Rate Related VS. Primary ST-T Changes:

A 56 year old black male presents to the Emergency Department via EMS, complaining of Chest Pressure, 10/10 pain scale. Pain started suddenly following sudden onset of palpitations, while mowing his lawn. All approximately 5 minutes prior calling EMS. Keep in mind, it was a hot and sunny day with temperature in the 90′s. He advised of prior episodes of chest pressure but never as severe as today’s episode. The pressure is generalized throughout his chest, and nothing seems to make it better.


  • Patent airway
  • Adequate ventilation with regular and equal chest expansion
  • Strong, irregular radial pulses with skin pink, warm and diaphoretic


  • Heart Rate: 206 beats/min
  • Respiratory Rate: 22 breaths/min
  • Non-invasive Arterial Blood Pressure: 141/102
  • SpO2: 98% on 3 lpm
  • Blood Glucose: 102 mg/dL


  • Hypertension (compliant)
  • Non-smoker, occasional alcohol consumption


EMS obtains the following 12 Lead ECG and transmitted to the ED:



Upon arrival to the ED, the following 12 Lead ECG was obtained:

Scan_20140918 (2)

What is your detailed 12 Lead ECG interpretation?

What is your course of treatment?

Do you think this patient requires Cath Lab activation?


The 360 Degree Heart – Part I

The hexaxial reference system.

If I asked you to imagine how the limb leads “look” at the heart, you would probably picture something like the image below:

Heart drawing courtesy of Dawn Altman from the ECG Guru website.

Notice those gaps in the limb leads? They don’t really exist. They’re an illusion.

This isn’t something that is commonly emphasized when the cardiac axis is being taught, but it’s absolutely vital to realize that in addition to each “positive” lead seen above, there is a corresponding “negative” lead in the opposite direction. These “negative” leads, which I denote with a (-) symbol, are literally nothing more than the original lead from the standard 12-lead ECG flipped upside down.

Mapped on the above hexaxial reference system we now have the coverage shown below:

Negatives + Segments


Now, in theory,  we have a full 360-degree view of the heart in the frontal plane. But how does this work in real life? Consider the 12-lead ECG below showing infero-posterior STEMI:

Infero-posterior STEMI

Infero-posterior STEMI


All we really care about for this discussion is the limb leads, so let’s focus on them and ignore the rest of the tracing:

1202 - EKG Crop


This is what it would look like if we arranged the limb leads as displayed in the first diagram:

1202 - Basic + EKG


Notice how there’s a gap between leads I and II? Also, aVR seems way out in right field, not connected to any of the other leads. Now we’re going to include the negative versions of each limb lead:

1202 - Full + EKG

Quite literally all I did was flip each complex displayed above so that it was the exact negative of what we originally saw. Then I displayed the inverted complex 180 degrees (directly opposite) its original position.

The above representation contains no more information that we see with the six standard limb leads, but it looks like we’ve doubled the amount of leads available. This is part of the beauty of the hexaxial reference system that doesn’t get emphasized enough.

Take a few minutes to appreciate how there is now a nice, smooth progression of the QRS complexes as you travel clockwise around the circle. Really, please do this:

Starting arbitrarily at lead I (it helps that it’s the most positive QRS complex), follow the circle clockwise. Appreciate how the QRS complex decreases in size as you go from (-)aVR to II to aVF to III to (-)aVL. Then, when you reach (-)I, the QRS is now at its most negative point. Continuing clockwise, the QRS complex now begins to gain amplitude until you end up back at lead I again.

Next, investigate the T-wave. Begin this time at lead III, where it is at its tallest. Like the QRS complex, as you travel clockwise the T-wave becomes more and more inverted until reaching its most negative point at (-)III. Continuing clockwise, it begins to gain size again until we arrive back at lead III.

Finally, can you guess how the ST-segment behaves?

Since this is a classic inferior STEMI from an RCA occlusion, the ST-elevation is maximal in lead III. Since it doesn’t matter which direction we go, let’s go counter-clockwise this time, starting again at lead III. Follow as the amount of ST-elevation decreases across leads aVF, II, and (-)aVR and turns into ST-depression. This is how reciprocal ST-depression works! It’s not due to “lateral ischemia,” but rather just the mirror image of the ST-elevation centered around lead III.

