In case you missed it this week:
Have a great weekend!
In case you missed it this week:
Have a great weekend!
This excellent case comes to us from Paramedic Jack Buckle. Thanks Jack!
You and your partner are in the middle of a busy shift, when you are dispatched to 37 year old male complaining of chest pain.
It's almost 2pm, and a balmy 78 degrees.
You arrive to a well kept house and find your patient sitting in his kitchen. He looks pale, but you don't notice any obvious distress.
"How can we help you today?"
"I just haven't felt well for a couple of days. No energy. Chills. And I've been nauseous."
"What made you call 911 today?"
"Well, to be honest, I started having some chest tightness today and I got really scared."
His discomfort, 6/10, is poorly localized and non-radiating. He describes it as "intermittent". It started when he was at rest, and began about 2 hours prior to calling 911.
After talking with your patient, you understand that he suffers from depression stemming from a rugby accident that left him with a severely painful back condition.
In fact, he has previously undergone L5-S1 fusion surgery. He takes several pain meds for this chronic condition.
Although he states that during a recent hospital stay (related to back pain) he had to be on the cardiac monitor (he doesn't know why), he denies any history of cardiac problems, and no allergies.
You acquire the following 12 lead ECG:
You are 14 minutes from the community hospital, and 22 minutes from the nearest PCI center.
YOU MAKE THE CALL:
What do you think is going on with this guy?
Where should you take him?
How should you treat him?
"For heaven's sake man, treat the patient not the monitor!"
Ahh, the angry cries appear every time we post a difficult case with a challenging ECG or treatment decision..
The attitude seems intractable, despite our best efforts.
Over a year ago, I wrote "Treat the Patient not the Monitor?", and not much has changed since!
So, I got to thinking. Where did this come from anyway? What were the intentions of the originators of "treat the patient not the monitor"?
In search of answers, I visited treatthepatientnotthemonitor.com, but surprisingly found nothing.
I am left only with my theories and opinions.
Back in the day, decades ago, I'm sure all of this wasn't an issue:
Pulse-ox? Portable cardiac monitor? I don't think so!
However, as the advent of portable medical devices made its way to EMS, educators and skeptics alike told cautionary tales about not treating "the monitor"– just look at your patient!
There are the classic examples we are all familiar with :
You put the pulse-ox on the patient with good color and no signs of respiratory distress and it reads 88%.
HE NEEDS O2 STAT! Well, of course not, because we treat patients not monitors!
Because measuring blood glucose is considered a "vital sign", you check it on an A/O patient (come on, you know some of you do it) and it reads 62.
HE NEEDS DEXTROSE STAT! Well, again, not so fast, because we are treating patients not monitors!
It is a good lesson, right? We do not treat numbers on a machine, we treat living breathing patients, and sometimes we just don't know what to do with the numbers.
By the way, cardiologists are having somewhat of a similar issue with high sensitive troponins. Because they are so sensitive, more patients without acute ischemic heart disease are showing positive readings, and now it is not clear what to do with all of them.
In Treat the Patient Not the Monitor -Part I, Rogue Medic writes that citing these words is "dangerous in the wrong setting". I couldn't agree more.
What exactly is the wrong setting? What is the right setting for that matter?
For starters, it comes back to our patient assessments. Can we assess a patient without the help of technology? Of course we can.
Will that assessment be as thorough and accurate as it could be? Well, maybe not!
Our technology is a key part of our assessment. If used in the correct setting, it adds information that we might not have been able to obtain otherwise.
The key word, though is "Context".
We should have a reason to use whatever technology we are using. In the setting of an AMS patient, getting a blood glucose reading makes sense to me. It is the proper context. If a patient is short of breath, pulse pulse-oximetry, or even better, capnography makes sense to me. If a cardiac etiology is the suspected cause of a patient's presentation, the monitor makes sense.
What does not make sense to me is the blind usage of this technology on every patient. I know it is done. I know people can make good arguments for that, but it doesn't work for me.
Here's why. Without the proper context, I feel like i might not know what to do with the results.
As I mentioned earlier, many medics routinely obtain blood glucose readings on every patient as a "vital sign".
My dilemma is this: Do I have a clinical reason to obtain this information? Will it alter the way I treat my patient?
