Dka or hyperosmolar nonketotic hyperglycemia?
Thanks for your respond in advance
C. Sillah
Macon , Ga
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Scott,
Can Calcium Chloride be given safely through an IO or is it risky like peripheral stick?
Thanks
Jeff
Party line is anything that can go IV can go IO, but you better be pretty sure of your IO being properly placed before giving CaCl. May be safer to use gluconate in these cases–that’s what I do unless it is a cardiac arrest.
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Hey Scott,
Wicked podcast as always, and I’m wondering about another possible myth with digoxin toxicity. I’ve been told about the “irritable myocardium” and no placement of CVLs other than femorals, as you could precipitate VF by tickling the already unstable myocardium with an IJ or subclavian. I can’t find any literature on this, do you know anything to support it?
Thanks,
Chris
Seems like another old wives’ tale. i have heard the same thing, but have never seen any evidence.
Hey Scott, After looking it up and checking Rosen’s and Goldfrank’s, I came upon this article, which seems to be the basis for the argument of no IJs/Subclavians: CLINICAL TOXICOLOGY7 31(2), 261-273 (1993) I’ve attached the key excerpt from the discussion here as well: “Safety of cardiac pacing in the treatment of digitalis intoxication was assessed in 39 pacing-treated patients from Groups 1 and 3. Fourteen adverse effects (36%) were recorded. These iatrogenic accidents were pacing-induced arrhythmias (6 cases), pacing defects (6 cases), and infectious complications (2 cases). The six pacing-induced arrhythmias occurred during or just after insertion (1 ventricular tachycardia, 3 VF) or subsequent to pacemaker adjustment (1 VA after a brief pause of pacing to study the underlying rhythm; 1 VF during reduction of ventricular rate from 80 bpm to 60 bpm). The six pacing defects occurred after ambulance transport (1 VA), external cardiac massage (1 patient), or accidental removal of the pacemaker by a confused patient, while no causes were found in three cases. The two infectious complications were staphylococcus epidermidis septicemias. One septicemia was complicated by fatal septic shock. Five out of these accidents (13 %) had a fatal outcome (2 VF, 2 VA, 1 septic… Read more »
Thanks.. Great discussion… what is the exact mechanism of Calcium in membrane stabilization ???
I know I am a little late to this post but I have seen references give doses up to 3 gms of Calcium Gluconate IV Push or 1 gram of Calcium Chloride. What I was trying to find if there was data to support these doses? I have tried to look at the AHA CPR guidelines back to 2000 and there is no reference of primary literature supporting them.
Thanks for the discussion and great job with the podcast.
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A patient with hyperkalemia and third degree AV block. which one should be the first priority- calcium gluconate or pacemaker??
Calcium chloride ASAP. No need for a pacer in most of these pts; the block resolves.
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In regards to the rate of administration of calcium-from the table in reference cited: the AHA guidelines reference: Shift potassium into cells: http://circ.ahajournals.org/content/112/24_suppl/IV-121.full Calcium chloride (10%): 500 to 1000 mg (5 to 10 mL) IV over 2 to 5 minutes to reduce the effects of potassium at the myocardial cell membrane (lowers risk of ventricular fibrillation [VF]) Although pharmacy guidelines may very, I believe that it is useful to reference the AHA source in support of one’s decision making. In terms of the evidence base that guides decision making in level and treatment, evidence based reviews indicate lack of evidence for many treatments example- Two studies investigated infusion of sodium bicarbonate for the management of hyperkalemia30,31 (Appendix 5). One reported a small absolute reduction in serum potassium from baseline of 0.47 (standard deviation [SD] 0.31) mmol/L (p = 0.001) at 30 minutes;31 in the other trial, there was no significant change in serum potassium at 30 and 60 minutes, relative to placebo.30 The trials of bicarbonate infusion had the lowest reduction in mean serum potassium among all single and combined modalities, including salbutamol and insulin. see: Management of patients with acute hyperkalemia Meghan J. Elliott, Paul E. Ronksley, Catherine M.… Read more »
I am glad you mentioned about using SC insulin rather than IV push insulin for routine hyperglycemia management, thank God! I’ve felt the same way for long time and it never made sense to see other docs pushing IV insulin to treat pure chronic hyperglycemia in ED. It never made pharmacokinetic sense to me. We don’t tell patients to get PICC line and push IV insulin at home forever for their diabetes every few hours during day and why are we pushing IV insulin for chronic hyperglycemia? It’s like pushing IV antihypertensives in ED to every anxious chronic hypertension patient who comes to ER every other week for hypertension after checking BP at Walmart automatic blood cuff machine during grocery shopping, as if that IV medicine at ER every other week is extremely essential to manage Pt’s chronic HTN. Thank you for validating my pet peeve and great blog again!
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