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

EMSToday2015-1
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!

The winner is . . . Steven Caho!

ipad_mini_ecg_challenge-1

Congratulations, Steven! If you’re reading this please contact me at ems12lead@gmail.com.

It’s not over, folks! There is still time to register for EMS Today 2015 and there will be one more drawing for an iPad mini! But hurry! Early bird registration ends Monday, January 19th!

Click HERE to listen while A.J. Heightman explain all the reasons you should attend EMS Today 2015!

AJVideoCapture

 

Hope to see you there!

See the previous blog posts:

Mark your calendars: EMS Today is back in Baltimore!

Register for #EMSToday2015 win and iPad mini! 

Adenosine given for a narrow-complex tachycardia over 150

This case comes to me from a paramedic trainee. Many elements have been altered to preserve anonymity. In the following, the narrative from the run-form is interspersed with questions that I put to the student afterwards.

I was trying to draw out how a student understood the evaluation and management of tachyarrhythmias. But I don’t think this case should be viewed as a reflection on any one student, preceptor, instructor, or even school.

Rather, I want to use this case to highlight some common beliefs about SVT, and the potential pitfalls. We’re looking for a constructive dialogue in the comments here, so keep it positive!

The Case

Run-Form:

“A 34 year-old male presented to EMS sitting upright in a chair. He was conscious, alert, oriented, states ‘I feel like a garbage truck is on my chest.’ Respirations rapid, pulse rapid and strong. Lungs clear bilaterally with slight shallow breathing. A rhythm strip shows sinus tach at a rate of 150.”

EKG_1

Sinus tachycardia, aprox 150 bpm.

Question 1. At this point, what was your overall impression, given his complaint and his rhythm strip?

Answer 1. “The initial impression was respiratory problem, given the rapid respirations. We noticed the tachycardia on the rhythm strip. At that point we knew we had a potentially unstable patient, but we hadn’t been convinced it was 100% cardiac yet. With the clear bilateral lung sounds we began to lean cardiac. The clinical impression then became a symptomatic SVT.”

Run-Form (cont.):

“Patient transferred to ambulance. BP 153/98, pulse 166, spo2 98% room air. At this time patient states he feels like he is going to pass out, monitor observed to be at a rate of 170.“

Question 2. You noted that the rate was higher at this point. How did this change your impression and treatment plan?

Answer 2 “The increase in rate drove us to a more aggressive treatment because the symptoms grew with the rate. However, we still wanted to try less invasive procedures to break or slow the rhythm to determine if the symptoms were solely from the SVT.”

Run-Form (cont.):

“IV established, and normal saline ran, O2 via nasal cannula. I asked the patient if he has ever been cardioverted, patient states ‘Yes, they gave me some drug that stops my heart in the hospital a couple years ago.’ Vagal maneuvers attempted to lower rate. 12-lead obtained shows sinus tach at 150 now post vagal maneuver.”

ECG_2

Question 3. The vagal maneuver lowered the heart rate. What did this demonstrate to you?

Answer 3 “The vagal maneuvers working for the short period of time drove us further down the SVT treatment plan, with the rhythm being refractory to fluids, O2 and now vagal maneuvers, and with the sudden increase in symptoms we proceeded to adenosine. “

Run-Form (cont.):

“Rate shortly returned to 170, patient began to feel impending doom and stating ‘I’m going to pass out.’ Patient now states constant crushing chest pain at an 8/10. 6 mg adenosine given.“

Question 4. Why was adenosine given? What was the hoped-for effect?

Answer 4 “The impending doom and feeling of passing out, coupled with the now constant crushing chest pain. The adenosine was given with the hope of relieving the symptoms, and breaking to rate to search for a possible underlying cause for this dysrhythmia.”

ECG_3

Pre-adenosine

During adenosine push

During adenosine push

Immediately post-push

Immediately post-push

Run-Form (cont.):

“Constant monitor print showed rate broke for brief period of sinus bradycardia and returned to a rate that did not exceed 135. Patient stated relief of chest pain, now a 5/10, still heavy crushing feeling. Patient no longer feels impending doom and states he no longer feels like he is going to pass out. Post medication 12-lead shows sinus tachycardia at 135.”

ECG_6

Question 5. Last question! Was the adenosine helpful?