Does he have a CVA or hypoglycemia? Of course, I'll check the BGL. But check it on everyone?
If i do this, what happens when I get a reading of 62 on an alert and oriented patient?
I have two choices:
Option 1: I treat the number and give my patient glucose. Well, I'm not going to do that, because my patient is not altered and doesn't need it.
So I go for Option 2: I simply ignore the number. Write is off as an "erroneous".
The problem is, If I am not going to use the reading I obtained, why am I getting it in the first place?
I don't use pulse-oximetry on everyone, and I don't routinely obtain a 12 lead on every patient encounter either for the same reasons.
I realize that right now, many of you are thinking, "see, even HE treats the patient and not the monitor!"
This is where i differ.
It all comes back to context. Clinical judgment means using all available information to assess the patient and find out what is going on. Of course, that does not mean blindly following the monitor, but it certainly does not mean ignoring it.
The reason "Treat the patient not the monitor" does not apply to the cardiac monitor is that used properly, it can give us information that we could not otherwise obtain. You can not look at a patient and determine whether or not he is having a STEMI.
Do we still examine our patients? Hands on, getting a feel for the pulse, their skin condition? Of course we do. But there is so much more to assess.
The fact is, there is no other surrogate for the monitor. We can not "look at our patients" and have an idea of what the monitor will reveal. That is quite different from blood glucose, NIBP, pulse pulse-oximetry, etc where there will be signs and symptoms of what those "monitors" will show.
The cardiac monitor? You just won't know until you apply it.
You might feel a slow regular pulse, but you don't know if it is Sinus Brady, Mobitz 1, or complete heart block.
That rapid pulse you palpated? Is it VT, AVNRT or A-Flutter?
Is there a STEMI, sending them straight to the cath lab?
Is that Brugada in your syncope patient?
Maybe it's WPW or ARVD!
To be blunt, in many cases you simply can't diagnose (yes we do that) your cardiac patient correctly without the monitor:
There are limitations to the cardiac monitor. They need to be troubleshooted like every other piece of technology. Part of our job is to be able to diagnose problems with the monitor, and not be led astray.
In "Reversals", Peter Canning writes about a case where the arm leads were put on reversed, and the rhythm looked like VT.
"The only thing going for me is that he doesn't look like he is about to die. I did not expect to see a rhythm like this. I look at it closer…I have the left and right arms mixed up. That'll do it."
If what you see on the monitor is totally out of left field, you have be a critical thinker and ask whether something could be wrong with the data. It happens some times. Leads are switched, cables break. That's part of clinical judgment, and our responsibility when using technology. You've got to have your "Spidey Sense" working at all times.
The limitations, however, do not overshadow the fact that we are supposed to figure out what is going on with our patients, and the cardiac monitor can play a crucial role in doing that.
I looked at many of the posts by Dr. Smith of Dr. Smith's ECG Blog looking for cases of "treat the patient not the monitor". Guess what I found? He actually uses the information on the monitor!
Dr. Mattu recently had his 100th video case presentation at his video blog. 100 videos? Why in heavens name would he do that when he could have just 1!
"This week, we have a very difficult case… squiggles here, some blipity-blips there… Oh hell with it, just look at your patient!"
That would be one short video series! In all seriousness, they present tough cases. Difficult ECGs. Why aren't they saying "Treat the patient not the monitor?
We (all of us) don't always like to hear it, but every time we throw our hands up and say "treat the patient not the monitor", it has more to do with our limitations than those of the monitor. It means, "help, I can't figure this thing out, so I'll just treat the patient until we get to the hospital".
That's what we do when we can't figure out what is going on. All of us.
Just know what it means when you do that. There was something on the monitor that you couldn't interpret. It is an opportunity to learn. That's what ems12lead.com is here for, and what other ECG blogs are here for as well.
"Treat the patient and the monitor".
Remember, it's all about the context!
As always, your comments are welcome!
This excellent case comes to us from our friends in the UK. The author wishes to remain anonymous, but we thank him for his contribution.
It is about 8am on a gorgeous Wednesday morning, when your Paramedic unit is dispatched to a 49 year old male, "chest pain".
You arrive at the bungalow of a summer resort and are greeted by an elderly couple.
"They don't look too bad", you think, but you are not that lucky.
