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The Trouble with Sinus Tachycardia

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Sometimes recognizing sinus tachycardia can give us fits.

What? Sinus tachycardia? One of the most basic rhythms?

The discussion that follows will highlight some of the difficulties sinus tach can present at high rates. The pitfalls of using the generalized term "SVT" will also be discussed. This discussion is not meant to imply that this issue is easy to navigate. It can get very difficult, and very dicey. The consequences of misinterpreting the rhythm and missing sinus tach can have very deleterious effects for our patients.

We are all good at recognizing sinus tachycardia at rates between 100-150, but when rates exceed 150 it seems to become problematic.

Is it difficult to recognize this?

No.

How about this one?

More difficult.

 

When sinus tachycardia occurs at high rates, our ability to correctly differentiate it from other types of SVT apparently decreases. P waves start to blend into the T waves. Instead of talking about discreet stand alone P waves, we talk about "notches" and "bumps". It is all too easy to look at a rate >150 and simply call it "SVT".

 

We know what sinus tach is: a sinus rhythm at rates faster than 100 (in adults), which is a normal physiological response to compensate for the increased needs of the body. I won’t spend time listing all of the possible causes, ranging from running around the block to septic shock.

AVNRT, a type of SVT that is responsive to Adenosine, is a re-entrant tachycardia that relies on a circuit through the AV node to sustain it. Block down the AV node, and the dysrhythmia terminates. Quite a bit different from sinus tach. Different mechanisms, different treatments.

Several case studies involving the above strips and ones like it have appeared on our FB page, and the FB pages of other EMS educational sites. What we have seen is that an alarming number of folks incorrectly identify sinus tachycardia as one of the other SVTs and want to treat with Adenosine or cardioversion.

Consider this rhythm strip that appeared on our page and another educational paramedic page:

The patient was a sick adult male, hypotensive. P waves are subtle, but they are there. Due to the rate, however,  a majority of providers (hundreds!) identified this as "SVT" and wanted to immediately cardiovert. 

Here is the followup ECG taken a couple of hours later. The patient was severely dehydrated and had received a few liters of fluid:

Now that the rate has slowed, sinus tach is clearly visible.

While we are discussing this, we should be clear about our terminology. Sinus tach is one of the Supraventricular Tachycardias. "SVT" is an umbrella term that represents a group of tachydysrythmias that originate above the ventricles. They will generally be narrow tachycardias, unless aberrant conduction is present. Some of the other types of SVT are AVNRT, AVRT, A-Flutter, A-Fib, junctional tachycardias and atrial tachycardia. Not only is sinus tach one of the SVTs, it is by far the most common SVT!

One of the issues that’s come to light is the fact that “SVT” is seemingly often taught as a “dysrhythmia” itself rather than what it really is: a group of dysrhythmias. I really don’t like the term “SVT” because it implies a diagnosis, when in fact it should motivate a provider to form a list of differentials and consider the H’s and T’s.

"Could this be sinus tach? A-Flutter? AVNRT?"

Treating "SVT" as a stand alone dysrhythmia leads folks to believe there is one “treatment” for SVT, when in fact the treatment is determined by which type of SVT the patient has.

What are we even taught about SVT?

Generally speaking these days, when students are taught SVT they are taught that a narrow tachycardia faster than 150 or 160 is "SVT". Simple as that.

How do we differentiate sinus tach from SVT?

That’s easy: rate!

If the rate is over 150 (some use 160), then it is “SVT and not sinus tach” and should be given adenosine or cardioversion! Quickly!

If you were taught that, raise your hand. Wow… that’s a lot of hands!

 

While we are on the subject, where did the rate limit of 150 or 160 come from?

I have NO IDEA. There does not seem to be any research I can find that even suggests that these numbers can be used to differentiate ST from other SVTs.

In fact, I could not find any research that demonstrates that absolute rate plays any part in differentiating ST from other SVTs.

All I could find is references to the guideline used to determine the theoretical maximum sinus tachycardia in healthy people: “220 – age”.

This “formula” is a guideline at best. It intends to illustrate that very young people can have ST at very high rates, and that as we age, it should be more difficult to achieve higher rates of sinus tach.  However, we deal with really sick patients, and theoretical guidelines are not good enough to help us with this issue.

What I know is what you all know. That medics are taught that at rates above 150, you can no longer see P waves, so you have to assume it is “SVT”.

“154= SVT”

“146= ST”

Easy as pie! Whether or not P waves are visible does not seem to factor into the equation.

 

Perhaps you don’t want to accept that these teachings do not seem to be based on anything concrete, but these are the facts. Sinus tach commonly exceeds rates of 150, and P waves are often discernable. More on this in a bit.

In any event, It is in this region of rates, between 150 and 200, where sinus tach is often mistakenly called “SVT”, and the risk of inappropriate treatment rises. Don’t believe it?

Before you can say “SINUS TACH”, I could show hundreds upon hundreds of comments left by medics stating that a rhythm “could not be sinus tach because the rate is over 150”.  And these comments were made by the medics who are motivated enough to visit educational sites and participate. 

The result of this is that too many medics are not correctly trained to deal with this issue. Sinus tach is unrecognized. The P waves are ignored, and the rhythm is labeled “SVT”, and the patient is in danger of suffering in more than one way:

For staters, they may receive an inappropriate treatment. A sick patient in sinus tach does not need to go through trials of adenosine, or even worse, cardioversion.  In addition to the discomfort, those treatments won’t work. Sinus tach is not a reentrant rhythm that relies on the AV node for its perpetuation, so adenosine or cardioversion won’t resolve the arrhythmia.

One of the most overlooked consequences of mistreating this rhythm is the fact that these patients are not getting the treatment they really need. These patients need lots of fluids. If medics are giving drugs and electricity, they certainly are not administering large boluses of NS.

It is easy to imagine how difficult the choice may seem. The sick patient in sinus tach will look shocky. He may have palpitations or chest pain, and may be altered. In other words, it will be very tempting to attribute the patient presentation to rate problem, even though the rate is compensating for their underlying medical issue.

Without a sound understanding of what sinus tachycardia really is, and what rate ranges are reasonable, it becomes much more difficult to make the right choice.

 

Probably right about now, some of you will want to blame ACLS for all of this. Consider the 2010 “Adult Tachycardia (with pulse)” algorithm [1]:

 

 

Box 1 states: “Heart rate typically greater than or equal to 150 if tachyarrhythmia”. 

What does that mean? What it seems to mean to a great many people is that a rate greater than 150 is "SVT".

If the patient appears unstable, we are performing synchronized cardioversion by box 4. There is no mention of sinus tach anywhere on this algorithm.

I’ll admit, I think that algorithm could be better. I think there should be a box that gets you out of that algorithm if sinus tach is recognized, similar to what appears on the ACLS Pediatric Tachycardia algorithm [2]:

 

 

Here, if the tachycardia is narrow, you are directed to one of two boxes which require you to assess for the presence of sinus tachycardia. I believe that a box like this in the adult algorithm would help clear up a lot of confusion.

In defense of the AHA, however, the simplified algorithm is based on the assumption that students have read the ACLS Provider Manual, on which the algorithm is based.

The following appears in the “Foundational Facts: Understanding Sinus Tachycardia” box on page 125:

           “Sinus tachycardia is caused by external influences on the heart, such as fever, anemia, hypotension, blood loss, or exercise. These are systemic conditions, not cardiac conditions. Sinus tachycardia is a regular rhythm, although the rate may be slowed by vagal maneuvers. Cardioversion is contraindicated.” [3]

Clearly, on page 125 of the ACLS Provider Manual, sinus tachycardia has been excluded from the adult tachycardia algorithm. It is a shame that fact is not reflected on the algorithm itself, because evidently a very large number of ACLS students do not read the manual and may incorrectly assume that rate is the determining factor.

 

I know some of you are thinking, “is this much to do about nothing? Is sinus tachycardia at rates above 150 as rare as an isolated posterior STEMI?"

We put this issue to the test. We brought in two well known electrophysiologists, Dr.’s John Mandrola and Mark Perrin, to shed light on this issue and share their perspectives with us. Readers of our blog will recognize them as past contributors and experts in their field.