While we’re at it, can you appreciate why aVL is the best lead for seeing reciprocal changes in inferior STEMI? In reality (-)III shows more ST-depression, but on the standard 12-lead aVL is the only lead that comes close to approximating (-)III, so that’s why we always look there for reciprocal ST/T-wave changes.

As a final exercise, see if you can appreciate how even the P-wave shows the same circular evolution.

I’ll be posting more on this topic over the coming weeks, but I just wanted to offer an initial understanding of what I’ll be getting into. I hope this helps, and if you have any questions please let me know in the comments.





Conclusion: “And then I gave her a NTG…”


From  Part 1: A 64 y.o. woman with typical symptoms of ACS was given nitroglycerin by the paramedic. Her ECG:


ECG Interpretation:
As noted by many of our astute readers, there is obvious ST-segment elevation (STE) in leads III and aVF. Lead II doesn’t show much STE, but relative to the small R wave it is striking. Reciprocal ST-segment depression (STD) is seen in leads I and aVL. This all points to an inferior-wall STEMI.

Because the STE in lead III >> STE in lead II, and given the prominent STD in lead I, the RCA is the most likely infarct-related artery. The T-wave inversion and STD in V2 suggest that the affected myocardum extends posteriorly. Contrast that with the isoelectric ST segment in V1 – this is a pattern found in right ventricular infarcts. It is estimated that up to about half of inferior MIs involve the RV.

Lead V4 in the second 12-lead is labeled as V4R, indicating that it was placed in the 5th intercostal space, midclavicular line, on the right side of the chest. STE in this lead is very specific for an MI involving the right ventricular wall, and confirms the initial suspicion.

So what happened after NTG was given?

She felt better!

In fact, she ended up getting a total of three doses of NTG from EMS, after getting a prophylactic 250 ml fluid bolus. Her pain came down to a “3/10,” while her BP actually increased, going up to 152/103. The medic had called in the STEMI after the first 12-lead, and she was immediately taken to the cath lab, where a right coronary artery occlusion was stented open. She recovered nicely, and will likely be back to Zumba-ing soon.

But nitro supposed to be bad in RV infarct, right?
As noted by numerous readers, the conventional physiologic understanding is that:

  • Up to 50% of inferior STEMIs also have ischemia/infarct of the RV
  • Ischemia of the RV produces acute “stunning,” or akinesis.
  • The loss of RV pumping makes the cardiac output exquisitely “preload-dependent.”
  • NTG, since it increases venous dilation, will reduce preload.
  • In turn, this can dramatically drop the cardiac output.

Based on these physiologic principles, both ACLS (free) and UpToDate (paywall!) warn against using NTG in patients with inferior MIs, and prohibit NTG use in confirmed RV infarct. However, neither source offers any references to support this.

In fact, I could only dig up one study that looked at the clinical outcomes in patients with RV MIs who received NTG.

The one study that showed NTG in RV MI causes hypotension
This was a retrospective study from 1989. The authors reviewed the charts of 405 patients admitted with MI, and looked at the 172 with an inferior MI. Of those patients, 38 had evidence of RV infarct, but complete records were available for 28 patients. (see figure below).

Reviewing the records it appeared that 20 (71%) patients developed hypotension “shortly after the administration of nitrates.”


Of course, this study has many shortcomings.

  • First of all, it was a retrospective chart review, with vague methods.
  • There was a lot of missing data!
  • Also, it only examined a pretty small number of patients.
  • Lastly, it only looked at inferior MIs, so we have no idea from this study what the rate of post-NTG hypotension is in anterior or lateral STEMIs. Higher, lower – no idea.

One BIG point – Contrary to the prediction offered by multiple commentators, however, none of these patients had a cardiac arrest associated with NTG!


So what does more recent evidence suggest?

Not every case of RV STEMI is sensitive to NTG.

