The role of 12 lead ECG in Pediatric Pulmonary Hypertension

A 10 year old male presents to the Emergency Department with complaint of substernal chest pain, 6/10, unable to describe the sensation but non-radiating, which started during a basketball game, while running.

Primary assessment:

  • Patent airway
  • Adequate respiratory effort with no signs of distress
  • skin is pink, warm and dry, with no signs of hypoperfusion

Pertinent medical Hx:

  • Chronic Interstitial Lung Diseases secondary to Human T-cell Lymphotropic Virus (HTLV)
  • Secondary Pulmonary Hypertension

No allergies reported

Medications:

  • Acetaminophen PRN
  • furosemide  20mg
  • Flovent

Baseline vital signs:

  • Heart rate: 112 beats/min
  • Respiratory rate: 24 breaths/min
  • SpO2: 97% on 2 lpm O2
  • Capillary refill: < 2 seconds

The patient is evaluated and admitted due to the current complaint and prior medical complications. The following 12 lead ECG is obtained:

 

1st

  • Sinus rhythm
  • Biatrial Enlargement or Abnormality
  • Right Ventricular Hypertrophy (R > 7mm in V1-2)
  • Rightward Frontal Axis (QRS axis approximately 121 degrees)
  • Right Precordial ST segment depression

As many prehospital and in-hospital providers are initially taught, ST segment depression and T wave inversion indicates myocardial ischemia. However, there are other conditions which can present with ST segment depression and T wave inversion, and not be ischemia related. These are commonly due to ventricular repolarization abnormalities, electrolyte imbalances such as Hypokalemia (low serum Potassium) and Hypomagnesemia (low serum Magnesium) and in the pediatric setting, Juvenile T waves or Juvenile T wave Inversion.

Reponarization abnormalities, such as the ones seen in ventricular hypertrophy, ventricular beats, Bundle Branch Blocks or ventricular paced rhythms, are knows as Secondary ST-T changes, which again, are not due to ishemia but the altered repolarization conduction. At times, it might be hard to differentiate between the two, however, in this case, the patient is admitted and diagnosed with Cor Pulmonale, treated Pulmonary HTN and mild Hypokalemia of 3.0 mEq/L following blood work. Cath performed show no structural coronary artery deffects or occlusion.

28 days later, the same patient presents to the Emergency Department complaining of chest pressure and is again admitted. The following 12 lead ECG is obtained:

first

  • Sinus rhythm
  • Biatrial enlargement or abnormality
  • Rightward Frontal Axis at 112 degrees
  • Biventricular Hypertrophy voltage criteria
  • Secondary ST-T changes

  An Echocardiogram study is performed wish showed mild dilated Right Atrium (RA) and dilated Right Ventricle (RV) with decreased RV systolic function and tricuspid valve regurgitation. Normal Left Ventricular function and size noted.

 The patient is admitted and treatment remained with Viagra (sildenafil) 20mg, Ambrisentan 10mg, Lasix 20mg and shceduled Bipap. Hemodynamic monitoring was established with Central Venous Pressures (CVP) and Pulmonary Artery Pressures (PAP) assessed and controlled.

16 days later, the following 12 lead ECG is obtained, with no complaint or symptoms:

Untitled

  •  Sinus rhythm
  • Biventricular Hypertrophy voltage criteria
  • Rightward Frontal Axis at 98 degrees
  • Secondary ST-T changes

This time, Echo showed thickened RV free wall with improved systolic function and tricuspid valve insufficiency. There is a dilated main pulmonary artery with normal branches. The LV remained within normal limits.

 

Take home value:

In the emergency medicine setting, a large portion of pediatric population will present with pulmonary and  cardiac related complications, which mostly arise from congenital etiology. The pulmonary and cardiac systems (Cardiopulmonary) are unavoidably related for normal physiologic function. Although RV forces are typically predominant in the early stages of life and often normalizes as the LV increases in workload and size, pathologic RV changes are one of the most common abnormal findings during pediatric ECG evaluation, which often, not only reflect cardiac abnormalities, but pulmonary system deffects.

For further, click on the link below:

Pulmonary artery pressures and ECG patterns

What it looks like: inferior STEMI

No mysteries here today – this is an inferior STEMI! But I thought that prehospital provider might like to see what happens “on the inside” during an MI.

The Case:

A 60-something female had a few days of feeling not quite right, so she did some Googling, and she began to worry about a heart attack. Therefore, when she acutely developed neck and jaw pain, she figured that her self-diagnosing was probably correct, and she called 911 without delay. Time from symptom onset to first medical contact (FMC) was about 30 minutes.