I asked Dr. Mandrola about the utility of the “220-age” formula, and here is what he had to say:

           “The old formula 220- age equals the max heart rate represents only an estimate. It can vary by up to 10-15%. That's a lot. Normally a 30 year-old would have a max of 190. But with the variation, ST could be as high as 200. I see tons of patients for 'tachycardia', that's supposedly abnormal. Often its just ST. The short answer is that human heart rates vary quite a bit–at the high and low end.”

I then asked him what we really want to know: how common is ST at rates above 150:

          “The sinus node is highly innervated with both sympathetic and para-sympathetic neurons. Adrenaline can easily push the sinus rate above 150. Stress, anxiety, fever, dehydration, drugs, heat, and many other things can do this.  

            If a patient has upright p-waves and the diagnosis is ST and is unstable, it's not because of a primary electrical disturbance. ST is a sign not a primary arrhythmia. Patients with ST should be resuscitated, but not with shocks, with fluids, oxygen and rest perhaps and comfort perhaps.”

 

I asked Dr. Perrin for his thoughts about using a rate of 150 as a cut-off between sinus tach and other types of SVT and he had this to say:

            “Thinking that ST has an upper limit of 150-160 is kind of crazy. The septic, those in congestive cardiac failure, people with pulmonary emboli, hemorrhaging patients, etc, etc… all of these could hit heart rates of 190-200 or higher.

                 It is an easy diagnosis to make as well – because the P will always be present. Perhaps if the rate is > 200 it may disappear into the T wave a little. The only real differential is atrial tachycardia/flutter, and this is pretty unlikely to destabilize a patient.”

We discussed the issue medics are having in the field with inappropriate treatments of sinus tachycardia. I asked if he had any first hand experiences with it:

           "In fact, I have found, anecdotally, that paramedics are quick to shock patients. I have misgivings about this, especially for narrow-complex rhythms. We live in a city. ERs are close by. Why shock so quickly? There's some data that shocks harm the heart.”

My sincere thanks to Dr.’s Mandrola and Perrin for their contributions. As always, peer sourcing is great way to gain additional insight and expertise.

Hopefully this discussion has been educational for those who thought that 150 was any kind of limit for sinus tachycardia. The fact of the matter is that sinus tach at rates between 150- 200 not only exists, but is not uncommon. We need to be better at assessing for sinus tachycardia, because it is the most common SVT. We need to make sure we are doing right by our patients, giving them what they need and keeping them our of harm's way.

We also need to be better educators and providers.

Some will say, "we are teaching to the Registry", or "we are teaching to ACLS".  

They will say, "in the real world, they will know what to do".

From what I have seen, it doesn't work like that. Providers fall back on what they were taught, which often happens to be incorrect.

It begs the question, why are we teaching something we know is not correct? That can't be good for anyone.

For those who didn't know this information before, you know it now. Let's see if we can change the way we educate and provide care in this area.

It seems to be a deeply rooted problem, ingrained in decades of education. Time for a change. I don’t know if the issue has been raised before, but we are raising it now. 

As always, I look forward to your comments!

 

_

Footnotes:

[1],[3]-  Advanced Cardiovascular Life Support Provider Manual

                  2011, American Heart Association

[2]             Pediatric Advanced Life Support Provider Manual

                  2011, American Heart Association

 

Posted by on April 30, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

“What’s wrong with Mr. Wilson?”

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It is a sunny January afternoon at the ER when you are called to see a 57 year old male complaining of feeling "really sick".

You find your patient lying in the bed in room 3. He looks pale and short of breath. You introduce yourself and ask him why he has come in today.

He says:

"About two weeks ago, I started feeling short of breath, with a cough. I got much more tired than usual. I went to see my doctor, who said I had an upper respiratory infection and prescribed me some antibiotics. I rested at home for a few days, and started to feel a little better. Then, I began to go downhill again. Felt so awful today, barely have enough energy to walk, so I had my wife drive me to the ER."

He tells you that he has a history of hypertension and is a pack a day smoker, although he is trying to quit., Prior to getting sick, he has felt pretty well. In fact, he tells you that he started a work out regiment to lose some of the excess weight he is carrying.

Your patient tells you he hasn't been eating or drinking well lately, and he is hypotensive at 86/58.

As you are running through your list of differentials, the tech hands you this 12 lead ECG:

 

 

You take a look at the ECG, and a couple of thoughts come to mind. You have an idea of what might have happened.

You tell Mr. Wilson that you want to run a few tests…

So, what do you think is wrong with Mr. Wilson?

 

Posted by on January 19, 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 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: , , , , , , ,

53 Year Old Male: Severe Leg Pain–Conclusion

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This is the conclusion to 53 year old male: Severe leg pain. You may wish to review the case.

Before we begin, my apologies for the delay in posting this conclusion. I live in coastal NY, and we got hammered by Hurricane Sandy. It has taken me a little time to get all caught up.

This is not an easy case. Our patient's chief complaint is of sudden onset of severe leg pain, and chest pain. Also notable is the measured hypertension.

Here is another look at the second 12 lead, which showed the following changes from the first:

There is sinus tachycardia, at a rate slightly above 100 bpm. There is physiologic left axis deviation. There are no signs of chamber enlargement, and the QRS is normal width. There is slight ST elevations in I and aVL, with ST depressions in the inferior leads, as well as V2 and V3.

At this point, our list of DDX should probably include:

  • DVT
  • Possible aortic dissection
  • STEMI

The patient's complaint sounds like it could be DVT, as many readers pointed out. We might expect to see swelling and redness as well, and this was not noted by the EMS crew. These signs and symptoms are not sensitive, however, as about 50% of people with DVTs will not have them. 

The patient is hypertensive, with chest pain, which led some of you to suggest an aortic dissection. Usually there is sudden onset of maximal chest pain, 10/10, with a "ripping" or "tearing" sensation. We do not have those typical signs and symptoms here by history. 

The patient does have ischemic signs on the 12 lead, consistent with lateral STEMI, but the patient's main complaint seems to be leg pain, not the chest pain.

 

So, how do we manage this patient? 

 

For starters, I think this is a tough patient to figure out. We have three good possibilities on our list of DDX, and two of them are immediately life threatening. 

I look at it this way, and of course it is with the benefit of hindsight. There seems to be more going on here than DVT, based on the patient's presentation, chest pain and 12 lead ECG. 

STEMI seems to be a reasonable assumption based on the 12 lead, but I would be thinking that as an atypical presentation (leg pain), this would almost be off the charts. It just doesn't seem like STEMI.

We also know that other conditions can cause ischemic changes on the ECG, and a dissecting aorta is one of them. 

Of course, O2 and IV access are indicated. NTG is a good possibility because it would be beneficial in either scenario. 

With that in mind, I would at least make sure we are transporting the patient to a hospital that can handle both STEMI and surgery for dissecting aorta. 

If a dissection progresses in a retrograde direction towards the aortic root, an acute total or partial occlusion of one of the main coronary arteries can occur. Usually, it is the RCA that is involved, but unusually, it can involve the left main. In the ED, heart rate and blood pressure will be controlled until surgery is performed. You can read more about this phenomenon here. 

As you have probably surmised by now, this was the fate of our patient. Once in the ED, a CT scan revealed a dissection of the ascending aorta. This dissection caused a partial occlusion of the LMCA. The patient underwent extensive surgery to repair the aorta. He was expected to make a strong recovery. 

We hope you enjoyed this unusual case! As always, comments are encouraged!

 

 

Posted by on November 26, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

53 Year Old Male: Severe Leg Pain

27 comments

This great case was sent in by faithful reader Bryan Brzycki, a Medic from Beaufort County. As usual, some minor information may be changed to protect patient confidentiality.

It's a cloudy fall morning when the tones go off and your unit is dispatched to the residence of a 53 year old male. 

When you and your partner arrive, you are greeted by the patient's wife, who leads you to your patient who is sitting on his couch in the living room.

He tells you that he was taking a shower this morning, and developed sudden onset of severe pain in his left leg. He feels discomfort throughout his leg. You inspect it, but do not notice anything abnormal. He tells you that no position seems to help the pain. You ask if he had any injuries that would account for the pain, and he can not remember anything, and that he has never felt anything like this before.

You ask about any other symptoms, and he tells you he also experienced some "mild" chest discomfort. He describes the leg pain as an 8/10, and the chest discomfort of a 3/10. You ask about any other symptoms and he denies anything else. 

