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HyperK and Shades of Grey: Myths and Facts about Hyperkalemia Part II

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Today we continue our discussion about the myths and facts of hyperkalemia with Dr. Brooks Walsh, author of the Mill Hill Ave Command blog. We also feature contributions from Dr. Stephen Smith, of Dr. Smith's ECG Blog.

If you would like to refresh your memory on Part I visit here.                                         

Dr. Walsh and I spoke about why he thought hyperkalemia presented such a challenge for EMS providers:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong and clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true."

With that said, let us continue with Myths and Facts about Hyperkalemia Part II:

 

Myth: The ECG shows a predictable sequence of changes as the potassium level increases

Experiments done on (presumably) healthy animals demonstrated a progression in ECG derangements as potassium levels were experimentally raised. A number of textbooks and review articles repeat this result, even though numerous human clinical studies have failed to replicate a linear relationship between the potassium level and specific ECG findings.

For example, one review article, much referenced in the EM literature, presents a table describing the correlations between potassium levels and expected ECG findings.

 

But the literature is full of case report that argue against such tidy correlations: here's a case of a woman with a potassium of almost 8, and complete AV block  but no QRS widening or T-wave tenting; here is a similar case with a K of 7.5; we even see that a patient can develop an AV block with a K level of just 5.5! On the other hand, here's a case of complete AV block with a narrow QRS, but a potassium of just 6.4.

We asked Dr. Stephen Smith about his experiences with this issue. He agreed and said he has seen patients go into VF after having only peaked T waves. You can see examples of this here.

So it seems better to avoid thinking that you can determine a specific potassium range on the ECG, but rather that it can suggest a generally elevated level. Any of the "expected ECG abnormalities" can occur at any level of potassium.

 

 

Myth: Calcium is a dangerous medication

Make no mistake – IV calcium can be a potent drug, but with potential benefits. And you should always refer to your local guidelines/protocols for the last word on when you can & should give it.  

But that being said, there is some concern voiced by clinicians about administering "one mustard box." Let's talk about 2 big concerns that people seem to have with giving calcium: skin necrosis and digoxin toxicity.

So, how worried should you be about skin necrosis? EMS usually carries calcium chloride, which has some potential to cause problems if it extravasates (calcium gluconate has a lower risk, and can be given subcutaneously for some problems). As a result, many people have a lot of concern about administering the medication, fearing the risks if the IV leaks or fails. 

Well, yes, you must assure yourself that you have a patent, free-lowing line in a big vein! But on the other hand, you have already been taking risks with injecting dextrose 50% and sodium bicarbonate, as both are known to cause skin necrosis. 

For example:

 

 Ann Emerg Med. 2006;48:236

This patient came into the ED with hyperkalemia, and was treated with IV insulin and dextrose (no calcium). 

Or how about this hand?

 

Ann. Surg. – November 1975

That's a neonate who was getting a D10% drip in his hand.

There are a small number of case reports of bad calcium extravasations, but that rare risk must be balanced against the immediate, and unpredictable, risk of life-threatening arrhythmias.

Some EMS-toxicologists may also point to the historical concern with digoxin toxicity, that calcium infusions could provoke a "stone heart," or cardiac tetany. A recent pig study had cast a lot of doubt on that thinking. And then a retrospective study was published in 2012 by Levine et al., which looked at patients with digoxin toxicity, some of whom were also treated with calcium. They found no effect on mortality – no "stone heart ' – and another myth was dispelled.

 

 

So you should feel comfortable giving calcium when you think you're dealing with hyperkalemia. But don't just take my word for it – listen to some medical experts!  

For example, from a nephrology paper:  

 "When uncertain of the importance of a raised potassium level, it is prudent to go ahead and administer calcium gluconate, as the downside risk is minimal."    Aslam 2002

Again, ECG master Stephen Smith:

"[G]iven the fact that calcium therapy is benign… when I suspect hyperkalemia I just given calcium immediately, even before I get the potassium back. … There are so many ways the ECG can manifest with severe hyperkalemia — life-threatening hyperkalemia. Again, the treatment is benign, and cheap! So how many life-threatening diseases can you treat benignly and cheaply?"

You can hear Dr. Smith expand on this by listening to him on  EMCRIT podcast 42.

 

 

Practical point: How to give albuterol for hyperkalemia

Albuterol may in fact have a role in the prehospital treatment of hyperkalemia. It works by shifting potassium from the serum into the cells.

Consider this case study abstract:

"Growing evidence suggests that there may be a role for albuterol in the treatment of patients with severe hyperkalemia…β2 agonist administration was found to be safe and was associated with a significant decrease in serum potassium levels. Therefore, β2 agonist therapy should be considered as an adjunctive treatment for patients with severe hyperkalemia."

Or this:

"In the doses used, nebulized albuterol therapy resulted in a prompt and significant decrease in the plasma potassium concentrations in patients on hemodialysis, and caused no adverse cardiovascular effects (Allon).

You can use an albuterol in a nebulizer, or can use levalbuterol if that's what you have (Pancu). And it doesn't have to be a neb – it can also be an MDI with a spacer (Mandelberg).

