Tuesday, May 29, 2018

Chest pain, Ventricular Paced Rhythm, and a Completely Normal Angiogram 3 Months Prior.

One of our graduates, Rochelle Zarzar, who is now an education fellow, sent me this from one of the hospitals she works at now:

An elderly woman presented with chest pain.  She had been nauseous the night before and did not feel well, then awoke 2 hours prior with chest pain.

She had had a completely normal angiogram 3 months prior.

Here is that angiogram report:
The left main coronary artery is normal.
Left anterior descending is a type 3 vessel and is normal.
Left circumflex is nondominant and normal.

The right coronary artery is dominant and normal.

The nurses immediately recorded an ECG.  This was 2 hours after the onset of CP:
What do you think?


There is a ventricular paced rhythm.  It is unusual in that the QRS is mostly positive in leads V1 and V2.  This suggests that it is a biventricular pacer that is timed to pace both ventricles simultaneously (only one spike).  There is concordant ST depression of at least 1 mm in V3 (+ Sgarbossa), and proportionally excessively discordant ST elevation in I and aVL, with reciprocal concordant ST depression in III and aVF (+ Smith modified Sgarbossa).  

So this is clearly an acute coronary occlusion (Occlusion MI, or OMI).

Remember: all you need for the diagnosis of OMI is for the Smith Modified Sgarbossa to be (+) in just one lead.  

Here it is positive in 3 leads.

They later found the old ECG:
Paced, with (as expected) all appropriately discordant ST segments
The change confirms the ECG diagnosis, which in any case should not be in question.

Rochelle made the diagnosis immediately:
"When they handed me that EKG, all I knew about her was the EKG itself and that she had chest pain, so I immediately called cardiology and activated the cath lab.  When I spoke to cardiology, they acknowledged the ECG changes but still doubted that it was a STEMI since she had a clean cath just 3 months ago.

"They told me to deactivate the cath lab and to check the troponin.  

"Troponin I later returned at 3.0 ng/mL."  

"I also had done a bedside echo in the meantime and I saw a new anterior/lateral wall motion abnormality and a new decrease in her EF (last echo in March showed EF of 55-60%)."  

"I called them back, they agreed that given the elevated troponin, that she should go to the cath lab."  

"Still, they did not want me to order heparin or ticagrelor since they were not convinced and thought maybe this could all be a stress cardiomyopathy." 

Here is the emergent cath report (I am uncertain as to the door to balloon time, or the exact delay to cath):  
· Right dominant coronary artery system
· The left main artery is severely diseased. There was subtotal occlusion with large thrombus in the distal segment of the left main with involvement of the ostia of the LAD, ramus, and LCX.  

Note: "Ramus" refers to "ramus intermedius", which is a variant of anatomy in which there is a large branch between the circumflex and the LAD, usually replacing the first diagonal of the LAD.

The ostium of the large branch off the ramus intermedius also was involved. The distal segments (minimal disease) and RCA (minimal disease) were similar to angiogram performed 3 months prior. 

Thrombectomy and Angiojet were performed into the LAD, ramus, and LCX. Flow was improved but not to TIMI 3. Stand alone PTCA was then performed for each of these segments but also could not restore flow completely. Therefore, stenting with a 3.0 x 20 mm Promus Premier drug eluting stent from the left main coronary artery into the LAD was successfully performed. The flow into the ramus and LCX remained poor, and thus kissing balloon inflations were performed in each of these branches. Additional stenting not performed due to the acuity of presentation and multiple side branch involvement.


The patient's subsequent course was complicated by cardiogenic shock, but she ultimately had a favorable outcome.

Embolism was suspected as the etiology; however, at the time she sent me this, the exact etiology had not been found.

Previous Normal Angiogram

There is little literature on the evaluation of apparent ACS, STEMI, OMI in patients with a previous normal angiogram.  The few studies I found are so small they are barely worth mentioning, except to say that it was rare to have new CAD soon after a totally normal angiogram.

1. Angiograms are "lumenograms."  You cannot see the plaque that is extraluminal, and pathology studies show that the vast majority of plaque is extraluminal.  Therefore, small amounts of luminal narrowing correlate with potentially very large occult plaque that could only be seen with intravascular ultrasound (IVUS) or with CT or MRI.

2. "Normal" was, in the past, used for coronaries with small nonobstructive (e.g., less than 50% stenosis) lesions.
--20-50% lesions progress and are known to fissure/ulcerate
--Over 50% (70%?) may be flow-limiting and correlate with stable angina.  Using fractional flow reserve can identify those who benefit from PCI.

3.  Most Acute MI occurs in plaque that is non-obstructive!  This is in spite of the fact that any given obstructive plaque is more likely to fissure and ulcerate and cause MI than any given non-obstructive plaque.  How is that possible?  Because the prevalence of minor plaque is so high!!  Many people walk around every day with nonobstructive plaque, and often multiple lesions in multiple arteries.  So even if a small percent of these plaques rupture, they result in a lot of acute MI over a population.