He has no significant history, takes no medications, and has no allergies. In fact, he tells you he just had his annual physical last month and he was given a "clean bill of health". 

Your partner applies the leads as you get a set of vitals. The patient is agitated and uncomfortable, telling you his leg is "killing him".

  • HR:  100 and regular
  • BP:  182/92 (right arm)
  • RR:  20
  • skin: warm and moist
  • lungs: clear bilat

Here is the 12 lead:

 

You try to sort out what is going on as you move your patient to the back of the truck. 

Although hard to connect it to the leg pain, he did mention some chest discomfort, so you give him 4 chewable ASA and begin transport.

You decide to acquire another ECG:

 

What do you think is going on with your patient?

 

Posted by on October 22, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , ,

59 Year Old Male–”Lifting Boxes”: Part II, with a twist!

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This is part II to 59 year old male–"Lifting Boxes". You may wish to review the case.

Let's review the ECG:

There is sinus rhythm at about 90 bpm. Some of you saw a slight bit of ST elevation in the inferior leads, and maybe an abnormal aVL. Perhaps? Perhaps not? V1-V4 look possibly abnormal, but there is an awful lot of artifact. There appears to be a bit of ST depression in V5-V6. Is this an ischemic ECG? Looks concerning from what we can decipher.

Sometimes on blog posts, we get used to crisp ECGs and tidy scenarios. Nothing wrong with that. Sometimes, though, our cases on the street just don't go like that. Often there is much to learn from those, but I digress.

 There are a couple of real concerns with this case;

  • As correctly pointed out in the comments, the quality of the ECG is poor. This leads to all sorts of interpretation problems. If we put effort into it, we can usually get a pretty good tracing. On occasion though, it can be tough.
  • Another issue is that the 12 lead was not acquired early on. The crew acquired the ECG in the ambulance after the following: assessment, history, physical exam, O2, ASA, bathroom break, change of clothes, etc. This is not what we are after, and we could miss important findings by waiting this long.

As most of the comments reflect, the timing of the ECG and poor quality make it tough to interpret, and tough to activate the cath lab. I know some of you saw findings that led to you say you would activate, but doing so based on this one poor quality ECG is tough to do. Just is. 

So off to the community hospital he went. 

Calls are run like this every day. We all know it. In fact, it is one of the reasons we discuss cases such as this.

Could this patient have benefited if the call was handled differently? 

Fortunately, we know that he did!

In a contrasting plot twist, this call was actually handled quite differently:

In reality the crew obtained the history and vitals previously mentioned. However, undaunted by the patient's reluctance they convinced him to allow a 12 lead to be acquired immediately. This is what they found:

Due to the patients girth and breathing patterns, it was difficult for the crew to acquire a totally clean ECG. However, this one clearly shows ST elevation inferiorly, as well as V5 and V6. We can also see ST depression in V2-V4 with tall R waves. There is also slight ST depression in aVL: Infero-postero-lateral STEMI. 

The crew acquired another 12 lead with V4R which revealed about 1mm of ST depression in V4R:

The ECGs were transmitted, and the patient was emergently transported to the cath lab, where he underwent PCI and had a successful outcome.

For comparison, note how much the ST segments resolved from the first 12 lead to the one acquired in the ambulance:

After just a short period of time from the first ECG,  obvious ST elevation in II and III has mostly resolved. Timing is everything!

The point of all of this is to clearly illustrate the importance of early 12 leads and good data quality. The prehospital care of this patient could have gone either way. We see it every day. How we handle those first minutes, and the quality of the data we acquire will have a huge impact on the care our patients receive.

What are your thoughts? I'm sure you have experiences similar to this one!

 

 

Posted by on September 20, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , , ,

88 year old female: Weakness

17 comments

This great case was submitted by Vince DiGiulio, EMT-CC; we highly recommend you read his wonderful blog The Medial Approach to Emergency Medicine. As usual, the case has been altered to protect patient and provider privacy.

You're working triage in a busy urban ED when an 88 year old female is brought in by her family. She is in a wheelchair and appears lethargic.

When you introduce yourself she comes around and is able to answer your questions, albeit with some hesitation. Her family reports that she is independent and lively at baseline and are concerned she is having a stroke.

You move her into a triage room and grab a set of vitals. Her breathing appears unlabored with an irregularly irregular pulse at her radials. You ask an ED tech to join you to help with acquiring an ECG.

  • Pulse: 80-100, irregularly irregular
  • BP: 122/83, auto-cuff
  • Resps: 22, unlabored, clear bilaterally
  • SpO2: 92% r/a
  • GCS: 14 (E3 V5 M6)
  • LAPSS: Negative

The ED tech runs a strip from the monitor after switching to Lead I as Lead II had small complexes.

All Over the Map - Rhythm Strip

You call back to the charge nurse and ask for a bed assignment and wheel the patient back with the help of the ED tech. In the room a 12-Lead ECG is acquired while a complete history is gathered.

  • PMHx: hypertension, hypercholesterolemia, Type II diabetes
  • Meds: lisinopril, Lipitor, glipizide, ASA, and a multivitamin
  • Allergies: PCN and Sulfa
  • Last In's/Out's: normal lunch, vomiting during the afternoon
  • Events: progressive lethargy and weakness after vomiting in the afternoon

The RN hands you a copy of the 12-Lead while she updates the electronic chart.

All Over the Map - 12-Lead

Given the 12-Lead you decide that a Lewis Lead should be acquired, as it may give additional insight into the underlying rhythm:

All Over the Map - Lewis Lead

The ED physician walks into the room and asks you one question, "does she has a history of atrial fibrillation?"

  • What is this patient's rhythm?
  • What are some potential causes of our patient's rhythm?
  • Does the Lewis Lead offer any potential insights into our pateint's rhythm?
  • Would this information change your treatment decision?
Posted by on September 11, 2012 • Filed under: ems-health-safety, ems-topics, patient-management • Tagged: , , , , ,

59 Year Old Male: “Lifting Boxes”

30 comments

This is part one of today's case study. As usual some information has been changed to protect patient confidentiality.

EMS is called to the residence of a 59 year old male, who's chief complaint is chest discomfort. 

As the crew enters the kitchen, they find the patient sitting in a chair surrounded by family members. He is not happy to see the crew.

He tells them he was doing some lifting of boxes all afternoon, and developed some chest pain, slightly left of center.

He took a break, and it started to get better. Now, 3/10 on the pain scale. He states he has no significant medical history.

The crew ask who called EMS, and he tells them his wife called because she thought he did not look good. He makes it clear that he is not happy with the EMS presence.

As they continue to speak with the patient, they put him on O2 and give him 4 baby ASA just in case. He tells them the discomfort happened earlier in the day when he was lifting boxes, and totally went away when he took a break. He expects nothing different this time. The discomfort does not move anywhere, no shortness of breath, no dizziness or lightheadedness. His wife tells them he was sweating, but he states that of course he was because he was lifting heavy boxes!

The crew takes a quick set of vitals:

  • HR:       90 and regular
  • BP:        148/86
  • RR:       18 regular
  • skin:      unremarkable
  • Lungs:  clear bilaterally
  • Spo2:    98% on O2

The patient's wife convinces him to go and get checked out for her sake. He relents. The crew decides to get him into the rig before he changes his mind, and defers further assessment until then. The patient is ambulatory, and insists on walking to the rig. On the way, he insists on going to the bathroom. Then changes his clothes for the hospital. The crew protests, but he states he will not go otherwise.

Once in the rig, the crew acquires the following 12 lead ECG:

 

The crew does not note anything too concerning, and considering the patient's story and lack of history, they transport him to the community hospital, without any additional ECGs.

CRITICAL QUESTIONS:

  • What are your interpretations of this ECG?
  • What if this was your patient? What would you have done differently?
  • Do you agree or disagree with how this call was handled?
Posted by on September 9, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , ,

Snapshot Discussion: 64 Year Old Male–Chest Pain

7 comments

This is the discussion for "Snapshot: 64 Year Old Male–Chest Pain".

First, let's talk about the patient presentation.What is concerning is the substernal chest pain, radiating to the shoulder and neck area. While this occurred about 30 minutes after exercise, it did not occur during exercise, so that is somewhat atypical. Still, enough red flags in the history to be very concerned.

