Sometimes recognizing sinus tachycardia can give us fits.

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

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

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

Is it difficult to recognize this?

No.

How about this one?

More difficult.

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

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

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

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

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

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

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

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

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

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

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

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

What are we even taught about SVT?

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

How do we differentiate sinus tach from SVT?

That’s easy: rate!

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

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

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

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

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

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

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

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

“154= SVT”

“146= ST”

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

We also need to be better educators and providers.

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

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

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

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

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

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

As always, I look forward to your comments!

_

Footnotes:

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

                  2011, American Heart Association

^{[2]             Pediatric Advanced Life Support Provider Manual}

                  ^{2011, American Heart Association}

EMS 12-Lead podcast – Episode #11 – Are we harming patients with oxygen?

In this episode of the EMS 12-Lead podcast we're joined by Kelly Arashin, ACNP, CCNS and Mike McEvoy, PhD, RN, CCRN, REMT-P at EMS Today 2013 in Washington D.C. We discuss the benefits and dangers of oxygen administration. 

Kelly is a dual boarded advanced practice nurse and Chair of the Hypothermia Steering Committee at Hilton Head Hospital in Hilton Head Island, SC.

Mike describes himself as a nurse, paramedic, firefighter, and medical college professor. He is also Chair of the Resuscitation Committee for University Teaching Hospital in Albany, NY.

Mike is the author of the article Can Oxygen Hurt? and taught an educational session at Physio-Control University entitled To Give Oxygen or Not: That is the Question. 

Tom Bouthillet, Kelly Arashin, Mike McEvoy at EMS Today 2013

Special thanks to Physio-Control, JEMS, PennWell, and the ProMed Network

You can also watch the video version.

See also:

Follow Kelly Arashin on Twitter at @BarefootNurse24

Visit Kelly's blog

Follow Mike McEvoy on Twitter at @McEvoyMike

Visit Mike's website

Subscribe to the EMS 12-Lead podcast on iTunes

Ivan Rokos, M.D. has referred to primary PCI for acute STEMI as “the most complex, multi-disciplinary, and time-sensitive therapeutic intervention in the world of medicine.”

The emphasis on door-to-balloon times, and more recently, first medical contact or EMS-to-balloon times has transformed how acutely ill patients suffering heart attacks receive timely reperfusion in many communities, because as we’re so often told, “time is muscle.”

While some believe that the emphasis on door-to-balloon times has unintended consequences, in our opinion the real-life stories of the men and women who build these systems of care illustrate the very best of what modern medicine has to offer.

A single 9-1-1 call (9-9-9 in the UK) triggers an awe-inspiring series of highly coordinated events that clearly demonstrate that despite all of our arguments about health care and how it should be paid for, when a fellow human being is in danger, we will work together to save that person’s life.

We will exercise exceptional caring and competence, and then return that patient to their family. We give them another chance.

That’s powerful.

Many of us in EMS (and other areas of medicine) love survivor stories because it makes us feel good to know we’ve helped another human being. That’s why we got into medicine in the first place. But then something happened. We became jaded. We became cynical. We saw the worst in people.

The Code STEMI Web Series is a salute to the individual EMTs, paramedics, nurses, and physicians who had the courage and the insight to change the status quo and build something very meaningful that directly influences whether our friends, neighbors, or even our family members live or die.

Change can be difficult. It can be painful. It takes us out of our comfort zone and sometimes it rearranges the pecking order. Yet, we must change, whether it’s allowing EMTs to acquire and transmit a 12-lead ECG, activating the cardiac cath lab at 3:00 a.m. Sunday morning, or learning how to reduce “door-in to door-out” (DIDO) times at Critical Access Hospitals so that heart attack patients have the best possible chance of survival.

As Michael Hibbard, M.D. reminds us, it’s not the strong who survive. It’s those who are most able to adapt to change.

Our most recent episode of the Code STEMI web series looks at the London Ambulance Service. It is the busiest, and arguably one of the best EMS systems in the world. We interview front line EMTs, paramedics, nurses, and physicians as well as survivors. We hope you enjoy watching it as much as we enjoyed filming it so you can share our enthusiasm for witnessing a job well done.

Seaon 2 of the Code STEMI Web Series is set to launch on March 7, 2013 at EMS Today in Washington, D.C.! This season starts out with our most exciting location ever — London, England as we feature the London Ambulance Service (LAS).

