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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: , , , , , , ,

Hyper-K and Shades of Grey

40 comments

Good morning all…

It's a beautiful fall Sunday morning, and you and your partner are enjoying an nice cup of coffee. But of course, the tones go off, and you are called to the residence of a 52 year old female, "sick". You recognize the address, you've been there before. 

Upon your arrival, you find your patient sitting in a chair in the living room. You remember her. She is a dialysis patient. She does not look well. 

She complains of not feeling well. She says she is weak, and has slight shortness of breath. You don't see any labored breathing or accessory muscle use, and she is able to speak in full sentences for now. Her respiratory rate seems ok, as does her pulse.

As you are getting your history, your partner gets a set of vitals. 

She tells you that she wasn't feeling great yesterday, and missed her scheduled Saturday dialysis (she is on a Tues-Thurs-Sat schedule). 

She thought she would be ok until Tuesday, but it didn't work out that way. She woke up today feeling really rotten and has been progressively feeling worse.

In addition to her renal failure, she also has a history of hypertension and asthma. She has no allergies. She says she has been compliant with her meds, and denies any chest pain or other aches/pains.

Her vitals are as follows:

  • HR         78 regular
  • BP         158/94
  • RR         20
  • SpO2     94 on room air
  • Lungs    very slight expiratory wheezes, but she states she always has that
  • Skin       unremarkable

You acquire an ECG that looks similar to this one:

image credit

You begin packaging your patient.

You are 20 minutes from the closet community hospital.

 

TODAY'S MISSION:

I am assuming most of you will recognize the above condition and know the available treatments for it. 

So, that is not the question.

The questions are these:

Do we treat this patient prehospitally? 

To be clear, the question is not "could we" but "should we"?

If we did, What would we use and why?

Is there a benefit to treating in the field versus waiting to hospital arrival?

 

**There is no obvious "right" answer to this… So, let's discuss it and see where we get. Have at it folks!

 

Posted by on November 30, 2012 • Filed under: ems-topics, patient-management, Training, training-development • Tagged: , , , ,

82 year old male CC: Shortness of breath – Conclusion

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This is the conclusion to 82 year old male CC: Shortness of breath.

Let's take another look at the 12-lead ECG.

This ECG shows a severe bradycardia.

We need to ask a couple of very important questions.

Is the patient stable or unstable?

The patient is unstable. In fact, the patient is periarrest.

We cannot be lulled into a false sense of security because the NIBP reads 142/122.

In the first place, that's an extremely difficult BP to believe.

I've seen this happen on more than one occasion. The last was a patient with a ruptured abdominal aortic aneurysm. Radial pulses were absent but the NIBP was reading very similar to this case (very high diastolic pressure with a narrow pulse pressure).

I tried to confirm it manually but I was unable to auscultate a BP in the back of the ambulance. Of course, the air conditioner and generator were running and the sirens were blaring. Let's face it. Sometimes it's not easy to auscultate a BP or breath sounds in the back of the ambulance!

I trusted my instincts and gave a fluid bolus. It turned out that the NIBP had given a spurious reading.

As I have mentioned before, I absolutely despise the mantra, "Treat the patient not the monitor!" I think it's one of the most misunderstood (and overused and abused) sayings in all of EMS.

A much better alternative is, "Correlate the monitor to the patient's history and clinical presentation." 

It's easy to second-guess or criticize the actions of someone else. I wasn't on this call, but tossing around a case like this gives all of us an opportunity to learn.

Very often I'm the one preaching to leave a patient alone and "do no harm". Too often EMS does more harm than good because we feel like we have to "do something" even though the patient is hemodynamically stable.

This is not one of those occasions.

So how do we determine our course of action?

2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 8: Adult Advanced Cardiovascular Life Support – Part 8.3: Management of Symptomatic Bradycardia and Tachycardia

There are some important statements here that deserve to be read very carefully.

"Electrocardiographic (ECG) and rhythm information should be interpreted within the context of total patient assessment. Errors in diagnosis and treatment are likely to occur if advanced cardiovascular life support (ACLS) providers base treatment decisions solely on rhythm interpretation and neglect clinical evaluation. Providers must evaluate the patient's symptoms and clinical signs, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, and signs of inadequate organ perfusion."

and

"Unstable and symptomatic are terms typically used to describe the condition of patients with arrhythmias. Generally, unstable refers to a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. Symptomatic implies that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases the provider must make an assessment as to whether it is the arrhythmia that is causing the patient to be unstable or symptomatic."

and

"[A] patient in septic shock with sinus tachycardia of 140 beats per minute is unstable; however, the arrhythmia is a physiologic compensation rather than the cause of instability. Therefore, electric cardioversion will not improve this patient's condition. Additionally, if a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient's condition. It is critically important to determine the cause of the patient's instability in order to properly direct treatment. In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself."