Here is another look at the 12 lead:

It is a regular sinus rhythm, at a rate of 65. The PRI is on the long side of normal at 200 ms, and the QRS is slightly wide at just over 100 ms. The axis is normal, and there does not appear to be anything causing secondary ST changes.

The question is, do we see signs of ischemia on this ECG?

This is not an obvious ECG, so as we would expect, many of you said yes, and many said no. Is this a normal ECG? We don't have an old ECG for comparison, but I would say this ECG is not normal.

Let's break it down. What jumps out at me most on this ECG are the morphologies in leads I and aVL:

 

 

There is almost 1 mm of flat ST depression in lead I, and a very notable T wave inversion in aVL.

While the T waves look large in leads III and aVF relative to the size of the QRS, there appears to be no ST elevation at this time.

Dr. Stephen Smith, of the famed Dr. Smith's ECG Blog, has written numerous times that depression and/or T wave inversions in aVL will often precede ST elevation in the inferior leads in IWMI.

Also see this recent case by Dr. Amal Mattu for another case on this subject.

Are there any other findings on this ECG that might support these concerns?

There is about 1 mm of ST elevation in V1. Could there be RV involvement? 

At the very least, I would be very concerned about a developing IWMI. The patient's discomfort is diminished, but not resolved. His complaints of "indigestion" are common with IWMI, and diaphoresis is another red flag.

Having said that, would I activate the cath lab based on this ECG? I have to say I would probably not activate based on this ECG alone.

I think this ECG is very concerning, but not yet diagnostic. I would certainly acquire serial ECGs and scrutinize the inferior leads for any subtle signs of change.

Dynamic changes would be a clincher. I would also treat with ASA and NTG, and would divert to PCI center if any changes in the ECG evolved.

This being a "Snapshot" case, we do not have follow up on this patient, or repeat ECGs. 

We run into this in the field often. The spectrum of ACS is far and wide, and we are often presented with borderline ECGs.

I think the best course is to treat based on what is best for the patient, and do serial ECGs!

Thanks for all of the insightful comments on this case!

Any additional thoughts?

 

 

Posted by on August 24, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

Discussion for “A Change of Pace: What Happened?”

4 comments

This is the discussion for "A change of Pace: What Happened?"  My apologies for the delay!

Pacemakers are amazing pieces of technology. They have evolved continually, and have given patients an increasing quality of life where none existed before.

However, with this amazing technology comes a level of complexity that also has not been seen before. These are remarkable devices, cable of many, many different types of functions. Sensing, pacing, defibrillating, single chamber, dual chamber, atrial paced, ventricular paced, cardiac resynchronization, etc… you get the idea. These are just some of the diverse functions that these devices can perform.

For us, we don't often know what type of pacemaker we are dealing with. And often, our patients do not know either! This created a dilemma for us, when we are confronted with an ill patient, and a pacemaker functioning in a way that we do not often see. Is it performing properly? Or is it performing inappropriately? Is the patient's complaint related to the pacemaker function, or the pacemaker reacting to the illness of the patient? To adequately answer these questions, we have to be able to figure our whether the pacemaker is functioning as it should, and why it is behaving this way.

To this end, I have enlisted the help of Mark Perrin, author of the EP Fellow blog. Peer sourcing is an amazing resource!

We'll go through these strips one at a time.

First, let's revisit the first ECG:

There appears to be a sinus rhythm at a rate of about 75bpm. The PR interval is about 240ms, and the QRS duration is slightly prolonged at about 110ms. There are pacing spikes that appear at the onset of the QRS. There also appears to be a fairly constant interval of 140ms between the P wave and the pacing spike.

So, what is going on here? Are the ventricles being paced by the pacemaker?

The first thing to understand is that the site of the pacing lead is normally in the right ventricle. Most of us already know that. However, what we may not all know is that the pacing lead sees "local activation", not the QRS that we see on the surface ECG. 

Mark Perrin: "A pacing spike on the beginning of the QRS is not uncommon. It usually occurs because of a right bundle branch block of a right ventricular conduction delay. The pacing lead is in the RV, therefore if there is delay to the right ventricle, activation of the LV (through a conducted P through the AV node) may occur just before the RV lead paces. The RV lead paces because it has not seen LV activation."

Essentially, there is an atrial sensing window of 140ms in this case. If there is a QRS that occurs within that sensing window, the pacing spike will be inhibited. If there is no QRS impulse sensed, the pacing lead will pace. Because of the conduction delay, the beginning of the QRS (which we see) is not seen by the pacer due to the conduction delay, so it paces, even though the ventricle is already responding to the P wave. What should happen, if this occurs, is that the pacing spike should always be near the beginning of the QRS. If it is, as it is in this case, nothing needs to be done, as this is what you could call a "normal variant".

What about the pause near the end of the strip, followed by the complex that looks different from the rest? You may also notice that the P wave looks a little different as well:

 

Mark Perrin: "This probably occurs because of a different degree of fusion between the conducted LV activation and RV pacing. The change in the apparent AV interval occurs again because the atrial lead sees "local" activation, not the P wave on the surface ECG. Therefore if the atrial activation occurs closer to the AV node it may start conducting to the ventricle before the wavefront reaches the atrial sensing bipole and triggers ventricular pacing. The opposite also occurs, i.e. atrial activation is further from the node, and reaches the atrial sensing bipole long before getting to the AV node."

Let's take a look at the second strip again:

This strip is a variation on the theme of the first. This strip has a mixture of the complexes seen on the first ECG, some with varying degrees of  fusion, plus a fully paced beat near the end of the strip. Why the fully paced beat here?

Mark Perrin: "The fully paced beat occurs (my guess) because the PVC before it invades the AV node thus delaying conduction down the node on the following beat."

Now on to the third ECG:

Here we see a fully paced rhythm at a rate of about 85bpm. Why the change from the prior rhythm to a fully paced rhythm?

To fully understand this, we have to remember a bit of physiology. In older people, or others likely to have diseased conduction systems, the "native" AV interval often increases when the heart rate increases. As the sinus rate increases, as in this case, the native AV interval also increases to the point where it is now longer than the pacemaker AV interval. Anytime the pacemaker AV interval is shorter than the native AV interval we won't see normal conduction anymore as the pacemaker takes over.

For this patient, these strips show normal pacemaker behavior. The main concept to remember is that the pacemaker does not see what wee see on the surface ECG. The pacemaker see local activation which may occur after the onset of the QRS in the ventricles, or after the onset of the P in the atria.

Many thanks again to Mark Perrin. I hope you have learned as much as I have in this case. I find pacemaker rhythms to be challenging but rewarding.  They can behave in so many different ways..Normally sometimes, and abnormally others. They really are incredible pieces of technology, and I one day aspire to really master the many ways in which they work. One day!

 

 

 

Posted by on August 3, 2012 • Filed under: command-leadership, Dispatch & Communications, ems-health-safety, ems-topics, mass-casualty-incident, patient-management, technology-communications-ems-topics, Training, training-development, training-fire-rescue-topics • Tagged: , , , ,

A Change of Pace: What Happened?

17 comments

Here is a challenging case this morning to stretch your mind…

You are called to a 71 year old male feeling "sick". He has not felt well for the past 24 hours. He describes feelings of "general aches and pains".

He has history of heart failure, for which he has an AICD.

His vitals are stable, and he does not appear to be in much distress.

Here are two continuous rhythm strips:

 

A short time later, his rhythm strip looks like this:

While in this rhythm, he reports that he feels "the same".

 

What is the rhythm in ECG #1?

What is going on in ECG #2?

What changed in ECG #3? And Why?

Looking forward to a good discussion!

Posted by on July 13, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , ,

Discussion for 51 Year Old Male: Chest Pain

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Here is the conclusion to 51 year old male: Chest Pain. You may wish to review the case.

Here is the ECG again:

 

There is a regular sinus rhythm at a rate of about 70. The QRS is narrow. The axis is normal, at about 15 degrees.

Let's take a look at the constellation of ST changes:

There is ST elevation in leads I, aVL, V2-V6. There is slight ST depression in III and aVF (and arguably in lead II) with ugly looking T wave inversions. Some of you also noted the suspicious looking Q waves in III and aVF.