A recent case report described the case of a patient with a clear isolated RV STEMI that presented with a blood pressure of 194/104. The right-sided leads were pretty diagnostic:


Despite this dramatic example of a RVMI, a “routine dose” of a NTG infusion did not produce hypotension. The authors conclude that “Not all patients with RVMI are hypersensitive to nitroglycerin.”

No difference in rates of post-NTG hypotension in inferior VS anterior/lateral STEMIs!

That case report may not be as unusual as the authors suggest! EMS researchers in Montreal were unable to find a difference in the rates of post-NTG hypotension between inferior STEMIs and non-inferior STEMIs. They looked at a total of 798 STEMIs that got NTG in the field. Both inferior and “non-inferior” STEMIs had about 8% rate post-MTG hypotension.

There were 461 patients with inferior STEMI in the study. Presumably, up to half of those (230) had a concurrent RVMI, and yet only 36 had post-NTG hypotension. This looks very different from the results from the 1989 study!

Patients without ACS often develop dramatic post-NTG hypotension

There are plenty of reports of patients developing hypotension after getting NTG, but who were NOT having an MI.

In a 1990 case report, a 36 y.o. male with chest pain received 2 NTG tabs. Despite an intially normal ECG, he dropped his BP down to 77/40, and developed a brief brady-asystole (figure below).  He recovered spontaneously, and ruled-out for ACS.

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

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

Lastly, I had my own experience with an elderly patient with epigastric pain, who developed profound bradycardia and hypotension after I personally gave her NTG. She quickly recovered, and had negative troponins.

The Bottom Line

Did I already mention that I’m not your medical director? If your protocols say “Don’t give nitro in inferior STEMI,” well, don’t do that!

But if give NTG to a patient with an initially negative ECG, and it turns out to be an inferior, you probably didn’t just cheat the reaper. And if your patient gets hypotensive after NTG, it doesn’t mean that you missed a RVMI!



64 y.o. Female with CP – “And then I gave her a NTG…”

My apologies for the faded ECGs. Turns out the medic (a recent grad from our hospital’s program) had been carrying them in his work pants for over a week, waiting to catch me in the ED. The  patient had been brought to another hospital, but he wanted to review the ECGs with me.

They had been called for a 64 year-old woman at a gym, who had been getting ready for her Zumba class. She described an abrupt onset of precordial chest pressure, 8/10, that radiated to the jaw and left arm. Of note, the Zumba instructor insisted “We hadn’t even started the class!”

  • PMHx: HTN, but no CAD.
  • Meds: ASA daily, Prevacid

Vital signs:

  • HR – 70
  • RR – 20
  • BP 150/84
  • SaO2 – 98% RA

Aside from mild sweating, the exam was unrevealing. A rhythm strip was obtained:


And then a 12-lead:


And then a second ECG, with nonstandard lead placement as noted:


At this point, the medic gave a sublingual dose of nitroglycerin.


Clearly, this is a STEMI. What coronary artery is probably involved, and what areas of the heart are likely affected?

What do you think happens next?

Conclusion to 80 Year Old Male: Fall

This is the conclusion to 80 Year Old Male: Fall. If you do not remember the particulars, check out the original post and then come back here to find the “answer” and summary.

Case Review

You arrived on scene to meet an 80 year old patient who was found on the floor after suffering what he described as a “trip and fall.” He had severe hip pain and for the most part presented as a straightforward hip fracture, plus or minus some ill effects of being on the ground for 48 hours. Worryingly, however, he could not describe the exact circumstances of how he ended up on the ground.

This should have immediately alerted you that he may have experienced syncope, not a mechanical fall. In fact, even elderly patients who can vividly describe how and why they fell should be screened for possible syncope. Even if it’s not intentional, the brain is good at filling gaps in information to form a cohesive story—especially if the patient doesn’t want to make a big deal about their fall in the first place.

Regardless of your reasoning, an EKG was performed, shown again below and annotated with a ladder diagram.

