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?
Summer is in full swing, and we are often asked about the best resources out there to learn more about ECG.
We decided to put together a list of "Editors' Picks" for some of our favorite "go-to" educational ECG resources.
Of course, this list is not comprehensive, and there are many outstanding books and sites that are not mentioned here this time around.
However, you have to start somewhere!
"12 Lead ECG: The Art of Interpretation" (Garcia and Holtz)
"Chou's Electrocardiography in Clinical Practice" (6th edition is recommended)
"Practical Electrocardiography" (Henry J.L. Marriott– Note: we recommend no later than the 8th edition– Marriott himself did not write later editions of the book)
"The ECG in Acute MI: An Evidence-Based Manual of Reperfusion Therapy" (Dr. Stephen Smith– Note: This book is solid gold, but very hard to come by since it went out of print.)
"Advanced ECG: Boards and Beyond" (Brendon Phibbs)
The World Wide Web:
Dr. Smith's ECG Blog– The Gold Standard
Life in the Fast Lane– The ECG Library is an invaluable resource
Dr. Amal Mattu's EKG Videos– Excellent weekly instructional videocasts
ECG Wave-Maven– Tons of practice ECGs to practice with from beginner to advanced. Detailed interpretations provided.
12 Lead ECG Challenge– Created by Tom Bouthillet
Editor's note: While listing the "12 Lead ECG Challenge" app could be seen as self-serving, I must tell you that this app is of such high quality and value that it simply can not be left off the list. I use it often. – David
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:
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
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"!
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 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?
EMS 12-Lead podcast – Episode #10 – Brooks Walsh, M.D. from the Mill Hill Ave Command blog
In this episode of the EMS 12-Lead podcast we're joined by Brooks Walsh, M.D., Emergency Physician and Editor of Mill Hill Ave Command and Doc Cottle's Desk. We discuss paramedic education, ECGs, blogging, science fiction doctors, "treating the patient and not the monitor", reperfusion therapy for acute STEMI, and preactivation of the cardiac cath lab.
Brooks Walsh, M.D.
Follow Brooks Walsh, M.D. on Twitter: @BrooksWalsh
Follow the Mill Hill Ave Command blog on Facebook
This is part II to 59 year old male–"Lifting Boxes". You may wish to review the case.
Let's review the ECG:
There is sinus rhythm at about 90 bpm. Some of you saw a slight bit of ST elevation in the inferior leads, and maybe an abnormal aVL. Perhaps? Perhaps not? V1-V4 look possibly abnormal, but there is an awful lot of artifact. There appears to be a bit of ST depression in V5-V6. Is this an ischemic ECG? Looks concerning from what we can decipher.
Sometimes on blog posts, we get used to crisp ECGs and tidy scenarios. Nothing wrong with that. Sometimes, though, our cases on the street just don't go like that. Often there is much to learn from those, but I digress.
There are a couple of real concerns with this case;
As most of the comments reflect, the timing of the ECG and poor quality make it tough to interpret, and tough to activate the cath lab. I know some of you saw findings that led to you say you would activate, but doing so based on this one poor quality ECG is tough to do. Just is.
So off to the community hospital he went.
Calls are run like this every day. We all know it. In fact, it is one of the reasons we discuss cases such as this.
Could this patient have benefited if the call was handled differently?
Fortunately, we know that he did!
In a contrasting plot twist, this call was actually handled quite differently:
In reality the crew obtained the history and vitals previously mentioned. However, undaunted by the patient's reluctance they convinced him to allow a 12 lead to be acquired immediately. This is what they found:
Due to the patients girth and breathing patterns, it was difficult for the crew to acquire a totally clean ECG. However, this one clearly shows ST elevation inferiorly, as well as V5 and V6. We can also see ST depression in V2-V4 with tall R waves. There is also slight ST depression in aVL: Infero-postero-lateral STEMI.
The crew acquired another 12 lead with V4R which revealed about 1mm of ST depression in V4R:
The ECGs were transmitted, and the patient was emergently transported to the cath lab, where he underwent PCI and had a successful outcome.
For comparison, note how much the ST segments resolved from the first 12 lead to the one acquired in the ambulance:
After just a short period of time from the first ECG, obvious ST elevation in II and III has mostly resolved. Timing is everything!
The point of all of this is to clearly illustrate the importance of early 12 leads and good data quality. The prehospital care of this patient could have gone either way. We see it every day. How we handle those first minutes, and the quality of the data we acquire will have a huge impact on the care our patients receive.