4. In the present age, "normal" should only be used for angiograms without any plaque at all.

5. "Non-obstructive" angiogram is often the terminology used when there is plaque, but it is not causing flow limitation (less than 50-70% narrowing).

6.  If the patient had a truly normal angiogram, then at 5 years from angiogram, new coronary disease is unlikely.  But this is based on very small studies.

7.  There are other causes of angina, myocardial infarction, and coronary occlusion [Spasm, "Syndrome X" (coronary endothelial dysfunction of small vessels), emboli, and others].  So, just because there was a truly normal angiogram does not rule out acute coronary occlusion (Occlusion MI, or OMI)

Normal Coronaries in Suspected Acute Coronary Syndrome:

The paragraphs below discuss the situation of patients with apparent MI who then go for an angiogram and it is found to be normal.  

These do NOT discuss the issue of a PREVIOUS normal angiogram in apparent ACS, as above.

Problem: In patients with apparent STEMI (ECG, troponin, echo) but who do not have occlusion on the ECG, and do not have visible thrombus or visible culprit, can there be unseen ruptured plaque that caused thrombus which then lysed?  Or are all these cases due to such entities as spasm, takotsubo, etc.

I called Tim Henry, Chair of Cardiology at Cedars Sinai in LA, and also the founder of the Level 1 STEMI program at Minneapolis Heart Institute (which has managed 7000 STEMI patients since its inception), and co-author of my EKG book.  He says that it would be very rare, but possible, to have a STEMI caused by thrombus from ruptured plaque that does not show a culprit lesion.  

Literature I found

The 4 articles below, about 8% of cases referred for primary angioplasty of STEMI have completely normal coronaries.  Many of these are false positive ECGs, but some are MI with due to spontaneous reperfusion.  If there is spontaneous reperfusion, the ECG will always show typical evolution or resolution.  

This case has an unequivocal ECG; it is clearly STEMI.  In cases in which the ECG is not unequivocal, absence of change over time proves it is not a STEMI.

By the way:
1) Non STEMI but with ST elevation due to non-AMI etiologies (early repol, LVH, etc.) is never documented in these studies.  
2) Furthermore, the mere presence of non-obstructive coronary disease, unless one sees a culprit lesion, does not prove that the symptoms were due to AMI.  
3) Troponin elevation is nonspecific.  Troponin is elevated in acute or chronic myocardial injury that is not MI, and also in type 2 MI).  The previous includes such entities as pulmonary embolism, myocarditis, stress cardiomyopathy, dilated cardiomyopathy, hypertensive cardiomyopathy, and more.  

Coronaries can now be evaluated with other means, such as intravascular ultrasound (IVUS).  Even when there is stenosis, most atherosclerosis is extraluminal.  It can be seen with IVUS, but not with a "lumenogram," which is what an angiogram is.  These atherosclerotic plaques can cause intralumenal thrombosis with STEMI.  If the clot lyses completely, the ischemia resolves and the angiogram may be normal.  This is what Tim Henry says would be rare.

Bibliography, with edited abstracts

There were 821 cath lab activations and 86% were treated by mechanical revascularization. In 76 patients (8.5%), no coronary artery stenosis was documented. Observations documented angiographically included coronary spasms (6.6%) and muscle bridges (5.3%). During a mean follow-up of 11.2±6.4 months, one patient developed an acute myocardial infarction requiring coronary intervention. All other patients were free of any cardiac event.

Article 2, full text

Of 898 patients who had cath lab activations for primary PCI, normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken.   None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain.

Characteristics of 690 consecutive patients with presumed STEMI referred for primary PCI.  87 (13%) had angiographically normal coronary arteries and were compared with patients with angiographically shown culprit lesions (control group; n = 594). Nine patients with significant coronary disease, but no identifiable culprit lesion, were excluded. Electrocardiograms (ECGs) from both groups were reviewed by 2 cardiologists blinded to angiographic findings.  On expert review of ECGs, 55% of patients in the normal coronaries group had ST-elevation criteria for STEMI (vs 93% in the control group, but the ECG was considered consistent with a diagnosis of STEMI by both observers in only 33% (vs 92% in the control group)   Left branch bundle block independently correlated with normal coronary arteries on multivariate analysis (odds ratio for STEMI 0.016).   The discharge diagnosis in the normal coronaries group was predominantly pericarditis (n = 72; 83%), but these were not adjudicated by the authors (Comment: I frankly don't believe it.  Many of these were probably normal variant ECGs).  Other diagnoses were myocarditis in 3 patients (3%), Takotsubo cardiomyopathy in 2 patients (2%), presumed coronary spasm secondary to intravenous drug abuse in 2 patients (2%), cryptogenic AMI in 1 patient (1%), dilated cardiomyopathy in 1 patient (1%), massive pulmonary embolus in 1 patient (1%), cholelithiasis in 1 patient (1%), and pneumonia in 1 patient (1%).

The most likely alternative diagnosis suggested by both observers for the non-AMI ECGs in the normal coronaries group was normal variant ST changes (25% observer 1 and 26% observer 2) and early repolarization abnormality (25% observer 1 and 14% observer 2). 

