IC established! We'll have several different sections reporting in - recent research, local topics, or highlighting areas of the Sponsor Hospital Council of Greater Bridgeport protocols.
*** Keep in mind - this website does not replace your protocols, and these posts do not reflect SHCGB or Bridgeport Hospital policies. This is a place to discuss research, controversies, or discuss possible future protocols. When in doubt, check your current protocols through the official source.
The facts: a 35 year old male, with no medical history, presented with 1 week of chest pain that became acutely worse 1 hour prior. It was a "squeezing" feeling that radiated down his left arm. He had some mild dyspnea, and 1 nitro made it somewhat better. Some smoking, no cocaine.
The ECG:
The computer interpretation used caps lock, had a lot of "***."
Cardiology was skeptical, but had him in the cath lab 30 minutes later. My resident put 50 cents down on a LAD occlusion, while I bet him a cup of (free) coffee that this was a classic first diagonal , or high lateral, STEMI. The two cardiology fellows agreed that we were both mistaken, and that they were certain to find a blocked circumflex. While the patient was in the lab the troponin came back as significantly elevated.
A few hours later, the cards fellow calls me back with the cath results.
Survey says!
No offense to Steve Harvey, but I'm a Dawson kinda guy.
Nada. Clean cath. "No significant fixed obstructive disease."
Interestingly, however, both ventriculography and an echo revealed hypokinesis of the high anterolateral wall, corresponding to the anatomy suggested by the ECG. He was given a diagnosis of focal myocarditis.
Focal Myocarditis
This isn't very common, but we can't say how uncommon. It is still uncommon enough to be worthy of case reports, at least in Texas. We know that about 3% of MIs have clean coronary arteries by angiography, but a number of those people have spasm or spontaneous reperfusion. The percentage may even be smaller with STEMI patterns, but we don't know.
The only way in the past to definitively diagnose myocarditis was through endomyocardial biopsy, which has a good number of shortcomings, in terms both of sensitivity, and of complications.
Advances in MRI techniques have enabled researchers to noninvasively study myocarditis. In a recent study it was found that 78% of patients who presented with an MI (64% with ST elevation), but a clean cath, had evidence of myocarditis on MRI.
Uh, yeah, I see it too...
Reciprocal changes
Now, I understand that the myocarditis can generate ST elevation, likely in the same manner that pericarditis does. I am really surprised, however, that our patient had such distinctive and appropriate reciprocal changes. Nonetheless, an ECG from a case report of myocarditis also shows reciprocal changes:
Pericarditis should never be assumed when there is even a hint of reciprocal ST depression. Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare. I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.
A great review article by Punja 2010 gives a few examples of ST elevation in myocarditis, but neither example shows reciprocal changes.
Nasty STE in myocarditis, but no ST depression
Sooo... Rare ECG finding? Not enough research? Incomplete diagnosis?
The Bottom Line
So, the next time you bring in that "for sure" STEMI, keep in mind there's a (3%*78%=) 2% chance it's myocarditis. Or higher. Or lower.
Medics aren't happy unless they're arguing about something.
Since most paramedics are 1) intelligent, 2) clever, and 3) convinced they are more clever than the other medic they're arguing with, they need an appropriate subject to engage in. The ideal topic should provide the opportunity for them to put their knowledge of physiology, gas laws, and hydrodynamics on display, but also allow them to parry with a quick "In my experience..." Ideally, there should be no clear empirical studies on the subject.
The "danger" of giving albuterol to a dyspneic patient who may have CHF is just such a topic.
Fortunately, a complete literature review on the topic easily will fit in one blog post, with plenty of room left over for a relevant case, complete with ECGs!
The Wheezer
"Hey Doc, you gotta see this guy next."
Generally I listen when an experienced nurse tells me that, so I went to see Mr Wheezer right then.
Not our patient.
He did not look good - sweaty, pale, working to breathe, with his second albuterol/ipratropium neb going. "I think it's my allergies," he says. So much for the patient telling me the diagnosis...
So I asked him to tell me about his "allergies." He'd been having some dyspnea on exertion over the past 2 weeks, with a nagging cough. But an hour ago, while at rest, he felt like his chest was being pressed in, right up into his jaw, and he had started sweating buckets. His breathing had worsened, and his wife called 911. He had a history of diabetes, hypertension, and stents in all 3 of the major coronary arteries.