What are your thoughts? I'm sure you have experiences similar to this one!
This is part one of today's case study. As usual some information has been changed to protect patient confidentiality.
EMS is called to the residence of a 59 year old male, who's chief complaint is chest discomfort.
As the crew enters the kitchen, they find the patient sitting in a chair surrounded by family members. He is not happy to see the crew.
He tells them he was doing some lifting of boxes all afternoon, and developed some chest pain, slightly left of center.
He took a break, and it started to get better. Now, 3/10 on the pain scale. He states he has no significant medical history.
The crew ask who called EMS, and he tells them his wife called because she thought he did not look good. He makes it clear that he is not happy with the EMS presence.
As they continue to speak with the patient, they put him on O2 and give him 4 baby ASA just in case. He tells them the discomfort happened earlier in the day when he was lifting boxes, and totally went away when he took a break. He expects nothing different this time. The discomfort does not move anywhere, no shortness of breath, no dizziness or lightheadedness. His wife tells them he was sweating, but he states that of course he was because he was lifting heavy boxes!
The crew takes a quick set of vitals:
The patient's wife convinces him to go and get checked out for her sake. He relents. The crew decides to get him into the rig before he changes his mind, and defers further assessment until then. The patient is ambulatory, and insists on walking to the rig. On the way, he insists on going to the bathroom. Then changes his clothes for the hospital. The crew protests, but he states he will not go otherwise.
Once in the rig, the crew acquires the following 12 lead ECG:
The crew does not note anything too concerning, and considering the patient's story and lack of history, they transport him to the community hospital, without any additional ECGs.
This is the discussion for "Snapshot: 64 Year Old Male–Chest Pain".
First, let's talk about the patient presentation.What is concerning is the substernal chest pain, radiating to the shoulder and neck area. While this occurred about 30 minutes after exercise, it did not occur during exercise, so that is somewhat atypical. Still, enough red flags in the history to be very concerned.
Here is another look at the 12 lead:
It is a regular sinus rhythm, at a rate of 65. The PRI is on the long side of normal at 200 ms, and the QRS is slightly wide at just over 100 ms. The axis is normal, and there does not appear to be anything causing secondary ST changes.
The question is, do we see signs of ischemia on this ECG?
This is not an obvious ECG, so as we would expect, many of you said yes, and many said no. Is this a normal ECG? We don't have an old ECG for comparison, but I would say this ECG is not normal.
Let's break it down. What jumps out at me most on this ECG are the morphologies in leads I and aVL:
There is almost 1 mm of flat ST depression in lead I, and a very notable T wave inversion in aVL.
While the T waves look large in leads III and aVF relative to the size of the QRS, there appears to be no ST elevation at this time.
Dr. Stephen Smith, of the famed Dr. Smith's ECG Blog, has written numerous times that depression and/or T wave inversions in aVL will often precede ST elevation in the inferior leads in IWMI.
Also see this recent case by Dr. Amal Mattu for another case on this subject.
Are there any other findings on this ECG that might support these concerns?
There is about 1 mm of ST elevation in V1. Could there be RV involvement?
At the very least, I would be very concerned about a developing IWMI. The patient's discomfort is diminished, but not resolved. His complaints of "indigestion" are common with IWMI, and diaphoresis is another red flag.
Having said that, would I activate the cath lab based on this ECG? I have to say I would probably not activate based on this ECG alone.
I think this ECG is very concerning, but not yet diagnostic. I would certainly acquire serial ECGs and scrutinize the inferior leads for any subtle signs of change.
Dynamic changes would be a clincher. I would also treat with ASA and NTG, and would divert to PCI center if any changes in the ECG evolved.
This being a "Snapshot" case, we do not have follow up on this patient, or repeat ECGs.
We run into this in the field often. The spectrum of ACS is far and wide, and we are often presented with borderline ECGs.
I think the best course is to treat based on what is best for the patient, and do serial ECGs!
Thanks for all of the insightful comments on this case!
Any additional thoughts?
Today we have a short "Snapshot" case…Just the down and dirty.
You are called to an urgent care center for a 64 year old male, CC of substernal chest pain, which radiated to the right shoulder and neck area. He states the discomfort feels a little like "indigestion".
This episode began just after finishing a 30 minute workout on the bike.
He denies any SOB or lightheadedness, but does admit to becoming diaphoretic. However, he does not know how much of that to attribute to the workout.
