68 y.o. male w/ weakness: conclusion – “Treat the monitor.”

But perhaps not the computer…

Recap of the case:

A patient with CHF, COPD, and diabetes called after falling, apparently due to weakness. Their ECG was recorded by the paramedic: STEMI_or_12-lead


The underlying rhythm is unclear, due to artifact, but there are very wide QRS complexes. The computer measures the QRS as 158 ms, which is clearly wrong. A conservative measurement in V1-V3 suggests a width of at least 200 ms. screenshot801

Such a wide QRS would be unusual for a bundle-branch block, as Dr Stephen Smith has pointed out. Of course, this could be a ventricular rhythm, but the classic sine-wave pattern (best seen in V1, and V5, V6) instead suggests severe hyperkalemia.


On the other hand, there is no bradycardia, there are no “tented” T-waves, and the absence of atrial activity is likely just due to pre-existing atrial fibrillation. But the wide QRS and characteristic QRST morphology overwhelmingly points to hyperkalemia.

Other examples of ECGs of severe hyperkalemia show much the same pattern:

Dr Smith's ECG Blog: "This is a quiz. The ECG is pathognomonic."

Dr Smith’s ECG Blog: “This is a quiz. The ECG is pathognomonic.

Dr Smith's ECG Blog: End-stage Hyper-K

Dr Smith’s ECG Blog: End-stage Hyper-K

Clinical course

The paramedic proceeded to a PCI center that was also “right around the corner,” so she fortunately did not have to make that decision! But she decided against requesting a prehospital activation of the cath lab, despite the computerized interpretation, feeling that hyperkalemia was far more likely. In the ED they repeated the ECG which demonstrated an unchanged pattern.


Same interpretation of *** *** ACUTE MI *** ***

A stat chemistry showed the potassium to be 9.

Treatments were started, and a subsequent ECG showed improvement in the QRS width.

Post-Tx ECG in EDNote, however, that tented T waves are now prominent, and that the more severe signs of hyperkalemia have begun to resolve.The patient was found to be in renal failure, likely due to sepsis from a pulmonary infection, and eventually recovered.

What about the *** MEETS ST ELEVATION MI CRITERIA *** message?

A number of readers suggested that proceeding to the more distant PCI center would be preferable. However, not a single person described the ECG changes that they felt could represent a STEMI on this ECG! While hyperkalemia is infamous for causing STE and STD that mimics ACS, occasionally with tragic results.

In one example from my experience, a patient in DKA presented with a K of 7.5. The ST segments normalized after calcium and insulin, and a subsequent angiogram was negative.


This patient didn’t need a PCI center. They needed calcium first, hopefully from EMS, and likely many grams of it, not just “one box and done.” They then needed insulin, probably fluids, and emergent hemodialysis. (I’m going to leave the sodium bicarbonate and Kayexalate/sodium polystyrene debate for another time…). Almost any hospital can provide these services.

Do not bypass a hospital when your patient has this ECG!

Myths about hyperkalemia

Dave Baumrind and I previously wrote about hyperkalemia, and it deserve re-reading, even if the title seems a bit… dated. In HyperK and Shades of Grey we discussed 4 myths regarding EMS evaluation and treatment of hyperkalemia.

TL;WR? Here’s a summary:

Myth: Dialysis patients tolerate hyperkalemia better than other people. – See more at: http://www.ems12lead.com/2012/12/31/hyperk-and-shades-of-grey-myths-and-facts-about-hyperkalemia-part-i/#sthash.Fbd6aMES.dpuf
  • MYTH: Dialysis patients tolerate hyperkalemia better than other people.
  • MYTH: If the ECG doesn’t show QRS widening, then the patient is at low risk.
  • MYTH: The ECG shows a predictable sequence of changes as the potassium level increases.
  • MYTH: Calcium is a dangerous medication.

Conclusion: Rate Related VS Primary ST-T Changes


This is the conclusion to our previous case, RATE RELATED VS PRIMARY ST-T CHANGES“. Check it out before you read the final portion.