The medical records of 941 patients undergoing coronary arteriography for presumed ACS within 48h of onset were critically reviewed. In 70 patients (7.4%, 35 males) no CAD was documented. Alternative substrates of acute myocardial ischemia included coronary artery anomalies (7 patients, 10%), coronary spasm (10 patients, 14.3%), spontaneous coronary dissection (2 patients, 2.8%), paradoxical embolism through a patent foramen ovale (4 patients, 5.7%), embolism from left atrium or calcified aortic valve (4 patients, 5.7%), imbalance between oxygen demand and supply (20 patients, 28.5%), mitral valve prolapse (11 patients, 15.7%). No alternative substrates were found in 12 patients (17.1%). Absence of CAD is an uncommon finding in patients undergoing coronary artery angiography for ACS.

Article 5.

Angina with Normal Coronary Arteries (JAMA 2005)

Detailed Analysis & Comments by KEN GRAUER, MD:
Excellent presentation by Dr. Rochelle Zarzar! The interesting feature of this case is documentation of a completely normal angiogram 3 months prior. This situation apparently dissuaded cardiology from the belief that the initial ECG here represented an OMI ( = Occlusion-related acute MI). Presumably, cardiology had an opportunity to view this initial ECG. We are not told if they were also sent a copy of the prior ECG on this patient. Realizing that “hindsight is 100% in the retrospectoscope” — in the interest of academic edification — I’ll go on record saying that cardiology made a big mistake. Sgarbossa and modified Smith-Sgarbossa criteria are indeed helpful — but they are primarily based on relative measurements. By far the most specific indicator of acute infarction in association with QRS widening from underlying LBBB and/or ventricular pacing — is the finding of ST segment elevation that “shouldn’t be there”. Regardless of the fact that the initial ECG in this case is paced — there just should NOT be the shape of ST elevation that we see in not only one, but 2 leads! ( = leads I and aVL) — nor should their be “mirror-image” reciprocal ST depression. There is often a “magic” reciprocal relationship between the ST-T wave in lead III and lead aVL whenever there is acute evolving infarction. This is “mirror-image” reciprocal relationship IS clearly present in this initial ECG, with confirmation that this is indeed REAL by the finding of reciprocal ST depression in the other 2 inferior leads. In an elderly patient who presents with new chest pain — the finding of these 5 abnormal limb lead ST-T wave changes is diagnostic of acute coronary occlusion, without need to first check serum troponin … The 2nd mistake made by cardiology in this case was either not to request the ECG done 3 months earlier (at the time of that normal cath) — or if they did request it, not to realize that despite slight variation in QRS morphology in the earlier paced tracing, and despite nonspecific ST-T wave abnormalities in a number of leads in this earlier tracing — there simply was NO “ST elevation where there should not have been” in the prior tracing. And, there is now ... GREAT case, and compliments to Dr. Zarzar for her excellent presentation!

Sunday, May 27, 2018

Weakness, head trauma, and an abnormal ECG

Written by Pendell Meyers, with edits by Steve Smith

A man in his 50s with history of CAD s/p CABG, CHF, and COPD presented after several falls attributed to acute generalized weakness.  Several had reportedly resulted in head trauma.  There was a normal neurologic exam.

Here is his ECG:

What do you think?

Sinus rhythm at around 60 bpm. There is STD with "down-up" T-waves in V2-V6, or more accurately T-wave inversion followed by large U-waves. The morphology is classic for hypokalemia. The computerized QT interval and QTc were 676ms and 663ms, which is really a measure of the Q-U interval instead of the QT interval. In other words, when the QT interval looks impossibly long, then you should check to see if what you thought was a T-wave is really a U-wave.

This ECG is not consistent with posterior ischemia given the overall morphology and U-waves, however you should remember to include posterior ischemia in your differential of STD that is maximal in V3-V4. More importantly, the patient has generalized weakness and no chest pain, SOB, or clear anginal equivalent.

Intracranial hemorrhage and/or Takotsubo ("stress") cardiomyopathy may present with STD and prolonged QT interval, but this is very different because of the U-waves.

We just presented an abstract discussing our ECG findings in hundreds of ICH cases (traumatic and non traumatic), and prolonged QTc and STD were the findings with the highest correlation to low GCS on arrival and death in this setting. I will be discussing these results in a separate post later.

The potassium returned at 2.6 mEq/L. Magnesium was 1.6 mEq/L. Head CT was negative. Two serial troponins were undetectable. Potassium and magnesium were supplemented, and his dose of diuretic was decreased. He did well.

Here is the patient's post-treatment ECG, with potassium = 3.8 mEq/L several hours prior to the ECG:

Computerized QT and QTc = 464 and 474 ms. There is still a tiny bit of dowsloping STD in V5-V6 with flat/inverted T-wave. This could be baseline, but it would not be possible to tell without a baseline ECG.

Here is the patients prior baseline ECG, two months prior to the presentation ECG:
Almost identical to the post-treatment ECG above.

See more examples to lock in the pattern recognition:

A woman in her 20s with syncope

Are These Wellens' Waves??

Look at These "T"-Waves

Why is this patient weak?