You can follow the series at First Responders Network or at CodeSTEMI.tv.

Special thanks to Physio-Control for sponsoring this web series!

Speaking of which, you can download the schedule for Physio-Control University at EMS Today by clicking here (PDF).

I'll be teaching an educational session called Hilton Head Island – Strengthening a Community's Chain-of-Survival. I'll explain how we achieved on of the highest cardiac arrest save rates in the nation (Utstein survival of 66% for 2012).

Hope to see you there! 

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:

ST-depression from ischemia does not localize.

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:

• Sometimes STEMI patients will have atypical symptoms.
• A single ECG is not enough to detect all STEMI patients, serial 12-Lead ECG's should be acquired on all patients who receive one.
• ST-depression from ischemia does not localize, localized ST-depression should be considered a reciprocal change until proven otherwise.

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:

• HR: 70 bpm, regular at the radials
• BP: 144/96
• RR: 18, unlabored, in no apparent distress
• SpO2: 95%
• ECG: "normal sinus, nothing out of the ordinary" (no 12-Lead was captured)

You perform a quick patient assessment prior to making any decisions:

• Onset: 21:00 the prior evening
• Provocation/Palliation: pain went away over night with sleep, came back after breakfast; nothing makes it better now
• Quality: "burning"
• Radiation: "straight thru to my back"
• Severity: 7 of 10
• Timing: constant burning

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.

• What do these 12-Lead's show?
• What are your next steps?
• Is indigestion a contraindication to aspirin administration?
• Are you glad this case does not involve a narrow complex tachycardia?

Since infographics are all the rage nowadays I thought we'd put some together for ECG interpretation.

I'm starting with left anterior fascicular block… well, just because!

I hope you find these to be useful!

See also: Left anterior fascicular block

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

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

He says:

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

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

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

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

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

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

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

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.

Happy New Year everybody!

We start 2013 with a continuation of our discussion about the field treatment of hyperkalemia. 

It might be helpful to review the first part of the discussion," HyperK and Shades of Grey" here. 

We are fortunate to have as a guest contributor Dr. Brooks Walsh of the Mill Hill Ave Command blog. An advocate of prehospital medicine, Dr. Walsh offers shares "Myths and Facts" of hyperkalemia with us. My sincerest thanks him for his valued contributions! 

I asked Dr. Walsh why he thought hyperkalemia presented such a challenge for EMS providers. Here is what he had to say:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong & clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true.

But rather than curse the darkness, I wanted to go over some newer perspectives on hyperkalemia. Now, I don't want to simply reiterate all the great material that Dr. Weingart talked about on EMCRIT, so you really ought to download his great podcasts on the treatment of hyperkalemia and on why Kayexalate is likely ineffective, if not outright dangerous. The podcasts are real short, so just play them right now.

With that said, I'd like to review a few topics in hyperkalemia that deserve more attention:

Myth: Dialysis patients tolerate hyperkalemia better than other people.

Medicine is funny. I mean, there are "facts" that "everyone knows," but that are surprisingly hard to prove in studies. This is sort of one of those kind of facts, with very little evidence, and plenty of "real world" experience. Should we continue to believe it?

Maybe. It kind of depends on what we mean by "tolerate." If we mean "don't show ECG signs of hyperkalemia," then maybe dialysis patients do "tolerate" hyperkalemia better than other people. 

It's kind of hard to answer this definitively, though, since ECG signs of hyperkalemia, especially in the moderate range (e.g. < 6.5), are often absent on the ECG on all patients. We just don't see that many patients, dialysis or no, with severe hyperkalemia. Even in a study that looked only at dialysis patients, the vast majority had a K < 5.2, and ECG changes were accordingly infrequent.

But it may also be that dialysis patients, in fact, do show fewer signs of hyperkalemia on the ECG than do other people. A study done back in 1967 looked at dogs that received IV potassium slowly or quickly (but ending up at the same blood level). The faster infusions caused more ECG and hemodynamic effects. It is possible that ESRD patients, with a presumably slow increase in potassium levels, show fewer ECG changes than, say, a patient with acute rhabdomyolysis.