"Our son has been complaining of chest pain and vomiting for a couple of days".
You are led back to a room where you find your 49 year old patient lying in bed.
His parents say they found him like this and called 911. They tell you he seemed ok when he went to bed last night.
Your patient is lying supine in bed, responds to verbal stimuli only, and it is difficult for you to make sense of his answers.
You note that he appears anxious and uncomfortable, with dried vomit on his shirt.
His airway seems clear, but his respirations seem quick and a bit shallow, although clear bilaterally. You put him on a non-rebreather.
The rest of the vitals are as follows:
While he is not adequately answering your questions, you are able to determine from his parents that he is an insulin dependent diabetic. You are unable to determine any other past medical history, medications, or allergies.
You check his blood glucose while your partner puts him on the monitor. The BGL reads "High".
Here is the 12 lead:
You are 15 minutes from the local community hospital, and 30 minutes to the PCI center by ground. Air transport to PCI is a possibility.
What's your differential diagnosis?
What does the ECG show?
What do you want to do about it?
The original presentation of this case appeared as "What's Wrong with Mr. Wilson?"… You can read the original post here.
Much has been written lately about RBBB abnormalities that were missed.
First, let's review the 12 lead of a typical RBBB. When learning to recognize abnormalities, we must first be intimately familiar with what "normal" looks like.
Editors note: Some astute readers may notice some subtle abnormalities of the ST segments here (so technically, not a normal ECG). I use this example to illustrate typical morphologies of the QRS complex:
*image credit LITFL
Typical features of an uncomplicated RBBB:
Instead of the typical rSR' pattern in V1, you may in fact see any of the following morphologies:
It is not abnormal to have a small amount of discordant ST depression in the right precordial leads. However, ST elevation in the right precordial leads is never normal. In fact, the ST segments should not be distorted enough in RBBB to cause ST elevation at all. This is precisely why RBBB does not confound STEMI interpretation in the way that LBBB does, where ST elevation may be a normal finding.
Now let's take a look at the 12 lead of our 57 year old male patient who complained of feeling "really sick":
Overall, this is an ugly ECG. There should never be any ST elevation, and certainly the Q waves in V1-V3 are very abnormal and significant.
If we look at a normal RBBB and our patient's ECG side by side, the abnormalities become obvious:
From the previously mentioned RBBB posts by Dr. Stephen Smith (links above):
Dr. Smith elaborates further on the Q waves:
"The wide Q waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle). This was common before the days of reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy"
The story of our patient:
The ECG recorded above was taken at admission to the cath lab. He was found to have a 99% lesion of his LAD. His ejection fraction was in the 30s.
He received a stent and a balloon pump, and was admitted to the ICU. His prognosis questionable.
Two weeks prior, he had started to feel very short of breath, along with a cough. On exertion, he felt "much more tired than normal".
After a few days he went to his PCP. His hx was significant for hypertension and smoking. It is unknown whether or not an ECG was acquired at that time.. He was, however, diagnosed with an URI and sent home with antibiotics.
He started to feel slightly better after a day or two, then began to decline again. He found himself without the energy to walk across the room. He had his wife drive him to the ED.
At the ED, they found him to be hypotensive (86/58) and not improving after the antibiotics. An ECG very similar to the one recorded above was acquired. Although it was not found to be diagnostic, there was concern that his issues could be cardiac. He was scheduled for a non-emergent cath a few days later.
At that time, the above ECG was acquired and the lesion was found.
For more information, be sure to read our series on RBBB:
It's a quiet Sunday afternoon when you're dispatched to a residence for a 77 year old female complaining of abdominal pain. Your dispatch notes indicates she was at the ED the day prior. Upon your arrival, you're met on the porch by the patient's son who directs you inside.
Your patient is sitting in a recliner, with mild respiratory distress, clutching her abdomen. Her skin appears a bit moist, and is warm when you touch her arm to feel for a radial pulse. When you ask her what is going on, she simply replies, "my belly won't stop hurting."
Your partner makes quick work of her vitals while you get the run down on her history.
Your general impression of the patient is she just looks unwell. Your partner relays her vitals.
Her son asks that you take her to the smaller, local hospital so, "she does not have to wait as long as she did at the ED yesterday." When you ask for her discharge instructions, he can only find the sheet which says Chest Pain and very generic information.