Answer 5 “I would have to say yes, the rate decreased and symptoms began to dissipate allowing for the patient to become more comfortable and the impending doom subsided.“

Conclusion

An echocardiogram and CT scan showed that the patient had a massive pulmonary embolus, blocking much of both pulmonary arteries. He had a history of PE and DVT, but was non-adherent with the anticoagulant medication.

Questions:

  1. Was this rhythm a “SVT?”
  2. Were the therapies (vagal maneuver and adenosine) helpful for diagnosis or treatment?
  3. What is the “ACLS approach” to the arrhythmia in this patient?
  4. What would your approach be?

 

The 12 Leads of Chistmas: V2

This article is the tenth in our latest series, The 12 Leads of Christmas, where each day we examine a new finding particular to an individual electrocardiographic lead.

 

Lead V2

I love V2.

It’s probably been my favorite lead to examine and ponder this past year. The cool thing is that it doesn’t seem all that special way at first. I mean, the precordial leads form what is essentially a smooth sigmoid curve across the chest; what could one lead tell us that’s so unique compared to its neighbors? As it turns out, in the right situation, V2 can hold some surprises.

01 - Sigmoid Precordials

I see math everywhere. Don’t worry, this image doesn’t have any real purpose; it just looks kinda cool if you’re into logistic functions. Image source.

So what’s so special about V2? Well, despite being commonly depicted as a plain anterior or septal lead, it would be much better described as a “high-anterior” or even “high-antero-lateral” lead. The high-lateral wall of the heart isn’t really well covered by the electrocardiogram so every bit of insight we can get on this area is vital. First though, what is the high-lateral wall?

Most folks reading this article will be familiar with the anterior, septal, lateral, and inferior walls.

Contiguous Leads

This chart is from an old article on our site discussing contiguous leads. I’ve left the former address at the bottom as a testament to how far we’ve come; both in our understanding of electrocardiography and in our design of graphics.

The problem with that classic teaching—well, aside from the fact that our obsession with identifying ST-elevation in “contiguous leads” is outdated and hurts patients—is that it vastly oversimplifies the way the electrocardiographic leads correspond to particular regions of the heart.

First, let’s clarify that for this discussion all we really care about is the left ventricle (LV), not the entire heart. In the structurally normal heart the LV myocardium constitutes the bulk of the QRS-T-complex we see on electrocardiogram, so for now we can ignore the effects of the atria and right ventricle (RV).

03 - LV Motion

The LV is shaped like a rugby ball or American football with one end lopped off. Image source.

It would be nice if the transverse, coronal, and sagittal views of the heart were perpendicular to its axes, similar to the animation above; but nature, while elegant, doesn’t like right-angles.

Instead, the LV is situated at an oblique angle, with the base pointed at roughly the right scapula and the apex towards lead V5.

04 - Coronal Section

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

This doesn’t complicate things too much when we’re dealing with the frontal plane—made up by the limb leads.

05 - Coronal Axis

Image source [modified].

Using the above illustration as a guide, I would theoretically re-associate the frontal leads with the regions of the heart as follows (clockwise from top) [these are only my terms]:

  • (-)aVF: Basal-lateral
  • (-)III: High-lateral
  • aVL: High-lateral
  • I: Low-lateral
  • (-)aVR: Low-lateral/Apex
  • II: Apex/Infero-apical
  • aVF: Infero-apical
  • III: Inferior
  • (-)aVL: Inferior
  • (-): Basal-septal
  • aVR: Basal
  • (-)II: Basal

Of course, there are still issues with this way of visualizing things.

First, there is the possibility for huge variation in individual anatomy—both how and where the heart sits in the chest and how the coronary arteries are distributed—so it’s not like the above associations are set in stone.

Second, because the heart is a continuous prolate spheroid (rugby ball), each region is contiguous with its neighbor. Add into this the fact that each “region” is somewhat arbitrarily defined and that results in a great deal of overlap.

Third, this perfect coronal cross-section of the heart is completely at odds with how the the field of cardiovascular imaging looks at things. While there are a variety of angles at which differing devices can examine the heart, most do so using the major and minor axes of the heart as references, not the axes of the body. In other words, echocardiography, cardiac MRI, perfusion scans, and other cardiovascular imaging modalities examine the heart using it as their point of reference, while the coronal, sagittal, and transverse planes we typically imagine (and see in non-cardiac CT scans) use the body as the reference and just happen to cut through the heart.

15 - Echo Regions

Consensus terminology for the regions of the heart, as correlated with cardiac MRI. These are polar maps of the heart, as if you were viewing the LV point-on from the apex and in-line with its major axis. Source.