A strange omission in the "streamlined" 2010 Adult Bradycardia With Pulse algorithm (that was present in the 2005 Bradycardia Algorithm) is the box that shows the Hs and Ts.

As Einstein is reported to have said, we must "make things as simple as possible but not simpler." 

Obviously we must correct hypoxemia.

However, if the rate does not bounce back we must consider other causes of the bradycardia.

In this case, the patient's potassium was very high (it turned out to be over 8.0).

I will grant you that this ECG does not show the classic "sine wave" or "Z-fold" pattern that is typical of life-threatening hyperkalemia (the QRS duration is well below 180 ms and there is no "merging together" of the S-wave and T-wave). On the other hand, there is very little risk to giving calcium and a huge upside potential for the periarrest patient.

Whether hyperkalemia was suspected or not, it would have been appropriate (according to the 2010 guidelines) to attempt to correct the heart rate using atropine, epinephrine, dopamine or transcutaneous pacing.

Would it have worked? I don't know.

Unfortunately, transcutaneous pacing is a skill that is poorly performed by all levels of health care providers. It is very unusual to see cases where patients were successfully paced using this technique. Far more often we see "false capture" with transcutaneous pacing.

This patient went into cardiac arrest in the cardiac cath lab while they were trying to insert a transvenous pacing lead.

Due to some kind of error, there was a significant delay in the lab. By the time they found out about the potassium level (a "critical value") it was too late.

You might recall the 58 year old male who was found unconscious at the bottom of the stairs. He was also suffering from life-threatening hyperkalemia and had a poor outcome.

Remember the ECGs from Rhythm Challenge #2?

In that case (which was far more obvious) hyperkalemia was also missed and the patient had a poor outcome.

The take-home message is that hyperkalemia can be profoundly life-threatening but it can't be treated if it's not suspected.

Consider this conversation between Stephen Smith, M.D. (from Dr. Smith's ECG Blog) and Scott Weingart, M.D. on the EMCrit podcast:

SW: "I know I've learned from being burned many times, that when I have a profound bradycardia or heart block, as my residents are getting excited to place in a pacer, even if the patient has no preexisting history, I do a trial of calcium chloride or calcium gluconate because I've just had so many cases where it turned out to be hyperkalemia. Is that your experience as well?"

SS: "That is my experience as well and I think it's very wise you're giving calcium before you start pacing. By far, more common than intrinsic causes of bradycardia and heart block is hyperkalemia — so common — and so frequently overlooked. It's a great imitator, I think. 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?"

I would like to thank our anonymous contributor for sharing this important case.

Posted by on May 3, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

Life-threatening hyperkalemia: do you recognize the ECG signs?

12 comments

I received a couple of interesting 12-lead ECGs from a semi-regular contributor who still wishes to remain anonymous (which is perfectly fine with me).

It was a transport from the emergency department to a tertiary care center for emergent dialysis.

Here are the 12-lead ECGs captured en route.

Potassium was 8.1.

Congratulations to this paramedic for using this transport as a learning opportunity!

Here are some ECGs from a recent case 76 year old female CC: Diminished LOC.

Potassium was 8.3.

Here are some ECGs from “Rhythm Challenge #2“.

I don’t remember the exact potassium level but it was above 8.0.

From 58 year old male CC: Unconscious.

I don’t think we ever got a potassium level on this poor fellow but he died.

Life-threatening hyperkalemia is something you can expect to see in the course of your career and it’s treatable!

It’s one of the few conditions (like D50 for insulin shock) that we can treat with IV meds (calcium gluconate or calcium chloride) and have an immediate therapeutic effect.

Take a close look at these ECGs and learn what to look for.

  • Undetermined rhythm (absent P-waves)
  • Non-specific intraventricular conduction defect
  • QRS duration > 180 ms
  • So-called “sine wave” or “Z-fold” appearance (merging together of S-wave and T-wave)

Throw in a history of renal insufficiency or renal failure, a missed dialysis appointment, use of potassium sparing diuretics, potassium supplements, etc., and you should be able to clinch the diagnosis.