Frightened, the patient drives himself to the local urgent care center .
Upon your arrival, the patient states that the discomfort had "just diminished", and that he now "doesn't feel too bad at all".
Vitals are within normal limits, and the patient does not admit to any significant history.
You acquire the following 12 lead:
What are your interpretations of this ECG? How concerned, if at all, are you?
The patient's discomfort has "diminished" by the time you arrive. How does this change affect your assessment and risk stratification of this patient?
You are 15 minutes from the local ED, and 40 minutes from a PCI center, although aviation may be available. How do you want to treat this patient?
This is the discussion for "A change of Pace: What Happened?" My apologies for the delay!
Pacemakers are amazing pieces of technology. They have evolved continually, and have given patients an increasing quality of life where none existed before.
However, with this amazing technology comes a level of complexity that also has not been seen before. These are remarkable devices, cable of many, many different types of functions. Sensing, pacing, defibrillating, single chamber, dual chamber, atrial paced, ventricular paced, cardiac resynchronization, etc… you get the idea. These are just some of the diverse functions that these devices can perform.
For us, we don't often know what type of pacemaker we are dealing with. And often, our patients do not know either! This created a dilemma for us, when we are confronted with an ill patient, and a pacemaker functioning in a way that we do not often see. Is it performing properly? Or is it performing inappropriately? Is the patient's complaint related to the pacemaker function, or the pacemaker reacting to the illness of the patient? To adequately answer these questions, we have to be able to figure our whether the pacemaker is functioning as it should, and why it is behaving this way.
To this end, I have enlisted the help of Mark Perrin, author of the EP Fellow blog. Peer sourcing is an amazing resource!
We'll go through these strips one at a time.
First, let's revisit the first ECG:
There appears to be a sinus rhythm at a rate of about 75bpm. The PR interval is about 240ms, and the QRS duration is slightly prolonged at about 110ms. There are pacing spikes that appear at the onset of the QRS. There also appears to be a fairly constant interval of 140ms between the P wave and the pacing spike.
So, what is going on here? Are the ventricles being paced by the pacemaker?
The first thing to understand is that the site of the pacing lead is normally in the right ventricle. Most of us already know that. However, what we may not all know is that the pacing lead sees "local activation", not the QRS that we see on the surface ECG.
Mark Perrin: "A pacing spike on the beginning of the QRS is not uncommon. It usually occurs because of a right bundle branch block of a right ventricular conduction delay. The pacing lead is in the RV, therefore if there is delay to the right ventricle, activation of the LV (through a conducted P through the AV node) may occur just before the RV lead paces. The RV lead paces because it has not seen LV activation."
Essentially, there is an atrial sensing window of 140ms in this case. If there is a QRS that occurs within that sensing window, the pacing spike will be inhibited. If there is no QRS impulse sensed, the pacing lead will pace. Because of the conduction delay, the beginning of the QRS (which we see) is not seen by the pacer due to the conduction delay, so it paces, even though the ventricle is already responding to the P wave. What should happen, if this occurs, is that the pacing spike should always be near the beginning of the QRS. If it is, as it is in this case, nothing needs to be done, as this is what you could call a "normal variant".
What about the pause near the end of the strip, followed by the complex that looks different from the rest? You may also notice that the P wave looks a little different as well:
Mark Perrin: "This probably occurs because of a different degree of fusion between the conducted LV activation and RV pacing. The change in the apparent AV interval occurs again because the atrial lead sees "local" activation, not the P wave on the surface ECG. Therefore if the atrial activation occurs closer to the AV node it may start conducting to the ventricle before the wavefront reaches the atrial sensing bipole and triggers ventricular pacing. The opposite also occurs, i.e. atrial activation is further from the node, and reaches the atrial sensing bipole long before getting to the AV node."
Let's take a look at the second strip again:
This strip is a variation on the theme of the first. This strip has a mixture of the complexes seen on the first ECG, some with varying degrees of fusion, plus a fully paced beat near the end of the strip. Why the fully paced beat here?
Mark Perrin: "The fully paced beat occurs (my guess) because the PVC before it invades the AV node thus delaying conduction down the node on the following beat."
Now on to the third ECG:
Here we see a fully paced rhythm at a rate of about 85bpm. Why the change from the prior rhythm to a fully paced rhythm?