80yo M - Fall - Laddergram

This ECG shows:

  • Sinus rhythm at 84 bpm (fairly regular, evenly spaced P-waves of normal morphology)
  • Prolonged PR-interval (PR-interval is about 220 ms)
  • Type II AV-block (see below)
  • Effective ventricular rate of 52 bpm
  • Right bundle branch block (QRS is about 140 ms wide; qR wave in V1; tall, narrow R-wave with shallow, wide S-wave in lead I and V6)
  • Left anterior fascicular block (mean QRS axis approx. -45 degrees (left axis deviation), rS waves in III and aVF, tiny initial q-waves in I and aVL)
  • Bifascicular block (RBBB + LAFB)
  • Left atrial abnormality (total P-wave duration of 120 ms (> 110 ms), terminal P-wave deflection in V1 of 80 ms (> 40 ms).

The most important finding here is the type II AV-block, often termed “second degree, type II” or “Mobitz II.” This finding greatly increases our suspicion that the reason the patient ended up on the floor because he experienced syncope secondary to an arrhythmia, not because he tripped.

Type II AV-block is most often associated with disease of the cardiac conduction system below the bundle of His, especially when it is associated with a bundle branch block. In this case, in addition to a simple RBBB, there is also evidence of impaired conduction in the left anterior fascicle, the combination of which is known as a bifascicular block.

There is also a slightly prolonged PR-interval that technically qualifies as first degree AV-block. When this is added to a bifascicular block some folks like to call it a “trifascicular block,” but this author does not use that term unless the PR-interval is markedly elongated. The overall picture is suggestive of extensive conduction system disease, so a bit of PR-prolongation is probably expected and usually seen in this setting. Also, “trifascicular block” is needlessly dramatic.

Assuming no contraindications and a decent chance for recovery from his hip surgery, the ECG suggests this a patient who will need a permanent pacemaker placed.

Prehospital Management

I’ve given this its own section because there was a bit of disagreement in the comments of the original case for how this patient should be managed. Here are my thoughts…

Starting with an easy issue, this patient is not significantly hypothermic. Though most modern oral thermometers aren’t very trustworthy when you get readings of 36.4 C or below, this is good enough for a start on this patient. The fact that a reading was obtained at all suggests this patient is not moderately or severely hypothermia. Definitions vary, but this temperature is not nearly low enough to account for the patient’s arrhythmia. Also, some suggested the presence of Osborn waves, but those are decidedly absent here. I think folks were confused by the RBBB. The only treatment necessary for this patient’s slightly low body temperature is the application of a blanket or two.

Next, the issue of the arrhythmia. Although it was probably related to his fall (likely secondary to syncope), the patient is experiencing no ill effects at the moment. His ventricular rate is reasonable and he has described no other incidents of syncope nor present symptoms. His blood pressure is elevated and his mentation is appropriate. There is no prehospital treatment indicated at this time. In all likelihood he will be admitted for a non-emergent implanted pacemaker in a day or two before hip surgery as long as the situation doesn’t change. Cardiologists don’t get excited about this EKG’s, and there is certainly no role for transcutaneous pacing at this point as the patient is stable and the block not pervasive.

It is likely the patient has experienced some acute kidney injury, if not secondary to rhabdomyolysis then at least secondary to dehydration. An IV with a normal saline bolus at a slow to moderate rate would be indicated. There is no reason to flood the patient with fluids prehospitally; you’re not going to make a huge difference in his kidney injury during a short transport and lab results from the ED will be able to better guide therapy.

Finally, let’s address the most debated point of this case: whether or not to administer opioid analgesics.

Opioids are not contraindicated in AV-block!

While very large doses—like those used in cardiac anesthesia—may be associated with sinus bradycardia (through a couple of different mechanisms), and there is a possibility of AV-block with toxic doses, the normal doses used for acute pain in the emergency setting will not affect this patient’s heart block significantly. Though there could be some minor slowing of the sinus rate due to reduction of the patient’s sympathetic response to pain; morphine, hydromorphone, or fentanyl will NOT worsen AV-block.

That said, this is an elderly patient with dehydration and decreased renal function; I would suggest titrating his dose of opioid up slowly. He’s going to be susceptible to the direct histamine release characteristic of the class (namely hypotension), though the effects seen with fentanyl and hydromorphone are low compared to morphine. Still, his vasculature is relatively depleted so any vasodilation is more likely to result in significant hypotension than we would see in an otherwise healthy patient—even if the effects are supposed to be “minimal.”


