From Precons to EMS 10 Awards and Nightwatch! #EMSToday2015

Wednesday, February 25, 2015

What an awesome day at EMS Today 2015! Kelly and I headed over to the Convention Center to get registered and ran into our very good friends Nick Nudell (@RunMedic), Chris Montera (@geekymedic), and Anne Robinson Montera (@CaringAnne).

Nick and I started the EKG Club many years ago as an email-based discussion group. It is now a thriving Facebook group that you should check out! We’ve also done some interesting consulting work together in the implantable medical device industry.

Chris and Anne are one of the “power couples” of EMS and are very influential in Community Paramedicine (more on that later).

Advanced Airway Cadaver Lab

After getting registered we headed over to the Advanced Airway Cadaver Lab which is put on by the Paragon Medical Education Group (@ParagonMedEd). It was really great because Kelly and I had met Jim Logan at a previous EMS 10 Awards event and got along great. I had also recently met Joe Holley, M.D. (@joeholley) on Twitter so they were expecting us. What an awesome experience!

As a side note, social media has become an indispensable tool at medical conferences!

Cadaver_Lab

Everyone in the cadaver lab was dressed in full PPE including mask, gown, gloves, and hair covers. So it was a surprise when I heard a British accent say, “Are you that blogger Tom?” I said, “Yes, I am!” Well guess what? It was Team London (#TeamLondon)! We started chatting and I couldn’t help but tell them how much respect I have for the London Ambulance Service. When I brought up the Code STEMI Web Series they said, “You know Mark Whitbread is here. He’s over at the Resuscitation Academy right now!”

It’s been 3 years so we had to head over and see it for ourselves!

Resuscitation Academy

The moment we walked into the Resuscitation Academy we were greeted by our good friend Mike Helbock (@medicme). Mike is one of the smartest guys I know and he is always very generous with his time and knowledge. Kelly and I had dinner with him when we were in Seattle and he told us all about the history of King County Medic One, how it got started, and how they operate. It was fascinating.

I said, “Hey Mike do you mind if I take some pictures?” and he said, “You can do anything you want!” which cracked me up.

As it turned out it was getting toward the end of the morning session and they were about to do a full code scenario. Guess who was right in the middle of the action? The one and only Mark Whitbread from the London Ambulance Service!

Resuscitation_Academy_Whitbread

If you haven’t seen the London episode of the Code STEMI Web Series you need to watch it. It’s an incredible system! It was great to see Mark but we had one more stop to make!

Advanced Community Paramedicine Workshop 

We arrived at the Advanced Community Paramedicine Workshop just in time to see a presentation about 2-1-1 San Diego and how it connects people who are struggling with appropriate resources. Immediately afterward our good friend Chris Montera (@geekymedic) talked about a case study from Eagle County Paramedic Services in Colorado.

Chris_Montera

After Chris’s presentation Kelly and I had a nice conversation with Matt Zavadsky (@MattZavadsky) from MedStar Mobile Healthcare. He’s a very well known guy in Community Paramedicine so it was nice to hear his perspective about 2-1-1 San Diego. Anyone who wants a nice introduction to Community Paramedicine can attend Introduction to Community Paramedicine today from 10:30 a.m. – 12:00 p.m.

Pratt Street Ale House

After a quick lunch at the Diamond Tavern (and another run-in with Team London) Kelly and I headed over to the Pratt Street Ale House where we met up with Thaddeus Setla (@setla), Scott Kier (@MedicSBK), Jeff Sorenson (@chicagomedic), Michael Herbert (@BigGermanMike), and several others (I hope they will forgive me for leaving them out). Things were just starting to get interesting when it was time for Kelly and I to head back to the room and get ready for the EMS 10 Awards.

Ted_Hayden_Pratt

Of course we just missed Hayden Drake (@paramedickiwi) from Team AUT!

By the way, the #EMSToday2015 hashtag on Twitter is really blowing up with some great stuff!

EMS 10 Awards

It’s always a real pleasure and distinct honor to share an evening with some of the greatest innovators in EMS and the EMS 10 Awards is a place where that is always guaranteed to happen! But, there’s one group that really stole the show and that was the crew from Nightwatch!