The paramedics had started the series of neb treatments he was receiving, and a quick exam revealed why - he had the loudest, clearest, most unambiguous wheezes I have ever heard. No crackles, no rhonchi, no upper airway crud fouling it up. Textbook wheezes. Even the greenest of EMT-B's, using a Fisher-Price stethescope, could confidently diagnose these wheezes.
"And an S3. He's definitely got an S3."
On the other hand, the first ECG looked like this:
That's pretty bad case of allergies. I looked at his old ECG:
No slam-dunk STEMI here. I grabbed the ultrasound, and took a look at the heart and lungs. No pericardial effusion, no signs of a PE, but when I looked at his lungs, I saw the shimmering artifact that suggests wet lungs. For an example (not my patient):
I took off the neb, and popped in a tab of nitroglycerin. Within 2 minutes he had his color back, he didn't't look so drenched, and he was breathing easier. Like a lightswitch - click! - he was improving.
I got cardiology involved pronto, before any labs, or even the chest x-ray came back. After they evaluated the patient and the ECG, they shared my concern, and were planning to take him for an urgent cardiac catheterization. Almost as an afterthought, we checked out the labs together.
Troponin - negative.
BNP - negative.
Huh.
We checked out the chest film - clear.
But the ball was rolling, and he went to the lab. Good thing, too, since he ended up having severe stenosis in his mid and distal LAD, as well as the circumflex, which all got new stents. The RCA, which previously been patent, was now totally and permanently occluded.
Soooo, that proves it was CHF, right?!? Well, he still had dyspnea after the procedure, though nowhere near as bad as before, so he got more tests and consults. I won't go through the details, but after being evaluated by 3 cardiologist, 2 pulmonologists, and one lowly ER doc, he had a diagnosis of "likely CHF."
This encounter made me consider a few questions:
How good are paramedics at diagnosing CHF?
The medic in my case only gave albuterol, no nitro or Lasix, and had not obtained an ECG, and so was clearly not considering CHF. But the diagnosis can be tough for physicians, even with all the clinical gizmos at our disposal.
With that in mind, how does the paramedic diagnosis of CHF stack up against the emergency physician's? Turns out, it's pretty good, within limits.
One study from 1995 looked prospectively at the paramedic's diagnosis compared with the ED physician diagnosis. Considering that the doctor had access to medical records, x-rays, labs, etc, the paramedics did fairly well, showing "good concurrence" with physician diagnosis. Another study looked at how well paramedics determined a cardiac cause of dyspnea. This could include angina or MI, as well as CHF, so it wasn't a perfect comparison, but the agreement between medic and doctor had a kappa of 0.71, or "good, approaching excellent."
A more recent, although retrospective, study looked only at the diagnosis of CHF. Interestingly, they studied all the patients whom the paramedic had given furosemide to, using this as a surrogate for a diagnosis. They then looked at the final diagnosis of the the emergency physician. Generally the medics did well, and the doctors agreed in 60 out of 94 cases.
The disagreements are thought-provoking though. Between pneumonia and COPD, a lot of furosemide was given to people to who didn't need it. Furthermore, there is evidence that suggests that treating pneumonia with diuretics is harmful.
Looking towards the future, however, if we can combine capnography and portable BNP analysis in the prehospital realm, EMS could end up being the gold standard for the ED to live up to!
How often does CHF present with wheezing?
Often enough!
In one study of older patients, it was found that about one third of patients had wheezing with their acute episode. Perhaps not surprisingly, these patients usually were smokers, had a prior diagnosis of COPD, and were using bronchodilators at home. Unfortunately, they did worse with their CHF events, going to the ICU at a higher rate, for instance.
There aren't too many other studies that study the rate of wheezing, but we can also look at the rate of albuterol/beta-agonist administration as a rough equivalent. In one study20% of patients got albuterol (in addition to other drugs), while in another study only 2% of CHF patients got albuterol (as the sole therapy).
I think this evidence suggests that there can often be a component of wheezing with acute episodes of CHF, but that "pure" wheezing, without other indications of of CHF, is pretty rare.