When you ask about her pain earlier, she denied any chest pain, however, to be prudent you obtain a 12-Lead:
You assist her to your stretcher, securing her with seat belts, and begin moving her to the truck.
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?
How about this one?
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”.
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 :
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 :
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.” 
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!
,- Advanced Cardiovascular Life Support Provider Manual
2011, American Heart Association
 Pediatric Advanced Life Support Provider Manual
2011, American Heart Association
This is the conclusion to 47 year old male: Holiday Indigestion. Thanks go to a long time reader Nicholas Eisele for this holiday case! Editor's Note: sorry for the delay, it helps to press "publish"!
When we left off, our patient was in the back of the truck with a burning sensation radiating to his back. We had run a 12-Lead ECG and our partner was wondering which facility you wanted him to drive to.
To answer that question, we should look at the 12-lead!
This 12-Lead shows a normal sinus rhythm at 70 bpm without ectopy or bundle branch block. A case could be made for incomplete right bundle branch block given a QRSd of ~110ms. Strikingly we have ST-depression in I, aVL, and V1-V5 with ST-elevation in lead III. Anytime you see flat or downsloping ST-depression in aVL you should look for elevation in the inferior leads (typically III). When present, it is almost certainly an inferior wall MI.
Many readers commented that the ST-depression in V1-V5 could be either a sign of a posterior wall MI or a "anterior ischemia". It is important to remember that ST-depression from ischemia does not localize! This concept is so important, I'm going to list it again:
Traditional evaluation of ST-depression has taught that focal ischemia may cause localized ST-depression, however, this is not the case. Subendocardial ischemia causes diffuse ST-depression and will not be found in a localized pattern. Any time you have localized ST-depression you must consider it to be a reciprocal change first!
In our case, we have ST-elevation in lead III which clinches the diagnosis of an inferior wall myocardial infarction with possible posterior extension. A subsequent ECG revealed evolving ST-elevation in the inferior leads:
Remember, all patients who receive one 12-Lead should at least receive a second 12-Lead! If you were not comfortable activating a STEMI from the first clean tracing, serial 12-Leads provide improved diagnostic sensitivity. A single 12-Lead may only identify ~80% of STEMI patients.
The paramedics in this case recognized this fact, activated a STEMI alert, and transported the patient to their nearest PCI center. The in-hospital ECG showed continued evolution of the IWMI with the most impressive elevation and depression of the patient's clinical course:
They achieved an impressive 83 minute first medical contact to balloon time with one stent placed in the RCA.
We hope you've enjoyed this case as much as we did, but more importantly this case presents some great teaching points:
Thanks go to a long time reader Nicholas Eisele for this holiday case! As always, details have been changed to protect patient privacy.
It is a blustery Christmas morning when you and your partner are dispatched for a 47 year old male with chest pain. Firefighters are already on scene obtaining a history and vitals when you arrive.
You check in with the officer in charge, a paramedic, and he reports that the patient has been having a "burning sensation" in the middle of his chest, going to his back. As it is Christmas morning and the patient's family is opening presents, the officer also relays the patient, "is likely going to refuse." He also relays that they witheld ASA due to the patient's "indigestion."
One of the firefighters gives your partner the patient's vitals:
You perform a quick patient assessment prior to making any decisions:
A focused history reveals no prior cardiac problems and that the patient takes no medications and has no allergies.
Given the patient's symptoms and possibility of a true cardiac problem you advise the patient that a trip to the hospital is worth it just to make sure he's not experiencing something serious.
After he sits down on your stretcher your partner begins placing electrodes for a 12-Lead as you gather four baby aspirin for the patient to chew.
You notice the artifact and hit print again, however, you decide you can run another one in the truck. After loading the patient your partner hands you the second 12-Lead, which is a bit cleaner than the first.
Not completely satisfied, you run a 3rd 12-Lead in the back of the truck.
Your partner asks which facility you'd like to go to.
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.
"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?
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.
This patient came into the ED with hyperkalemia, and was treated with IV insulin and dextrose (no calcium).
Or how about this hand?
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."
"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).
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.
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!
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
"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.
"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"!
This is the conclusion to our Name that ECG case: 66 year old female, resolved chest pain.