Nightwatch_Kelly

Left-to-right: Titus Tero (@NightwatchTitus), Dan Flynn (@Nightwatch_Dan), Kelly Arashin (@BarefootNurse24), Keeley Williams (@nightwatchmedic), Holly Monteleone (@NightwatchHolly), and Nick Manning (@Nightwatch_Nick)

It was impossible to not be impressed. They are a very genuine, and very gracious, group of top-notch EMS professionals! They really do the EMS profession and the City of New Orleans proud. Ken Bouvier is doing something right. That is obvious! Don’t miss your opportunity to meet the crew from Nightwatch. They will hanging out with the good folks from Physio-Control (@PhysioControl) at Booth 804.

There’s much more to say about the EMS 10 Awards and the very deserving awardees but I must get ready for my first-ever JEMS Editorial Board meeting which is sure to be interesting!

Stay tuned. This conference is just getting started! Follow me on Twitter at @tbouthillet.

A visit to Johns Hopkins #EMSToday2015

Tuesday, February 24, 2015

We arrived a day early into Baltimore and decided it would be a good idea to visit what is arguably the nation’s best hospital. Johns Hopkins Hospital’s core values include Excellence & Discovery, Leadership & Integrity, Diversity & Inclusion, and Respect & Collegiality and you sense when you’re walking around that it’s more than just lip service.

johnshopkins

I’ve written many times about Peter Pronovost and The Science of Safety (everyone in medicine should be required to watch the video). It’s not an accident that one of the world’s foremost experts in patient safety calls Johns Hopkins home!

The history in this place is incredible. It was originally built in 1889. The Rotunda, which is now part of the Administrative Building, houses a towering statue of Jesus known as Christus Consolator. It is a powerful presence. Passers-by including patients, family members, medical students, residents, and surgeons reverently touch the statue. You can’t help but wonder about them. What challenges do they face? What complex cases are they participating in?

Christus_Consolator

Here in a hospital famed for modern medicine, a 10-and-a-half-foot marble statue of Jesus rises beneath its historic dome. Elsewhere, such a prominently featured religious symbol might be cause for controversy. But at Hopkins Hospital, “Christus Consolator” has managed to defy its traditional symbolism and garner respect from nearly all who pass.

Long a source of solace and hope for patients and families, the Christ statue also has meaning for hundreds of employees. For many it signifies healing, hope and compassion; for others, it means faith and tradition and even freedom. To a few, it is simply a work of art, or even a throw-back to a less tolerant time. Muslims, Jews, Christians, atheists-all interpret the statue in ways that feel right for them. [Source]

Rotunda_JohnsHopkins

Towering above the statue is the Rotunda. Legend has it that the term “grand rounds” or “making the rounds” originated here as physicians had to climb a winding staircase that exited at each floor into the circular hallway under the dome.

On the way back from Hopkins we ran into our good friend Mike McEvoy @McEvoyMike at the Marriott Inner Harbor.

mcevoy_arashin_bouthillet

You might remember Mike from one of our most popular EMS 12-Lead podcasts Episode #11: Are we harming patients with oxygen? We finished up the night with food and adult beverages in the lobby.

This morning we’re off to visit the Advanced Airway Cadaver Lab, the Resuscitation Academy, and the Advanced Community Paramedicine Workshop!

Are you following the #EMSToday2015 hashtag on Twitter? You should be! That’s where I found out from @hp_ems that the EMS 10 Award winners for 2014 were posted online!

hp_ems

Head on over and check it out! The EMS 10 Awards are tonight and this is usually the highlight of the trip.

Stay tuned for more updates from EMS Today 2015!

The Calm Before the Storm! #EMSToday2015

In case you haven’t heard the good folks at PennWell and JEMS have selected yours truly as the Official Blogger of EMS Today 2015.

Kelly_Tom

The #EMSToday2015 hashtag is already buzzing! My wife Kelly @barefootNurse24 and I @tbouthillet flew into Baltimore yesterday and it was fun to follow our international colleagues gearing up for the JEMS Games!

TeamAUT

Here we have Hayden Drake @paramedickiwi from #TeamAUT (New Zealand) and a “stow away” which I choose to believe is the amazing kakapo (a critically endangered flightless parrot with a remarkable story).

Team_London

Here we have Dan @Daniel_Barnwall, Dean, and Steve from the London Ambulance Service #TeamLondon!