To fully understand this, we have to remember a bit of physiology. In older people, or others likely to have diseased conduction systems, the "native" AV interval often increases when the heart rate increases. As the sinus rate increases, as in this case, the native AV interval also increases to the point where it is now longer than the pacemaker AV interval. Anytime the pacemaker AV interval is shorter than the native AV interval we won't see normal conduction anymore as the pacemaker takes over.
For this patient, these strips show normal pacemaker behavior. The main concept to remember is that the pacemaker does not see what wee see on the surface ECG. The pacemaker see local activation which may occur after the onset of the QRS in the ventricles, or after the onset of the P in the atria.
Many thanks again to Mark Perrin. I hope you have learned as much as I have in this case. I find pacemaker rhythms to be challenging but rewarding. They can behave in so many different ways..Normally sometimes, and abnormally others. They really are incredible pieces of technology, and I one day aspire to really master the many ways in which they work. One day!
Here is a challenging case this morning to stretch your mind…
You are called to a 71 year old male feeling "sick". He has not felt well for the past 24 hours. He describes feelings of "general aches and pains".
He has history of heart failure, for which he has an AICD.
His vitals are stable, and he does not appear to be in much distress.
Here are two continuous rhythm strips:
A short time later, his rhythm strip looks like this:
While in this rhythm, he reports that he feels "the same".
What is the rhythm in ECG #1?
What is going on in ECG #2?
What changed in ECG #3? And Why?
Looking forward to a good discussion!
Here is the conclusion to 51 year old male: Chest Pain. You may wish to review the case.
Here is the ECG again:
There is a regular sinus rhythm at a rate of about 70. The QRS is narrow. The axis is normal, at about 15 degrees.
Let's take a look at the constellation of ST changes:
There is ST elevation in leads I, aVL, V2-V6. There is slight ST depression in III and aVF (and arguably in lead II) with ugly looking T wave inversions. Some of you also noted the suspicious looking Q waves in III and aVF.
Pericarditis and Early Repol were put forth as possibilities. Remember though, that neither of those will have reciprocal changes (excepting myocarditis, which may present as STEMI). Here, we have reciprocal changes inferiorly. If you were inclined to be thinking about STEMI mimics in this case, those changes should put ischemia at the top of the list. In addition, as some of you pointed out, the ST changes do not look like Early Repol, and the amount of ST elevation here is alarming.
The crew in this case, along with the physician, decided this was STEMI. The patient was given Heparin, ASA, anti-emetics, and Morphine. His condition improved enroute, and his BP climbed to 124/75.
Upon arrival at the hospital, he was taken directly to the cath lab. There was a complete blockage of the LAD.
Here is the cath lab image showing the blockage:
Here is the image after revascularization:
I don't know about you, but I always find these images amazing. Fortunately, our patient was discharged from the hospital to cardiac rehab a few days later. He was expected to recover nicely.
Enjoy the holiday!
Here is a great case submitted by faithful reader Niels, a Paramedic in Germany. As always, some minor information may have been changed to preserve patient confidentiality.
Our case today takes us overseas, to the German countryside. It's a clear blue Monday morning, 11:40 am, when you and your partner are called to a 51 year old male complaining of chest pain. You are dispatched parallel to an Emergency Physician (in Germany, every ALS call is dispatched with an ALS ambulance and a doctor).
On arrival, you find a male patient lying in bed. He appears to be very diaphoretic an pale. He tells you he is very athletic and fit, but today is "feeling horrible". He says his "chest is killing him", and he admits to being nauseous, with several bouts of vomiting.
O,P,Q,R,S,T: He tells you he woke up with the pain, and it seemingly came out of the blue–he was feeling fine the night before. Nothing seems to make the pain, which he describes as "crushing', feel better. In fact he can find no position of comfort. You seem to be compiling "red flags" as he tells you that the substernal pain also radiates to his left arm. He rates it a 4 or 5 out of 10, and says it began about 15 minutes before EMS was called. You ask if he's ever had this happen before and he says no.
As your partner starts to apply the electrodes, you continue your HPI and vitals. He has no real medical history, although he did smoke but quit ten years ago. He takes no meds. He does tell you that he saw his general physician last week for becoming "short of breath" during his workouts. Pneumonia was ruled out.
You give him 4 baby ASA, and acquire the following 12 lead ECG:
Ok, this is not what you are used to seeing. In addition, the speed is 50mm/sec. Thanks to the studio magic of Christopher Watford, here is the same ECG "stitched" together in the familiar format, speed adjusted to 25mm/sec:
A few moments later, the Physician arrives. He wants to know the status of the patient, and what you see on the ECG.