66 year old female, resolved chest pain.
Welcome to another installment of Name that ECG! Remember, this is a cold read and your job is to interpret the ECG to its fullest.
66 year old female, resolved chest pain.
What are your differentials?
Posts which include any permutation of the phrase "treat the patient not the monitor" will be deleted and their author beaten with a LifePak 5.
This is the conclusion to Name that ECG: 51 year old male.
51 year old male, palpitations.
Welcome to another exciting installment of Name that ECG. Remember, your job is to interpret the ECG to its fullest; we'll leave the treatment for somebody else!
51 year old male, palpitations.
What are your differentials?
Posts which include any permutation of the phrase "treat the patient not the monitor" will be deleted and their author fed to trauma hungry EMT students.
These are the findings for our Name that ECG case: 88 year old male, weakness.
(click for a marked up image)
Today our goal is to interpret the ECG to its fullest from a "cold read" perspective. We're giving you the patient's age, chief complaint, and ECG…and that's it!
88 year old male, weakness.
What are your differentials?
Posts which include any permutation of the phrase "treat the patient not the monitor" will be deleted and their author will be reassigned to the unit that never gets off shift on time, you have been warned.
Good morning all…
It's a beautiful fall Sunday morning, and you and your partner are enjoying an nice cup of coffee. But of course, the tones go off, and you are called to the residence of a 52 year old female, "sick". You recognize the address, you've been there before.
Upon your arrival, you find your patient sitting in a chair in the living room. You remember her. She is a dialysis patient. She does not look well.
She complains of not feeling well. She says she is weak, and has slight shortness of breath. You don't see any labored breathing or accessory muscle use, and she is able to speak in full sentences for now. Her respiratory rate seems ok, as does her pulse.
As you are getting your history, your partner gets a set of vitals.
She tells you that she wasn't feeling great yesterday, and missed her scheduled Saturday dialysis (she is on a Tues-Thurs-Sat schedule).
She thought she would be ok until Tuesday, but it didn't work out that way. She woke up today feeling really rotten and has been progressively feeling worse.
In addition to her renal failure, she also has a history of hypertension and asthma. She has no allergies. She says she has been compliant with her meds, and denies any chest pain or other aches/pains.
Her vitals are as follows:
You acquire an ECG that looks similar to this one:
You begin packaging your patient.
You are 20 minutes from the closet community hospital.
I am assuming most of you will recognize the above condition and know the available treatments for it.
So, that is not the question.
The questions are these:
Do we treat this patient prehospitally?
To be clear, the question is not "could we" but "should we"?
If we did, What would we use and why?
Is there a benefit to treating in the field versus waiting to hospital arrival?
**There is no obvious "right" answer to this… So, let's discuss it and see where we get. Have at it folks!
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:
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!
This is the conclusion to a 51 year old female CC: Near Syncopal Episode. If you haven't read the first part we highly recommend it!
When we left off, our crew was attending to a 51 year old female who had almost passed out in a stadium tunnel during a college football game. We received a few questions as to the type of football, which could be important to the diagnosis, so we will clarify that this was an American Football game.
Our crew had found her to be hypotensive, first bradycardic and then tachycardic, with concerning changes on the 12-Lead. A nasal cannula at 4 L/min was initiated and they established bilateral IV's and were rapidly infusing nomal saline to restore perfusion.
Let's take a look at the initial rhythm strip:
The initial rhythm strip shows a narrow complex tachycardia at ~130 bpm, without clear P-waves. Retrograde P-waves can be seen in numerous complexes T-waves, leading to a presumptive diagnosis of a junctional tachycardia.
The longer rhythm strip shows sinus complexes followed by runs of junctional tachycardia. Astute readers will note Wenckebach conduction of the retrograde P-waves!
This finding alone would be highly concerning given our patient's present condition and history, however, when we move onto the 12-Lead her diagnosis is clinched:
The initial 12-Lead ECG again shows a junctional tachycardia, with markedly hyperacute T-waves and ST-elevation in the anterior precordials with downsloping ST-depression in the inferior leads. The degree of which the T-waves tower over the R-waves in V4 is truely impressive!