But the ability to avoid ECG changes isn't the "tolerance" we care about in hyperkalemia - we really care about the potential for patients to go into cardiac arrest. Hyperkalemia, regardless of ECG signs, puts the patient at risk for fatal arrhythmias. If you have either lab results or ECG evidence of hyperkalemia, that patient needs to be treated immediately – on that, most experts agree. I couldn't find any mention in the literature that suggests otherwise. For example:

                   "We emphasize that despite the absence of ECG changes of hyperkalaemia in ESRD, hyperkalaemia is still a     potentially life-threatening condition." –Aslam 2002

Or

"Some experts advocate calcium administration in patients whose serum potassium is >6.0–6.5 mm, even in the absence of EKG changes." –Putcha 2007 

 

Myth: If the ECG doesn't show QRS widening, then the patient is at low risk.

Some clinicians are under the impression that you can wait to treat the hyperkalemia until the QRS is "incredibly widened," showing huge sine-waves.  An ECG that shows "just T-waves" is presumably at lower risk, in this view.

Except that's not how it works, according to the experts. As these nephrologists explain:

                 "Five medical textbooks (two nephrology, two internal medicine, and one emergency medicine) advocate calcium gluconate in all hyperkalemic patients with EKG changes. "

Or this critical-care nephrologist:

                "It is apparent that neither the EKG nor the [potassium level] alone is an adequate index of the urgency of hyperkalemia,… hyperkalemia should be treated emergently for 1) K > 6.5 mmol/L or 2) EKG manifestations of hyperkalemia regardless of the [level]." –Weisberg 2008 "Management of severe hyperkalemia"

We asked Dr. Smith about his experiences with this topic, whether he has seen patients arrest without going through the ECG transition to widened, sine wave ECGs. His response as well was that "I have seen v-fib with peaked T waves only" on the ECG.

Stay tuned for "Myths and Facts Part II"!

This is the conclusion to our Name that ECG case: 66 year old female, resolved chest pain.

66 year old female, resolved chest pain.

Rhythm:

• Rate: atrial rate of ~55 bpm, ventricular rate of ~55 bpm
• Regularity: regular
• P-waves: sinus (upright in I and II), associated 1:1 with the QRS
• PRi: 140 ms
• QRS duration: 90 ms

Bonus points:

• Axis: -45 degrees, left axis deviation, LAFB
• Bundle Branches: normal conduction
• QTc: normal (<1/2 R-R interval), 420 ms (Bazett's Formula)
• ST/T-waves:
  • T-waves: flipped T-waves in aVL, biphasic V2-V5 consistent with Wellen's Syndrome
  • ST-elevation: none noted
  • ST-depression: none noted

Differentials:

• Normal sinus rhythm in a patient with Wellen's Syndrome
  • Possible high-grade stenosis of the LAD with recent reperfusion

Notes:

• Wellen's Syndrome should be regarded with the same importance as a STEMI during assessment and transport.

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.

Rhythm:

• Rate?
• Regularity?
• P-waves?
• PR interval? Associated?
• QRS width?

Bonus points:

• Axis?
• QTc?
• ST/T-wave changes?

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.

On Monday, the American College of Cardiology Foundation and the American Heart Association released the 2013 Guidelines for the Management of ST-Elevation Myocardial Infarction. Their last updates to these guidelines were in 2004 and 2006, so this is an important milestone.

If you have been following our blog and podcast, most of the changes will not be earth shattering. We have long been advocates of evidence based STEMI care, which has put us at the bleeding edge as the guidelines take time to catch up. What does this mean for you, our readers?

Our readers have been ahead of the game! We're constantly impressed by your breadth and depth of knowledge.

The 2013 guidelines makes these changes, which we've covered before, to the identification of STEMI:

• "New or presumed new" Left Bundle Branch Block is no longer an indication for a STEMI.
• Providers should use Sgarbossa's criteria to diagnose STEMI in the presence of LBBB. (Editor's Note: we're going to go ahead and add that our readers should take this one step further and utilize Smith's modification to Sgarbossa's criteria.)
• Isolated ST-depression in V1-V4 is an indication of a posterior STEMI.
• Widespread ST-depression with ST-elevation in aVR is an indication of proximal LAD or LMCA occlusion. (Editor's Note: the evidence points more towards this being an indication of 3-vessel disease or near occlusion of the LAD/LMCA.)
• Hyperacute T-waves, e.g. de Winter ST/T-wave changes, are an early indicator of a STEMI.