Posted by on March 13, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

76 year old female CC: Diminished LOC – Discussion

29 comments

Here’s the follow-up to 76 year old female CC: Diminished LOC.

Be sure to check out all the awesome comments on the case!

Let’s take another look at the 12-lead ECG.

There’s something very unusual about this heart rhythm.

It’s slow, there are no P-waves, and the QRS complexes are extremely wide (> 200 ms).

Could this be a ventricular rhythm?

Sure. It’s possible. But this is wide even for a ventricular rhythm.

The morphology is consistent with a nonspecific intraventricular conduction defect.

Whenever I see an ECG like this I immediately think, “Hyperkalemia!”

Other possibilities include:

  • Tricyclic anti-depressant overdose (note the tall R-wave in lead aVR)
  • Other sodium channel blockers (Class 1a antiarrhythmics, tramadol, diphenhydramine, etc.)
  • The effects of prolonged myocardial ischemia (end stage of big MI, PE, or respiratory arrest)

Special thanks to Dr. Smith from Dr. Smith’s ECG Blog for helping me refine this list of differentials.

Another interesting feature of this case is the multiple ecchymotic areas on the body and the pulseless R foot. This could suggest a coagulopathy or renal failure.

Additionally, I liked David’s theory about rhabdomyolysis contributing to hyperkalemia.

Would I have given this patient calcium? Absolutely!

It couldn’t hurt and it might help.

We often have to make decisions in the field based on incomplete information.

It’s the “fog of war”.

As Carl von Clausewitz wrote:

“The great uncertainty of all data in war is a peculiar difficulty, because all action must, to a certain extent, be planned in a mere twilight, which in addition not infrequently — like the effect of a fog or moonshine — gives to things exaggerated dimensions and unnatural appearance.”

So what was the outcome?

This patient went into cardiac arrest at the emergency department and was not successfully resuscitated.

If we find out the exact cause of death we’ll let you know.

*** UPDATE ***

The patient’s potassium level was 8.3 (Critical High).

Here’s the raw data.

Thanks again to Randy for the great case!

Posted by on February 18, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

58 year old male CC: Unconscious – Conclusion

14 comments

Here is the conclusion to 58 year old male CC: Unconscious.

This was an unusual case with an unfortunate outcome.

Let’s look at the heart rhythm again.

The rhythm is slow and irregular with strange looking complexes. At first glance it’s difficult to distinguish QRS complexes from T-waves. It looks like a pre-morbid rhythm.

However, on closer inspection we can see that the QRS complex is present but near isoelectric. The QRS duration is > 200 ms which is extremely abnormal. Whenever you see a QRS complex > 200 ms you should suspect hyperkalemia!

In addition, when the S and T-waves merge together and the ST-segment becomes non-distinct you’ve moved into what is sometimes referred to as the “sine wave” ECG. This is an ominous finding.

Unfortunately, at the time this ECG was recorded (several years ago) our paramedics weren’t trained to recognize hyperkalemia. It’s one of the many ways the paramedic profession has evolved throughout the course of my career.

However, they knew the heart rhythm was “bad” and they wanted to see something a little bit less scary on the monitor so they elected to perform transcutaneous pacing (TCP).

Did they achieve capture? Let’s take a look.

They did not achieve capture, although I can understand whey they thought they had intermittent capture.

A shows the morphology of the underlying rhythm. B shows a (presumed to be) transcutaneously paced QRS complex. It is classic for false capture. C shows a “phantom” QRS complex (caused by pacing artifact) that coincidentally falls directly on top of the (unsensed) native QRS complex. This makes it appear as though capture has been achieved. D shows a “phantom” QRS complex falling in the absolute refractory period of the underlying rhythm (proving beyond any shadow of a doubt that these QRS complexes are the result of pacing artifact).

So what ended up happening?

The patient survived to arrival at the emergency department. However, during transfer of care the emergency physician asked that the TCP be turned off so that he could examine the underlying rhythm.

Moments later the patient was shocked x2 by his ICD and the resultant heart rhythm was asystole.

He was not successfully resuscitated.

It was later that they found out the potassium level was > 9 mEq/L (I don’t remember the exact value).

I don’t know why this patient’s ICD shocked him. I was not present when the device was interrogated. But I suspect that it may have been confused by the TCP.

If I am ever faced with a situation in the future where I feel that TCP is indicated and the patient has an ICD I will be contacting Online Medical Control and asking permission to disable tachy therapy with a ring magnet.