In this case the patient received IV hydromorphone for his pain, was admitted for pacemaker placement the next day, and received his new hip soon after that. He experienced no lingering complications from his stay except for slightly decreased renal function and was discharged to rehab in good condition.


“Bad heartburn” – Conclusion


In “Bad Heartburn” – 82 y.o. female without chest pain, the paramedic had obtained an ECG on an elderly woman who only complained of mild “heartburn.” An initial ECG was obtained:

STE in II, III, aVF, STD in aVL and V2-V4. Also, the T wave is fully inverted in V2 and V3.

ECG interpretation :

The degree of ST elevation is significantly higher in lead II than lead II, which usually supports an RCA occlusion. Furthermore, there is mild ST depression in lead I, also typical for RCA occlusion. There is apparent sinus arrest, with a junctional escape rhythm, which suggests that the SA nodal artery (usually a branch off the RV) is involved.

The ST depression and T wave inversion in V2 and V3 suggest an acute posterior infarct.

Grauer's "mirror test" suggests acute posterion MI.

Grauer’s “mirror test” suggests acute posterion MI.

The “classic” pattern of high R waves and upright T waves is actually not representative of acute occlusion – for more on this, read this discussion on old versus “new” teaching on recognizing posterior MIs. We do not see ST elevation in aVR or V1 that would suggest a concomitant RV infarct, however.

Patient Course:

Although the protocols did not require a computerized interpretation to verify a STEMI, the absence of “typical” ischemic symptoms made a prehospital cath lab activation modestly more difficult to justify. Since the computer interpretation algorithms may miss a STEMI up to half of the time, the medic obtained a second tracing less than a minute later:


Ah, that makes more sense…

The ED was contacted while EMS was still on scene, and medical direction quickly agreed with alerting the cath lab, despite the atypical symptoms. As noted before, ASA was given, but NTG was withheld. Ten minutes later, during transport, the medic shot a repeat ECG with V4R.


No STE in V4R, which suggests against an RV infarct.

The patient stayed in the ED for 10 minutes while the cath team was assembling, and a repeat ECG was obtained.

screenshot743Angiography results:

A complete occlusion of a LEFT-dominant circumflex was found during PCI, and was successfully stented. A transvenous pacer was placed, but was used only for a brief period. The patient recovered well.

Some discussion points:

1. You will miss STEMIs in the elderly unless you do them on practically everyone.

A study conducted in an ED found that, in patients over the age of 79, you should get an ECG on any patient with chest pain, dyspnea, altered mental status, upper extremity pain, weakness, syncope, nausea/vomiting, or abdominal pain. And even then they missed a bunch of STEMIs!


2. The computer interpretation can be falsely negative.

In a recent study using Lifepak-12 monitors, the computer only diagnosed a STEMI in 58% of the cases, while another study found that the computer got 69% of the STEMIs. Despite the high quality of the first tracing (no artifact or baseline wander), the computer missed an ECG pattern that most medic students would recognize after their first day of cardiology class!

3. Nitroglycerin probably would have been fine, but it likely isn’t worth the bother.

Aspirin therapy, fibrinolysis, and percutaneous coronary angiography have all been demonstrated to reduce mortality. Nitroglycerin, despite an appealing rationale, has not been shown save lives. Reduction of discomfort should be a goal of EMS, of course, but there isn’t much evidence that nitro does much more than that.

Okay, but what if a medic elected to give a tab or 2 of NTG to this patient – would this be harmful? Despite the standard teaching that RV MI must be ruled out before giving nitro to a patient with an inferior MI, the current data is reassuring.

I go over this in more depth in my post “Nitroglycerin – Old and New: Pt 2“, but the boiled-down version is:

 The Bottom Line

Although computers are pretty good at playing chess, they aren’t always right about STEMI diagnosis. Be very suspicious of atypical symptoms, and grab an ECG. And whether or not you give NTG, this patient needs emergent reperfusion!