The honest answer is we probably would not have written a post about these guidelines if it were not for the following gem, buried on page 10 in the section on Regional Systems of Care (emphasis mine):

"For patients who call 9-1-1, direct care begins with FMC, defined as the time at which the EMS provider arrives at the patient’s side. EMS personnel should be accountable for obtaining a prehospital ECG, making the diagnosis, activating the system, and deciding whether to transport the patient to a PCI-capable or non–PCI capable hospital."

Folks, a joint task force of cardiologists has just placed the responsibility for the diagnosis and activation of a STEMI in the hands of EMS providers!

Many systems are already ahead of the game when it comes to STEMI care, but others lag behind.

We've taken responsibility for the care of cardiac arrest victims and now is the time we acknowledge the critical role we play in STEMI care.

• Does your system acknowledege paramedic diagnosis of STEMI?
• Are you ready to take on the responsibility of diagnosis and activation of STEMI?

This is the conclusion to Name that ECG: 51 year old male.

51 year old male, palpitations.

Rhythm:

• Rate: ventricular rate ~185 bpm, unknown atrial rate
• Regularity: regular
• P-waves: none appreciated
• PRi: N/A
• QRS duration: ~200 ms

Bonus points:

• Axis: inferior, +90 degrees
• Bundle Branches: V1-negative, wide-complex
• QTc: not appreciable
• ST/T-waves:
  • T-waves: appropriate discordance in all leads
  • ST-elevation: not readily interprettable
  • ST-depression: not readily interprettable

Differentials:

• Ventricular tachycardia

Notes:

• Subtle dissociation of the atria may be visible in the ST/T-waves in II and III.
• It is unlikely that this rhythm is anything but ventricular tachycardia.
• The ST-segments in aVL are arguably excessive, potentially indicating an ACS cause of this tachycardia.

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.

Rhythm:

• Rate?
• Regularity?
• P-waves?
• PR interval? Associated?
• QRS width?

Bonus points:

• Axis?
• QTc?
• ST/T-wave changes?

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)

Rhythm:

• Rate:
  • Atrial rate of ~120 bpm, appreciated in V1-V3
  • Ventricular rate of 33 bpm
• Regularity: regular atrial and ventricular activity
• P-waves:
  • Appreciable in V1-V3, unknown if sinus but rate is consistent with sinus tachycardia
  • The P-waves may or may not be associated with the QRS complexes, if they are it is a 4:1 association
• PRi: if associated, high-normal at 210 ms
• QRS duration: possibly slightly prolonged at 120-130 ms (V3 and V6 are widest)

Bonus points:

• Axis: -45 degrees, pathologic left axis deviation (down aVF, up I, down II), LAFB
• QTc: normal (< 1/2 R-R), 351 ms (Bazett's)
• Bundle Branches: V1-positive (qR), R in Lead I, RS in V6, IVCD
• ST/T-waves:
  • T-waves: biphasic T-waves in II/aVF/V6, flipped T's in I/aVL/V3-V5,
  • ST-elevation: possible ST-E in V1-V3
  • ST-depression: possible ST-D in I

Differentials:

• Sinus tachycardia or atrial tachycardia with:
  1. 4:1 2nd Degree AV Block and IVCD
  2. 3rd Degree AV Block with a junctional escape rhythm (IVCD)
  3. 3rd Degree AV Block with a ventricular escape rhythm

Notes:

• A longer rhythm strip from V2 would better highlight the degree of AV block present
• A septal MI may be the cause of our patient's heart block and condition

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.

Rhythm:

• Rate?
• Regularity?
• P-waves?
• PR interval? Associated?
• QRS width?

Bonus points:

• Axis?
• QTc?
• ST/T-wave changes?

What are your differentials?

Posts which include any permutation of the phrase "treat the patient not the monitor" will be deleted, 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:

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

You acquire an ECG that looks similar to this one:

image credit

You begin packaging your patient.

You are 20 minutes from the closet community hospital.

TODAY'S MISSION:

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

So, that is not the question.

The questions are these:

Do we treat this patient prehospitally? 

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

If we did, What would we use and why?

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

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

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

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

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

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

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

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

• DVT
• Possible aortic dissection
• STEMI

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

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

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

So, how do we manage this patient? 

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

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

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

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

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

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

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

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

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

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.

• LOC: alert to verbal (GCS E3 V5 M6)
• Pulse: weak radials at 50 bpm
• BP: 80/50
• RR: 14, shallow, clear lung sounds
• SpO2: 92% r/a
• BGL: 68 mg/dL (3.8 mmol/L)

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.