Finally, the idea that there is a single electrical center of the heart (where the arrows of the axes cross in the coronal image) is flawed. We can approximate an electrical center, as I have, but because the entirety of the LV doesn’t contract simultaneously (see the asymmetrical motion in the gif earlier in this post), the “electrical center” of the heart actually moves through the course of the cardiac cycle.

06 - Electrical Center

Click image to enlarge. It took me forever to find a paper discussing this topic, but here’s the source.

But what does all of that have to do with V2?

“I told you that story to tell you this one,” (a questionable reference at the moment).

As tough as it is to get the frontal leads right in regards to infarct localization, they’re downright simple compared to the precordial leads. You see, the forefathers of electrocardiography had the good sense to give us the limb leads to form a nice, standard coronal plane. Recognizing the need to examine the heart in more than one plane, they later devised the precordial leads to examine the heart in the transverse.

…but they weren’t be content with just looking at a single transverse plane, which is how an engineer would devise the system. Instead, the precordial leads were designed to follow the flow of the heart, from the cephalad base to the more caudal apex. This makes sense and certainly has benefits, but it plays absolute havoc with the field of vector electrocardiography and our ability to visualize how the individual leads relate to different regions of the heart.

What we end up with isn’t actually a plane at all, but rather six separate views of the heart at varying angles with regards to the the “electrical center.” V1/V2 sit at one level, V4–V6 at another, and V3 in the middle (see the first image in this post).

Most illustrations of the transverse plane depict the precordial leads as below:

07 - ECG Anatomy LITFL

An incorrect representation of the electrical planes and axes. Image source.

It’s a beautiful image and gets some of the basics right, but there is also a lot wrong with it. [I don't mean to single out this one instance; almost every diagram I've seen performs the same over-simplification.]

As an example of why this format breaks down, consider for a moment inferior STEMI’s due to RCA occlusions (either proximal or distal, it doesn’t matter). They almost always present with an injury vector of 110–120 degrees; meaning the ST elevation is maximal in lead III and essentially points at lead III.

08 - 0825 - 70yo F - 01

An EKG!? In this blog about EKG’s?? It’s about time. Anyway, most folks would call this an “infero-lateral” STEMI; but why would the lateral wall be involved in an inferior STEMI due to an RCA occlusion? I would term this an infero-apical-septal STEMI, but that’s a discussion for another day.

If that pretty diagram was correct, why on earth would the above EKG also display ST-elevation in V4–V6 (the classic “infero-lateral” STEMI [flawed terminology])? That question bothered me for years until I discovered the work of Dr. Antonio Bayés de Luna and figured out where I was going wrong. [Sadly, I don't have time to directly address this question here, but the simple explanation is that everything you know about leads V4–V6 is wrong.]

So what’s the right way of displaying the precordial leads?

That’s actually a pretty tough feat. A single transverse plane doesn’t do them justice, especially when you consider the moving electrical center of the heart, individual variation in cardiac anatomy and orientation, individual variation in surface landmarks, and technician variability in electrode placement (the precordials are very dependent on exact and consistent placement).

Sadly, given the time constraints of getting this post together, I haven’t been able to put together a great illustration or 3-dimensional model (or find someone who can), but I’ll make it happen someday. This will have to do for now:

09 - CXR Cardiac Anatomy Precordials Marked

All six precordial leads fanning out from the approximate electrical center (purple dot). Original image source [modified].

You can see that all six leads fan out from the heart. Try to visualize an elliptical plane whose edge touches V1 and V4–V6 . Though V3 is a little out-of-plane, V2 is the only lead that really falls out from the rest; it’s directed much more superiorly than the others in that regard.

It’s a very subtle point and hopefully the rest of the post will make it more clear, but it is vital to what makes V2 so unique.

If you were to imagine the LV as a football or rugby ball (or prolate spheroid) again, its major axis is what it spins around when it spirals. The major axis of the LV runs from roughly V4 or V5 and is directed towards the right scapula. With regard to that axis, V2 is the most superior precordial lead we have.

What would happen if we encountered an injury vector that was perpendicular the rough plane formed by V1 and V4–V6; towards the left shoulder and tilted just a bit anterior?

We don’t have to imagine this, however, because it is an electrocardiographic pattern we encounter from time to time during isolated “high-lateral” STEMI.