Diabetic Ketoacidosis: is there hypokalemia?

Saturday, May 26, 2018

RBBB and inverted hyperacute T-wave in V3. Do not let negative posterior leads dissuade you!

An elderly male with history of MI 10 years prior called 911 for chest pain.

Here is the prehospital ECG:
What do you think?
Computer only noted RBBB.

There is sinus rhythm with RBBB.  There is a bit of ST elevation in III and aVF, with reciprocal ST depression in aVL.  This is a subtle inferior MI. 

Is there more?

In RBBB, there should be some ST depression in V1-V3, discordant to (in the opposite direction of) the R'-wave.  But unless there is a huge R'-wave (as in RVH), this ST depression should not exceed 1 mm.  And the inverted T-wave should be proportional.

Here there is more than 1 mm of ST depression in lead V2, and the inverted T-wave in V3 is hyperacute.  This is posterior STEMI.

Moreover, look at V6.  There is ST elevation with a hyperacute T-wave (there should never be STE in RBBB!).  This is lateral STEMI, which supports the diagnosis of posterior STEMI.

Frequently, in posterior STEMI, one can see subtle STE in lead V6.

I knew this was an inferior posterior MI, so I activated the cath lab.

We recorded an ED ECG:
There is now more STE in inferior leads.
The inverted hyperacute T-wave in V3 is more pronounced.
The ST depression in V2 and V3 is more profound.
Interestingly, the STE and hyperacute T-wave in V6 are not evident. 

Just for my own interest, I recorded posterior leads.  Unfortunately, that ECG was lost.

But what I want to share with you is that there was no ST elevation in posterior leads!  And this cannot be blamed on reperfusion, because leads V1-V3 were recorded simultaneously with V7-V9,  and they were identical to the above ECG.

Once you have made the diagnosis of posterior MI (with or without associated inferior or lateral MI), you should not believe negative posterior leads.  They are often falsely negative!


Posterior leads are recorded through a lot of impedance of the intervening lungs, and the voltage simply many not be adequate.  It is true that the QRS is also very small in posterior leads, so (as always), proportion is the most important element.  That is why the "criteria" for posterior leads is only 0.5 mm.  However, in this case, there was not even 0.5 mm of STE.

Another ECG was recorded:
It is looking somewhat better.
The T-waves are not as deep in V2 and V3
There is some terminal upright of the T-waves in V2 and V3, typical of reperfusion.

Angiogram report:

Culprit Lesion (s):
99% thrombotic occlusion of the mid-circumflex, which is the culprit lesion for the patient's acute chest pain syndrome
70% in-stent restenosis of the pRCA

Severe disease of the distal/apical LAD

Echo report:

The estimated left ventricular ejection fraction is 40-45 %.
Regional wall motion abnormality - inferior.

Regional wall motion abnormality - lateral.  (remember that posterior (inferobasal) is now called "lateral" in echocardiography)

Post reperfusion ECG:
This is a normal RBBB.

More posts:

Beware confusing the diagnosis of posterior STEMI by using posterior leads...

Thursday, May 24, 2018

ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma

This patient had a head injury and was unconscious.  He was found without respirations or pulse.  Prehospital CPR resulted in ROSC.  He remained comatose.

Here is his initial ED ECG:
What do you think?

There is sinus rhythm at a rate of about 75.  There is ST depression in right precordial leads, with deep T-wave inversions.  This is what catches the eye.

What SHOULD catch your eye?

Whenever there is abnormal repolarization (abnormal ST segments and T-waves), the FIRST thing you should do it look for abnormal depolarization.

In fact, don't even get distracted by ST-T waves!  Even before you look at them, look at the QRS.

Is it normal?  Abnormal?  Is there an abnormal axis?  Abnormal voltage?  Abnormal R-wave progression in precordial leads?   Abnormal Q-waves?  RBBB?  LBBB?  Etc.

You should read the ECG systematically!

Look for:

Rhythm, rate
P waves
PR interval  
QRS Duration (IVCD? RBBB? LBBB? Paced?)
QRS Axis 
Abnormal Q waves
R-wave progression

Only then do you look at:

ST segments
T wave axis (inversion?)
Size of T-waves, whether upright or inverted
QT interval

Only THEN should you look at the ST-T.

But let's be realistic!!

Realistically, our eyes are drawn to the ST-T.  We can't help ourselves.

Therefore, we have to be aware that the ST-T is dependent on the QRS.

In this case, there is a deep S-wave in lead I.  There is right axis deviation.

Whenever there is a right axis, you should think about right ventricular hypertrophy.  (There is also large voltage consistent with LVH.)

How would you verify that??

Look at the R-wave in V1.  If is it abnormally large, you have RVH until proven otherwise.

So I looked for it and, lo and behold, there it is!  A large R-wave in V1.

Now it is useful to know that these ST-T morphologies are CLASSIC for RVH.

I knew immediately that all of this was due to chronic RVH with secondary ST-T abnormalities.  I was not concerned for ischemia at all.

In other words, all these findings were old and had nothing to do with the patient's present condition.