What do you tell him?
This is the discussion to "What Happened?" You may wish to review the case here.
Ok, let's review the initial 12 Lead:
Just about everyone picked up on the infero-posterior STEMI.
Where it got interesting for me, was determining what the rhythm was! At first glance, the rhythm was for the most part regular (note the computer interpretation of Atrial Fibrillation with RVR!) and narrow, with a rate just a touch faster than 100. I did not see P waves before most of the QRS complexes, and I initially thought it was a junctional tachycardia.
As the STEMI was most likely due to an RCA occlusion, it is not surprising to have conduction disturbances. The pause, followed by an apparent sinus beat (circled in red above), had me wondering if this was indeed junctional with a sinus "escape" after the pause, or some kind of sinus rhythm with AV block.
In keeping with our spirit of "Peer Sourcing", I ran this strip by electrophysiologist Dr. Nick Tullo, of the ECG Academy.com. A review done by Life in the Fast Lane of Dr. Tullo's excellent academy can be found here. This is the conversation I had with Dr. Nick about this rhythm:
Me: Thanks for the help Dr. Nick. Now, what the heck is this?? Junctional, or sinus/AV block?
Dr. Nick: I would call it "Atypical Wenckebach" –essentially 13:12. You can see a sinus P following the fourth beat, and then a similar pause just before the end of the tracing. The pause is less than two times the previous R-R, and the PR of the second beat following the pause is longer than the PR that interrupts the pause (what you are calling accelerated juntional is really sinus rhythm with a first degree AV block, but you can't see the P easily because it's buried in the previous T). In the setting of acute IWMI it's due to the same high-vagal-tone mechanism that would cause the usual 3:2 or 4:3 Wencheback (or even complete heart block in some patients) but the AV node is mostly keeping up.
Me: Wow… OK! But, how do we know it's not a junctional rhythm with a sinus beat escaping from the pause?
Dr Nick: You have to look hard for the P waves. If it was a junctional rhythm you'd see consistent P's at the end of the QRS or maybe in the very early part of the ST segment. If I'm right, the P wave will be on the T-wave somewhere and not always in the same spot (since it's not directly connected to the previous QRS). Granted, the ST elevation makes it hard to see the Ps. But I see the answer clearly:
Look at V5…see how the first beat has a concave upslope of the T wave while the second beat looks like it has a bump on it? That bump is the P wave. Assuming that the R-R interval midway through the "junctional rhythm" is equal to the atrial rate (since the PR doesn't change midway through an Atypical Wencheback cycle) measure back from the visible P preceeding the third beat in V5…doesn't it land right at the bump? The reason the T looked concave the beat before that is because that P wave is on the peak of the T.
I've put together some graphics to help illustrate the important points.
First is Lead V5, which Dr. Nick referenced, blown up. I've done the same with lead II. Note the subtle morphology changes in the two T waves. This is the last P wave of the cycle, which does not conduct. the P wave following the pause is the first of the cycle, and has the shortest PR interval:
I know, you're thinking, "Really? Do those little blips/bumps really measure out?" Don't take my word for it. I've got one more illustration to show you. I took a mid cycle R-R interval (1), as Dr. Nick suggested, and used that to measure back and see where the P wave should be in leads II and V5 (2,3):
As you can see, right on cue, those blimps/bumps are right where the P wave should be. And there we have it: 13:12 Atypical Wenckebach, with a PVC at the very end of the strip.
My sincere thanks to Dr. Nick Tullo for his help with this case, and kudos to Jason, who expertly picked up on this in the comments section.
Now for the second 12 Lead:
The patient was treated with thrombolytics (TNK), and as many of you commented the resulting rhythm was an accelerated idioventricular rhythm (AIVR). AIVR appears similar to VT, but slower (slower than 120). In the thrombolytics era, this transient rhythm was noted to be a marker of reperfusion, although not all patients with a reopened coronary artery have AIVR. When it appears it rarely causes hemodynamic instability, and usually requires no treatment. For more information about AIVR, see here.
Of course, you will notice that I have circled several leads in the 12 lead above. In keeping with this case, in which nothing seems to be typical, you will notice that in fact the ST segments have not resolved during the AIVR. The inferior ST elevations remain, as do the ST depressions in V1-V4, and aVL.