This was the initial 12 lead ECG obtained by EMS prior ED arrival:

Scan_20140922 (5)There is an irregularly irregular tachycardia with no signs of P waves, which the Lifepak 15 determined to be Atrial Fibrillation with Rapid Ventricular Response (RVR), however, V1 also appears to have the presence of Flutter waves, so the possibility of A-flutter is present. There is evidence of subendocardial ischemia, seen as generalized ST segment depression and slight ST segment elevation in aVR. There are also signs of Left Ventricular Hypertrophy (LVH). There is normal frontal axis with good R wave proggression.

Remember there are multiple things that can cause an irregularly irregular rhythm, not just A-Fib, such as:

  • Wandering Atrial Pacemaker
  • Multifocal Atrial Tachycardia
  • A-Flutter with variant conduction
  • Premature impulses

Although this patient presented with Chest Pain and considered unstable by “ACLS guidelines”, no other changes where noted by field personnel, and Syncronized Cardioversion was not performed. This patient was placed on O2 at 15 Lpm via Non-rebreather mask, peripheral IV access obtained and given 324mg ASA.

This was the first 12 lead ECG obtained in the ED:

final ed 1

The ST segment depression is evolving in both precordial leads (V3-6) and frontal plane (limb leads), however the rhythm remains irregularly irregular.


Now, lets get to the main question: Are these primary ST segment changes, meaning, due to ischemia (occlusion/vasospasm), or are these rate related changes?

All of these are possibilities, when we take into consideration, age, medical history, signs and symptoms and other risk factors. Certainly, Left Main Coronary occlusion, Multi-vessel or 3 vesssel diesease and Proximal LAD occlusion, can cause these generalized ST segment changes when there is partial blood flow reduction to all these areas, however, most likely, there is no complete occlusion, as this would lead to infarction causing ST segment elevation over time, and most of these cases do not survive. It is just tough to accurately determine the cause with this rate.

The patient was treated with 20mg Diltiazem followed by 10mg over 1 hr,  .25mg Digoxin followeand a total of 10 mg Morphine for chest pain with overall resolution of both rhythm and pain.

For furhter on Digoxin, click on the link:  Understanding Digoxin

This is the post-treatment 12 lead ECG:

Scan_20140922There is a sinus rhythm with minimal LVH voltage criteria, supported by Left Atrial Enlargement or Abnormality (LAE or LAA). The R wave progression has not changed, but the ST segment depression has resolved.

All Primary ECG changes have resolved after rate reduction and no coronary artery abnormalities were found during angiography.


 Elevated heart rates have been found to increased Myocardial Oxygen Consumption (MvO2) progressing to cardiac ischemia, reducing Cardiac Output, exacerbate other complications such as Congestive Heart Failure and increasing discordant ST segment elevation in LBBBs among other findings.




68 y.o. male with weakness: “Treat the monitor, not the patient?”

A recent graduate of our hospital’s paramedic program brought this case to me. Leigh works for Stratford EMS, an excellent local service in Southwestern Connecticut.

(A quick note on the specific details of the case: This patient did not necessarily come to my hospital. Additionally, several features of the case have been altered; some to preserve anonymity, others to simplify the case. The ECGs and other essential aspects are unchanged.)

The Case:

EMS was dispatched for a 68-year-old male with altered mental status. On arrival, however, they found the gentlemen to be alert but disoriented. Per the patient, his legs just “gave way,” and he fell onto the floor. His family found him 30 minutes later, still on the floor, too weak to stand. They called 911.

PMHx: Atrial fibrillation, COPD, CHF, DM2

Meds: Carvedilol, HCTZ, furosemide, metolazone, spironolactone, warfarin, Januvia, Advair, Spiriva
Vital Signs:

  • HR – 91
  • BP – 134/78
  • RR – 24
  • SaO2 – 93% RA
  • BG – 74 mg/dL (4.1 mmol/L)


  • Gen: Appears ill
  • Skin: No bruises/abrasions
  • Lungs: Diminished bilaterally
  • Cardiac: No gross murmurs
  • Neuro: Weakness bilateral legs


A rhythm strip was obtained:


A 12-lead was obtained:


The *** MEETS ST ELEVATION MI CRITERIA *** notification catches your eye, of course!


The nearest 24/7 PCI center is 20 minutes away, while a smaller community hospital (fibrinolysis only, but has an ICU, etc.) is “just around the corner.” What is your transport destination?

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!