I’m really looking forward to the JEMS Games! You can see some highlights here (along with a list of all of the teams competing this year).

JEMS_Games_Highlights

Tomorrow I’m looking forward to covering the Advanced Airway Cadaver Lab @ParagonMedEdu, the Resuscitation Academy, the Advanced Community Paramedicine Workshop, and the EMS 10 Awards!

Of course, last night Kelly and I headed over to Frank & Nic’s West End Grille for some crab dip and Natty Boh! It’s good to be back.

NattyBoh

Stay tuned!

The 12 Leads of Christmas: V3

This is the eleventh and penultimate article in our latest series, The 12 Leads of Christmas, where each day we examine an individual electrocardiographic lead.

Lead V3

Sorry about the huge delay since the last post in this series—work, life, and teaching took over for a few of weeks.

Today we’re going to discuss V3, and there’s no way I can do that without talking about isolated posterior myocardial infarction. Of all twelve, fifteen, eighteen, or even twenty leads you may examine on the ECG, V3 usually shows the most prominent ST/T-wave abnormalities during isolated posterior STEMI. Sometimes V2 is more dramatic, or less often V4, but in the grand scheme of things the ST-depression we see during acute posterior injury tends to be centered on V3.

The good news is that the word is out about posterior STEMI. Thanks to the work of folks like Bob Page, Amal Mattu, and many others, most prehospital and in-hospital emergency medicine providers are aware of the diagnosis—including the use of posterior leads V7–V9.

This article presumes that you know how to identify both acute (ST-depression in V2–V4) and old (tall R-waves in V1–V3) posterior MI. If you’re not comfortable with the diagnosis just yet, I suggest checking out these other resources instead. This is a pretty advanced discussion aimed at folks who are already strong at reading ECG’s.

Okay, so isolated posterior STEMI usually presents with ST-depression that is maximal in V3. To be honest, this is all a setup for the next post on V6, so with that V3 learning pearl out of the way, our real goal is to examine just what causes an isolated posterior STEMI on the ECG.

As a word of warning: this is a longer post than I usually like, but I promise it’ll take less time to read than the years I’ve spent working it out myself.

 

The Posterior Wall

Before even examining the ECG, however, let’s identify the posterior wall of the heart.

It seems like a simple task—the posterior wall should be the part of the heart directly opposite the anterior chest—but if we learned anything from our analysis of V2, it’s that the terminology used to describe the regions of the heart isn’t straightforward. In fact, the very existence of a “true posterior wall” has been hotly debated (point/counter-point).

Our human obsession with representing nature as simplified models never seems to go quite as smoothly as we would like.

00 - xkcd Teaching Physics

Click image for the original post on xkcd.

 

Recall that when we discuss the localization of MI’s using the standard 12-lead, the only walls of the heart we really care about are those constituting the left ventricle (LV). The right ventricle (RV) and atria are left out of this discussion because they usually exert little effect with regards to ST and T-wave changes in the structurally normal heart. Removing those bits, what we’re left with is a prolate spheroid (an American football or rugby ball) with one end lopped off.

03 - LV Motion

Image source.

As shown in the gif above, there are five main regions of the heart: the anterior (ANT), septal (SEPT), inferior (INF), and lateral (LAT) walls… and the apex (APEX).

It would be nice if the heart was oriented at right angles to the patient’s torso, but sadly for us that is not the case. Instead it is rather oblique, with the base typically pointed towards the patient’s right scapula and the apex aimed downward towards V4 or V5—though this can vary depending on individual anatomy.

02 - Heart and Lungs

Image source. Used with the permission of illustrator Patrick J. Lynch.

The problem with setting the heart at an oblique angle is that now the nice, simple naming system used on the football gif is no longer intuitive (wtf, evolution!?).

Rather than pointing straight ahead, the apex points to the left and somewhat downward. That’s simple enough.Prolate Spheroid - Apex

 

The inferior wall is the only true wall that retains roughly the same orientation. In both cases it is the most caudal, resting on the diaphragm.Prolate Spheroid - Inferior

08 - VLA and Transverse Inferior Wall

[Left] Transverse view of the chest with a red line showing the path of the vertical long axis. [Middle] Vertical long axis view of the heart. [Right] Inferior wall of heart highlighted in green. Image modified from this source.