When asked about this, Dr. Smith, of Dr. Smith's ECG Blog had this to say: "This is one of the few cases of AIVR I've seen that was not associated with reperfusion."
In this case, our patient failed thrombolytics. He was immediately sent for rescue PCI. Unfortunately, we don't have any additional information.
There was a lot of information in this discussion. I sure learned a lot!
I look forward to your comments, and as always, thanks for reading!
A 68 year old male, with no significant medical history, presents to the local ED (non-PCI) with chest pain. He had been doing some gardening, when he suddenly felt chest discomfort (8/10), non-radiating with diaphoresis. His wife drove him to the ED. Once there, he was given ASA and NTG, and the following ECG was acquired:
His vitals were as follows:
After a short time, the patient was given another treatment and entered the following rhythm:
Here at the EMS 12-Lead Blog, we love case studies.
We love to post them, you love to read them, and many of you love to comment on them.
Not only on this blog, but on other very good blogs that are out there as well. I think it’s a great way to learn, and share ideas in this era of Web 2.0. What I want to discuss today is one comment I often see:
Treat the patient, not the monitor!
Before we start, I want to be clear about a couple of things.
First, I understand that ECG interpretation is hard. Really hard. To become proficient it takes countless hours, months, and years of study. Whatever my opinions, I am certainly not trying to suggest it is easy or routine. I make mistakes like everybody, and I will still run a difficult strip or 12-Lead by people who know more than I do for help with the interpretation.
Second, when we are talking about treating the patient not the monitor, we are not talking about defibrillating a live patient with tremors because it looked like VF on the monitor. “Oops, guess I should have looked at my patient”. No, that’s not what we mean.
Often, when someone writes, “just treat the patient, not the monitor”, what he or she really means:
I can not figure out all of these squiggly lines, so I am going to ignore them.
Hey, I get it.
Hell, I’ve been there, and so has everybody else. In fact, I am still there sometimes. Everybody has a patient whose ECG is challenging, and takes them as far as they can go with their interpretation skills. It does not mean that we should devalue the importance of the ECG just because we are having trouble interpreting it.
If we want to evolve into clinicians instead of technicians, we have to use all of the relevant tools at our disposal. When it comes to potential cardiac patients, our cardiac monitors can be some of our most important tools. These relatively small machines can give us a ton of important information, and arguably we can not really have a full picture of what is happening with our patient if we can not interpret what we see on the monitor.
Does what we see on the monitor really matter that much?
Consider your tachycardic patient, who looks sick with poor color, but an Ok mental status and a reasonable pressure. Are we looking at,
Do you want to give fluids? Or perhaps adenosine, amiodarone, or Cardizem?
How are you going to determine what treatment he needs?
Oh that's right, by interpreting the ECG.
There is really no getting around it. I suppose you could just transport everyone to the hospital and let them deal with it, or wait until they become unstable enough that you have to shock them. But is that the optimal patient care we want to deliver?
Even if you decide all you can or should do is take the patient to the hospital, you have to ask what type hospital do they need?
Want to hold off on NTG? Give fluids? How are you going to know?
Again, by interpreting the ECG.
How about your syncope patient. Anyone up for WPW, Brugada, or another arrhythmia?
See what I mean?
When it comes to cardiology, I really don’t think we can separate the patient from the monitor. I mean, they are hooked up to the darn thing anyway!
But even figuratively, what we see on the monitor is part of their history, part of their present illness, and very often contains the answers that we could get no other way. We are talking about cardiac patients who for the most part, look very similar, although the underlying problem can be anything we can see on the ECG from normal tracings, to arrhythmias and STEMIs and everything inbetween.
If you're good, you just might pick up something that saves their life. We see countless cases sent in by you–our readers–of patients who might not be here today if it wasn't for their prehospital ECG interpretation!
When we get that voice in our heads, the one that tells us not to focus on the squiggly lines and just look at our patient, we should listen to what that voice is really trying to tell us: that we don't know what it means, and we need to learn more.
There is no shame in that. In fact, I would take it as a sign of a good provider. To acknowledge what we need work on, and try to improve. That’s all we or our patients can really ask!
If you spend time reading Dr. Smith's ECG Blog or some of the electrophysiology blogs, one thing you will never see is "treat the patient not the monitor." That's because this is a false choice.
So let's start a trend whenever you come across a tough case study, and leave a helpful comment:
Treat the patient AND the monitor!