Is there a danger in giving albuterol to a patient with CHF?
My patient ended up getting stented for cardiac ischemia. It seems reasonable to wonder if the 2 neb treatments, in addition to being ineffective, might have exacerbated the ischemia, causing harm. However, looking at the clinical evidence is difficult, as much of it doesn't apply to emergency medicine, let alone paramedicine.
For example, there are a number of studies that analyze the harm associated with use of bronchodilators in patients who have diagnoses of both COPD and CHF. These studies, however, follow patients over months to years, and aren't very relevant.
One ICU study looked at the degree of tachycardia or number of tachyarrhythmias after albuterol neb treatment. They actually did not find much negative effect on the vital signs.
Well, what about studies in the ED or prehospital that look at truly relevant outcomes? Surprisingly, there only appear to be 2 relatively useful clinical studies available to guide us.
The first was a case-control study done in 1992, by Wuerz. They looked at about 500 dyspneic patients who had received prehospital treatments. They found that it was pretty bad to treat asthma or COPD, for example, with Lasix. However, when they looked at the 9 CHF patients who were mistakenly treated with beta-agonists, they found, reassuringly, that "none died."
The second study (Singer 2008) was bigger, using registry data on about 11,000 CHF patients treated in the ED. The nice thing about using such a data source is that you can get a lot of patients, and find associations. The bad news is that you often can't explain what you do find.
Such is the case with this study. About 20% of the patients received beta-agonists, either by EMS or in the ED, but had no pre-existing history of COPD or asthma. They used some statistical rejiggering to try and make fair comparisons, since CHF patients with a history of COPD are not exactly like CHF patients who don't have COPD. I won't bore you with the details, but that's what they mean by "adjusted with propensity analysis" on the following table.
Now, there wasn't any apparent difference in mortality, discharged alive form the ED, or ICU admission - that's what all those big red Xs mean. There was, however, an increased rate of intubation in those CHF patients who were treated with bronchodilators, but who had no history of COPD.Same for BiPAP and inpatient mechanical ventilation.
So what does this all mean? Now, this study wasn't randomized, and it really only shows an association, not cause and effect. The authors state (emphasis is mine):
Inhaled bronchodilator use in these heart failure patients without chronic obstructive pulmonary disease appeared to be associated with worse outcome. Because of the observational nature of these data, we cannot determine whether these patients’ outcomes were worse because they were more severely ill or because of a directly harmful effect of the inhaled bronchodilator.
However, this association persisted after adjustment for propensity score and standard risk factors for mortality. This finding suggests that inhaled bronchodilators may have contributed to the poorer outcomes observed in heart failure patients without chronic obstructive pulmonary disease who were treated with bronchodilators.
Or may not have contributed - we just don't know. The authors allow that treatment with bronchodilators may just a marker for bad CHF, but not a cause of bad CHF. I'm sympathetic to that point of view.
The Bottom Line
If you're pretty sure the patient has CHF, they need nitro and CPAP. Lasix is old school, and might hurt people when you're wrong about the diagnosis, and there is no evidence that albuterol will help with edema.
On the other hand, if you get fooled by wheezes, don't feel too bad. It might not have helped, but it probably didn't do much of anything at all.
Quick post today, concerning a very common error I see both in EMS and ED patients - misplaced ECG leads. I would call this a pet peeve (as the techs and nurses I work with are well aware!), except that a peeve does not usually carry significant clinical implications.
An article in the curent issue of EMS World argues for the acquisition and transmission of prehospital ECGs by BLS crews. No argument there - that is exactly what happens in the ED. A tech acquires the ECG and runs it to me. If your system allows for easy transmission of ECGs, and if paramedics are scarce, this would be a common-sense approach to take.
Unfortunately, an accompanying illustration distracts from the main message.
Another clue to V1 & V2 misplacement is their location relative to lead V4. Given that V4 should be located in the fifth ICS, the large vertical distance between V2 and V4 in the illustration suggests misplacement of V1 and V2 as well.
A second apparent error is that V3 is shown slightly medial to V2.
It should properly be placed halfway in between leads V2 and V4.
Why is this important?