The ECGs

EMS captured an initial 12-lead:

ST elevation in III and aVF, reciprocal ST depression in aVL. Again, NOT a mystery.

ST elevation in III and aVF, reciprocal ST depression in aVL. Again, NOT a mystery.

The medics immediately called for cath lab activation. Because of the off-hours presentation, the patient was evaluated in the ED while the team assembled. A second ECG was obtained:

Muy_obvio_ED

No changes – still bad.

Since the patient was comfortable, and her condition was stable, we did an echocardiogram for education’s sake.

The Echos:

When a portion of the heart is ischemic, it doesn’t move very well. It’s like an area of the heart is paralyzed, and the echocardiogram can be as good as the ECG in showing ACS, and sometimes it’s better!

Let’s take a look at two views of the heart moving. First,imagine you chopped the heart in two, like a loaf of bread. Since the left ventricle is shaped like a hollow tube, you would be looking at a ring of myocardium. This is the short-axis view:

screenshot898

From my friends at Yale http://www.yale.edu/imaging/echo_atlas/views/short_axis_lv.html

The right coronary supplies the muscles from about “6 o’clock” to “9 o’clock,” also supplying blood to the posterior papillary muscle marked in the picture. Our patient’s short-axis view showed:

Watch this for a while, and you might note that the area from 6 to 9 o’clock isn’t moving that great. Let me highlight that part of the image:

Red arrows = not contracting well

Red arrows = not contracting well

Let’s take another look at the heart. This time, instead of slicing the heart like a loaf of bread, we’re slicing it like a bagel! This is called the apical 4-chamber view, since the apex of the heart is at the top, and we see all 4 chambers of the heart:

Again, from Yale http://www.yale.edu/imaging/echo_atlas/views/four_chamber.html

Again, from Yale
http://www.yale.edu/imaging/echo_atlas/views/four_chamber.html

The RCA supplies the wall in between the LV and the RV, while other arteries supply the apex. Our patient:

If you look at the septum, you see it isn’t contracting when the other side of the LV is. Let me highlight that area with red arrows:

screenshot891

Red arrows = actually moving the WRONG way during systole.

 Follow-up:

Our patient had such a brief interval from FMC to balloon inflation that her troponin never turned positive. Nonetheless, we have both ECG and echo evidence of a large potential infarct that was treated before it could do serious damage.

Conclusion to Snapshot Case: 85yo M – Chest Pain

This is the conclusion to the Snapshot Case from a couple of days ago. If you haven’t already done so, I suggest reviewing the very brief initial case description.

Here again is the EKG from Tuesday’s case.

01 - 85yo M

This tracing is nearly pathognomonic for true occlusion of the left main coronary artery (LMCA), resulting in a “left main STEMI.”

Since this a Snapshot case with no follow-up this diagnosis cannot be confirmed, but it is a rather unique pattern I have yet to see mimicked by any other form of ACS. I’m not surprised that few, if any, readers were familiar with this presentation. It is not commonly taught, and in fact I only came across it from seeing a few cases and reading case reports. Let’s review the pattern of ST-deviation that we are seeing…

First, consider the limb leads.

There is massive ST-elevation in leads I and aVL with massive reciprocal ST-depression in leads II, III, and aVF. This pattern is consistent with STEMI of either the left main (LMCA), left anterior descending (LAD), or circumflex (LCx) coronary artery. Though there is really no way to differentiate them using the limb leads alone, the magnitude of the ST-elevation—enough to produce a true “tombstone” pattern in I and aVL—certainly suggests a large area of ischemic myocardium consistent with the LAD or LMCA.

For those following my 360 Degree Heart series, here’s what the leads look like displayed in that fashion (though it adds nothing to the diagnosis here).

360 Degree Layout

Though informed by the limb leads, the probable diagnosis here resides in the precordial leads. The ST-elevation is maximal in V2 and extends out to V4–V6 with reciprocal ST-depression in V1.

This pattern could be somewhat consistent with an isolated lesion in the LAD but there is a problem: a typical LAD occlusion should not have ST-depression in V3, especially if there is ST-elevation extending all the way out to V6. Seeing no ST-elevation in V3—maybe even a little ST-depression—when there is a large amount of ST-elevation in the rest of the classic “anterior” leads is a big issue. It’s right to consider that perhaps V2 and V3 have been swapped, but based on how the rest of the tracing plays out I can tell you that is not the case here.

The pattern could also be considered consistent with an LCx culprit, and the large amount of ST-elevation in V2 certainly suggests that (V2 is a “high-lateral” lead, believe it or not), but there is a bit too much elevation in V4-V6. Though this latter territory is often considered part of the lateral wall (a pun?), it’s actually pretty low [caudal] on the heart compared to the area the LCx and its branches typically serve and is really part of the antero-apical region supplied by the LAD.