This area, better described as the basal-antero-lateral territory of the heart, can be perfused by with the first diagonal off the LAD (D1), the ramus intermediate branch off the left main (RI), or an obtuse marginal off the left circumflex (OM1). As a result, nailing down the exact culprit artery is nigh-impossible on the ECG, but when there an isolated occlusion of one of these arteries it can present as an incredibly subtle STEMI.

What you’re looking for is an injury vector directed high and to the left (roughly -60 degrees, but there’s a good deal of wiggle room due to the variable anatomy), which will create subtle ST-elevation in aVL with more pronounced ST-depression in lead III. There may also be elevation in lead I or depression in aVF.

What gets really interesting, and the whole reason we’re having this in-depth discussion, is that precordial leads will all show minimal changes or maybe some ST-depression…

…all except for V2!

It seems like a non-physiological pattern at first, and you might be tempted to think there was a lead switch, but that’s just not the case.

10 - CXR Cardiac Anatomy Precordials Vector Marked

The typical injury vector in isolated “high lateral” STEMI, perpendicular to the plane formed by most of the precordial leads. V2 is the exception. Original image source [modified].

As shown above, most all of the precordial leads are perpendicular to the injury vector seen with this type of STEMI. When a lead is perpendicular to a vector it cannot see it. V2, however, is exceptional because it is just superior enough to the plane that lies perpendicular to the injury vector that it actually manages to “see” a bit of it.

Here are some examples.

11 - 0815 - 86yo F - 01

Typical STEMI isolated to the “high-lateral” territory. V2 is the only precordial lead showing ST-elevation, while the marked ST-depression in lead III tells us there is ST-elevation pointing away from there—towards the left shoulder.

Here’s the above ECG arranged “360 Degree Heart” fashion.

12 - Negatives + Heart + ECG

Here’s another…

13 - 1016 - 50yo M - 01

Here’s another similar ECG. See if you can spot the pattern.

And one more, super subtle tracing…

14 - 0054 - 52yo M - 01a

This one is extremely subtle, even in V2, but it follows the same pattern.

 

The subtlety of these ECG’s is one of the reasons why this territory of the heart is often considered “electrocardiographically silent.” It’s not silent in the above tracings—it’s whispering “STEMI”—you just need to listen closely.

 

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: V3
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! 

Register for #EMSToday2015 win an iPad mini! 

The 12 Leads of Christmas: V5

This article is the ninth in our latest series, The 12 Leads of Christmas, where each day we examine a new finding particular to an individual electrocardiographic lead.

Lead V5

We’re getting into the home-stretch in our little series. I wasn’t entirely sure if we were going to make it through since a few of the leads, though they are useful, don’t bring much that is particularly unique to the table. V5 is one of those—like aVF and V4—and while there is still plenty to discuss, it’s not as exciting as lead III, aVL, or aVR.

Don’t lose faith, however, as I have saved three of my favorites—V2, V3, and V6—for last.

Anyway, let’s get on with this V5 business.

One of my favorite tricks for showing off to new techs (and letting them know that I’m keeping an eye on their work) is to guess that they were sloppy with their precordial lead placement without even seeing the patient. How do I do that?

V1 is a good place to start, looking for signs of incomplete right bundle branch block that could mean the lead was placed too high on the chest.

Another common error, however, is to bunch up leads V4-V6 on the anterior chest. Despite personally training many of the techs in my department, I still see this setup way too often:

01 - Apollo Torso Electrodes Incorrect

Crazy precordial electrode placement. V1 and V2 are way too high (cephalad) and wide (lateral), V4–V6 are bunched up on the anterior chest, and V3 is in no man’s land. Image source.1

 

It’s hard to make a 2D diagram that displays proper electrode placement—especially when you can’t directly visualize the ribs—but a much better setup is shown below:

02 - Apollo Torso Electrodes Perspective Correct

Correct precordial electrode placement. V1 and V2 are parasternal, in the 4th ICS; V4 is in the mid-clavicular line, 5th ICS; V3 is halfway between V2 and V4; V5 is on the same horizontal level as V4, in the anterior-axillary line; V6 is on the same horizontal level as V4 and V5, in the mid-axillary line. Image source.1

03 - Axillary Lines Torso Electrodes Perspective Correct

A lateral view of V4–V6, showing their relationship to several anatomical landmarks. Image source.

 

How does V5 fit into the picture?