Misplacement of ECG leads, and especially V1 and V2, are common. One study compared the accuracy of cardiac techs, compared with nurse, physicians, and even cardiologists. No one, except the techs, came out looking too good.
The ovals represent the range of misplacement for each lead, broken down by training level. Ref.
These errors are not trivial. "Pseudo-infarction" patterns can be generated from incorrect lead placement, leading to erroneous cardiac catheterization lab activation, cost, and diversion of resources. In the example below, simply moving the V1 and V2 leads from the 4th ICS, then to the 3rd, and then the 2nd, produced ECG changes which the computer interpreted as suggestive of ACS.
Another example - you can see how an rSR' pattern is falsely generated as V1 and V2 are moved from the 4th ICS (in B-1) to the 3rd ICS, and then 2nd ICS (in B-3).
(Interesting aside - placing the leads in a higher ICS is used to assess for an occult Brugada pattern, But this is sort of a specialized technique, and I leave it to the electrophysiologists.)
A recent post from Captain Chair Confessions highlighted the importance of proper lead placement, not only with regard to accuracy, but also in assuring that EMS appears professional and competent. I second that, but I have to acknowledge that many paramedics likely learned the incorrect position from preceptors within the hospital. Heck, in one of the studies mentioned above, the cardiologists were the people least likely to properly position V1 and V2!
So, kudos to David Howerton and the other authors on making a good argument for ECG acquisition as a BLS skill! But strive to demonstrate proper lead placement - it makes a difference
In the last 2 posts, I reviewed recent studies that looked at the decision to obtain a prehospital ECG, and a novel method to teach STEMI identification to novice ECG readers. This leads to the last installment in this trilogy: How often does EMS mistakenly activate the cath lab? For that matter, how good are emergency physicians?
(Side note: This is the second paper I have reviewed that has Jon Studnek as an author. He's a paramedic who also has a PhD, and is faculty at Carolinas Medical Center. He writes a lot, and I probably could fill all of my posts with reviews of his publications.)
AKA "Dr. Medic"
This study uses data from the Reperfusion of Acute Myocardial Infarction in Carolina Emergency Departments (RACE) program in North Carolina. This program has already been shown to improve time to PCI or lytics for patients with a STEMI, as well as other process measures. While recent data on actual patient outcomes is mixed, there is no doubt that this ambitious collaboration has brought some order to the notoriously fragmented emergency health care system in the U.S.!
The investigators used data from the 14 hospitals in North Carolina that acted as the receiving centers for STEMI patients transferred for emergent percutaneous coronary intervention (PCI).They looked at sub-groups of patients, broken down in three different ways:
Patients who first presented to a PCI center, or to a non-PCI center;
Patients who had the cath lab activated by EMS, or in the ED; and
Patients who used EMS, or those who "walked in" to the ED.
Because of the size of the program, they were able to look at a total of almost 4000 catheterization lab activations. That's one of the main strengths of this study - they have a lot of data.
Another aspect of the study that gives it some "real-world" applicability is how they defined an "inappropriate" activation of the cath lab. While other authors have described a "clean cath" as an inappropriate activation, the authors acknowledge that there are many scenarios where PCI for presumed STEMI is appropriate, despite the 20/20 hindsight of a negative cath. Takotsubo cardiomyopathy, for example, often requires an emergent angiogram to clarify the diagnosis.
So, instead they defined an inappropriate cath lab activation "If catheterization was canceled because of ECG reinterpretation or if the patient was deemed not to be a candidate" for PCI. Clinical factors, such as age or DNR status, were used to determine candidacy.
The overall results, comparing paramedics and ED physicians were that 15% of activations were inappropriate:
They analyze the results further, breaking down the data into the subgroups described above. The group of interest is all the patients who were transported by EMS, and had their initial activation by EMS. In other words, none of these patients were "walk-ins," but it included both patients who were brought to PCI and to non-PCI centers (initially).
They compare these activations against all the patients who had cath lab activation performed by the ED physicians (both at PCI centers and non-PCI centers), with patients who either came in by EMS or car.
There are a couple different ways to analyze these results, but overall the physicans performed better that the medics. Well, 7+ years of training ought to pay off somewhere, and and incremental accuracy in ECG interpretation is a reasonable expectation.