Obviously there are a lot of lessons to be learned from this case.

See also:

Transcutaneous pacing (TCP) – The problem of false capture

Transcutaneous pacing (TCP) with a Lifepak 12

Using capnography to confirm capture with transcutaneous pacing (TCP)

Transcutaneous pacing (TCP) for asystole

Ineffective or inappropriate ICD shocks – Part I

Ineffective or inappropriate ICD shocks – Part II

Ineffective or inappropriate ICD shocks – Part III

Rhythm Challenge #2 (Hyperkalemia)

Posted by on December 20, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , ,

41 year old male CC: Chest pain – Answer

17 comments

Thank you for all of the excellent comments on this case! I was delighted to see such a high level dialog when I checked my blog this morning.

Normally I would to answer each of you individually, but since there are 22 comments (so far) I thought I would try a different strategy and post the answer, along with tips for the correct interpretation of this ECG (at least in the context of “STEMI / not a STEMI” while you are out in the field).

This was not a STEMI.

It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.

First, let’s look at the 12-lead ECG and make the case for LVH.

You’ll recall from my previous posts on the topic that I’ve said it’s more important to recognize the so-called “strain pattern” than the voltage criteria.

The reason is simple.

If the “strain pattern” isn’t causing a problem (mimicking an acute anterior STEMI) then you’re waisting your time calculating the QRS voltage.

This ECG has the general appearance of “T-wave discordance”. In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality.

In this case, the most likey cause is left ventricular hypertrophy.

I say “generally appearance of T-wave discordance” because it’s not true in every lead. That’s why I mentioned in a previous post that there are “some caveats”.

When I’m looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).

Let’s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not “T-wave discordance” is present.



With those leads removed, are the T-wave deflected opposite the QRS complexes?

Absolutely!

Could that be a coincidence?

Highly unlikely!

The high lateral leads in particular are showing a very typical looking strain pattern.

This can be a problem because it could easily be mistaken for “lateral ischemia” or reciprocal changes secondary to acute STEMI!

Does this ECG meet the voltage criteria for LVH?

Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it’s right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.

But I don’t think that’s important.

The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?

The answer is yes.

Remember, we’re looking at the ST-segments and the T-waves together.

At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.

Let’s blow this up a little bit.



When we use the TP-segments as a baseline, we can see that it’s debatable as to whether or not lead V1 shows more ST-elevation, but it’s obvious that lead V2 shows a more pronounced ST-T wave abnormality.

The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within “normal” at 419 ms.

I don’t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was “on the high end of mild hyperkalemia” (so I’m guessing between a 6 and 7).

Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.



There isn’t much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you’ll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more “broad-based”.

This was a very difficult case. So what can we learn from it?

In my mind, it’s very simple (and it needs to be simple for field use — complicated equations involving calipers are not simple).

T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.

Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STE-mimic!

I hope we can continue our useful discussion about this ECG! I look forward to reading more of your comments.

See also:

41 year old male: CC: Chest pain

Posted by on May 26, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

41 year old male CC: Chest pain

27 comments

A 41 year old male is pulled over during morning rush-hour by sheriff’s deputies.

He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.

The patient is awake, alert, and oriented to person, place, time, and event.

His skin is pink, warm, and moist.

He appears acutely ill and anxious.

He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.

Onset: 1 hour ago while sleeping.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as a poorly localized “fullness” or “pressure”.
Radiate: The patient cannot tell whether or not the pain radiates.
Severity: The patient reluctantly gives the pain a 7/10.
Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.

Vital signs are assessed.

Resp: 20
Pulse: 76
BP: 138/78
SpO2: 99 on RA

The cardiac monitor is attached.



A 12-lead ECG is captured.



What is your analysis of this ECG?

Does anything about it concern you?

Is this a STEMI?

Why or why not?

Note: This 12-lead ECG was captured in the back of an ambulance with the motor and generator running, but it shows excellent data quality.

See also:

41 year old male: CC: Chest pain – ANSWER

Posted by on May 24, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

Rhythm Challenge #2

37 comments

Here’s an interesting rhythm strip that was captured in the days before my EMS system had 12-lead ECG monitors.



What do you think?

*** Update 01/20/2010 ***




Here is the rhythm strip taken on arrival at the hospital.



Here is the 12-lead ECG that was captured at the hospital.



Does that change anything?

Posted by on January 20, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,