When you follow the R-wave progression across the precordial leads, in a normal adult ECG there should be a tiny R-wave in V1 with a larger S-wave. Though V2 usually has a larger S-wave than V1, as you move from V2 to V6 the S-wave will get smaller and often disappear while the R-wave will grow in height—these transitions should be rather smooth from one lead to the next.

20 - R-wave Progression

Notice how the R-wave reached its maximum height between V4 and V5, and while there will still be a sizable R-wave in V6, it is not as large as V5′s. Below are a few normal ECG’s with proper electrode placement:

04 - 1424 - 20yo M

Note the smooth precordial R-wave progression that reaches its maximum in V5. Also not the disappearance of the S-wave by the time we get to V6. This won’t happen every time but when present it’s a good sign that the electrode has been place far enough posterior.

05 - 0816 - 10yo M

Again there is a smooth precordial R-wave progression with the maximum R-wave amplitude in V5.

06 - 1265 - 13yo M - 01

Again there is a smooth R-wave progression with the tallest R-wave in V5 and no S-wave in V6.

 

When V4–V6 are bunched up on the front of the chest you end up with V5 close to where V4 is supposed to be and V6 ends up where V5 was supposed to be. As a result, the maximum R-wave height occurs in V6 instead of V5 and there will often be a residual S-wave still present in V6 as well. Here are some examples:

07 - 0575 - 63yo M - 01

There is a normal, if somewhat early, R-wave transition on this EKG. This is the baseline for the same patient as the next tracing.

08 - 0575 - 63yo M - 03

This is the same 63yo male as the prior tracing but notice how much slower the R-wave develops across the precordium. The maximum R-wave size is in V6 and there is still an S-wave present there.

09 - 0042 - 70yo F

There is a very poor R-wave progression on this EKG with no sign of old anterior infarction, LAFB, or other abnormalities. It is pretty safe to assume the PRWP is due to electrode placement.

10 - 0020 - 58yo F

Not only is there a poor R-wave progression, there is an rSr’ complex in V1, suggesting this technician made multiple errors when performing the EKG.

11 - 0045 - 49yo M

This is the EKG of a morbidly obese patient showing a poor R-wave progression. Most of the time this would simply be attributed to the patient’s body habitus, but in this case there is a subsequent tracing showing a normal R-wave progression. The PRWP here is just due to improper electrode placement.

13 - 0056 - 16yo M

Poor R-wave progression due to improper electrode placement (confirmed with direct observation) in a 16yo. There is also a large first degree AV-block, unrelated to the PRWP.

15 - 0025 - 21yo F

Another case where the largest R-wave is in V6 with no good reason for this 21yo to show a PRWP. There is also a subtle rSr’ in V1, again suggesting more than one electrode placement error.

16 - 0007 - 53yo M

More of the same.

17 - 0218 - 17yo M

Again an unexplained PRWP, and again there is an rSr’ pattern in V1 that is highly suggestion of improper electrode placement. Noticing a pattern?

18 - 0869 - 14yo M

Yet another young person with no reason to show this poor of an R-wave progression. Lead V4–V6 are practically identical, suggesting that they were placed very close together.

 

We also refer to this finding of a poor R-wave progression as “clockwise rotation.” If you imagine you’re looking at a transverse cross-section of the heart from below, it’s as if the heart has been rotated in a clockwise direction. In the above cases the heart hasn’t been rotated clockwise, the electrodes have been rotated counter clockwise, resulting in the same net-effect.

21 - 800px-Rwaveprogression

Normal R-wave progression. Image source.

22 - 800px-Reduced_rwaveprogression

Clockwise rotation of the transition-zone. Image source.

There are a lot of causes of poor R-wave progression (aka “clockwise rotation”) aside from improper precordial electrode placement. One of the most common is obesity, but that is also a common reason for placing the left-precordial leads too close together on the anterior chest, so it’s hard to determine which obese patients have a true PRWP unless you perform the EKG yourself. It is also seen with COPD, left anterior fascicular block (LAFB), anterior myocardial infarction, among other things.

All of the cases shown above were performed on patients with no other cause for their PRWP progression, leaving improper precordial electrode placement as the most likely culprit. Additionally, you may notice that most of the EKG’s are a bit faded. That’s because most of these cases were collected several years ago, before my hospital instituted a somewhat structured EKG training program. While I still see sloppy EKG’s from time to time, they are nowhere near as common as they were when I first started and, as a result, I’m glad to see most of the examples in my collection are several years old.