 

 

The anterior wall of the heart is actually the most superior, and while it is tilted a fair bit ventral towards the chest, I really think that life would be a whole lot easier if we just called it the superior wall. Plus, it’s pretty much directly opposite the inferior wall, so… yeah.Prolate Spheroid - Anterior

[Left] Transverse view of the chest with a red line showing the path of the vertical long axis. [Middle] Vertical long axis view of the heart. [Right] Anterior wall of heart highlighted in green. Image modified from this source.

 

 

The septal wall is still what separates the cavity of the LV from that of the RV, but you may notice that it is also quite anterior, angled towards the patient’s right pectoral. An argument could be made that it is just as “anterior” as the true anterior wall, but I want to change the name of that region anyway so I guess we can keep this one the way it is.

Prolate Spheroid - Septal

10 - 4-Chamber Septal

4-chamber (quasi-transverse) view of the heart with the septum highlighted.

 

 

And finally, the lateral wall. You’ll notice that it’s not pointed toward directly lateral—or perpendicular to the anterior chest wall—as its name would suggest, but rather a bit posterior. That turns out to be important…

Prolate Spheroid - Lateral

4-chamber view of the heart with the lateral wall highlighted.

 

Having listed all the major territories of the heart, where is the posterior wall? Well, as mentioned earlier, that question is debated. It’s not included as one of the seventeen segments of the heart currently described by the AHA, but since it’s a term we commonly throw around—especially in electrocardiography—and it doesn’t look like that’s changing any time soon, we should probably figure out where it has gone.

07 - 17 Sections

The sections of the heart as standardized by the AHA. In this diagram the left ventricle is view in-line with its axis, centered on the apex (segment 17). [Source]

 

Just as with Jurassic Park and so many mid-century B-movies, the thoughtless (but cool!) march of science is to blame for this mess.

This is an imperfect review, but as best I can piece it together, the story goes that electrocardiography was the only game in town for localizing ischemia for most of the 20th century. As a result, the regions of the heart were described based on how infarction Q-waves were distributed on the ECG. Leads II, III, and aVF “look” downward, therefore an infarction in those leads was called an inferior MI. Likewise, the electrodes for V2–V4 are located on the anterior part of the torso, so Q-waves in those leads were said to correlate to anterior MI. Lastly, since I, aVL, V5, and V6 tend to “look” towards the lateral aspect of the torso, Q-waves in that distribution were thought of as corresponding to lateral MI.

In that world it would make sense for an infarction on the “back of the heart,” opposite the anterior wall,  to be called a posterior infarction. And so tall R-waves in the right-precordial leads—reciprocal to Q-waves in the opposite territory—were said to correspond with posterior MI.

Now, I realize that hardly anyone discusses Q-wave MI’s anymore. We’re starting there because most of the literature that developed our current terminology predates the 1980′s and 90′s, and thus was only concerned with Q-wave MI’s. ST-elevation was recognized as an ischemic phenomenon before those decades but since thrombolytics, coronary angiography, and PCI (our STEMI management options) are all relatively modern developments, chronic Q-wave MI’s were the main concern for most of the 20th century.

Then echocardiography (and nuclear imaging… and CT… and MRI… and other advanced imaging modalities) came on the scene and messed up our simple naming system. Offering a multitude of views of the heart, it became clear that more than three or four basic regions were needed to fully describe the walls of the left ventricle. And, with these new images, the frame-of-reference shifted from indirect landmarks on the chest to ones based on direct visualization of the heart.

When you’re looking at an echocardiogram you don’t think in terms of the sagittal, coronal, and transverse planes that we typically use, but instead consider the axis formed by the “tube” of the left ventricle and how the walls relate to that.

As we showed before, the heart sits at an oblique angle in the chest—not really lining up with the walls of the torso. Now that the heart can be examined in isolation—no longer constrained by torso anatomy or landmarks—using it’s own anatomy as the reference,  the anterior wall is no longer truly anterior nor the lateral wall truly lateral. But we’re here to talk about the posterior wall, so what happened there?

It was assimilated.

In the minds of most cardiologists the classic posterior wall, sometimes called the “true posterior wall,” was (and still is) thought of as being the infero-basal section of the LV (section #4 on the AHA’s “bull’s-eye” diagram above). We will call that the “classic posterior wall” in this article.