• What is your diagnosis? What are your next steps?
• What does the first rhythm strip show?
• What does the 12-Lead show?
• What does the long rhythm strip show?

This is the discussion for 63 year old male CC: Substernal Chest Pain, brought to you by Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. Be sure to review the first part!

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!

• Did you catch the posterior STEMI?
• Does your service allow you to activate a posterior STEMI?

Today we're presenting a case from our friend Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. In fact, this case is being presented both for his readers and for ours! We hope you like it.

You're working ED triage when a 63-year-old man walks in complaining of substernal chest pressure that had awoken him from sleep 2 hours prior. He denied any radiation of the pain, but complained of some mild presyncopal symptoms. His wife reported that he had had intense diaphoresis at home. He reported having a similar episode 1 year ago, but a subsequent stress test was negative. 

You obtain a quick history:

• PMHx: HTN, type 2 diabetes mellitus
• Meds: irbesartan, insulin
• Allergies: NKDA 

A quick set of vitals are obtained:

• HR: 90 
• BP: 145/123 (NIBP)
• RR: 16, unlabored
• SaO2: 98% r/a

The physical exam reveals a patient with mild sweating, but no JVD. His lungs are clear, there are no cardiac murmurs, and he does not have any lower extremity swelling or tenderness.

You obtain a STAT 12-Lead ECG:

The patient is taken back to a bed, 324mg of aspirin is administered, an IV is started, and labs are drawn. The patient receives 0.4 mg SL nitroglycerin and 5 mg morphine, both without relief. Metoprolol is given for the patient's hypertension and a heparin drip initiated. Cardiology was consulted and believed the ECG to be non-specific. 

Per the ED physician, an ECG is performed 15 minutes later to assess the right side of the heart. Note that all of the precordial leads were reversed (e.g. V2R = V1):

Due to persistent chest pain, a nitroglycerin drip is initiated and titrated up to 132 mcg/min without improvement in chest pain. A loading dose of clopidogrel is given.

An hour after presentation the ED physician asks for a posterior ECG:

Labs return a troponin of 0.05 (normal is < 0.04). A CBC and basic chemistry panel were essentially negative.

• What does the first ECG show? Is it diagnostic?
• Do the right-side and posterior leads help with diagnosis? 
• If this is a STEMI, what coronary artery is likely involved? 

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

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

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

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

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

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

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

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

Here is the 12 lead:

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

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

You decide to acquire another ECG:

What do you think is going on with your patient?

This is the conclusion to our case 24 year old male: "Anxiety Attack". Be sure to read Part I before the conclusion!

When we left off, our providers were on scene with a young man, in custody, who was pale and had a radial pulse too fast to count. A narrow complex tachycardia was present on the monitor to which our patient helpfully pointed out, "it's SVT".

Let's find out if our patient is right!

The initial rhythm strip shows a regular, narrow complex tachycardia at approximately 200 bpm. Differentials include SVT (e.g. AV Nodal Reentrant Tachycardia and Orthodromic AV ReciprocatingTachycardia), atrial tachycardia, atrial flutter, and atrial fibrillation. However, given the rate, it would seem unlikely to be flutter, and given the near dead-on regularity it excludes atrial fibrillation.

The 12-Lead ECG confirms much of what we saw in the initial rhythm strip. We have a regular, narrow complex rhythm at 200 bpm. Retrograde P-waves are appreciable in leads II, III, aVF, and V1. These P-waves are often termed pseudo-S or pseudo-R' waves, and are most commonly seen in AVNRT. However, ST-elevation in aVR during SVT is a sign of orthodromic AVRT.

Regardless of mechanism, it is safe to say that our patient was right! He is currently experiencing SVT.

The treating paramedic also came to this conclusion and began treatment by lying the patient down and attempting vagal maneuvers. The patient was coached to bear down and then to blow through an empty 10 cc syringe, both without effect:

An 18 gauge IV was established in the left antecubital fossa. 6 mg of adenosine was then administered rapid IV push followed by a 20 cc normal saline bolus flush. The following was captured:

This rhythm strip shows an interruption in the AV nodal reentry circuit with a conversion to a sinus tachycardia.