Later, it was confirmed from outside records that this patient has pulmonary hypertension from Eisenmenger's syndrome.


One might think that these are central nervous system T-waves, but they are not.  Here are some examples of CNS T-waves:

Bizarre T-wave Inversions in a Patient without Chest Pain

Here are Ken Grauer's comments:

KEN GRAUER, MD Wrote the Following:
GREAT case — with the most important point emphasized being the need for systematic ECG interpretation. We are not told the age of this patient … — but I’ll presume it is an adult. I would add the following points to those made by Dr. Smith:
  • i) It does not matter which system you use for ECG interpretation — as long as you automatically apply YOUR system to the interpretation of EACH and every ECG that you see. Unless this is done religiously — it is all too easy to miss important findings (as many of you probably did for this ECG …); 
  • ii) Being “systematic” does NOT slow you down. On the contrary, in addition to organizing your thinking and clarifying what you know for certain, and which ECG findings you might be uncertain about — with a little practice, being systematic will dramatically SPEED UP your interpretation — because you will no longer be going back-and-forth repeating your assessment of various findings; 
  • iii) WHATEVER system you use — you must interpret intervals (PR/QRS/QT) early in the process — because if there is a conduction defect (ie, wide QRS) that you fail to recognize, the criteria for assessment of ALL parameters that follow will change; 
  • iv) I favor a system that sequentially assesses 6 key parameters = Rate-Rhythm-Intervals (PR/QRS/QTc)-Axis-Chamber Enlargement-QRST Changes. 
  • v) The purpose of the “R” in QRST Changes, is so that you do not overlook the finding of a dysproportionately tall R wave in lead V1, like we have here. Putting together the findings we have for this ECG — this >10mm tall R wave in lead V1, together with RAD (right axis deviation) and the anterior ST-T wave depression — suggests probable RVH and/or pulmonary hypertension. But this tracing does NOT suggest “pure” RVH — because there is also a surprisingly deep S wave in V1 (which is typically absent with pure RVH), as well as tremendously increased biphasic QRS amplitude (≥50mm) in V2,V3 and V4 ( = Katz-Wachtel phenomenon) — which strongly suggests LVH as well as RVH ( = biventricular hypertrophy).

Saturday, May 19, 2018

A middle aged man with ST depression and a narrow window of opportunity

Written by Pendell Meyers

I received a text at 18:13 of an ECG taken several minutes prior, with no clinical information and only the question "De Winters?"

Here is the ECG:

What would you tell the treating team???

I responded at 18:14 PM:

"I think it's posterior STEMI (OMI) instead of de Winter. Cath lab immediately is indicated."

I clarified further:

"De Winter would need hyperacute T waves (not present here), and would indicate acute occlusion of the territory in the affected leads; so if there was de Winter in anterior leads, that would mean the anterior wall is the one involved. Here we have isolated posterior STD, with no hyperacute T wave, so that's OMI of the posterior wall. Posterior wall may have hyperacute T's if posterior ECG is recorded."

Let's go back in time and see the full case play out.

A middle aged man with HTN, DM, and CAD (with two prior stents) presented for chest pain, shortness of breath, and palpitations that started several hours ago (2-3 hours) while walking his dog. He was triaged at 17:34, had normal vital signs except tachycardia, was not in cardiogenic shock, and had this ECG obtained:

There is atrial fibrillation with rapid ventricular response at about 150bpm. There is massive ST depression in leads V2-V3, with smaller amounts of STD in V4-5, I, II, III, and aVF, with obligatory reciprocal STE in aVR. The J point in V6 is isoelectric (or perhaps even a little elevated), which would be unusual in the case of widespread supply/demand mismatch ischemia because there would normally also be STD in V6; the fact that V6 is isoelectric implies that there is relative STE in this lead.

When there is rapid AF and diffuse STD with elevation in aVR, the differential does include rate-related demand ischemia (supply/demand mismatch), as well as non-occlusive ACS in the setting of three vessel disease or left main disease, as well as OMI.

However, the fact that the STD is so much greater in V2-V3 than the other leads with STD suggests that it is in fact primary STD (posterior elevation) with superimposed widespread STD from supply/demand mismatch in the setting of rapid AF. Additionally, STD in V1 is almost never present in the case of diffuse STD from global supply/demand mismatch ischemia, whereas STD in V1 is commonly present in posterior OMI.

Also, remember that the rule of thumb "STEMI (or OMI) does not produce tachycardia unless the patient is in cardiogenic shock" does not apply to patients who have an arrhythmia which bypasses the normal physiologic determiners of heart rate, such as atrial fibrillation or flutter. Any patient with underlying AF who has an acute severe illness of almost any etiology may have rapid ventricular response due to catecholamine surge or other responses to illness. So this rule of thumb does not apply to our patient in this case.

The treating team was concerned for OMI vs. rapid AF with rate related ischemia, so they very appropriately administered aspirin and IV rate controlling medications over approximately 20 minutes and collected repeat ECGs.