04 - Lateral Illustration Inferobasal Wall

Postero-lateral view of the heart (imagine you’re looking from lead V7) with the infero-basal (classic posterior) wall highlighted on the cross-section. Images modified with the permission of illustrator Patrick J. Lynch. [left] [right]

Vertical long axis view from a cardiac MRI. The green arrow points to the infero-basal (classic posterior) wall. While the center and right images give the impression that this segment is located directly opposite the anterior chest (and thus truly “posterior”), the image on the left demonstrates that this view of the heart is actually captured at an oblique angle. The red line follows the heart’s central axis and represents the plane forming the “long-axis” images we see to the right. Image modified from this source.

Depiction of a parasternal long-axis section of the heart, a common echocardiographic view. The infero-basal (classic posterior) wall is highlighted. Images modified with the permission of illustrator Patrick J. Lynch. [left] [right]

There are, however, a few issues with calling that the “true posterior wall.”

You know how everyone says that a tall R-wave in V1 and V2 is a sign of old posterior infarct; being reciprocal to a “posterior” Q-wave? When they say that, the usual implication is that there is an infarction of the infero-basal wall we just described. Dr. Antoni Bayés de Luna, a true master of electrocardiography (and I don’t toss that term around lightly), has headed a couple of papers deconstructing why that may not be the case. He instead argues that V1 is reciprocal to the lateral wall, not the “classic posterior wall,” and in his papers MRI correlations have shown the EKG sign of a tall R-wave in V1 to be very specific for lateral wall infarction (excluding non-infarction causes of a tall R, of course).

He believes we should be calling the basal-lateral wall the “posterior wall,” not the infero-basal wall.

22 - 4-Chamber Basal-lateral Diagram Angled

4-chamber view of the heart. Arrow points to the basal segment of the lateral wall (therefore the basal-lateral wall). Image modified with the permission of illustrator Patrick J. Lynch. [Source]

 

It makes some intuitive sense . If you have a Q-wave originating from the classic posterior wall (aka the infero-basal wall), drawing a vector away from that region through the “electrical center” of the heart would put you near V3 or V4. According to Bayés de Luna’s logic and research, infarction of this posterior wall still gives you a tall reciprocal R-wave, except that it shows up best in V3.

12 - MRI Infero-basal Q
R-wave vector from an infarction of the infero-basal wall.

19 - Bayes Infero-basal

Figure 3 from Bayés de Luna’s paper on posterior wall terminology. There is an infero-basal (“classic posterior”) infarction with a tall R-wave in V2–V3, but no tall R-wave in V1. [Source]

 

If, on the other hand, you draw a line (R-wave vector) from the basal section of the lateral wall through the “electrical center” of the heart, you would end up near V1. Likewise, in Bayés de Luna’s research, patients with an infarction of this basal-lateral wall on MRI were more likely to show a tall R-wave in V1.

R-wave vector from an infarction of the basal-lateral wall.

20 - Bayes Basal-lateral

Figure 4 from Bayés de Luna’s paper on posterior wall terminology. Note the tall R-wave in V1, corresponding to an infarction of the basal-lateral wall. [Source]

 

But his arguments all have to do with completed Q-wave MI’s; how does that correlate to the acute STEMI’s we care about?

It’s more the principle of the matter that is important for now.

You see, regardless of whether a “true posterior wall” exists, there is still an electrocardiographic entity of acute posterior STEMI. I almost think of it as a “syndrome,” with a certain constellation of signs (right-precordial ST-depression chief among them) that, when seen together, produce the posterior STEMI syndrome. Even if there is no consensus regarding the exact anatomy on echocardiography or MRI, there are still patients who present with ST-depression confined to the right precordial leads and ST-elevation on posterior leads V7–V9. They have an acute coronary lesion.

That much is a certainty.

Isolated posterior STEMI due to an acute thrombotic lesion in the LCx.

Isolated posterior STEMI due to an acute thrombotic lesion in the LCx.

It really doesn’t matter if the ischemic territory is the “classic” infero-basal wall or Bayés de Luna’s basal-lateral wall—in a purely electrocardiographic sense the patient is experiencing an isolated posterior STEMI. The ECG doesn’t care if they have a posterior wall or not; there is an “injury vector” (ST-elevation) directed towards the patient’s back and we choose to call that a posterior MI.