Pericarditis and Early Repol were put forth as possibilities. Remember though, that neither of those will have reciprocal changes (excepting myocarditis, which may present as STEMI). Here, we have reciprocal changes inferiorly. If you were inclined to be thinking about STEMI mimics in this case, those changes should put ischemia at the top of the list.  In addition, as some of you pointed out, the ST changes do not look like Early Repol, and the amount of ST elevation here is alarming.

The crew in this case, along with the physician, decided this was STEMI. The patient was given Heparin, ASA, anti-emetics, and Morphine. His condition improved enroute, and his BP climbed to 124/75.

Upon arrival at the hospital, he was taken directly to the cath lab. There was a complete blockage of the LAD.

 

Here is the cath lab image showing the blockage:

Here is the image after revascularization:

 

I don't know about you, but I always find these images amazing. Fortunately, our patient was discharged from the hospital to cardiac rehab a few days later. He was expected to recover nicely. 

Enjoy the holiday!

 

 

 

 

Posted by on July 4, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , ,

51 Year Old Male: Chest Pain

20 comments

Here is a great case submitted by faithful reader Niels, a Paramedic in Germany. As always, some minor information may have been changed to preserve patient confidentiality.

Our case today takes us overseas, to the German countryside. It's a clear blue Monday morning, 11:40 am, when you and your partner are called to a 51 year old male complaining of chest pain. You are dispatched parallel to an Emergency Physician (in Germany, every ALS call is dispatched with an ALS ambulance and a doctor).

On arrival, you find a male patient lying in bed. He appears to be very diaphoretic an pale. He tells you he is very athletic and fit, but today is "feeling horrible". He says his "chest is killing him", and he admits to being nauseous, with several bouts of vomiting.

O,P,Q,R,S,T: He tells you he woke up with the pain, and it seemingly came out of the blue–he was feeling fine the night before. Nothing seems to make the pain, which he describes as "crushing', feel better. In fact he can find no position of comfort. You seem to be compiling "red flags" as he tells you that the substernal pain also radiates to his left arm. He rates it a 4 or 5 out of 10, and says it began about 15 minutes before EMS was called. You ask if he's ever had this happen before and he says no.

As your partner starts to apply the electrodes, you continue your HPI and vitals. He has no real medical history, although he did smoke but quit ten years ago. He takes no meds. He does tell you that he saw his general physician last week for becoming "short of breath" during his workouts. Pneumonia was ruled out.

  • HR:     67 and regular
  • BP:     92/57
  • RR:    28, a bit labored
  • Skin:  cool and moist
  • Lungs Clear, SpO2 99% on room air

You give him 4 baby ASA, and acquire the following 12 lead ECG:

Ok, this is not what you are used to seeing. In addition, the speed is 50mm/sec. Thanks to the studio magic of Christopher Watford, here is the same ECG "stitched" together in the familiar format, speed adjusted to 25mm/sec:

A few moments later, the Physician arrives. He wants to know the status of the patient, and what you see on the ECG.

What do you tell him?

 

Posted by on June 20, 2012 • Filed under: ems-health-safety, patient-management, Training, training-development • Tagged: , , , , ,

“What Happened?”–Discussion

1 comment

This is the discussion to "What Happened?" You may wish to review the case here.

Ok, let's review the initial 12 Lead:

Just about everyone picked up on the infero-posterior STEMI.

Where it got interesting for me, was determining what the rhythm was! At first glance, the rhythm was for the most part regular (note the computer interpretation of Atrial Fibrillation with RVR!) and narrow, with a rate just a touch faster than 100. I did not see P waves before most of the QRS complexes, and I initially thought it was a junctional tachycardia.

As the STEMI was most likely due to an RCA occlusion, it is not surprising to have conduction disturbances. The pause, followed by an apparent sinus beat (circled in red above), had me wondering if this was indeed junctional with a sinus "escape" after the pause, or some kind of sinus rhythm with AV block.

In keeping with our spirit of "Peer Sourcing", I ran this strip by electrophysiologist Dr. Nick Tullo, of the ECG Academy.com. A review done by Life in the Fast Lane of Dr. Tullo's excellent academy can be found here. This is the conversation I had with Dr. Nick about this rhythm:

Me: Thanks for the help Dr. Nick. Now, what the heck is this?? Junctional, or sinus/AV block?

Dr. Nick: I would call it "Atypical Wenckebach" –essentially 13:12. You can see a sinus P following the fourth beat, and then a similar pause just before the end of the tracing. The pause is less than two times the previous R-R, and the PR of the second beat following the pause is longer than the PR that interrupts the pause (what you are calling accelerated juntional is really sinus rhythm with a first degree AV block, but you can't see the P easily because it's buried in the previous T). In the setting of acute IWMI it's due to the same high-vagal-tone mechanism that would cause the usual 3:2 or 4:3 Wencheback (or even complete heart block in some patients) but the AV node is mostly keeping up.

Me: Wow… OK!  But, how do we know it's not a junctional rhythm with a sinus beat escaping from the pause?

Dr Nick: You have to look hard for the P waves. If it was a junctional rhythm you'd see consistent P's at the end of the QRS or maybe in the very early part of the ST segment. If I'm right, the P wave will be on the T-wave somewhere and not always in the same spot (since it's not directly connected to the previous QRS). Granted, the ST elevation makes it hard to see the Ps. But I see the answer clearly:

Look at V5…see how the first beat has a concave upslope of the T wave while the second beat looks like it has a bump on it? That bump is the P wave. Assuming that the R-R interval midway through the "junctional rhythm" is equal to the atrial rate (since the PR doesn't change midway through an Atypical Wencheback cycle) measure back from the visible P preceeding the third beat in V5…doesn't it land right at the bump? The reason the T looked concave the beat before that is because that P wave is on the peak of the T.

I've put together some graphics to help illustrate the important points. 

First is Lead V5, which Dr. Nick referenced, blown up. I've done the same with lead II. Note the subtle morphology changes in the two T waves. This is the last P wave  of the cycle, which does not conduct. the P wave following the pause is the first of the cycle, and has the shortest PR interval:

I know, you're thinking, "Really? Do those little blips/bumps really measure out?" Don't take my word for it. I've got one more illustration to show you. I took a mid cycle R-R interval (1), as Dr. Nick suggested, and used that to measure back and see where the P wave should be in leads II and V5 (2,3):

As you can see, right on cue, those blimps/bumps are right where the P wave should be. And there we have it: 13:12 Atypical Wenckebach, with a PVC at the very end of the strip.

My sincere thanks to Dr. Nick Tullo for his help with this case, and kudos to Jason, who expertly picked up on this in the comments section.

Now for the second 12 Lead:

The patient was treated with thrombolytics (TNK), and as many of you commented the resulting rhythm was an accelerated idioventricular rhythm (AIVR).  AIVR appears similar to VT, but slower (slower than 120). In the thrombolytics era, this transient rhythm was noted to be a marker of reperfusion, although not all patients with a reopened coronary artery have AIVR. When it appears it rarely causes hemodynamic instability, and usually requires no treatment. For more information about AIVR, see here.

Of course, you will notice that I have circled several leads in the 12 lead above. In keeping with this case, in which nothing seems to be typical, you will notice that in fact the ST segments have not resolved during the AIVR. The inferior ST elevations remain, as do the ST depressions in V1-V4, and aVL. 

When asked about this, Dr. Smith, of Dr. Smith's ECG Blog had this to say: "This is one of the few cases of AIVR I've seen that was not associated with reperfusion."

In this case, our patient failed thrombolytics. He was immediately sent for rescue PCI. Unfortunately, we don't have any additional information.

There was a lot of information in this discussion. I sure learned a lot! 

I look forward to your comments, and as always, thanks for reading!

Posted by on June 2, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , , , ,

What Happened?

49 comments

A 68 year old male, with no significant medical history, presents to the local ED (non-PCI) with chest pain. He had been doing some gardening, when he suddenly felt chest discomfort (8/10), non-radiating with diaphoresis. His wife drove him to the ED. Once there, he was given ASA and NTG, and the following ECG was acquired:

His vitals were as follows:

  • HR:    104 and regular
  • BP:     118/68
  • RR:     20 and regular
  • Skin:   cool, pale and clammy
  • Lungs: clear bilaterally
  • SpO2:  99% on O2

After a short time, the patient was given another treatment and entered the following rhythm:

 

  • What do you think happened?
  • What is the rhythm?
  • What do you think they did next?
Posted by on May 24, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development, Uncategorized • Tagged: , , , , ,

Treat the patient not the monitor?