However, you can't even conclude this from the data presented, since an activation may have been deemed "inappropriate" because of a patient's DNR code status, say, or severe comorbidities (e.g. sepsis, or terminal disease). Specifically, we don't have the break-down for ECG accuracy versus judging cath lab candidacy for the 2 groups - it may well be the case that medics are just as good as emergency physicians at reading ECGs, but the physicians are better at judging which patients actually warrant an emergent catheterization.
The last table emphasizes the point that, while this sort of study is great at generating statistically-significant results, there is a lot of "granularity" that is not accessible to us.
Clearly, not all EMS agencies or EDs are equal - some systems are better than others. In this table, note the range of appropriate activations:
There are few EMS agencies and EDs who are evidently did not generate a single inappropriate activation! However, a 100% appropriate activation rate may also suggest a system that is too restrictive, and is missing too many STEMIs.
On the other hand, it is concerning that some EDs, even at the big hospitals with cath labs, have a "false-positive" rate of 25%. Similarly, some EMS agency inappropriately activates the cath lab 1/3 of the time!
The Bottom Line
This isn't a study that you can use to change your clinical practice in the next shift. It isn't even very useful at changing practice at your EMS agency or ED. However, it points the way to doing the more practical research, by highlighting important aspects.
For example, how do paramedics at different agencies decide to activate the cath lab, and how do these methods correlate with accuracy? Could a closer look at the 65% - 100% range in appropriate activations suggest a "best practice" for EMS? Should we rely more on intensive continuing education for paramedics? Alternatively, should there be more emphasis on computerized and/or human algorithms for ECG interpretation?
Furthermore, since the "Not Cath Lab Candidate"group accounted for such a large proportion of the inappropriate activations (4.3%), might their be a better way to anticipate this exclusion? To a large degree, the cardiologist is the individual who is deciding the patient's candidacy for the cath lab, and it is often difficult for the emergency physician, let alone the paramedic, to anticipate their decision. I'm not sure that the accuracy of prehospital STEMI activation should be judged using such "soft criteria."
So, more research is called for, as usual. But this paper serves as a very useful guide for the future.
Just when a paramedic student has started to feel somewhat confident about rhythm interpretation, she is introduced to the other 11 leads.
First off, the leads are organized even worse than the QWERTY keyboard. Inferior leads are the left of anterior, the lateral leads are in two different places, and aVR sits there all by itself, like a chump.
Then there are all the depressions and elevations, T waves flipping around, ischemia vs infarct. And then someone shows you how to pick up on a posterior MI by flipping the paper over. Madness, I tell you.
In particular, identifying a STEMI can be difficult, even if ST segment elevation is clearly seen. For example, the following ECGs all show ST segment elevation, but...
1. Not a STEMI
2. Not a STEMI either
3. Nope.
But with a fairly undramatic ECG like:
4. Bingo - Occlusion of the proximal LAD
The first first three ECGs demonstrate 3 common cause of ST elevation that we see in EMS or the ED, so-called "mimics" of STEMI. Now, there are a host of rules and criteria to help you diagnose each of these mimics, but it's hard to learn all of these, and to feel confident about them.
Is there a simpler way to achieve ECG excellence? Some short-cut to Jedi-level ECG mastery other than slogging through hundreds of tracings?
Perhaps a training montage?
Well, no.
But there are a few different ways to develop pattern recognition, and switching up the methods can put things in perspective. Hartman and colleagues have helped the novice ECG student tremendously with a new, focused approach to ECG interpretation. While this does not replace experience, practice, and feedback on interpretations, it's a good alternative way to tackle ECGs.
The rule has 4 steps, and we'll tackle them in that order
1. Is there ST elevation in at least 2 related leads?
The first rule specifies a minimum amount of elevation: 1-2 mm in two anatomically related leads.
It doesn't take long before a paramedic student identifies their first patient with ST elevation. Okay, granted, it's usually not an actual STEMI that they find, since the majority of ST elevation found in the ED or by EMS is not a STEMI. Typically, ST elevation will be due to any number of "mimics," such as left bundle branch block (LBBB), left ventricular hypertrophy (LVH), early repolarization (ER), as well as a number of other conditions. Surprisingly, if you look at all the patients who come into the ED with ST elevation, only about 1 in 7 patients have a true STEMI!