A repeat 12-Lead was obtained by the crew:

The post-conversion 12-Lead shows a sinus rhythm without delta waves, epsilon waves, or acute ST/T-wave changes. The computerized interpretation notes a short PR interval of 98 ms, however, this author reads the PRi as normal at ~120ms. If an accessory pathway is present, conduction is concealed on the patient's baseline 12-Lead.

The patient was transported by the crew without incident and was lost to follow-up by EMS. However, this case shows that sometimes our patients will know exactly what is wrong, which underscores the importance of obtaining a good history.

• What conditions could this patient have which caused his SVT?
• What treatments may this patient receive if he continues to suffer from SVT?

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.

See also:

Mill Hill Ave Command

Dr. Cottle's Desk

Follow Brooks Walsh, M.D. on Twitter: @BrooksWalsh

Follow the Mill Hill Ave Command blog on Facebook

Subscribe to the EMS 12-Lead podcast on iTunes

This is the conclusion to our three part case series, 62 year old male: Chest Discomfort. Before reading the conclusion, we suggest you check out Part I and Part II. Thanks again to Vince DiGiulio, EMT-CC for this wonderful case!

When we last left off, our patient had experienced a resolution of his chest pain accompanied by changes on his 12-Lead ECG. The ED physician had called cardiology, but they were unimpressed. Are we comfortable with this?

Let's review our patients'  first 12-Lead.

We have a narrow complex, regular rhythm at 90 bpm consistent with a normal sinus rhythm. Flat or downsloping ST segments are visible in leads III and aVF. Additionally, ST-Elevation is present in leads V1 through V4. As some readers pointed out, this is diagnostic for an Anterior Wall Myocardial Infarction. There are also some subtle hints that this is not a normal variant:

• Dr. Smith included in the comments that the R-wave amplitude of V2-V4 is only 10 mm. In cases of AWMI, a loss of precordial R-wave amplitude is often noted.
• If you compare the T-waves in V1 and V6, you'll note that they are much larger in V1 than in V6. Dr. Henry J. L. Marriott describes this finding as a "loss of precordial T-wave balance." Dr. Mattu covers this in depth in his excellent video New Tall T-Waves in V1.

The most important point is that there is no other explanation for our patient's ST-Elevation. There is no LVH or BBB present and Early Repolarization is a diagnosis of exclusion in a 62 year old patient.

Regardless, any patient with chest pain should be evaluated with serial ECG's. During our patient's second 12-Lead, he happened to be pain free:

Our repeat 12-Lead shows a normal sinus rhythm, with the development of terminal T-wave inversions in leads V1-V4. Several of our readers correctly pointed out that these are the hallmarks of the eponymous Wellens' Syndrome (or Wellens' Warning). Interestingly enough, the computer's interpretation now displays *** ACUTE MI ***.

So what is the importance of this finding?

In 1982, Hein JJ Wellens identified two types of abnormal T-waves associated with critical, proximal LAD stenosis. The first type, not seen in our case, features deeply inverted, symmetric T-waves in the anterior precordial leads. The second type, featured above, are characterized by biphasic T-waves. In his seminal study, Wellens found that these electrocardiographic patterns were most often seen during pain free periods. Subsequent studies showed that nearly every patient with Wellens' Syndrome had blockage in the LAD, ranging from 50-100%!

So what happened with our patient?

Our patient continued to experience transient episodes of chest pain. His troponin-I levels returned at 1.09 ng/mL 20 minutes after the pain-free ECG. Recognizing Wellens' Syndrome, the ED physician had the patient transferred directly to the cath lab for immediate PCI.

Key points highlighted by this case:

• Obtain Serial ECG's!
• A single ECG diagnostic for STEMI is indication for cath lab activation.
• Resolution of chest pain is not a reason to withold aspirin.
• Wellens' Sydrome strongly suggests an advanced degree of LAD stenosis and requires urgent evaluation.

References

• Dr. Smith's ECG Blog – Wellens' Syndrome
• de Zwann C, Bar FW, Wellens HJJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982; 103:730-736. [PubMed]
• Parikh KS, Agarwal R, Mehrota AK, Swamy RS. Wellens syndrome: a life-saving diagnosis. Am J Emerg Med 2012; 30:255e3-255e5. [PubMed]
• Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med 2002; 20(7):638-43. [PubMed]

This great case comes from a long time reader who wishes to remain anonymous. As always, details have been changed to protect patient and provider privacy.