8 comments

Here at the EMS 12-Lead Blog, we love case studies.

We love to post them, you love to read them, and many of you love to comment on them.

Not only on this blog, but on other very good blogs that are out there as well. I think it’s a great way to learn, and share ideas in this era of Web 2.0.  What I want to discuss today is one comment I often see:

Treat the patient, not the monitor!

Before we start, I want to be clear about a couple of things.

First, I understand that ECG interpretation is hard. Really hard. To become proficient it takes countless hours, months, and years of study. Whatever my opinions, I am certainly not trying to suggest it is easy or routine. I make mistakes like everybody, and I will still run a difficult strip or 12-Lead by people who know more than I do for help with the interpretation.

Second, when we are talking about treating the patient not the monitor, we are not talking about defibrillating a live patient with tremors because it looked like VF on the monitor. “Oops, guess I should have looked at my patient”. No, that’s not what we mean.

Often, when someone writes, “just treat the patient, not the monitor”, what he or she really means:

I can not figure out all of these squiggly lines, so I am going to ignore them.

Hey, I get it.

Hell, I’ve been there, and so has everybody else. In fact, I am still there sometimes. Everybody has a patient whose ECG is challenging, and takes them as far as they can go with their interpretation skills. It does not mean that we should devalue the importance of the ECG just because we are having trouble interpreting it.

If we want to evolve into clinicians instead of technicians, we have to use all of the relevant tools at our disposal. When it comes to potential cardiac patients, our cardiac monitors can be some of our most important tools. These relatively small machines can give us a ton of important information, and arguably we can not really have a full picture of what is happening with our patient if we can not interpret what we see on the monitor.

Does what we see on the monitor really matter that much?

Consider your tachycardic patient, who looks sick with poor color, but an Ok mental status and a reasonable pressure. Are we looking at,

  • Sinus tach? 
  • SVT? 
  • VT? 
  • A-Flutter?

Do you want to give fluids? Or perhaps adenosine, amiodarone, or Cardizem?

How are you going to determine what treatment he needs?

Oh that's right, by interpreting the ECG.

There is really no getting around it. I suppose you could just transport everyone to the hospital and let them deal with it, or wait until they become unstable enough that you have to shock them. But is that the optimal patient care we want to deliver?

Even if you decide all you can or should do is take the patient to the hospital, you have to ask what type hospital do they need?

  • Do we just treat them all as a STEMI and take them to the PCI center?
  • Is it just a baseline finding and their local hospital is Ok?
  • Is it an isolated posterior STEMI that we're not seeing?

Want to hold off on NTG? Give fluids? How are you going to know?

Again, by interpreting the ECG.

How about your syncope patient. Anyone up for WPW, Brugada, or another arrhythmia?

See what I mean?

When it comes to cardiology, I really don’t think we can separate the patient from the monitor.  I mean, they are hooked up to the darn thing anyway!

But even figuratively, what we see on the monitor is part of their history, part of their present illness, and very often contains the answers that we could get no other way. We are talking about cardiac patients who for the most part, look very similar, although the underlying problem can be anything we can see on the ECG from normal tracings, to arrhythmias and STEMIs and everything inbetween.

If you're good, you just might pick up something that saves their life. We see countless cases sent in by you–our readers–of patients who might not be here today if it wasn't for their prehospital ECG interpretation!

When we get that voice in our heads, the one that tells us not to focus on the squiggly lines and just look at our patient, we should listen to what that voice is really trying to tell us: that we don't know what it means, and we need to learn more.

There is no shame in that. In fact, I would take it as a sign of a good provider. To acknowledge what we need work on, and try to improve. That’s all we or our patients can really ask!

If you spend time reading Dr. Smith's ECG Blog or some of the electrophysiology blogs, one thing you will never see is "treat the patient not the monitor." That's because this is a false choice.

So let's start a trend whenever you come across a tough case study, and leave a helpful comment:

Treat the patient AND the monitor!

Posted by on May 19, 2012 • Filed under: ems-health-safety, Training, training-development, Uncategorized • Tagged: , , , ,

Snapshot Discussion: 32 year old Male–Chest Discomfort

28 comments

Here is the discussion for the Snapshot Case: 32 year old male–Chest Discomfort. Sorry for the delay.

If you recall, we have a young patient, a 32 year old male, with a heart rate too rapid to count. He is alert and oriented, and has a good pressure (126/70). He has been in the following rhythm for at least two hours:

 

So, what do we know about the rhythm? It is wide and fast, with a rate of 262. Since wide + fast = VT until proven otherwise, you couldn't be faulted for running it as VT.

Unfortunately as a "Snapshot Case", we don't know the outcome of this patient. However, our mission was to come up with a differential for this rhythm, so I'll share some thoughts:

  •  A-Flutter with 1:1 conduction: With rates approaching 300, it would be appropriate to consider it. I don't see any evidence of flutter waves though.
     
  •  SVT with LBBB aberration: The QRS is wide, but not that wide at 130 ms. V1 is negative, and there are monomorphic R waves in leads I and V6.   This is typical morphology for LBBB. Also, let's look at a clear QRS, from lead III:

           

           You can see that the initial downstroke of the QRS is sharp, and occurs in less than 20 ms. This as well favors SVT/LBBB over VT. If it is SVT, it could be either AVRT (WPW) or AVNRT.

  • VT: The rhythm is wide and fast, and it is possible that this is VT. The QRS is not that wide but it could still be fascicular VT (but I would have expected RBBB morphology) or RVOT VT (which would not have RBBB, but then I would expect the inferior leads to be positive not negative). It doesn't seem to meet any criteria that rule in VT (no initial R wave in aVR, concordance, etc), but that does not rule out VT. And then there is the sharp initial deflection of the QRS, instead of a slower activation. And of course the patient's age and history do not favor VT.

All in all, I think any of the above are reasonable in this case. We can't know for sure, but I lean towards SVT with LBBB aberration, probably rate related, unless he happens to have LBBB as a baseline.  You may have other thoughts, and I'd love to hear them!

As far as treating the patient, his mental status is good, his pressure is good, and he has been tolerating this rhythm for at least two hours. I think he's a good candidate for a trial of Adenosine, which might reveal the answer. If that fails, there is Amiodarone, cardioversion, or diesel as far as my protocols go. 

With no clear cut answer, I'm sure you all will have some good thoughts to add to this discussion. Sometimes, we just don't know for sure, but we still have to hone our skills of considering our differentials.

Thanks for reading, and I'm looking forward to your comments!

Posted by on May 17, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , , , , ,

Snapshot: 32 year old male–chest discomfort

46 comments

Here's a new snapshot case straight from the UK… We have a 32 year old male, normally fit with no history whatsoever. He has had a stressful week (personal issues), and decided maybe a 4 mile run might help. It didn't. When he returned home, he developed sudden onset of chest discomfort, and decided to lie down for bit. After a couple of hours, he wasn't feeling better and called 911.

While he is alert and oriented, he is also anxious and diaphoretic. Lungs are clear bilaterally, but the RR is elevated at about 30. Pulse is too fast to count, but the BP is 126/70. He describes the chest discomfort this way: "I feel like someone is punching me in the chest!" It is substernal, non-radiating, and rated a 5/10. His only other complaint is a touch of lightheadedness.

Here is the rhythm strip and 12 lead:

Your mission, should you choose to accept it, involves coming up with a differential diagnosis for our patient, and stating which factors favor one diagnosis over another. Oh, just one more thing… How do we treat him?

We look forward to your excellent responses!

Posted by on April 30, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , ,

63 Year Old Male: “Dental Pain”

34 comments

Here is an interesting case submitted by Adam Frederick, NREMT-Intermediate.  As usual, some details have been changed to protect patient confidentiality.

EMS is called to the local Urgent Care for a 63 year old male complaining of upper jaw pain related to "dental work". He had made two trips to the dentist this past week for pain related to "work done on a crown". Both times the dental work was in order, and the dentist could not find a reason for the  jaw pain. Today, while walking on the treadmill at the local fitness center, the jaw pain returned. He drove to urgent care because the dental office was closed. 