On the other hand, if you don't have some ST elevation, the patient probably doesn't have a STEMI. (Yeah, we're going to miss a true posterior or a proximal left main. This rule is for the novice reader, okay?)
No ST elevation, so not a STEMI.
2. Is the QRS a normal height?
The heart, over a period of years, responds to hypertension by bulking up and adding muscle mass. This process results in LVH, which, in the long run, isn't good. It shows up on the ECG as deep S-waves in V1 and V2, and high R-waves in V5 and V6.
In the short term, though, it mainly serves to distract us, as it can produce ECG findings that can look a lot like a STEMI. If we look at ECG #1 above, we see ST elevations in leads V2 and V3. Could these represent a STEMI?
Likely no, for several reasons. Now, a lot of the reasons involve interpretation of subtle, qualitative signs - the morphology of the ST segments and T waves, "notching" of the J-point, reciprocal changes, etc. it just doesn't "look" like a STEMI, but you need to read hundreds of ECGs to feel comfortable with those.
It is far simpler to count the big boxes. Rule #2 boils down 3 sub-steps:
First, look at the S-waves in V1 and V2. Pick the deepest one, and count the big boxes.
Next, look at the R-waves in V5 and V6. Pick the highest one, and count the big boxes.
Last, add those two numbers. If it is over 7 big boxes, the ST elevation is probably due to LVH
7 big boxes equals 35 little boxes, or 35 mm. Count the small boxes if you prefer, or if the you're near the cutoff. Looking at ECG #1 as an example, and counting the little boxes, we find:
So, about 40 mm, or 8 big boxes, so likely not a STEMI.
3. Is the QRS a normal width?
Rule #3 is simple - If the QRS is over 0.12 seconds long, don't call a STEMI.
Probably the most common cause of dramatic ST elevation is the LBBB, as in ECG #3 above. You can also see the same pattern if the the patient has a pacemaker.
Now, the experienced and sophisticated paramedic knows that there is a way to interpret the LBBB for signs of STEMI, but even the "simplified" rules for determining STEMI in LBBB are somewhat complicated. Many paramedics are familiar with the rule, but the new paramedic shouldn't be expected to make this call. If the patient has a pacemaker, it's even more unreliable to interpret the ECG.
4. Is there ST depression in at least 1 lead?
Rule #4 - if there is no ST depression, do not call a STEMI.
Most students have learned that you should look for reciprocal ST depression in a STEMI. Unfortunately, because of the non-intuitive, non-anatomic way that the ECG is arranged, it isn't clear which leads are "opposite" each other. And the patterns of depression can vary a lot, depending on which coronary artery is occluded. For example, an "inferior" STEMI may or may not have depressions in I and aVL; it depend on whether the culprit artery is the RCA or the obtuse marginal.
A much simpler criterion for reciprocal depression is any ST depression on the ECG. This would eliminate, for example, ECG #2 above. Although the computer interpretation was STEMI, it is a classic example of early repolarization, or possibly pericarditis (less likely, as the ECG did not evolve). Another example from my ED is this ECG:
27 y.o., prior dx of pericarditis
Just like ECG #2, there is diffuse ST elevation without any ST depression. Not a STEMI.
Applying the rule
Let's take another look at ECG #4:
Okay, going through the rules:
Rule #1 - Over 1 mm of ST elevation is seen in both V1 and V2, which are anatomically contiguous.
Rule #2 - The S-wave in V1 is about 1 big box deep, while the R-wave in V5 is 3 big boxes high. That's a total of 4, so the QRS height is normal.
Rule #3 - The QRS looks narrow, about 0.100 seconds wide.
Rule #4 - There are ST depressions in the lateral leads, most notably in V5.
So we see that this simple 4-step rule, intended to assist the novice paramedic, actually picks up a STEMI that the computer missed!
The Bottom Line
This elegant method of ECG interpretation, although intended for the student, can be very useful for the experienced paramedic as well.
The glucose-insulin-potassium study is grabbing all sorts of attention, out of all proportion to the underwhelming results (see here and here for analysis). There is nothing in that paper that a paramedic can use in the foreseeable future, let alone on the next shift. Folks in EMS tend to be very practical, and the use of that drug combo is still very theoretical.