But we’ll describe why Bayés de Luna is probably right…

 

The Distributions

I quote Bill Cosby yet again: “I told you that story to tell you this one,” (and, a month later, it’s still a questionable reference).

There seem to be three major causes of the “posterior infarction syndrome.” Don’t call it that though—no one will know what you’re talking about:

  1. Obstruction of a dominant right coronary artery (RCA) or a dominant left-circumflex artery (LCx). The two look pretty similar from the left ventricle’s point-of-view and are often indistinguishable on the standard 12-lead, so we’ll list them as one cause.
  2. Obstruction of a non-dominant LCx.
  3. Obstruction of a branch off the LCx–regardless of dominance.

In my experience, posterior STEMI from a dominant RCA or dominant LCx culprit (situation #1) is almost always accompanied by signs of inferior STEMI.

13 - 1309 - 01

Typical infero-posterior STEMI due to a proximal occlusion of the right coronary artery.

Infero-posterior STEMI due to acute obstruction of a dominant left circumflex artery.

Infero-posterior STEMI due to acute obstruction of a dominant left circumflex artery. Can you tell the difference from the preceding ECG? Yeah, me neither.

 

Sometimes it’s subtle—just a bit of straightening of the ST-segments with a slightly early take-off of the J-points in III and aVF, as seen below—but it’s unusual to see an RCA occlusion produce a truly “isolated” posterior STEMI.

Subtle infero-posterior STEMI due to acute obstruction of the RCA.

Subtle infero-posterior STEMI due to acute obstruction of the RCA. Note the straightening of the ST-segment in leads III and aVF with an early take-off and prominent ST-depression in aVL.

Same patient as the last ECG, but this time both the inferior and posterior injury are more evident.

Serial ECG from the same patient but this time the inferior injury is more evident.

 

The reason why you almost always see inferior STEMI when the dominant artery is obstructed has to do with what defines the anatomy: the “dominant” artery is the one that gives rise to the posterior descending artery (PDA); also called the posterior interventricular artery.

Image reproduced from Gray's

Image reproduced from Gray’s Anatomy: The Anatomical Basis of Clinical Practice. [1]

27 - Gray's Coronaries Dominance_edit

Image reproduced and modified from Gray’s Anatomy: The Anatomical Basis of Clinical Practice. [1]

 

Though individual anatomy varies, the PDA’s job is to supply blood to the inferior portion of the septum—especially the basal-septal territory.

Image from this article.

Image reproduced from this article (PDF).

 

And here is the key: despite its name, the posterior descending artery does not supply either vision of the posterior wall that we discussed before. Its main concern is the septum, and while it does its job well, it doesn’t over-extend itself to reach the infero-basal or basal-lateral walls. An isolated occlusion of the PDA will produce a picture that looks either like a pure inferior STEMI (or rarely an infero-anterior STEMI)—not a infero-posterior or isolated posterior STEMI.

Infero-anterior STEMI due to isolated occlusion of a "wraparound" posterior descending artery (PDA). Image source.

Infero-anterior STEMI due to isolated occlusion of a “wraparound” posterior descending artery (PDA). Image source.

So, the posterior wall is not supplied by the posterior descending artery.

In a right-dominant circulation, at least part of the nebulous “posterior” territory can be supplied by a extension off the end of the RCA called the right postero-lateral artery (PLA); also known as the retro-ventricular artery. Sometimes it’s just a nub extending past the PDA or even absent, but sometimes it can be quite large. It typically supplies a portion of the inferior wall and on occasion can even extend through the LCx’s usual territory on the lateral wall.

Posterior view of the heart. The "posterior" territory of the heart is highlighted in yellow.

Posterior view of a heart with right-dominant circulation. The “posterior” territory of the heart is highlighted in yellow. Image modified from Lippincott Williams & Wilkins “Atlas of Anatomy.” [2]

To produce a posterior STEMI via the RCA with a right-dominant circulation (shown above), you can either block the postero-lateral artery by itself (a rare event) or any portion the RCA that feeds it (the usual case). As we just described, however, if you block the RCA that feeds the postero-lateral artery, you’re also going to cut off blood-flow to the posterior descending artery—forcing an inferior infarction!