In this case the real lynchpin for me is V3. A lot of findings are pointing towards an LAD culprit but that sudden loss of elevation in V3 sticks out like a sore thumb. I’m left to conclude that there should be anterior ST-elevation in V3 with our LAD occlusion but some other force is acting to cancel it out; that force is posterior STEMI from a LCx occlusion as well. Combine the anterior ST-elevation of an anterior STEMI with the posterior elevation of a large posterior STEMI and they can cancel one-another out, leaving a net of almost no ST-deviation.

So what we have here is a mixed STEMI picture with features consistent with both LAD and LCx occlusion, and that’s exactly what is causing it. The LMCA supplies both the LAD and the LCx, so a true occlusion of the left main essentially creates a STEMI of both those territories. [You could also have a dual-culprit STEMI with culprits in both the LAD and LCx but that is rather rare, even when compared to LMCA STEMI.]

Also consistent with LMCA STEMI is the presence of right bundle branch block (RBBB) and left anterior fascicular block (LAFB) in a pattern of bifascicular block. Given the marked STEMI this is probably an acute finding and fits the picture of ischemia involving a massive area of the myocardium (and is also associated with a markedly increased mortality).

“But LMCA occlusion presents with diffuse ST-depression and ST-elevation in aVR and V1!”

Despite the extremely prevalent teaching, that finding is actually what you see with diffuse NSTEMI, sometimes involving the LMCA, and usually with a less-than-total culprit lesion; whereas what we see here is LMCA STEMI with a complete or near-complete occlusion of the LMCA. For more on the diffuse subendocardial ischemia seen in LMCA NSTEMI see my prior post here.

“I still don’t believe you.”

That’s fine, but I highly suggest checking out these other cases with very similar patterns of ST-deviation.

Image from Panel A of the NEJM article linked here.1

Invasive Cardiology

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.2 There is significant ST-elevation in V3, likely due to a non-obstructed RCA supplying the posterior wall instead of the LCx.

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.3 Similar to the prior tracing there is massive ST-elevation in V3.

Image reproduced from this linked case at Dr. Smith's ECG Blog.

Image reproduced from the case linked at Dr. Smith’s ECG Blog.4

Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.5

 References:

  1. Dwyer N, Kanani R. Images in clinical medicine. Left main coronary artery thrombosis. N Engl J Med [Internet]. 2012 Apr 5 [cited 2014 Dec 12]; 366:e21. Available from: http://www.nejm.org/doi/full/10.1056/NEJMicm1105065
  2. Joumaa MA, Davis T, Rosman H. Acute left main coronary artery occlusion: a catastrophic problem with poor prognosis. J Invasive Cardiol [Internet]. 2006 Jun [cited 2014 Dec 12]; 18(6):E179-80. Available from http://www.invasivecardiology.com/articles/acute-left-main-coronary-artery-occlusion-catastrophic-problem-poor-prognosis
  3. Goktekin O, Unalir A, Gorenek B, Kudaiberdieva G, Cavusoglu Y, Melek M, Aslan R, Timuralp B. Traumatic Total Occlusion of Left Main Coronary Artery Caused by Blunt Chest Trauma. J Invasive Cardiol [Internet]. 2002 Aug [cited 2014 Dec 12]; 14(8):463-5. Available from http://www.invasivecardiology.com/articles/traumatic-total-occlusion-left-main-coronary-artery-caused-blunt-chest-trauma
  4. Smith, SW. Dr. Smith’s ECG Blog [Internet]. Minneapolis; 2008-2014. The difference between Left Main occlusion and Left Main insufficiency. 2014 Aug 2 [cited 2014 Dec 12]. Available from http://hqmeded-ecg.blogspot.com/2014/08/the-difference-between-left-main.html
  5. Fiol M, Carrillo A, Rodríguez A, Pascual M, Bethencourt A, Bayés de Luna A. Electrocardiographic changes of ST-elevation myocardial infarction in patients with complete occlusion of the left main trunk without collateral circulation: differential diagnosis and clinical considerations. J Electrocardiol. 2012 Sep; 45(5):487-90.

Register for #EMSToday2015 win an iPad mini!

Here’s a blog post so promotional that it may crash Facebook’s throttling algorithm!

zuck_not_worried

In case you weren’t aware, the EMS Today conference is back in Baltimore and is scheduled to take place  February 25-28, 2015. In my last blog post I wrote about some of the reasons I love Baltimore and why I believe it’s the “spiritual home” of EMS Today (even though I really enjoyed Washington, D.C.).