While at urgent care, he reported to the nurse that the pain began about 45 minutes ago, and seemed to worsen when he did strenuous activity. He thought it odd that today he had some chest discomfort as well, but felt it was probably due to his anxiety.

EMS arrives to find the patient in exam room 2. He looks pale, and his skin is cool and moist. He reports jaw pain of 8/10, and substernal chest pain of 4/10. History is significant for hypertension and anxiety. He takes Lipitor, ASA, and Metoprolol daily. He has no known allergies. His vitals are as follows:

  • HR: 90 and regular
  • BP: 180/114
  • RR: 16
  • Skin: cool/moist/pale
  • Lungs: clear bilaterally
  • Spo2: 98% on supplemental oxygen

You apply your cardiac monitor and acquire the following rhythm strip and 12 lead ECG:

 

Prior to EMS arrival, the patient was given 4 baby aspirin, but now refuses nitro and the IV. He states he "doesn't know what all the fuss is about", and that he "just wants to go home", and you get the feeling that he just might refuse transport.

  • What do you tell your patient?
  • Are you concerned about the ECG? If so, why?
  • How would you treat this patient, and where would you like to take him?
Posted by on April 10, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , , , ,

Discussion for 58 year old male CC: Epigastric pain

6 comments

This is the discussion for our "Snapshot" case, 58 year old male CC: Epigastric pain. You may wish to review the case before continuing.

Thanks to all of you, we had a lot of great comments!

Many of you had wished we had a rhythm strip to analyze… keep in mind, this 12 lead is a continuous ten second strip, long enough to analyze the rhythm.  Learning how to interpret rhythm off of a 12 lead is a good skill to have!

So, let's review the 12 lead:

So what do we know? We have a bradycardic rhythm with a rate of about 36.  There are visible P waves. The comments were mostly split between 2nd degree AV block type 1 (Wenckebach) , 2nd degree AV block type 2 (Mobitz II),  and 3rd degree block (CHB).  So, which is it? One very important thing to remember about 2nd degree blocks type 1 is that they will be irregular due to the dropped QRS.  In this strip, some considered that there may have been a lengthening QRS and dropped beat, leading to a conclusion of Wenckebach.  However, if you map out the QRS complexes, they are regular.  That pretty much eliminates 2nd degree type 1. There is no constant PRI, which would eliminate 2nd degree type 2 from the differentials, and that leaves 1st or 3rd degree blocks.  At that point, it becomes apparent that it is a 3rd degree block. Rhythms like this can be tricky, unless you look for all of the P waves. In this case, they are easiest to see in V3 and V4.  You should get used to marching them out.  You will find that many are "hidden" in T waves and just after the QRS complex, and may be missed unless mapped out, as I've done below: 

The other interesting thing about this rhythm is that the QRS complexes are not wide, as we might expect, but narrow. What does this mean? It means that the escape beats are not coming from the ventricles, but from the AV node or high in the HIS system.  As we know, these beats will perfuse much better than ventricular beats, and no doubt helped this patient remain more stable.

Next, we have to ask a question:  Is the complete heart block is the primary problem, or secondary to something else? Most of you recognized the inferior STEMI, with ST elevations in the inferior leads, and reciprocal depression in leads I and aVL.  Also, notice the ST depression in leads V1-V4.  This is not reciprocal depression, but rather posterior involvement as well! So we have an infero-posterior STEMI, with probable RVI.  You could do a 15 lead, but if you don't, he is already going to the cath lab:

A few things to keep in mind:

  • Patients suffering an IWMI often present with epigastric discomfort or burning.
  • As the RCA usually supplies the SA and AV nodes, AV blocks and bradycardias are common.
  • IWMI often extend to the RV and posterior portions of the heart.

The last thing to discuss is how we would treat this patient.  What about atropine? As was mentioned, atropine is not usually indicated in high degree heart blocks.  However, if the escape is coming from the AV node, atropine could possibly be effective, but not likely. I'm not sure the unapposed sympathetic response is what we are after in this case anyway.

How about pacing? Same issues, plus the discomfort of the electrical therapy.  Our patient is mentating well, and while his pressure is not very high (92 systolic), it is not terrible either. Fluids would be a good option here, and I think i would hold off on pacing unless he was shocky and the fluids didn't help.

It is important to remember that memorizing the ACLS algorithm is quite a bit different from applying it to our patients.  We have to decide what the primary problem is and what will fix it. In this case, the primary problem is an occluded artery, which needs to be opened immediately.  The arrhythmia is secondary to this problem, not the other way around. Some of are teetering on the edge, and the wrong treatment could push them over.  We must always balance the benefit we expect from our treatment against the risk of what could go wrong if we do it.  Is it worth it? Is it in the best interest of our patient? For this reason, we may decide not to give meds or pace, even though it could be justified under the "algorithm". 

Unfortunately, we don't have any follow up or additional information to wrap this case up. But I can tell you this: Patients are complicated. Much more complicated than algorithms. We face grey areas and decisions that are not always easy.  That is what makes medicine so interesting… and challenging.

We hope you enjoyed this interesting case. Thanks for reading, and keep up the good work!

Posted by on March 14, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , , , , ,

Snapshot: 58 year old male CC: Epigastric pain

74 comments

From time to time, we may have an interesting ECG, but without enough information (including final diagnosis) or additional ECGs to make a full case study.  In these instances, we will share the ECG and whatever information we have in our "Snapshot" series.  As always, some information may be changed to protect patient confidentiality.  Hope you enjoy!

Our first "Snapshot" involves a 58 year old male, with a chief complaint of epigastric pain. This pain has gone on for three days, and EMS is called by his girlfriend after "a couple" of syncopal episodes. Upon your arrival, he is alert and oriented, with an auscultated BP of 92/50, and a palpable radial pulse of 36. RR was 18, with an SpO2 of 95% on room air and clear lung sounds. He does, however, look anxious and is cool and diaphoretic. He complains of some shortness of breath, which he attributes to his epigastric pain. He has no significant medical history.

Here is the 12 lead ECG:

 

 

So, 

What do you think is going on here?

What would you do about it?

Posted by on March 5, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , , , ,

Discussion to 63 year old female CC: Chest Pressure

2 comments

This is the discussion to 63 year old female CC: Chest Pressure.  You may wish to review the case.  Also, you may wish to review the two part discussions about WPW here and here.

Thanks to those who commented for some very insightful comments!

Let's revisit one of the pre-conversion 12 Leads:

We can see an irregularly irregular WCT rhythm (note the conversion to narrow complex A-Fib at the end of the lead II rhythm strip).  Our list of differentials should include:

  • A-Fib with RVR and aberrant conduction
  • A-Fib with WPW
  • Slightly irregular VT

As it turns out, this patient was diagnosed with new onset A-Fib with WPW.  Apparently, at least one other member of the family had it as well.  However, i do not think this case was at all obvious.  While the pre-conversion ECGs had an "appearance" of A-Fib with WPW, it was not as irregular and "bizarre" as we have typically seen. I think leads V2 and V3 showed morphologies that appeared most familiar to us when it comes to A-Fib/WPW:

If we determine that A-Fib is present (irregularly irregular rhythm), we must try to determine if it is A-Fib with aberrant conduction vs. WPW.  How can we tell? If it is aberrant conduction, we would expect to see the same morphology of the QRS complex, and a ventricular rate that is not unreasonably fast. If we see changing QRS morphologies, and the shortest R-R intervals that are 250 ms or less, WPW is suspected. In this case, the rhythm appeared to be irregularly irregular, but not grossly, as in other cases.  Also, the morphologies were not as bizarre as we have seen in past cases.  The rate was very fast in spots, however, which supported an accessory pathway.

What was also quite confounding, however, was the post-conversion ECG, which as many of you correctly pointed out, did not show any obvious signs of WPW. On the flip side, there was the predominant R wave in V1, and the Q waves in leads III (most notable) and aVF, possibly showing a "pseudoinfarct" pattern:

 

This was a complex case.  One of the great things about web 2.0 is the ability to "peer source." I forwarded this case to a few electrophysiologists who were kind enough to offer their insights on this case:

Dr. John M, of the Dr. John M blog, left some awesome comments in the comments section of this case. I strongly urge you to read his comments.  To briefly summarize, he believes the rhythm is "AF with intermittent conduction over an infero-post accessory pathway." As to why there is no obvious pre-excitation present on the post conversion ECG, he says the pathway is "left sided and away from the septum; in other words, it is geographically distant from the AV node. Second, this patient has a really good AV node- as evidenced by a short PR interval despite an onslaught of AV nodal blocking drugs." He also adds, "it's not uncommon for accessory pathways to conduct intermittently when injured or aged, or suppressed with meds." This summary does not do justice to his comments. Make sure you read them in the comments section!