But how much to we give? Of the medics who are savvy enough to want to use Albuterol to treat hyperkalemia, few of them know the effective dose needed to treat.

You can give 5mg (McClure), 10, or even 20mg (Allon), if you are using a nebulizer. The dose of 10-20 mg seems to be the dose most often used. 

Perhaps you realize that the "standard dose" we use to treat bronchoconstriction is 2.5mg/3ml. It is problematic to consider loading at least 4 doses into a small volume nebulizer. That's not really going to work. 

Albuterol does come prepared as 2.5 mg/0.5ml. Now we are talking about 2 ml's, which is much easier to manage and a better choice for treating hyperkalemia.

Is it worth stocking multiple doses of Albuterol? Perhaps. It is not going to be the first line treatment for hyperkalemia, so the decision will vary by system. Needless to say, if you are going to treat with Albuterol, make sure you have an effective way to do it.

 

We hope you have enjoyed this short series on the Myths and Facts about Hyperkalemia. 

My thanks again to Dr. Brooks Walsh, as well as Dr. Stephen Smith for their valued contributions.

As usual, all comments and opinions are encouraged!

Posted by on January 14, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

HyperK and Shades of Grey: Myths and Facts about Hyperkalemia Part I

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Happy New Year everybody!

We start 2013 with a continuation of our discussion about the field treatment of hyperkalemia. 

It might be helpful to review the first part of the discussion," HyperK and Shades of Grey" here. 

We are fortunate to have as a guest contributor Dr. Brooks Walsh of the Mill Hill Ave Command blog. An advocate of prehospital medicine, Dr. Walsh offers shares "Myths and Facts" of hyperkalemia with us. My sincerest thanks him for his valued contributions! 

I asked Dr. Walsh why he thought hyperkalemia presented such a challenge for EMS providers. Here is what he had to say:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong & clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true.

But rather than curse the darkness, I wanted to go over some newer perspectives on hyperkalemia. Now, I don't want to simply reiterate all the great material that Dr. Weingart talked about on EMCRIT, so you really ought to download his great podcasts on the treatment of hyperkalemia and on why Kayexalate is likely ineffective, if not outright dangerous. The podcasts are real short, so just play them right now.

With that said, I'd like to review a few topics in hyperkalemia that deserve more attention:

 

Myth: Dialysis patients tolerate hyperkalemia better than other people.

Medicine is funny. I mean, there are "facts" that "everyone knows," but that are surprisingly hard to prove in studies. This is sort of one of those kind of facts, with very little evidence, and plenty of "real world" experience. Should we continue to believe it?

Maybe. It kind of depends on what we mean by "tolerate." If we mean "don't show ECG signs of hyperkalemia," then maybe dialysis patients do "tolerate" hyperkalemia better than other people. 

It's kind of hard to answer this definitively, though, since ECG signs of hyperkalemia, especially in the moderate range (e.g. < 6.5), are often absent on the ECG on all patients. We just don't see that many patients, dialysis or no, with severe hyperkalemia. Even in a study that looked only at dialysis patients, the vast majority had a K < 5.2, and ECG changes were accordingly infrequent.

But it may also be that dialysis patients, in fact, do show fewer signs of hyperkalemia on the ECG than do other people. A study done back in 1967 looked at dogs that received IV potassium slowly or quickly (but ending up at the same blood level). The faster infusions caused more ECG and hemodynamic effects. It is possible that ESRD patients, with a presumably slow increase in potassium levels, show fewer ECG changes than, say, a patient with acute rhabdomyolysis.

But the ability to avoid ECG changes isn't the "tolerance" we care about in hyperkalemia - we really care about the potential for patients to go into cardiac arrest. Hyperkalemia, regardless of ECG signs, puts the patient at risk for fatal arrhythmias. If you have either lab results or ECG evidence of hyperkalemia, that patient needs to be treated immediately – on that, most experts agree. I couldn't find any mention in the literature that suggests otherwise. For example:

                   "We emphasize that despite the absence of ECG changes of hyperkalaemia in ESRD, hyperkalaemia is still a     potentially life-threatening condition." –Aslam 2002

Or

"Some experts advocate calcium administration in patients whose serum potassium is >6.0–6.5 mm, even in the absence of EKG changes." –Putcha 2007 

 

Myth: If the ECG doesn't show QRS widening, then the patient is at low risk.

Some clinicians are under the impression that you can wait to treat the hyperkalemia until the QRS is "incredibly widened," showing huge sine-waves.  An ECG that shows "just T-waves" is presumably at lower risk, in this view.

Except that's not how it works, according to the experts. As these nephrologists explain:

                 "Five medical textbooks (two nephrology, two internal medicine, and one emergency medicine) advocate calcium gluconate in all hyperkalemic patients with EKG changes. "

Or this critical-care nephrologist:

                "It is apparent that neither the EKG nor the [potassium level] alone is an adequate index of the urgency of hyperkalemia,… hyperkalemia should be treated emergently for 1) K > 6.5 mmol/L or 2) EKG manifestations of hyperkalemia regardless of the [level]." –Weisberg 2008 "Management of severe hyperkalemia"

We asked Dr. Smith about his experiences with this topic, whether he has seen patients arrest without going through the ECG transition to widened, sine wave ECGs. His response as well was that "I have seen v-fib with peaked T waves only" on the ECG.