Have you been thinking about attending?

Good news! If you register through one of the JEMS/PennWell EMS blogs, you not only receive a $100.00 discount from the regular price ($15.00 in addition to the $85.00 early bird registration discount) but you will also be entered into a drawing to win an iPad mini!

If that sounds lame, think again, because the drawing will be limited to the just the folks who register through an EMS blog and there will be two drawings; one at the end of December and one at the end of January. As of today there are only three blogs participating (including EMS 12-Lead) so I’m guessing the odds will actually be pretty good for this type of drawing.

To enter, visit the (>>> registration page <<<) and enter the promo code EMS12LEAD during checkout.

It’s that easy! You will be automatically entered into the drawing. If one of our followers wins the iPad mini we will announce it here (and through our social media channels).

ipad_mini_ecg_challenge

As a side-note, the 12-Lead ECG Challenge App looks amazing on iPad and iPad mini! The cost is only $5.99 and it makes a great Christmas gift! (Apple iOS, Android, Amazon, Web-Based). Educators can also use the app in the classroom setting or for continuing education! Contact Limmer Creative for details.

Remember to follow the #EMSToday2015 hashtag on Twitter! We’re hoping to arrange a meet-up!

Snapshot Case: 85yo M – Chest Pain

Snapshot cases are EKG’s where we do not have good patient follow-up—or sometimes even clinical information—but still feel there are worthwhile learning points to convey.

This is an old case we’ve actually featured on the blog before, but today we’re going to do so with a different focus.

This ECG is from an 85-year-old male, presumably experiencing chest pain.

01 - 85yo M

Don’t worry about the rhythm. I’m going to keep the presentation simple this time because the tracing is actually pretty particular to a specific pathology.

This patient is experiencing a STEMI. Where is the culprit lesion?

 

Mark your calendars: EMS Today is back in Baltimore!

EMS_Today_2015

Those of you who miss the Pratt Street Ale House, Slider’s Bar and Grill, Pickles Pub, “Natty Boh”, Maryland crabcakes, the Inner Harbor, and Fell’s Point will be glad to know that EMS Today is back in Baltimore Feb 25-28, 2015!

I like the Smithsonian as much as the next guy (all right, probably more than the next guy) but Baltimore feels like the spiritual home of EMS Today! That’s probably because of all the great times we’ve had there in years past. Remember “EMS 2.0″ and solving the world’s problems over a couple of beers at Uno’s Pizza? Were we naive back then? Prescient? A little of both?

The world has changed, EMS has changed, and many of the faces and names have changed, but I’m okay with that! In rugby the real action is in the “second phase of play.” Let’s not just go back to Baltimore to recapture the magic of those days, let’s go back to Baltimore and create some new magic.

Things to do (highlights):

  • Keynote address will be delivered by none other than Gordon Graham
  • Ride along with Baltimore City Fire Department (space limited)
  • Check out the Physio-Control podcast studio and say hi to Jamie Davis
  • Watch the JEMS Games (congrats to Cumberland County EMS for their win last year)
  • Check out the latest innovations in the Exhibit Hall
  • Observe an autopsy at the Maryland Office of the Medical Examiner
  • Attend the Advanced Community Paramedicine Workshop
  • Participate in the Advanced Airway Cadaver Lab
  • Attend NEMSMA’s EMS Officer Leadership Workshop
  • Take advantage of the rare opportunity to attend the Resuscitation Academy on the east coast!
  • Watch Team EMS 12-Lead win the STEMI showdown! (just kidding – would rather one of YOU win the STEMI showdown!)

We will highlight some of our favorite breakout sessions in the next couple of weeks.

You can review all of the pre-conference workshops (>>> here <<<).

In the meantime here’s some exciting news to help you “pull the trigger” on EMS Today!

For a limited time (until January 19) you can take advantage of early bird registration. That confers a significant discount.

In addition you can use:

Promo code: EMS12LEAD

For an additional $100.00 discount on your registration!

Basically that means that if you were to (>>> register right now <<<) as a full delegate with a gold passport you would pay $340.00 instead of the regular price of $525.00 (plus whatever precons, workshops, or special events have additional cost).

earlybird

EMS_Today_Promo_Code

That’s a substantial discount!

We are not the only ones offering a promo code but to be honest it’s nice to see JEMS and PennWell getting the EMS bloggers a little more involved in event planning and social media strategy! You can show your support for Team EMS 12-Lead by using the EMS12LEAD promo code when you register.

You should also follow the #EMSToday hashtag on Twitter before, during, and after the conference! We’re hoping to arrange a meet-up!

See also:

Conference schedule

Speaker list

Events schedule

Special events