When I looked through the issue of American Heart Journal that has that much-hyped study, though, I found another paper, one that appears more more useful. What's more, you can start using the results today, and could plausibly save a whole lot more lives (or at least myocardium) than with the "cardiac cocktail."
Ironically, the evidence is better for this cocktail in cardiac disease.
"A Prioritization Rule for Obtaining a 12-Lead ECG"
So, when do you decide to get an ECG on a patient in the field? If they have chest pain, sure, but probably not in all chest pain. And you're probably sharp enough to grab an ECG in the old guy with new nausea or dypsnea. But are you missing some STEMIs? Are you getting too many ECGs, and wasting your time? Someone outta do a study.
Well, Glickman et al. did, and I'll boil down the results that you can use on your next shift.
A very, very deep interest in binary recursive partitioning...
The problem in emergency departments, just like in the field, is that a lot of STEMI patients do not show up with the classic chest pain symptoms. However, we want to identify all these STEMIs, but we also don't think we should get an ECG on everyone - it would just slow everything down. You also want a rule that is straightforward enough for a range of "non-physicians;" RNs, techs, and medics. (That being said, the results were very instructive for this physician.)
The researchers used a database of patients who came to a ED in North Carolina in 2007 and 2008, and looked at two things: who was diagnosed with a STEMI, and what the triage note listed as the chief complaint.
Funny: they used a computer program to search the triage notes for chief complaints, and called it the Emergency Medicine Text Processor (EMT-P).
Anyway they categorized the chief complaints of the 6464 patients who were diagnosed with a STEMI, then grabbed the records of about 3.5 million other patients who were matched to those same chief complaints, as well as age, gender, and other stuff. They found out a few important things.
1. Chest pain is less common in older folks with STEMI.
This is already well-known, but they have a good pair of graphs that make the point clear. Age has a huge impact on the predominant symptom that people feel with a STEMI.
There is a small difference between men and women, but it's the age-effect that is so evident here. For example, women under 50 years of age have chest pain as their chief symptom about 85% of the time, while men over the age of 70 only note chest pain around 70% of the time. In other words, chest pain can be more common in women if you look at different age groups.
2. Think: ≥ 30, ≥ 50, and ≥ 80 years old.
When they fed all the data through C3P/EMT-P, they came up with a rule for deciding if you should get an ECG, based just on the age and chief complaint. They broke it down by 3 age groups, as noted above:
I want to emphasize the last bit there - this is a rule designed to assist non-physicians in screening a large number of patients rapidly, but it is constructed to supplement clinical judgment, not replace it.
Another way I might phrase the rule is:
Anybody over 30 y.o. with chest pain gets an ECG,
Anybody over 50 y.o with chest, head, and upper extremity complaints,
Anybody over 80 y.o. with any torso complaints (except maybe isolated diarrhea...)
This seems pretty inclusive - it's hard to see how an 81 y.o. in the ED would not get an ECG! Regardless, some people will get missed. The sensitivity of the rule is only 92% sensitive.
So, who were these 8% of STEMIs whom the rule would miss?
Who gets missed by this rule?
Again, a helpful diagram:
It misses younger patients, even the ones with chest pain.
It misses the young-ish patients with dyspnea.
It misses the 50-79 year-olds with GI presentations.
It misses the > 70 crowd that presents with... fever?!
Fever? Seriously, you can't win.
The Bottom Line
One way that EMS can save lives is to identify STEMI patients in the field, followed by proper triage and notification. But you can only identify a STEMI if you get an ECG. This paper shows us how wide a net we have to cast in order to catch most of them.
Use the decision rule to prompt you or your partner to do more ECGs. And even when the rule doesn't necessarily call for a 12-lead, listen to your gut and follow your clinical suspicion.
The results of the IMMEDIATE trial have been popping up repeatedly today on Facebook, partly because I "like" a few EMS FB pages, and also because one of the authors (Hi Carin!) is a FB friend (IRL too!).
Here's an example of the way the trial is being described:
"Cut the risk of death in half." Sounds great!