Stay tuned for "Myths and Facts Part II"!

 

Posted by on December 31, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

Top 10 myths about prehospital 12 lead ECGs

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A recent thread at JEMS Connect has reminded me how many myths are circulating about prehospital 12 lead ECGs.

1.) If you're close to the hospital, performing a prehospital 12-lead ECG is a waste of precious time.

The prehospital 12-lead ECG is an important triage tool. The closest hospital is not necessarily the closest appropriate hospital! In addition, just because you're close to a PCI hospital doesn't mean you can't save 15 minutes of ischemic time by giving the hospital early notification that you've identified a STEMI patient.

2.) Prehospital 12-lead ECG monitors are incapable of capturing diagnostic quality 12 leads.

As long as the low frequency (high pass) filter is set to 0.05 Hz (which happens automatically when you capture a prehospital 12-lead ECG) then you will record accurate ST segments. A more important issue is data quality and lead placement, which is a training issue (and a credibility issue).

3.) It's important for the ED staff to perform another 12 lead ECG to confirm that it's really a STEMI.

I don't care if the ED staff performs another 12 lead ECG as long as the cath lab has already been activated based on the prehospital 12-lead ECG and they are already taking advantage of parallel processing (for those patients who show obvious STEMI in the field). However, there's nothing "magic" or "special" about the ED's 12 lead ECG. Serial ECGs can be extremely important, but mostly for suspected ACS patients with nondiagnostic (or borderline) ECGs on initial presentation. If they're waiting for their own 12 lead ECG before activating the cath lab, then they're wasting valuable time.

4.) If ST segment elevation resolves by the patient's arrival at the hospital, then it's not a STEMI, and the patient doesn't need an emergent cath.

Should you wait for the cardiac biomarkers to come back positive before sending the patient to the cath lab? I'm not sure that's a good idea. The case I posted last month shows that even when ST segment elevation resolves by arrival at the hospital, the patient can still have an occlusive thrombus in an epicardial coronary artery.

5.) Nitroglycerin is contraindicated for patients with suspected right ventricular infarction.

Not all patients with inferior STEMI have RV involvement, and not all patients with RV involvement develop the hypotensive syndrome. Consider the vital signs, the heart rhythm, and the physical exam, and treat accordingly. Sometimes the patient just needs a preemptive fluid bolus.

Update: The new 2010 AHA ECC Guidelines say to use NTG "with extreme caution, if at all" in the setting of suspected right ventricular infarction. It's not quite "contraindicated" but that's a strong statement! What do I say? "Use your brain!"  There's no substitute for sound clinical judgment! 

6.) Prehospital 12-lead ECGs are important tools to help distinguish between VT and SVT with aberrancy.*

If you're using QRS morphology to "rule in" VT, then be my guest! If you're using it to justify giving a CCB to a patient with a wide complex tachycardia, then I think you're crazy. That's not to say that I don't capture 12 lead ECGs for all patients who present with cardiac arrhythmias, because I do. Documenting the arrhythmia is very important. Sometimes it even helps with the diagnosis. But I do not base my treatment decisions on QRS morphology and neither should you.

7.) If the hospital ignores the prehospital 12-lead ECG then there's no point in performing one.

I'm sympathetic to this view, but it's a defeatist attitude. You should capture a prehospital 12-lead ECG with the first set of vital signs, prior to oxygen and nitroglycerin. That way, when you "clean up" the 12 lead ECG prior to arrival, you can hand them a picture of what the patient looked like prior to your intervention. It's hard to imagine that a board certified EM physician would ignore that. In any case, the ECG should be made a part of the patient's record, because the cardiologist may care.

8.) It's easy to identify STEMI on the prehospital 12-lead ECG.*

Technically this isn't a myth. It is easy to identify a home run STEMI on the prehospital 12-lead ECG. However, that should not be interpreted to mean that reading a 12 lead ECG is easy, or that just because you've been taught to identify an obvious STEMI with reciprocal changes that you can read an ECG as good as a physician. You might be able to, but you probably can't. Identifying ST segment elevation on the 12 lead ECG is easy! Differentiating between true STEMI and the STE-mimics can be difficult. Sometimes very difficult.

9.) It's impossible to identify STEMI in the presence of LBBB.

Sure you can. You can use a modified form of Sgarbossa's criteria and you can perform serial ECGs. A moving ST segment suggests dynamic supply vs. demand characteristics consistent with ACS. Is it difficult? It's more difficult. Impossible? Hardly.

10.) Axis determination is "nice to know" information but you don't really "need to know" it.

That's like saying "paramedics don't really need to know how to read a 12 lead ECG." That's fine, if that's really your opinion. Just don't complain when you're asked to transmit the ECG for physician interpetation.

* Technically not a myth but requires qualification.

Posted by on April 21, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,