The crew immediately recognized the extensive anterior wall infarct with cardiogenic shock, and given the concurrent finding of a junctional tachycardia presumed there to be gross insult to the AV nodal tissue. They placed defibrillation pads on the patient and helped the arriving crew package the patient. The patient was able to follow commands and 324 mg aspirin was given PO. After 1 liter of fluid the patient remained hypotensive and another bolus was started. Oxygen was titrated to maintain an SpO2 of >96%.
Eventually the patient stated she had some dull pressure in her chest, but otherwise denied pain or shortness of breath. An early STEMI notification was given and while enroute to a STEMI receiving center the crew ran multiple 12-Leads, capturing the evolution of the myocardial infarction.
In this 12-Lead we can clearly see periods of alternating tachycardia and bradycardia, an ominous sign given the evolving MI. V5 and V6 were removed and adjusted closer to V4 and V7 so that defibrillation pads could be placed.
The patient was taken directly to a cath lab suite and found to have a 100% occlusion of the LAD and after the placement of a stent the patient's ECG normalized and her hypotension resolved.
This case illustrates the amazing evolution of an extensive anterior myocardial infarction and highlights the role the LAD can play in AV nodal function. We hope you enjoyed these ECG's as much as we did!
This case comes from a reader who wishes to remain anonymous, as always details have been changed to protect patient and provider privacy.
You're working an overtime shift at a college football game on a hot Saturday in August, when a man flags down your crew. You head on over and are directed into one of the stadium tunnels to a female laying on the ground with bystanders pouring cold water onto her.
One of her friends reports she felt hot and dizzy while watching the game and came into the tunnel to, "cool off." She then said she felt faint and her legs gave out from underneath her and she fell to the ground.
You introduce yourself and ask the patient how she feels, however, while her eyes track you appropriately she is very lethargic and slow to answer. Her friends are unaware of any medical problems your patient may have.
Your partner obtains a set of vitals while you place the patient on the monitor.
Your event jump bag lacks all but basic trauma and IV supplies so you request an ALS unit meet you on location. Your partner establishes an IV and hangs a bag of fluids. The rhythm strip prints out.
Noting a difference in rate, you ask your partner to recheck her radial pulses. He confirms they are now at 120/min and weak; you direct him to place a BP cuff around the liter bag and to work on a second line.
Your partner asks, "should we give her anything for her blood sugar?"
A quick history from the patient reveals no major medical problems, takes no medications, has no allergies, and she denies any history of diabetes. You acquire a 12-Lead ECG as the ALS unit checks on scene.
Multiple rhythm changes are noted on the monitor and a long strip is printed.
The ALS crew asks you for a report as you help place her on their stretcher.
When we last left off, our patient was a 63 year old male complaining of substernal chest pain which awoke him from sleep. We obtained standard, right-sided, and posterior ECG's which cardiology deemed non-specific. Our patient continued to have persistent chest pain even after maximal therapy.
Coronary catheterization was performed later that morning, and a total occlusion of the first obtuse marginal (OM1), a branch of the circumflex artery, was found. A drug eluting stent was placed, and his subsequent hospital course was unremarkable.
Could we have guessed this from the start? Let's take a look at his ECG's again:
Reviewing our patient's first ECG we see horizontal ST segment depression of 1 mm was seen in II and aVF, 3 mm ST depression in V2, and 1 mm ST depression in V3 and V4, all with upright T waves. An early R-wave transition was noted, with a height of 13 mV and an R/S of 1 in V2. Lead III showed T wave inversion.
The right-sided ECG featured only ST segment depression and inverted T-waves.
Reviewing the posterior leads, we see some interesting changes. Notably ST segment elevation of 0.5 mm in V7 and V8, and an unchanged appearance of the limb leads.
So, Dr. Walsh, what can we take away from this case?
Devoted readers of EMS 12-Lead will already know much about posterior MI, so I'll just do a brief review of the basics. I encourage you to search for the tag "posterior STEMI" for more information. As always, Dr. Stephen Smith's website also has plenty of examples and teaching about posterior MIs.
There is a small amount of controversy about what anatomic area of the heart a "posterior" MI actually affects. Some have suggested that the infarct is actually in the infero-basal region, while others have evidence that it should be viewed as a lateral infarct.