At 18:08, the rhythm changed and the rate decreased to about 110bpm, but the patient complained of ongoing chest pain and dyspnea. Here was the ECG at that time:

The rhythm is not entirely clear because there are not definite P-waves, but it is certainly regular and therefore not atrial fibrillation. Now the diffuse STD is resolved, leaving very focal STD from V1-V5, maximal in V2-V3 consistent with classic, obvious posterior STEMI (a very obvious case of OMI).

The treating physicians saw the focal STD in the anterior leads and were considering posterior STEMI vs. possible de Winter's pattern. They texted me at 18:13 and my opinion was posterior STEMI.

At 18:15 a Code STEMI was called, and the cardiology team responded immediately. Unfortunately they believed that the STD was more likely to be caused by rate-related ischemia from rapid AF. They advised the ED team to give nitrates and cardizem drip.

Because they were not convinced, the ED team performed a posterior EKG while the cardiologists were at beside, approximately 15 minutes after the last ECG:

It appears that leads V2 through V6 have all been moved to a posterior location, though it is unclear exactly where they were placed on the chest, or which leads are supposed to represent V7-V9. Regardless, it is irrelevant because ALL leads show diagnostic STE, confirming posterior STEMI. 

Somehow the cardiologists were still not impressed by this posterior ECG. They cancelled the Code STEMI and asked the ED team to administer nitro drip and let them know what the troponin shows.

At 18:41, the first troponin T (drawn at 17:40) returned significantly elevated at 0.44 ng/mL. The patient had ongoing pain.

Code STEMI was called a second time.

The cardiology team responded and this time agreed to take the patient to the lab. He had a delay of 87 minutes from the first, appropriate Code STEMI (18:15) to arrival in the cath lab at 19:42.

Here is what they found:

Normal RCA.
The left main coronary artery branches into a very small LAD (the vessel going vertically down the image) which has a 50% ostial stenosis, and a LCX which is 100% occluded at the ostium.

Arrows at the site of LCX occlusion.

Another view, showing the relatively small LAD in the upper half of the image, and the empty territory of the occluded LCX in  the lower half.

Arrows show the site of LCX occlusion.

A wire has crossed the ostial LCX lesion and you can now see the large vessels distal to the occlusion.

Arrows show the site of the (prior) LCX occlusion.

The epicardial vessels are now open, revealing an enormous territory supplied by the occluded LCX. As you can see, an Impella (cardiac output assist device) has also been placed, as the patient has gone into cardiogenic shock on the table.

Arrows highlight the territory that had been occluded.

 The patient became progressively more dyspneic, hypoxic, and hypotensive during the procedure, despite opening the artery as shown above. An Impella was placed for assisting cardiac output, and the patient was intubated.

Remember, the angiographic result does not ensure that the actual downstream myocardium is receiving blood supply. Only the clinical symptoms and ECG can show whether there is true reperfusion on a cellular level.

So what do you expect to see on his repeat ECG? You are looking to see if he shows signs of reperfusion vs. "No Reflow Phenomenon" (in which the ECG changes progress as if there was no reperfusion at all, because there is either no reperfusion at the level of the cells, or reperfusion was too late and the infarct is already irreversible). See the diagram below for the patterns of reperfusion vs. continued occlusion.

 Here is the patient's post-intervention ECG:

What do you make of this? Why are the anterior T-waves so big now?

This ECG shows posterolateral reperfusion. The large T-waves in V1-V3 are reciprocal to massive negative reperfusion T-waves in the posterior leads (remember: the diagram above assumes you are looking at leads directly over the site of the infarct). The inverted T-wave in V6 and I is indicative of lateral reperfusion. So this ECG is evidence that the infarct was not yet complete at the time of cath, and that there was truly successful reperfusion on a cellular level as well as the angiographic level.

Despite reperfusion, the patients troponin T peaked at over 32 ng/mL at just under 24 hours from presentation (extremely high troponin, indicative of enormously large territory of infarction). It is impossible to convert this directly to troponin I, however our experience suggests a roughly 10:1 conversion between troponin I:T, so for those of you using contemporary troponin I assays, this patient would be predicted to have a troponin I of over 300 ng/mL.

Unfortunately the patient's course was complicated by acute renal failure requiring dialysis, and the patient ultimately passed away 7 days later of a combination of complications.

It is plausible that he may have had a better outcome if his duration of acute coronary occlusion had been reduced, but we can't know for sure. But we can make sure to learn from his case and deliver reperfusion therapy as rapidly as possible to those with diagnostic ECGs.

Learning Points:

You must advocated for your patients with OMI, because the STEMI guidelines and some current practice patterns do not. Even though this particular case does have STD diagnostic of "posterior STEMI," this is not actually recognized formally as an entity in our current ACC/AHA 2013 STEMI guidelines, despite the fact that it is recognized in other ACC/AHA documents). There are no formal recommendations for posterior STEMI in the 2013 STEMI guidelines, not even millimeter thresholds for STE in V7-V9 as are given in other documents.

Posterior OMI may manifest on the classic 12-lead ECG as STD proportionally maximal in leads V2-V4.