Dr. Wes, of the Dr. Wes blog, had this to say: "Sure looks like pre-excited AF (pre-conversion), and normal (no pre-excitation) post-conversion. Could he still have an accessory pathway? Of Course. If the accessory pathway is lateral enough, he may not reach the AP antegrade from the sinus node before the ventricle is activated via the AV node. Hence, no pre-excitation is seen." He adds that anything that would delay conduction in the AV node may reveal the pre-excitation.

Mark P, author of the Electrophysiology Fellow blog, offered this: "The WCT is very suggestive of a pre-excited AF, probably a left posterior AP. True, there is no obvious delta on the resting ECG, but there is a slurred Q wave in III and aVF (negative delta), and the dominant R wave in V1. So, putting it all together, a resting ECG suggesting a left post/lat AP and a tachycardia ECG (notice how the Q in III and aVF is exaggerated in this ECG- a negative delta) also suggests AF with a left post/lat."

So, we seem to have a consensus among the electrophysiologists, and i appreciate their contributions to this case greatly!

A few take home points:

  • Social media and the ability to "peer source" is awesome.
  • Seeking "expert opinions" leads to great knowledge and learning.
  • There is much more to WPW on the ECG than what is "classically" taught.
  • These cases are complex and can be missed in the ED. 
  • Learn as much as you can about these conditions–you just might save a life.

Hope you enjoyed this case! Comments and feedback are always appreciated.

 

Posted by on February 29, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development

My experience at the Resuscitation Academy

2 comments

 

Back in October, I was fortunate to attend the Resuscitation Academy in Seattle, WA. As many of you already know, the Academy is run by Seattle Medic One and King County EMS, with the goal of improving survival from out of hospital cardiac arrest. EMS directors, managers and medical directors convened for a three day "mini-fellowship" program, immersing ourselves in lectures and discussions about developing strategies we could bring back to our own communities.

I returned home inspired and motivated. As the STEMI/Cardiac Arrest Coordinator for my agency, I was eager to affect change. My original plan was to write this post back then. In the words of David Hiltz, a fellow RA alumnus, I knew I would "drink the kool-aid". I just wanted to know how long it would last.

Would I, after several months, be just as motivated and inspired as I was when I returned from the Academy?

I am.

This was a tremendous opportunity to learn from the best. Medic One and King County EMS are well known for their impressive survival to discharge rates from witnessed VF arrests of cardiac origin (they classify asystole and PEA as a different disease process).  Their survival to discharge rates, north of 50%, top any list I have seen. Of course, detractors will question the "narrow" definition used to achieve those rates, and in fact I did pose that very question to Dr. Mickey Eisenberg himself on day one.

When asked about this, he acknowledged the question, and told me simply that he invited any system to use the same narrow definition, and see where they stack up. I was impressed with his candor, and the accessibility I had to the minds of such esteemed Physicians.

In addition to Dr. Eisenberg, our faculty included Drs. Tom Rea, Leonard Cobb, Peter Kudenchuk, and others.  You may recognize their names from some of the major studies that shape our practice. We discussed such topics as "Measuring Performance and QI", "Dispatcher Assisted  CPR", "High Performance CPR", "Cardiac Arrest Registries", "Response Times", "The ineffectiveness of ACLS" (yes you read that correctly), and "Community CPR". There were other engaging topics as well.

They also like to speak in mantras:

  • "Pick the 'low hanging fruit'"
  • "Change happens iteratively"
  • "Measure and improve, measure and improve"
  • "Performance, not protocol"

There are two more mantras that I think impressed me the most.  The first is what they call their "Culture of Excellence".  And it is easy to see why. This is a high functioning system, with leaders in academics and research who are intimately involved in their delivery of patient care. No matter how much success they seem to have, they do not rest on their laurels.  They continually measure and research, striving to be better. They set goals that seem unrealistic to many, but very realistic in Seattle/King County.

Did I hear someone say 70% survival to discharge rates?  Every cog in their machine from the doctors and administrators to the medics I spoke with all work together for one common goal… which leads me to the last mantra which impressed me so much: "Everybody in VF survives."

"What? Well, they don't where I come from," was a common thought running through the room. And of course, even in King County not everyone survives sudden VF arrest.  But the message is clear: they expect them to survive.  "Hearts too good to die", as they say. Even though not everyone survives, the expectation is that sudden VF arrest is a treatable entity. Get the care to them in a timely fashion, and deliver it expertly, and they will survive. And when they don't, they do QI until they can find out why they didn't survive. Lessons learned are added to the mix and the cycle continues.

I could not wait to return to my system, full of ideas and hope. To me, Seattle/King County serves as a beacon to what is possible. As Tom Bouthillet is fond of saying, "a system achieves exactly what it is designed to achieve". If you want different results, you have to change your system. If I had my way, it could be done top down, on a larger scale. Why settle for little steps, agency by agency, when it can be changed on a "system" level by the highest administrators. Of course, system design, politics, geography all play a role in the character of each EMS system.

It is up to all of us to decide the best way to get the job done in our own systems. Some may achieve this in a top down approach, and others may have to start at the bottom, at the agency level, and go up and out from there. Either way, the important part is setting change into motion. Get some momentum going. Aim for the top, and don't settle for less.

That is what I have been working on since I have returned. As they say at the Academy, "it's not complicated, but it's not easy either." We have made a commitment to measuring performance, We have stepped up our QI of cardiac arrests, including structured debriefings, and utilization of data from our cardiac monitors. And of course, we have focused our training on what works, namely CPR skills and defibrillation, trying to increase our compression fractions as much as possible.

A culture changes when you start looking at and talking about issues in a different way. Time will tell how long it will take for us to see meaningful changes in our survival rates. Armed with the attitude and lessons learned at the Resuscitation Academy, I know we will get there. A culture of excellence starts somewhere, and it might as well start with us.

 

Posted by on February 27, 2012 • Filed under: administration-leadership, ems-health-safety, ems-topics • Tagged: , ,

63 year old female CC: Chest Pressure

29 comments

Here's a case from a faithful reader who wishes to remain anonymous.  As usual, some information has been changed to protect patient confidentiality.

You are called to transfer a 63 year old female from a community hospital to a large medical center.

Upon arrival at the local hospital, you are confronted with chaotic scene. You see your patient, now resting, and are told she presented with chest pressure and palpitations a couple of hours ago, was also becoming obtunded, and her family had stated she had not had any any similar episodes in the past. Her vitals are as follows:

  • Pulse:   200 and irregular
  • BP:   132/76
  • RR:   22 regular
  • Eyes:   Pearl
  • Skin is cool and dry

They hand you an ECG and tell you she presented in the following rhythm:

And with the following history:

  • She had sudden onset of chest pressure and palpitations, which began while she was doing some work around the house.
  • Nothing changed the discomfort
  • felt like "pressure" and "palpitations"
  • No radiation
  • she rated the pressure as a 7/10
  • began one hour prior to presentation
  • No allergies to medications
  • She takes a "pill for blood pressure", name unknown
  • Past medical history significant only for hypertension
  • had a normal breakfast and lunch
  • She can not recall any specific trigger for the episode

In the ED prior to your arrival, she had received the following treatments:  Lopressor, Amiodarone, Magnesium Sulfate, Heparin, Lidocaine, Morphine and Versed.

None of these treatments changed the patient's rhythm:

The patient's mentation continued to decline, and her BP started to crash. After three attempts, she was successfully cardioverted. Here is the post-conversion 12 Lead:

You transport your patient, now stable, to the medical center without incident.

So, now the key questions:

  • What was the presenting rhythm and why?
  • What is the post-conversion rhythm and why?
  • What are the best treatment options for this rhythm?

See also:

Conclusion to 63 year old female CC: Chest pressure

Posted by on February 22, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , , , ,