Nitroglycerin - Old and New: Pt 2

A paramedic from AMR in Bridgeport told me about an interesting patient he treated recently. And by "interesting," I mean "briefly terrifying." He was bringing in a 75 y.o. male with chest pain, and had given the patient aspirin, and acquired an ECG. 

I scribbled on it. It's not a clue.

A few things on the ECG bothered him, and the patient's symptoms suggested ischemic symptoms. Since the vital signs were fine, he then gave 1 tab of nitroglycerin (NTG) under the tongue. 

Within 90 seconds, the patient became pale, sweaty, and described feeling pretty awful. The blood pressure bottomed out in the 70s, and the medic noted a drop in the heart rate. He acquired ECG #2:

Small change.

Fortunately, a dram of atropine and a jigger of normal saline rapidly fixed the bradycardia and hypotension. 

Concerned that he had "unmasked" a right-ventricular MI, he then obtained a third ECG, this time with V4R, to interrogate the right side:

TV4 is V4R - rest of precordial leads are the usual.

The rest of the transport was uninteresting, as well as his time in the ED. Although he was admitted, his ECG didn't show any changes from prior, and his troponins were negative. No MI.  
So what happened here? Does the second ECG suggest a cause of the bradycardia? For that matter, what about the first and third ECGs? In what way was the NTG involved?

I'll discuss a few basic questions about NTG-related hypotension, and also discuss an interesting new study out of Montreal, before finishing up with an infrequent adverse effect of nitro.

Why are we concerned about giving NTG during an AMI?
As most paramedic students would be able to tell you, we're worried mostly about MIs that involve the inferior wall, since about half of these involve the RV. Since infarctions of the RV tend to make the patient very sensitive to preload-reducing drugs, it is commonly taught to avoid NTG if there are signs of an inferior infarct. A small study from 1989, for example, looked at a group of patients with diagnosed inferior-wall MI, and found that evidence of RV involvement was strongly associated with NTG-related hypotension.

Many people recommend that you grab an ECG before giving NTG to a patient with suspected cardiac ischemia. While there are different reasons offered for this, the typical reason is to look for an inferior MI, and thus avoid hypotension caused by an RV infarct. 

(On the other hand, Dr Smith is concerned that NTG could "mask" a STEMI - read "Wait until after the ECG to give Nitroglycerin." Pretty dramatic example!)

So, given the apparent importance of this advice, is NTG-related hypotension common?

How often do patients drop their BP after NTG?
Not often!

For instance, a study from 1994 looked at 300 EMS patients that got NTG for CHF or chest pain, and only 4 developed a SBP < 90 mmHg. That's only 1.3%, and even those 4 patients did fine after the NTG wore off.

Another study looked at over 1,500 patients who received NTG from EMS, and only 12 patients had significant adverse hemodynamic effects - only 0.7% of the total.Some folks had some big drops in their BP, but nobody died. Similarly, only 1 patient out of 288 in a third study had hypotension. That patient improved with a 300ml NS bolus.

Okay, so reactions are rare. When these do happen, though, do they predict anything about a presence or location of an MI?

Does a hypotensive reaction to NTG predict an inferior-wall MI? (Breaking news!)
This comes from an abstract presented at the 2013 NAEMSP Scientific Assembly, and so should be considered preliminary. Nonetheless, it appears to be an interesting addition to the nitro literature. (The whole abstract is copied at the bottom of the post)

Researchers in Montreal searched their EMS database for patients who had been transported for suspected ACS. They then picked out the patients who ended up being diagnosed with a STEMI, and who had also received NTG from EMS. Although these patients got prehospital ECGs, the EMTs weren't trained to read them - just to acquire and and transmit. They likely were not able to identify a "likely RV infarct," and were not instructed to withold NTG from anybody based on the ECG. This amounted to about 800 patients over a 2 year period. 

The researchers divide the ECGs into inferior-wall STEMIs and non-inferior-wall STEMIs, and looked at what giving NTG did to either group. They found two things:

• First, patients with an inferior-wall STEMI were more likely to have hypotension initially.  
• Second, after they got NTG, patients with an inferior MI were not more likely to have hypotension, or even a significant drop in BP.

Although you should be cautious if you have a hypotensive patient with huge ST elevations in V4R, it's not clear that the evidence suggests that we routinely need ECGs before giving NTG. 

So what happened to our patient with the bradycardia and hypotension? 

The Bezold-Jarish reflex
He fainted. You can also call it a vasovagal reaction, or a triggering of the Bezold-Jarish reaction, but it's all basically your standard faint

Well, maybe not just like that, but pretty darn close. He never actually "passed out," but given his vitals and symptoms, he wouldn't have stayed upright for long. Fortunately, he was already laying down on a stretcher, so he never lost consciousness. Staying supine when you brady down is a pretty good policy. 

But there's other evidence besides the vital signs that suggest  a vasovagal mechanism, and not a preload-sensitive cardiac ischemia. Take a closer look at the second ECG:

Sinus activity has been totally suppressed, and the rate has dropped down to a typical junctional speed. This is an AV dissociation, rather than 3rd degree block, since the ventricular rate (39) is higher than the atrial rate (0). The QRS hasn't widened at all, suggesting the block is at or above the level of the AV junction. As I noted in a previous post, these are the classic features of a vasovagal bradycardia & syncope.  

The Bezold-Jarish reflex is the likely mechanism, where initial tachycardia triggers a strong burst of activity from the vagal nerve, dropping the blood pressure and suppressing the SA and AV nodes.

From the Cardiology & CCU FB page

The (relative) hypovolemia that you might see when someone gets too much NTG, especially with an RV infarct, would be more likely to produce a compensatory tachycardia, and wouldn't usually produce such dramatic AV blocks.  

Is this something new and rare that I've stumbled across? Sadly, no. There are numerous case reports describing hypotension and bradycardia after giving NTG to patients, many of whom were shown not to be having any MI at all, let alone an RV infarct.

For example, in a 1990 case report, a 36 y.o. male received 2 NTG tabs in the course of a work-up of chest pain. Despite an intially normal ECG, he dropped his BP down to 77/40, and developed a brief brady-asystole. 

His vitals improved without drugs or IV fluids, and his labs and stress test ruled-out MI.

Another case report from 2007 (free access!) describes a similar sudden-onset junctional bradycardia and hypotension in a 60-y.o. male after NTG administration. Further back in ancient history (1981), a case series of 4 patients with this same pattern of bradycardia with hypotension and a narrow-complex bradycardia without sinus activity were described.

In yet another case, a 54 y.o. woman with chest pain (who ultimately ruled-out for MI) was given NTG for chest pain, and developed bradycardia. She described "lightheadedness and malaise," but never dropped her blood pressure.

Atropine (despite the blood pressure) helped the heart rate normalize.

The Bottom Line 
So now that I've described all these nasty bradycardias, should you withhold that next dose? Probably not. Even with EMS giving NTG to thousands of patients in the studies above, the rate of serious adverse effects is ≤ 1%. Those reactions also tend to be transient as well.

I should also point out that the SHCGB Guidelines do not require an ECG before NTG. After all, patients take this medication on their own all the time. On the other hand, they are not calling 911 every day, so the prudent paramedic should be getting ECGs early and often!


________________________________________________________  
103. DOES PREHOSPITAL ADMINISTRATION OF NITROGLYCERIN FOR CHEST PAIN CAUSE HYPOTENSION IN ACUTE INFERIOR WALL STEMI? A RETROSPECTIVE COHORT STUDY
Dave Ross, et al. Urgences-sante; Hopital du Sacre-Coeur de Montreal Montreal
Background. Patients with inferior ST-segment elevation myocardial infarction (STEMI), associated with right ventricular infarction, are potentially at higher risk of developing hypotension when administered nitroglycerin (NTG). However, current basic life support primary care paramedic (PCP) protocols do not differentiate location of STEMI prior to NTG administration.  
Objective. We sought to determine whether NTG administration is more likely to cause hypotension (systolic blood pressure <90 mmHg) in inferior STEMI compared with non-inferior STEMI.  
Methods. We conducted a retrospective chart review of prehospital patients with chest pain of suspected cardiac origin and computer-interpreted prehospital electrocardiograms (ECGs) indicating “acute MI.” Computerized interpretation was performed by the GE Marquette 12SLR-Zoll E Series. Patients were treated by PCPs. We included all local STEMI cases identified as part of a provincial STEMI registry project. Charts were reviewed by trained data extractors using a predefined instruction list. Univariate analysis was used to compare differences in proportions of hypotension after NTG administration, drop in systolic blood pressure greater than or equal to 30 mmHg, and hypotension on initial prehospital blood pressure between patients with inferior wall STEMI and those with STEMI in another region (non-inferior).  
Results. Over a 29-month period, we identified 1,466 STEMI patients. Of those, 798 (54.4%) had complete data and received NTG. Hypotension occurred after NTG in 36 of 461 inferior STEMIs and 29 of 337 non-inferior STEMIs, 7.8% vs. 8.6%, p = 0.69. A drop in systolic blood pressure greater than or equal to 30 mmHg occurred in 23.5% of inferior STEMIs and 23.8% of non-inferior STEMIs, p = 0.91. Initial hypotension was noted in significantly more inferior STEMIs compared with non-inferior STEMIs, 9.9% vs. 4.9%, p = 0.005. Interrater agreement for chart review of the primary outcome was excellent (kappa = 0.94). 
Conclusion. Patients with chest pain and inferior wall STEMI on their computer-interpreted prehospital ECG who receive nitroglycerin do not seem to develop hypotension more frequently than patients with STEMI in other territories, although they are more commonly hypotensive on presentation. Current PCP protocols for NTG administration in computer-interpreted prehospital ECG STEMI appear to be safe.

Bradycardia - Traumatic etiology?

When the patient has bradycardia, you run through a short differential. Electrolytes, MI, drugs,.... trauma? How does that work?

The patient
A trauma alert was rolled into room 5 at the 'Port. A 45 year-old male, restrained driver in a roll-over, who had been ambulatory on EMS arrival. He was mildly intoxicated, denied any significant medical problems. His vitals were normal both prehospital and in the ED. (The trauma alert was due to mechanism, not his condition.) 

His exam was notable for a rather large laceration to his scalp, with a correspondingly large blood clot at the head of the backboard.

"He probably smells my dog!"

The bleeding was controlled, and the evaluation continued. 

While we were getting the chest x-ray, however, we noted that his heart rate, which had intially been around 70-80, started slowing down. 60, 50, 40, down to the 30s! 

His blood pressure, which had also been normal, plunged down to a systolic BP of around 50 mmHg. His ECG showed this:

An old ECG was entirely normal. Interestingly, the patient, in a supine position the whole time, denied any symptoms whatsoever, and was moderately amused by our concern.

Discussion
So what happened to his heart? 

Well, we should worry first about ischemia- or infarction-related bradycardia. An inferior MI is notorious for causing 1° and 2° AV blocks, most of which resolve on their own. These bradycardias manifest with a narrow QRS, since the block involves the AV node, but not the bundle of His, etc. They usually get better in a few days, on their own.

By contrast, anterior MIs may involve an infarct of part of the ventricular conduction pathways. The patient will have a wide QRS and a high-grade 2° or 3° AV block. These are bad, and need permanent pacemakers!

Although you should think of hyperkalemia when you see bradycardia, there was little else to suggest it. He denied any medications, so digoxin, beta-blockers, and calcium-channel blockers seemed unlikely, especially given how quickly the rhythm had developed after normal prehospital vital signs.

Perhsps I should be clearer about how the bleeding from the scalp was controlled. Since the wound was large, and the bleeding brisk, a number of staples were rapidly placed.

NOT an approved wound closure technique. (credit)

Let's take a closer look at the ECG. Like I said before., he gradually slowed down to 34. 

Sinus activity is almost extinguished - I can only find 2 P-waves, preceding beats #1 and #3. The QRS is narrow, suggesting a junctional rhythm, albeit much slower than you would expect (usual junctional rate is 40-60). You can't really call it complete heart block, since there is so little atrial activity; instead, it's just called AV dissociation.

Putting all this together, it appears he had a cardioinhibatory/reflex syncopal episode; i.e. he fainted. The placement of the staples likely triggered a strong vagal reflex, which inhibited both the sinus node (almost no P-waves) and the AV node (junctional bradycardia). 

Fortunately he was already supine when it occurred!

Inappropriate stapling technique.

The treatment
He got atropine 0.5 mg IV, and a liter of NS on a pressure bag. His heart rate corrected quickly, coming up to about 80, but his blood pressure took a few more minutes to come up! He was admitted, and did not have any more bradycardic episodes. 

Bottom line
 No harm, no foul, as they say. But I do think we're going to be more enthusiastic about using lidocaine in the trauma bay, however!

Two interesting recent EMS calls.

I don't have a deep analysis of a recent study, or a recent change to the protocols, or even my thoughts on some EMS controversy

I do, however, have a gross picture and an interesting EKG! Both of these come from patients brought in by the same long-time medic at American Medical Response in Bridgeport.

First, the EKG.

The patient was an elderly lady, brought in from an nursing home, with a low blood pressure, but not looking "shocky," or at least not yet. Although there was no chest pain or other obvious cardiac complaints, and no arrhythmias, the medic nonetheless (wisely) obtained a 12-lead.

Of course, shooting an EKG, like any other  data point you obtain in the field, has been compared to picking your nose in public - namely, what do you do with the results?

So what would you do with this booger? Extra points if you find the occult STEMI.

The medic, correctly, did not call for cath lab activation.

Now the picture!

Same medic, bringing in a 80-ish year-old women who, because of dementia and multiple strokes, has had her diet restricted to pureed & thickened foods. Unfortunately, her husband, while preparing dinner, turned his back for just a moment while preparing himself a meal. When he turned back she wasn't breathing so well, and was starting to look a little blue-ish.

Not quite this bad.

By the time the patient showed up at the ED, however, she had a mild dry cough, but had her reassuringly pink skin color back!

The paramedic, not sure if we fully appreciated what had happened, held aloft with his MacGill forceps the spoils of the hunt:

Gross.

Nonetheless, a nice save! I have no idea how this lady managed to stuff a piece of meat that size into her mouth, let alone get it down into her epiglottal zone. Definitely a case that required on-scene, definitive, airway management.

Okay, that's it - no deep topics today.

But the next post will be more "meaty," I promise.

Did the machine miss something big?

I'm going out on a limb here, since I don't have the cath report yet. But I'm getting it soon, so we will have some closure on this!

The case:
A 68 year old male called 911 for "10/10" chest pain, and took aspirin before EMS arrival. Nitroglycerin was given by the medic, but it dropped the BP. Some normal saline took care of that, and transport was expedited.

The first ECG:

Computer interpretation: "Widespread ST-T abnormality suggests myocardial injury/ischemia"

Literally seconds later, the monitor showed a burst of activity:

A repeat ECG then showed:

No further events enlivened transport to the tertiary-level, primary-PCI facility.

So what does the first ECG show?
This ECG suggests a proximal LAD occlusion in two different ways, and justifies cath-lab activation, in my view.

The first pattern is likely familiar to astute 12-lead ECG readers. There is widespread depression throughout the ECG (II, III, aVF, and V3-V6), and ST elevation in aVR. Such a pattern indicates either severe 3-vessel disease or severe occlusion of the left main artery.

The second indication of LAD occlusion is not as well-known. Note the upsloping pattern of ST depression in the precordial leads.  This is distinct from the horizontal or downsloping pattern that you often find with a posterior AMI.

For example, this posterior MI demonstrates horizontal ST depression:

Source

Another example of a posterior MI shows a downsloping pattern of the ST segment:

Source

By contrast, in our ECG we have a sharply upsloping ST segment. Furthermore, it terminates in a tall, fairly sharp, T-wave.

DeWinter "waves"
Back in 2008, de Winter and a few other authors described a ECG pattern that they had seen in 2% of anterior AMIs. Interesting, all of the patients with this pattern had occlusions of the LAD in the proximal region - a very serious blockage that could infarct a good chunk of myocardium.

[T]he ST segment showed a 1- to 3-mm upsloping ST-segment depression at the J point in leads V₁ to V₆ that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R-wave progression. In most patients there was a 1- to 2-mm ST-elevation in lead aVR

They offered 8 examples of the precordial ST-T pattern:

Interesting looking ST segments and T-waves! Comparing these examples to our patient, looking at a blow-up of the precordial leads:

Upsloping ST-segment depression? Check.
Tall, positive, symmetrical T waves? Check.
Loss of R-wave progression? Check.
Normal-width T-wave? Check.
ST-elevation in aVR? Check.

So even without the 20/20 hindsight that blogging affords me, I'm anticipating a proximal LAD occlusion.

The final ECG
It appears the ST segments have normalized - both the ST elevation in aVR, and the ST depressions in multiple leads have returned to baseline. Even though this spontaneous reperfusion is an encouraging development, the patient still requires emergent angiography in my opinion, given the high likelihood of a dangerous, unstable lesion.

The Bottom Line
There - you know what I know now. Do you see anything that points to an alternative diagnosis, another concomitant problem, or different management?

I'll dig up the final results, and and them in the comments in a few days.

Importance of the Prehospital ECG

I've talked about the evidence for liberal and frequent ECGs in the field. This, however, is not a literature review, but a "real-world" example.

A patient was brought into the ED recently, treated by Milford Fire. Fortunately for the patient, paramedic Eric Mohr was on duty, and did some nice ALS work.

EMS Course
 An elderly female had developed chest pain, abruptly, while asleep. It wasn't a mystery - she described "squeezing" pain that radiated to the jaw. The first ECG, from onscene, was not exactly a stumper either:

*** THE LP-12 IS VERY EAGER TO TELL YOU SOMETHING ***

Like I said, not subtle.

Transport was intiated, aspirin was given. They were just about to patch in and call for a cath-lab activation, but decoded to grab one more ECG as evidence. (Note the change in time - they switched to an LP-12 that hadn't been adjusted for daylight savings.)

Huh, no more STEMI. Or anything, really.

Furthermore, the patients pain was starting to resolve as well. Aside from brief period of sinus bradycardia that resolved with atropine, the patient's symptoms continued to improve.

In the ED
By the time they reached the ED, she was almost symptom-free. Our ECG was consistent with that of EMS - very, very normal.

More normal than mine. Seriously.

Tell me if you see anything there - I didn't.

Since the patient was now utterly symptom-free, with a normal ECG, I put her in a bed near the desk, and checked in every 10 or so minutes to see if she was feeling anything changes.

About an hour later, she reported the same feeling in her chest and jaw, and I grabbed another series of ECGs:

 

Hmmm. I wasn't sure if the one little change I was seeing was real, so we grabbed V4R (PDF download there). I don't have the actual ECG of that lead (by then there was practically a sheaf of tracings, and it got lost in the pile), but it stuck in my memory. Let me draw it for you:

V4R - According to the courtroom artist

As I described it to the cardiologist, "It's only about 0.25 mm, but that ST segment just wants to come up!"

This ridiculous interpretation of mine made sense to cardiology, and the cath lab was activated, despite the absence of classic STEMI criteria, and a patient whose symptoms had again resolved.

"Classic" STEMI criteria, from Rokos 2010.

Good thing too. She ended up having a 99% occlusion of the RCA.

From this episode, I think there are 2 lessons to take away.

EMS needs to grab ECGs early and often.
If Eric hadn't obtained that initial ECG, this would have been a far more difficult case. It was pretty clear from the onset that she had troubles with her inferior wall. This would have been very difficult to demonstrate solely on the subsequent ECGs, however.

Look at aVL
For this, I give all the credit to Stephan Smith. One of his frequent teaching points is that ST depressions or T-wave inversion in aVL is often the herald, the very first ECG indication of an impending inferior wall STEMI.

He has made this point recently, as well as on numerous prior occasions. Go read those, and look at the tracings, and see how the cases unfolded with EMS and in the ED. Pay special attention to how the emergency physician and cardiology approached the situation. These aren't straightforward cases, and goes beyond "STEMI 101."


The Bottom Line
Yes, it's true that you expect to see reciprocal changes in aVL and perhaps lead I, with an inferior wall MI.

But in a patient with ischemic-type symptoms, and no ECG changes expect for this pattern in aVL, keep your eyes open for ECG evolutions. Run a couple more strips. Grab some right-sided leads. Tell med control to meet you at the door to discuss the situation.

See you at 4 AM!

Not yer usual STEMI.

The facts: a 35 year old male, with no medical history, presented with 1 week of chest pain that became acutely worse 1 hour prior. It was a "squeezing" feeling that radiated down his left arm. He had some mild dyspnea, and 1 nitro made it somewhat better. Some smoking, no cocaine.

The ECG:

The computer interpretation used caps lock,  had a lot of "***."

Cardiology was skeptical, but had him in the cath lab 30 minutes later. My resident put 50 cents down on a LAD occlusion, while I bet him a cup of (free) coffee that this was a classic first diagonal , or high lateral, STEMI. The two cardiology fellows agreed that we were both mistaken, and that they were certain to find a blocked circumflex. While the patient was in the lab the troponin came back as significantly elevated.

A few hours later, the cards fellow calls me back with the cath results.

Survey says!

No offense to Steve Harvey, but I'm a Dawson kinda guy.

Nada. Clean cath. "No significant fixed obstructive disease."

Interestingly, however, both ventriculography and an echo revealed hypokinesis of the high anterolateral wall, corresponding to the anatomy suggested by the ECG. He was given a diagnosis of focal myocarditis.

Focal Myocarditis

This isn't very common, but we can't say how uncommon. It is still uncommon enough to be worthy of case reports, at least in Texas. We know that about 3% of MIs have clean coronary arteries by angiography, but a number of those people have spasm or spontaneous reperfusion. The percentage may even be smaller with STEMI patterns, but we don't know.

The only way in the past to definitively diagnose myocarditis was through endomyocardial biopsy, which has a good number of shortcomings, in terms both of sensitivity, and of complications.

What could go wrong with this?

Advances in MRI techniques have enabled researchers to noninvasively study myocarditis. In a recent study it was found that 78% of patients who presented with an MI (64% with ST elevation), but a clean cath, had evidence of myocarditis on MRI.

Uh, yeah, I see it too...

Reciprocal changes

Now, I understand that the myocarditis can generate ST elevation, likely in the same manner that pericarditis does. I am really surprised, however, that our patient had such distinctive and appropriate reciprocal changes. Nonetheless, an ECG from a case report of myocarditis also shows reciprocal changes:

Turning to Stephan Smith's ECG Blog for some wisdom, I found this observation in "Is it MI or pericarditis?" (There's a lot of overlap between pericarditis and myocarditis, and many people link them on a spectrum; e.g myopericarditis.):

Pericarditis should never be assumed when there is even a hint of reciprocal ST depression.  Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare.  I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.

A great review article by Punja 2010 gives a few examples of ST elevation in myocarditis, but neither example shows reciprocal changes.

Nasty STE in myocarditis, but no ST depression

Sooo... Rare ECG finding? Not enough research? Incomplete diagnosis?

The Bottom Line

So, the next time you bring in that "for sure" STEMI, keep in mind there's a (3%*78%=) 2% chance it's myocarditis. Or higher. Or lower.

The most difficult step in obtaining an ECG.

Quick post today, concerning a very common error I see both in EMS and ED patients - misplaced ECG leads. I would call this a pet peeve (as the techs and nurses I work with are well aware!), except that a peeve does not usually carry significant clinical implications.

An article in the curent issue of EMS World argues for the acquisition and transmission of prehospital ECGs by BLS crews. No argument there - that is exactly what happens in the ED. A tech acquires the ECG and runs it to me. If your system allows for easy transmission of ECGs, and if paramedics are scarce, this would be a common-sense approach to take.

Unfortunately, an accompanying illustration distracts from the main message.

Source

In an unfortunate twist, there are two errors of lead placement here. These errors are both common and possibly clinically significant.

The problems.

First, I believe V1 and V2 are located too high on the chest.

These leads should be located in the forth intercostal space (ICS), which in males is often within a fingerbreadth of the horizontal nipple line.

Reference

Another clue to V1 & V2 misplacement is their location relative to lead V4. Given that V4 should be located in the fifth ICS, the large vertical distance between V2 and V4 in the illustration suggests misplacement of V1 and V2 as well.

A second apparent error is that V3 is shown slightly medial to V2.

 It should properly be placed halfway in between leads V2 and V4.

Why is this important?

Misplacement of ECG leads, and especially V1 and V2, are common. One study compared the accuracy of cardiac techs, compared with nurse, physicians, and even cardiologists. No one, except the techs, came out looking too good.

The ovals represent the range of misplacement for each lead, broken down by training level. Ref.

These errors are not trivial. "Pseudo-infarction" patterns can be generated from incorrect lead placement, leading to erroneous cardiac catheterization lab activation, cost, and diversion of resources. In the example below, simply moving the V1 and V2 leads from the 4th ICS, then to the 3rd, and then the 2nd, produced ECG changes which the computer interpreted as suggestive of ACS.

Reference

Another example - you can see how an rSR' pattern is falsely generated as V1 and V2 are moved from the 4th ICS (in B-1) to the 3rd ICS, and then 2nd ICS (in B-3).

Reference

(Interesting aside - placing the leads in a higher ICS is used to assess for an occult Brugada pattern, But this is sort of a specialized technique, and I leave it to the electrophysiologists.)

Source

The Bottom Line

A recent post from Captain Chair Confessions highlighted the importance of proper lead placement, not only with regard to accuracy, but also in assuring that EMS appears professional and competent. I second that, but I have to acknowledge that many paramedics likely learned the incorrect position from preceptors within the hospital. Heck, in one of the studies mentioned above, the cardiologists were the people least likely to properly position V1 and V2!

So, kudos to David Howerton and the other authors on making a good argument for ECG acquisition as a BLS skill! But strive to demonstrate proper lead placement - it makes a difference

An Alternative Method of ECG Interpretation

Just when a paramedic student has started to feel somewhat confident about rhythm interpretation, she is introduced to the other 11 leads.

First off, the leads are organized even worse than the QWERTY keyboard. Inferior leads are the left of anterior, the lateral leads are in two different places, and aVR sits there all by itself, like a chump.

Then there are all the depressions and elevations, T waves flipping around, ischemia vs infarct. And then someone shows you how to pick up on a posterior MI by flipping the paper over. Madness, I tell you.

In particular, identifying a STEMI can be difficult, even if ST segment elevation is clearly seen. For example, the following ECGs all show ST segment elevation, but...

1. Not a STEMI

2. Not a STEMI either

3. Nope.

 But with a fairly undramatic ECG like:

4. Bingo - Occlusion of the proximal LAD

The first first three ECGs demonstrate 3 common cause of ST elevation that we see in EMS or the ED, so-called "mimics" of STEMI. Now, there are a host of rules and criteria to help you diagnose each of these mimics, but it's hard to learn all of these, and to feel confident about them.

Is there a simpler way to achieve ECG excellence? Some short-cut to Jedi-level ECG mastery other than slogging through hundreds of tracings?

Perhaps a training montage?

Well, no.

But there are a few different ways to develop pattern recognition, and switching up the methods can put things in perspective. Hartman and colleagues have helped the novice ECG student tremendously with a new, focused approach to ECG interpretation. While this does not replace experience, practice, and feedback on interpretations, it's a good alternative way to tackle ECGs.

Abstract. If you want a pdf, message me at Facebook.

The rule has 4 steps, and we'll tackle them in that order

1. Is there ST elevation in at least 2 related leads?

The first rule specifies a minimum amount of elevation: 1-2 mm in two anatomically related leads.

It doesn't take long before a paramedic student identifies their first patient with ST elevation. Okay, granted, it's usually not an actual STEMI that they find, since the majority of ST elevation found in the ED or by EMS is not a STEMI. Typically, ST elevation will be due to any number of "mimics," such as left bundle branch block (LBBB), left ventricular hypertrophy (LVH), early repolarization (ER), as well as a number of other conditions. Surprisingly, if you look at all the patients who come into the ED with ST elevation, only about 1 in 7 patients have a true STEMI!

On the other hand, if you don't have some ST elevation, the patient probably doesn't have a STEMI. (Yeah, we're going to miss a true posterior or a proximal left main. This rule is for the novice reader, okay?)

No ST elevation, so not a STEMI.

2. Is the QRS a normal height?

The heart, over a period of years, responds to hypertension by bulking up and adding muscle mass. This process results in LVH, which, in the long run, isn't good. It shows up on the ECG as deep S-waves in V1 and V2, and high R-waves in V5 and V6.

In the short term, though, it mainly serves to distract us, as it can produce ECG findings that can look a lot like a STEMI. If we look at ECG #1 above, we see ST elevations in leads V2 and V3. Could these represent a STEMI?

Likely no, for several reasons. Now, a lot of the reasons involve interpretation of subtle, qualitative signs - the morphology of the ST segments and T waves, "notching" of the J-point,  reciprocal changes, etc. it just doesn't "look" like a STEMI, but you need to read hundreds of ECGs to feel comfortable with those.

It is far simpler to count the big boxes. Rule #2 boils down 3 sub-steps:

• First, look at the S-waves in V1 and V2. Pick the deepest one, and count the big boxes.
• Next, look at the R-waves in V5 and V6. Pick the highest one, and count the big boxes.
• Last, add those two numbers. If it is over 7 big boxes, the ST elevation is probably due to LVH

7 big boxes equals 35 little boxes, or 35 mm. Count the small boxes if you prefer, or if the you're near the cutoff. Looking at ECG #1 as an example, and counting the little boxes, we find:

So, about 40 mm, or 8 big boxes, so likely not a STEMI.

3. Is the QRS a normal width?

Rule #3 is simple -  If the QRS is over 0.12 seconds long, don't call a STEMI.

Probably the most common cause of dramatic ST elevation is the LBBB, as in ECG #3 above. You can also see the same pattern if the the patient has a pacemaker.

Now, the experienced and sophisticated paramedic knows that there is a way to interpret the LBBB for signs of STEMI, but even the "simplified" rules for determining STEMI in LBBB are somewhat complicated. Many paramedics are familiar with the rule, but the new paramedic shouldn't be expected to make this call. If the patient has a pacemaker, it's even more unreliable to interpret the ECG.

4. Is there ST depression in at least 1 lead?


Rule #4 - if there is no ST depression, do not call a STEMI.

Most students have learned that you should look for reciprocal ST depression in a STEMI. Unfortunately, because of the non-intuitive, non-anatomic way that the ECG is arranged, it isn't clear which leads are "opposite" each other. And the patterns of depression can vary a lot, depending on which coronary artery is occluded. For example, an "inferior" STEMI may or may not have depressions in I and aVL; it depend on whether the culprit artery is the RCA or the obtuse marginal.

A much simpler criterion for reciprocal depression is any ST depression on the ECG. This would eliminate, for example, ECG #2 above. Although the computer interpretation was STEMI, it is a classic example of early repolarization, or possibly pericarditis (less likely, as the ECG did not evolve). Another example from my ED is this ECG:

27 y.o., prior dx of pericarditis

Just like ECG #2, there is diffuse ST elevation without any ST depression. Not a STEMI.

Applying the rule

Let's take another look at ECG #4:

Okay, going through the rules:

• Rule #1 - Over 1 mm of ST elevation is seen in both V1 and V2, which are anatomically contiguous.
• Rule #2 - The S-wave in V1 is about 1 big box deep, while the R-wave in V5 is 3 big boxes high. That's a total of 4, so the QRS height is normal.
• Rule #3 - The QRS looks narrow, about 0.100 seconds wide.
• Rule #4 - There are ST depressions in the lateral leads, most notably in V5.

So we see that this simple 4-step rule, intended to assist the novice paramedic, actually picks up a STEMI that the computer missed!

The Bottom Line

This elegant method of ECG interpretation, although intended for the student, can be very useful for the experienced paramedic as well.