Regardless of the name, however, it generally is the result of an occlusion of the left circumflex coronary artery (link to cool animation). This territory is generally regarded as "electrically silent" in the standard ECG leads. As such, diagnosis relies on indirect evidence in the standard leads, as well as the use of non-standard "posterior" ECG leads.
So, how can we be Posterior STEMI Rock Stars, Doc?
For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:
- Horizontal ST depression in V1-V4
- Tall, broad R waves (>30ms)
- Upright T waves
- Dominant R wave (R/S ratio > 1) in V2
So, a typical posterior STEMI looks like this:
Inferioposterior STEMI courtesy of LifeInTheFastLane.
Note the ST elevations in the inferior and lateral leads; in general, a posterior MI usually shows signs of a STEMI in either of these two regions the majority of the time. It's pretty obvious that evidence of STEMI in one area (e.g. inferior) certainly strengthens suspicion for a posterior MI.
However, here's an example of a posterior MI that does not show any inferior or lateral involvement:
Posterior STEMI without inferiolateral changes. (PubMed)
Using posterior leads (V7-V9) can show ST elevation, but the magnitude may not be as dramatic as that seen in the "usual" STEMIs. Many experts consider, for example, 0.5 mm of elevation to be significant, instead of the usual > 1 mm criteria, and that elevation in just one lead is sufficient.
So what's wrong with the conventional thinking?
There's a short-cut way to diagnose a posterior MI, that involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.
For example, a blow-up of lead V2 from the isolated posterior MI above (the second ECG) looks like this:
It fulfills all the criteria I reviewed above, so it's a classic example of how we currently define a posterior MI. And if we "flip" it, we get this:
Yep Doc, that looks like a regular STEMI now!
For many people (MDs included!), the diagnosis of a posterior MI starts, and ends, with this flipping.
I'll tell you what has always bothered me though. Look at the R-wave in the un-flipped image. This is just the mirror image of the Q-wave, and our "flipped" image reinforces that. In fact, the Q-wave in our flipped image looks pretty darn old, like the MI has progressed far along already.
Furthermore, the T-wave in our "flipped" image hardly looks hyper-acute. In fact, it looks like the T-waves are in the process of returning to baseline, another indication that our "classic" posterior MI is old.
Here's an example of an subacute/old inferior MI, for comparison. Also note the resolving, partially inverted, T-waves in III and aVF:
Old Inferior MI courtesy of LifeInTheFastLane.
It looks instead like our description of posterior MI is training us to look for old, completed MIs!
Let's look at this from another angle. Look at this typical inferior STEMI, and focus on lead aVF:
That's a classic STEMI, no doubt. Tiny Q-waves, tall T-wave – everything suggests that this is very acute.
Now, instead of being lead aVF, let's pretend it were lead V9. What would the "flipped" view of this lead be? Let's flip it and see!
This view shows a small R-wave, and a fully inverted and deep T-wave. Now, if we take a look back at the criteria listed above for a posterior MI, however, it would not meet much of the description of a posterior MI we listed before.
We're teaching people to pick up on old posterior MIs, and training them to miss the acute presentations.
Interesting, so how can we avoid this, Doc?
Well, I may have had this thought kicking around in my head, but some cardiologists actually wrote down these thoughts! Birnbaum et al. just published the article Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. This wasn't a prospective controlled trial, but they managed to get 13 cardiologists to agree on a few things.
One of those was that our standard description of the morphology of posterior MI on the ECG is likely wrong. Helpfully, they proceed to describe what we ought to be looking for!
After reviewing the usual evolution of LCx-occlusion MI, they conclude that the standard definition, that relies on tall R-waves and upright T-waves is:
… the late “mirror image” of fully evolved ST-segment MI (STEMI) (Q waves with terminal T-wave inversion) and not the acute phase of STEMI.
By contrast, they give an example of what they consider to be an acute posterior STEMI:
If we blow up lead V2…
…we see that there is a small R-wave, and fully inverted T-waves, and an R/S < 1. It meets none of Brady's criteria above. But if we flip it…
It looks like a regular ol' STEMI!
Bring it home for us, doc.
The usual description of posterior MI may be in need of revision. The posterior leads, however, remain useful to reveal acute cardiac ischemia.
Thank you again to Dr. Brooks Walsh for this case and his insight into posterior STEMI!
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".
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?