You're dispatched on an ALS quick response vehicle by law enforcement requesting EMS to check up on a subject. Dispatch notes indicate officers were called reference a domestic disturbance and have two subjects in custody. A BLS ambulance just around the corner from the call checks on scene and requests ALS continue.

You're directed into a small apartment by an officer and find the BLS crew obtaining vitals from a young man, who appears pale, seated on a couch, uncuffed. The officer says, "he started complaining of chest pain and his hands tingling after we arrested him, might be an anxiety attack. He and his girlfriend really got into it."

You check in with the BLS crew who are obtaining his vitals and introduce yourself to the patient. He looks up at you and simply states, "It's SVT."

One of the crew looks up and nods his head while giving the vitals:

• Pulse: too fast to count
• BP: 118/64
• Resps: 18, unlabored
• SpO2: 94% r/a, cap refill normal
• JVD: moderately elevated

A quick assessment is made:

• Signs and Symptoms: Palpitations and SOB
• Allergies: None
• Medications: None
• PMHx: "I've had SVT a lot, like twice already this month."
• Last In's and Out's: Dinner
• Events: verbal altercation with girlfriend

During your exam the BLS crew has placed the patient on the monitor for you:

As it prints out, you tell one of the officers that he's definitely a patient and will be going with you to the hospital.

A 12-Lead is acquired:

• Is this patient actually in SVT?
• What is your treatment plan?
• What sort of medical problems could this patient have?

This is part two of the three part series, 62 year old male: Chest Discomfort. As before, clinical details have been altered for educational purposes and to protect patient and provider privacy.

• What does the patient's 12-Lead show now?
• This 12-Lead was acquired while the patient was pain free, are they in the clear?
• What are your next steps for this patient?

This another great case study from Vince DiGiulio, EMT-CC. As always, some details have been changed to protect patient privacy.

It's Monday night and you're working triage in a busy emergency department. The waiting room is full when a very pleasant 62 year-old man presents to the desk with a chief complaint of chest discomfort. You sit him down in a wheelchair while he gets registered and perform a quick "eyeball" examination.

The patient is a well-appearing middle-aged male in no acute distress, who actually appears younger than his stated age. He is alert, oriented, and answers all questions appropriately, with skin that is warm and dry and a strong radial pulse that's not too fast or too slow. His breathing is unlabored and he states that he has been experiencing some minor chest discomfort for around for two days.

You figure that he's not going to collapse in the lobby and leave to speak with the triage RN while he signs some paperwork. The two of you decide to bring him back to the dedicated ECG nook, where the nurse will perform a triage assessment while you obtain vitals and run a quick ECG.

• Onset: 2 days ago
• Provocation/Palliation: He cannot describe any provoking factors, but states "I usually rest and it eventually goes away"
• Quality: Midsternal chest pressure
• Radiation: None
• Severity: "Not bad at all, maybe a 3 out of 10."
• Timing: Intermittent, with spells lasting for 10 minutes or so and possibly increasing in duration more recently. The current episode has lasted at least 15 minutes.

Using an automated monitor, you obtain the following vitals:

• Pulse: 92 bpm
• BP: 147/88 on his left arm
• Resps: 20, unlabored, and clear bilaterally
• SpO2: 96% on room air
• Temperature: 37.1 C (98.8 F) orally

At the same time, the nurse elicits the following information:

• Signs/Symptoms: Intermittent midsternal chest pressure x 2 days. No diaphoresis, nausea, vomiting, SOB, or dizziness.
• PMHx: No significant medical history besides well-controlled HTN and an appendectomy in his 20's
• Meds: "some blood pressure medication"
• Allergies: NKDA
• Last In's/Out's: Dinner
• Events: "This discomfort started a couple of days ago. It comes and goes, but my wife wanted me to get checked out and I finally gave in after dinner when it started to return."

You run the following 12-Lead:

There is no old ECG in your electronic medical record for comparison, and when you walk back to the main department, you cannot find a physician to look at the tracing. One is performing an I&D of a peritonsilar abscess, while the other is probably with a patient somewhere but MIA.

Every room is filled, most of the hallway beds are occupied, and there is certainly a line forming at the front desk while you're wandering around in back.

• Are you concerned about this ECG?
• Do you need to pull a physician away from someone else to look at it?
• Does he need to jump to the front of the queue and get a room right away?
• If you were in the field, how would you treat and transport this patient?