Also, since a well-developed postero-lateral tends to supply a good portion the inferior wall—not just the infero-basal segment—even an isolated PLA occlusion could still result in a mixed infero-posterior STEMI.

As you see, it’s rather hard to create an isolated posterior infarction via the RCA, so that kind of rules-out the right side of the circulation as the culprit for most isolated posterior STEMI’s. What about when there’s a left-dominant circulation?

Posterior view of a heart with left-dominant circulation. The “posterior” territory of the heart is highlighted in yellow. Image modified from Lippincott Williams & Wilkins “Atlas of Anatomy.” [2]

If you block the LCx with a left-dominant circulation you can cause ischemia to the posterior territory, but just as with the RCA during right-dominance, you’re also going to affect the posterior descending artery downstream and the branches before it that supply the inferior wall; again causing an infero-posterior STEMI.

So, yet again, that really limits our ability to create an isolated posterior STEMI.

CONCLUSION: The real culprit

Getting to the heart of the matter, there are two main acute lesions we see that cause an isolated posterior STEMI pattern on the ECG:

  1. Acute obstruction of a non-dominant LCx.
  2. Acute obstruction of an obtuse marginal (OM) off the LCx, or similar artery.

The purple arrow points to an acute lesion in the LCx while the yellow territory is the ischemia downstream.

The purple arrow points to an acute lesion in the LCx while the yellow territory is the ischemia downstream. You can see how it affect mainly the mid and basal portions of the lateral wall, perhaps also reaching a bit of the infero-basal wall. Image modified from Lippincott Williams & Wilkins “Atlas of Anatomy.” [2]

 

The purple arrow points to an acute lesion in an obtuse marginal artery while the yellow territory is the ischemia downstream. Image modified from Lippincott Williams & Wilkins “Atlas of Anatomy.” [2]

As shown above, these regions tend to correspond to the basal-lateral wall of the left ventricle. There’s a lot of overlap between both the artificially segmented “walls” and the various arterial supplies, however. The LCx and its branches can also supply blood to other territories—the “classic” infero-basal segment, the mid-anterior wall, even the apex (among others)—but we’re talking in generalities here, and in general the yellow region above is the one we care about for isolated posterior STEMI.

And this is why we’ve come so far.

All of the prior nonsense was just to pave the way for the following statement: Isolated acute posterior STEMI is almost always caused by a culprit lesion in either the non-dominant circumflex itself or an obtuse marginal artery off either a dominant or non-dominant circumflex.

In our next post we’re going to get into some more practical aspects of diagnosis isolated posterior STEMI, but to show why the above statement is (mostly) true, we had to examine:

  • How the regions of the heart got their names, and why they are inaccurate.
  • Why the proper “posterior” wall may actually be the basal-lateral wall.
  • Why the right coronary artery and its branches cannot usually create a region of ischemia isolated to the “posterior” territory, whether infero-basal (classic posterior) or basal-lateral.
  • Why, even if the infero-basal territory is ischemic (regardless of culprit), the inferior wall is also usually affected, producing an infero-posterior STEMI.

I hope that walk-through was enlightening, and hopefully it will pay dividends when we start to examine some real-world ECG patterns of isolated posterior STEMI later this week.

The Evidence

Though I pieced together the above post from seeing a lot of cases and studying a lot of coronary anatomy, it’s not all made up. In addition to numerous case studies, there are a few papers that have examined the infarct-related artery in isolated posterior STEMI and all have shown that, in the preponderance of cases, the culprit is either the LCx or one of its obtuse-marginal branches.

 

I hope you’re enjoying our 12 Leads of Christmas series. You can check out the rest of the posts below (updated as new posts come out):

12 Leads of Christmas: Lead I
12 Leads of Christmas: Lead II
12 Leads of Christmas: Lead III
12 Leads of Christmas: aVL
12 Leads of Christmas: aVF
12 Leads of Christmas: aVR
12 Leads of Christmas: V1
12 Leads of Christmas: V2
12 Leads of Christmas: V4
12 Leads of Christmas: V5
12 Leads of Christmas: V6

 

*** EMS Today 2015 is coming Feb 25-28, 2015 ***

Mark your calendars: EMS Today is back in Baltimore! 

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Adenosine for sinus tachycardia: Try to avoid this!