 

References

  1. By Unknown (original by Onatas?) (User:Bibi Saint-Pol, own work, 2007-02-08) [Public domain], via Wikimedia Commons.
  2. Häggström, Mikael. “Medical gallery of Mikael Häggström 2014“. Wikiversity Journal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 20018762.

 

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: V3
12 Leads of Christmas: V4
12 Leads of Christmas: V6

 

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

Mark your calendars: EMS Today is back in Baltimore! 

Register for #EMSToday2015 win an iPad mini! 

The 12 Leads of Christmas: V4

This article is the eighth in our latest series, The 12 Leads of Christmas, where each day we examine a new finding particular to an individual electrocardiographic lead.

Like aVF, V4 is a tough lead to discuss on its own. It’s part of the natural flow of the complexes across the precordium and it is certainly nice to have, but because it’s so closely related to V3 and V5 there isn’t a whole lot that makes it unique. The two topics we’ll discuss today involve, but are not isolated, to V4.

First off, I can’t discuss V4 without mentioning the work of our blog’s good friend and mentor, Dr. Stephen Smith, on differentiating early repolarization from subtle anterior STEMI. The formula he and his team derived uses the R-wave amplitude in V4 as one of the three variables in an equation that can be utilized as a decision-aid in the evaluation of these difficult EKG’s.

A series of cases displaying how and when to use the formula can be found here on his site.
The article describing the derivation of the formula can be found here (free full text!).
A simple form for calculating the value is available on the right-hand sidebar of Dr. Smith’s site.
Alternatively, a simple calculator is also available on the MDCalc site.

Earlier this year he was nice enough to feature a case of mine that really shows off the utility of the formula (among other lessons). Here’s a link to the full case description, while the image below is merely a teaser.

01 - 1386 - 75yo F - 01

Early repolarization or subtle anterior STEMI? Check out the link above to find out.

 

Another time V4 becomes useful is when you see a wide QRS complexes on the EKG but aren’t sure whether they’re due to a paced or native rhythm.

Most of the time you can see pacemaker spikes in several leads but, especially with aggressive filter settings, it’s also not unusual for those pacer spikes to be nearly invisible. Since most ventricular pacing wires are inserted into the RV apex, it turns out that the leads closest to that location are also the ones best suited to capture evidence of it firing.

Due to variability in individual anatomy and positioning of the pacing lead it doesn’t always work out but, in my experience, ventricular pacing spikes are usually best seen in V3–V5 region, so I typically center my scrutinization around V4. Atrial spikes, on the other hand, are usually best seen in V1 and V2, closer to where those wires are placed. Here are some examples of the former:

02 - 0862 - 83yo F - 08

They’re super subtle but V4 is the only lead in which ventricular pacer spikes are visible.

03 - 1314 - 76yo M

Ventricular pacer spikes are visible in V3–V5 but most visible in V4.

04 - 0855 - 66yo M - 03

Subtle ventricular pacer spikes are only visible in V3 and V4.

05 - 0275 - 78yo F

Subtle ventricular pacer spikes only visible in V4–V6. Interestingly, though the computer is usually pretty good at spotting PM’s, in this case it only picks up the atrial spikes.

06 - 0269 - 84yo M

Subtle ventricular pacer spikes in V3–V6, best seen in V4.

07 - 0635 - 82yo M

There’s a decent amount of artifact but there are also ventricular pacing spikes visible in V3 and V4 (in this case V3 > V4).

 

Another easy way to increase the visibility of pacer spikes is to increase the adjust the filter settings of the electrocardiograph. Depending on the particular machine you’re using this range in difficulty from easy to hard but it’s still worth knowing how to do—even is it’s only changed on rare occasions.

09 - 1450 - 75yo F - 01b

This EKG was printed with a filter bandwidth of 0.05–40 Hz. 40 Hz is a more aggressive low-pass filter than most guidelines recommend for diagnostic use (usually 100 or 150 Hz), but in the emergency setting I find the clarity that setting offers outweighs the small effects it has on the size of complexes.

08 - 1450 - 75yo F - 01a

This is the same exact ECG printed with a higher frequency low-pass filter (300 Hz vs 40 Hz). As you can see there is increased artifact but the pacer spikes are much more visible.Unlike the prior cases, in this instance V3–V5 are not the best leads for seeing the ventricular pacing spikes.

 

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: V3
12 Leads of Christmas: V5
12 Leads of Christmas: V6

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