The result they are describing, to be specific, is that 8.7% of the people getting the placebo had a cardiac arrest, or died while they were hospitalized, while only 4.4% of the patients getting the study drug did. That's either an (absolute) difference of 4.3%, or about a (relative) 50% decline.
Such an effect would be stunning. In the years after thrombolytics and aspirin were introduced, the incremental benefits of new therapies for AMI have been getting smaller and smaller. This result here would blow the others out of the water.
For instance, back in 1988, it was shown that either the use of aspirin or of thrombolyticsreduced the risk of deathin MI by about 2-3% over placebo. The combination was better of course.
After that, it's been harder to show that the more complicated and expensive therapies save that many more lives. When we send a patient to the cath lab for an AMI (instead of giving a thrombolytic in the ED), for example, there isn't that huge a benefit. One recent analysis suggested that, overall, you could only find a 0.7% difference in mortality (6.6% vs 5.9%) between lysed patients, and those that went for PCI. A lot of money for not much gain.
So, if this combination of glucose, insulin, and potassium (GIK) could cut mortality in AMI from 6.6% to, say, 3.3%, it would be freakin' amazing.
"I bet there's a catch. There's always a catch."
Well, I don't mean to be an Eeyore, but the perhaps we should wait for, yes, "further study." I offer three reasons why:
1. They weren't studying mortality.
The principle outcome they were studying was whether the initial presentation of ACS would progress to an MI, or it would be an "aborted" MI. This is the outcome that they believed had the most biochemical and clinical justification, and they clearly thought that it had a reasonable chance of being demonstrated.
It turns out there was no difference in the percent of people who progressed to completed MI - the GIK infusion did not help, at least not here. So the trial is negative for the real primary outcome.
2. There were 12 secondary outcomes.
Look at the table of the results:
Remember: the outcome they staked the success of the trial on was the one at the top: "Progression to MI," for all participants. The rest are a bunch of secondary outcomes, and they don't count to the same degree as the primary outcome.
Analogy: A friend is flipping a coin, and you call heads. That's your primary outcome of interest. But if you also say to your friend "Okay, I call heads, but I also call it if you drop the coin, if it flips over 5 times in the air, if your phone rings in the next 30 seconds, or if your nose starts to itch in the next 10 seconds.
Now, you may be wrong about heads, but say your friend's nose does indeed start to itch in the next 10 seconds? Will he concede defeat? What will he say?
"No pick! NO PICK!"
Most likely your friend will point out that the most relevant and important prediction you made was heads vs tails. Furthermore, you called out such a long list of other items that you were almost certain to come up with a positive result. He will insistent on another coin toss, where the primary outcome is now nose-itching, not heads or tails.
The same holds in statistics and study design, and is also why the authors state in their conclusion (my emphasis):
"The primary end point was not significantly different between groups, and the observed favorable results of GIK were based on prespecified but secondary end points, although biologically plausible and consistent with preclinical studies. The study tested one primary hypothesis, 3 major secondary, and 6 other secondary hypotheses. All were prespecified and no adjustment for multiple comparisons among the secondary end points was made; thus, reported significance levels should be considered approximate. Accordingly, given the lack of complete consistency of the findings, and the modest P values for most of the statistically significant findings, it would be appropriate to describe the observed favorable effects on the secondary outcomes as generating clinically testable hypotheses for evaluation in larger cohorts."
3. 30 day mortality seems pretty important too...
Ok, say you can take the "cardiac arrest or in-hospital mortality" results at face value. What, then, shall we make of the 30-day mortality? It was shown to be basically the same in both groups.
We just saw this discussion take place last month. A study from Japan showed that giving epinephrine in cardiac arrest got people to the hospital with ROSC more often, but the 30-day mortality was no different (We'll leave the neuro results alone for now.).
It would be nice if epi put all the dots on the right side of the graph. But it doesn't.
So, say the results are right - people don't die or arrest in the hospital as often, but they still die in the first 30 days just as often. Now, maybe everyone's hospital stay was over 30 days, but I doubt it.
Still feel excited?
Bottom line:
I believe that EMS has an essential role in managing ACS, of course. But, as it stands, giving this mixture to your ACS patients is not yet ready to be added to your drug box.