Diffuse supply/demand mismatch ischemia, such as during atrial fibrillation with rapid ventricular response, may manifest widespread STD, but this will usually be proportionally maximal in V4-V6. Additionally, I have never seen a case of widespread STD from supply/demand mismatch with STD in lead V1 (whereas V1 is involved in posterior STEMI). Changes due to diffuse supply/demand mismatch without ACS should resolve within 10-30 minutes of resolution of the condition causing abnormally increased demand.

A delay of even just 1 hour may have been the difference between life and death in some cases such as this. Whether the patient meets STEMI criteria is irrelevant; what matters is whether the patient has an acutely occluded coronary artery that could be opened emergently in order to improve the outcome of acute MI.

The diagnosis of OMI (or STEMI) does not rely on troponin, and should be made based on clinical findings and the ECG if possible. Furthermore, troponin T level of 0.44 ng/mL does not differentiate between early-mid OMI and supply/demand mismatch from rapid atrial fibrillation with underlying structural heart disease. Our troponin assay, for example, usually does not even start to elevate from zero until at least 2-4 hours after onset of acute coronary occlusion. This period of time is in fact the most valuable for the patient, as they have the most at risk but salvageable myocardium. The whole idea of "STEMI" or "OMI" is to prevent the cells affected by acute coronary occlusion from becoming measurable troponin if possible.

The ECG predicts reperfusion on a cellular level better than the angiogram, possibly even better than the patient's symptoms. Without understanding the progression of ECG findings in continued acute occlusion vs. reperfusion, you may not understand whether your patient has had successful intervention, and more importantly you may not know when the patient has re-occluded.

Posterior leads may help convince others of diagnostic STD maximal in V2-V3, but are not mandatory for diagnosis.

Friday, May 11, 2018

A young man with lightheadedness and bradycardia, and an impatient AV node.

A healthy 20 y.o. man presented with lightheadedness. 

There are great comments I've now posted at the bottom from Ken Grauer and Jerry Jones.

The symptoms began about 2 weeks prior and were exertional. He stated that he plays on a college basketball team and he noticed over the previous 2 weeks that every time he exercised with the team he felt lightheaded. 

There was no actual history of syncope. He had had no associated chest pain, shortness of breath or palpitations. He had had no symptoms at rest or associated with positional changes. No history of similar symptoms previously. No history of heart or lung disease. There was no family history heart problems, sudden death, drowning, deafness. He did not take any medications.

Here is his ECG:
What do you think?
The treating physicians diagnosed complete AV block.

There is a narrow complex bradycardia at a rate of about 42.  It is hard to determine if there is a P-wave before the first complex, as that complex is at the edge of the tracing.  

The 2nd complex definitely does NOT have a P-wave in front, nor does the 3rd or 4th.  However, the 5th has a P-wave which is followed very shortly (at less than 120 ms) by a QRS.  The 6th has a slightly longer PR interval, and the 7th and 8th longer still.  

The longest of the PR intervals is the 7th.

What is this rhythm?  Is there AV block?  

No!  At least we see no evidence of block here.  There is no P-wave which does not conduct.  This is AV dissociation.  But not all AV dissociation is due to AV block.  In this case, it is "Isorhythmic Dissociation."  The sinus node and the AV node just happen to be discharging at the same rate, and also coincidentally are happening at about the exact same time.  

The AV node is too impatient to wait for the sinus beat to conduct.

Let's look at it again with annotation:
The P-wave in complex 7 probably conducts (red line is PR interval).
But I cannot prove this!
The black lines in complexes 6 and 8 are exactly the same length as the red line in the 7th.
You can see that the QRS initiates before the end of the black line in 6 and 8.
Thus, the AV node is firing before the impulse from the sinus node had a chance to arrive.
So the AV node was too impatient to wait for AV conduction.

For complexes 2, 3, and 4, the P-wave is hidden in the QRS.
Complex 5 has a preceding P-wave, but the very short PR interval makes it obvious that the QRS fired before that sinus impulse had a chance to conduct.
Beyond rhythm, the ECG is completely normal for a young man, with early repolarization (see classic J-waves in II, aVF, V4-V6)

Could there be AV block?  Yes, it is possible, and we cannot disprove AV block based on this ECG. But we have no reason to think there is AV block.

If the AV node is firing, why are there no retrograde P-waves?  Because the sinus node fires before the impulse from below can reach the atrium.  The ascending impulse from the AV node meets the descending impulse from the sinus node and they block each other.

How could we demonstrate absence of AV block?    Just have the patient do a bit of exercise to increase his sinus rate to a rate faster than the AV node rate.  

Another ECG was recorded later in the ED:
There is a slightly faster sinus rate now, almost 50, and now all P-waves are conducting.
This shows that the J-waves were indeed J-waves, not hidden P-waves

Clinical course:

The patient was admitted because of concern for intermittent complete AV block.

A walk test showed appropriate responsiveness of the sinus node with good AV conduction.

An echo was normal.