This is the feedback I gave the student on this case. (Recall that this was a young adult male who presented with dyspnea, chest pain, as well as pre-syncope, whose initial ECG showed a brisk tachycardia which went up to the 170s at points):

At 150, about to speed up.

Bottom line:

“As you point out, this was sinus tachycardia. When you have sinus tachycardia, you have to look for causes and treat those. I encourage you to read David Baumrind’s excellent essay on this topic for a different explanation. Here’s mine.

Sinus Tachycardia

“Sinus tachycardia can be caused by hypovolemia, cardiogenic shock, hypoxia, thyroid storm, cocaine intoxication, alcohol withdrawal, or massive pulmonary embolism. Sinus tachycardia is not an arrhythmia, it’s a symptom. The patient is telling you – through their vital signs – that their body is being stressed by something. You have to figure out what this stress is, and treat that.

You (the student) did all the right things to address the sinus tachycardia; getting a history and physical to suggest causes, performing a few tests to catch things the exam didn’t reveal, and trying a few interventions (like oxygen and fluids) that can act as therapy as well as being diagnostic.

 

The patient had a massive PE, as well as moderate thyrotoxicosis. There was little in the exam or ECG to suggest these, so transport to the ED with supportive care was about the best you could have shot for.

The big thing to know about thyrotoxicosis and about PE  is that adenosine doesn’t help either of those.

Adenosine

“What is adenosine used for? For briefly blocking off the AV node from conduction when the patient has a reentrant rhythm. The most common examples of reentrant rhythms are AVRT and AVNRT, but we usually just lump them together as PSVT. Many people just shorten this to SVT, although this is sloppy medical language.

What is SVT?

“But,” you might say, “this was SVT, because it was over 150 bpm!” This is not true at all, and not what ACLS says.

  • First off, many cases of PSVT/AVNRT/AVRT have a heart rate under 150. There are two examples at my blog – go check it out!
  • Second, many patients with sinus tachycardia have a HR over 150, as you well know. If they have severe symptoms, chest pain, feelings of doom, shortness of breath, whatever – you have to figure out the cause, and treat it (E.g. with fluids, oxygen, intubation, benzos – whatever is appropriate for the clinical context).

Heck, when I run up from the cafeteria, my heart rate gets up over 150, just from the unexpected physical effort. The treatment isn’t adenosine; I just have manyto rest for a moment! Go back and look at the ACLS chapter. It suggests that a narrow complex tachycardia is unlikely to be the primary cause of hemodynamic problems if the HR is under 150. That means, if the patient is crashing, a tachycardia of 140 (whether it’s AF, PSVT, MAT, whatever) probably isn’t the reason they’re crashing. I.e.; the hemorrhage/hypoxia/sepsis is the problem, not the rhythm itself. For some odd reason though, this has been profoundly misinterpreted by some in the EMS community. I assure you, no physician I know believes “HR > 150 means SVT.”

Don’t block the AV node in sinus tach.

“So, this patient had a clear-cut sinus tachycardia. Adenosine was not indicated – in fact it is contraindicated. Your paramedic preceptor should have been encouraging you to look for the cause of the sinus tachycardia. And it isn’t just adenosine – you don’t want to use any AV blockers in this situation.

  • Metoprolol is only indicated for the treatment of sinus tachycardia in a few unique circumstances (e.g. thyroid storm).
  • Calcium-channel blockers are almost never indicated in sinus tach, and the potential to harm is significant. For example, if you give diltiazem to a patient in cardiogenic shock (and sinus tachycardia), you might as well have shot them in the head. (Yes, I have seen this happen. Not good.)

Thanks anonymous student for your help with this post!

Thank you for being very open about your thinking in this case. I know that you are (were?) very proud about this case, and no one likes to hear that they were off in their judgment. However, when I’ve made mistakes in the past, I’ve endeavored to keep other folks from doing the same thing. You keep doing the same!”

An expert is a person who has made all the mistakes that can be made in a very narrow field.” Bohr

The first iPad mini goes to . . . #EMSToday2015

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Well, apparently at least one of you registered for EMS Today 2015 using promo code EMS12LEAD during checkout.

How do I know this? Because I was recently notified by our friends at PennWell that the first drawing for an iPad Mini is complete!

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