Learning Point:

1. Complete AV block is only one etiology of AV dissociation.  Isorhythmic dissociation is another.

2. Isorhythmic Dissociation is a benign condition.

Here is a very nice article on AV dissociation:

Here is a nice article on Isorhythmic Dissociation: http://circ.ahajournals.org/content/circulationaha/42/4/689.full.pdf

Here is a nice example of Isorhythmic Dissociation with a Laddergram:

Here are other examples of Isorhythmic Dissociation:

Sudden weakness with bradycardia and bizarre T-waves

Here are other posts on AV dissociation and AV block

AV Dissociation Lecture by K. Wang (28 minutes)

A Mystery Rhythm, Explained by K. Wang's Ladder Diagram.

Atrial Flutter. What else?? (AV dissociation with block)

Great comments from Jerry Jones and Ken Grauer:


Great case! In my classes I emphasize recognizing the difference between 3rd degree AV block and simple AV dissociation because the implications and the resulting workup and treatments are so different. It's unfortunate how many people interpreting ECGs think 3rd degree AV block is defined by AV dissociation (obviously, it isn't!).

I do take issue with the sentence "There is no P-wave which does not conduct." Actually, there is only one P wave that conducts (the capture beat) and it results in the slightly shorter R-R interval toward the end. I think a better way to phrase the sentence would be that "there is no P wave that failed to conduct that did not have an obvious reason for not conducting." All but one P wave arrives at the AV node or His bundle during the effective refractory period. As you well know, it isn't the AV dissociation that defines 3rd degree AV block - it's the failure of a P wave to conduct when there is no reason for it NOT to have conducted.

This is, indeed, isorhythmic dissociation but it is sometimes referred to as dissociation by interference (the other two types being dissociation by default and by usurpation). What's unusual here is that the atrial rate is slightly faster than the ventricular rate which is a situation typically seen with 3rd degree AV block. You can, however, see this in the interference type of AV dissociation. So the old adage that "if the atrial rate is faster than the ventricular rate, then it must be 3rd degree AV block" is simply not always true.

Thanks for a very informative and educational site.

  1. Hi Jerry. This tracing is even more complex than it at first seems. Although in the 1st ECG, the sinus P wave rate is faster than the junctional escape rate toward the end of the tracing — I believe it most probably was SLOWER before these last few beats in the 1st ECG. Closely comparing QRS morphology of the escape beats to me suggests that a sinus P wave occurs just before onset of the QRS of beat #4; and just after the QRS of beat #3. I think the very slight elevation of the notch at the end of the QRS of beat #2 is due to the occurrence of a sinus P wave, which (if I am correct), would indicate that the sinus rate was indeed SLOWER than the junctional escape rate earlier on in the tracing. Of note — P wave morphology preceding the last beat ( = beat #8) in this 1st ECG is different (ie, flatter) than sinus P waves — which I believe is due to takeover by a low atrial rhythm. I believe this premise is supported by the 2nd ECG, for which P wave morphology in the long lead II is clearly different (flatter and notched) compared to P wave morphology in the 1st ECG for the sinus P waves. So as I suggested in my earlier Comment (from May 12) — I think the underlying rhythm in this case is marked sinus bradycardia + sinus arrhythmia — which results in switch of the pacemaker site between EITHER an AV nodal escape focus at 42/minute OR a low atrial escape. What remains to be shown (stated, but not documented in the initial presentation) — is whether there will or will not be an appropriate response to exercise in this previously healthy 20-year old who did present with exertional symptoms of “lightheadedness” (which of course is not “normal” for a 20-year old). THANKS as always for your insightful comments! I thought this was a GREAT case for discussion!

Hi Ken! Always great to hear from you and get your input. I agree that this is a very complex tracing but I want to avoid reading too much into it. I think you are absolutely correct in that this is a sinus brady with sinus arrhythmia that has been usurped by a junctional pacemaker, most likely arising in the His bundle rather than the AV node or NH transition. While a focal ectopic atrial tachycardia is not that uncommon, an atrial escape rhythm is very, very uncommon - mainly because whatever (probably parasympathetic input) is causing the sinus brady almost always has the same effect on the areas of the atria with escape pacemaker activity. A junctional pacemaker in the His bundle would be affected very little - if at all. Regarding the conduction of the sinus (or atrial) impulses, after reviewing the first tracing again, I think there is a very strong argument that only the last two P waves conducted and they may even be P' waves (certainly the last one is, as you pointed out). I don't think the 3rd-from-last P wave conducted because - using my calipers - the QRS that follows it is right on time for the junctional escape rhythm. Plus, even though the PR interval is 0.20 seconds, that is not enough time for this AV node to conduct. The last two PR intervals are visibly longer than 0.20 seconds and so are the PR intervals in the final ECG. There are two kinds of "normal" PR intervals: the textbook normal (0.12 - 0.20 sec) and then whatever is "normal" for the patient. The last two QRS complexes are definitely out of sync with the junctional rhythm, so I think they were conducted. To say the 3rd-from-last QRS conducted, one would have to rely on coincidence and I always try to avoid invoking magic, divine intervention and coincidence as an explanation for a dysrhythmia. Admittedly, this can be difficult at times!

Hi Jerry. Thanks for your additional comment. Just to clarify — I never said (or meant to imply) that beat #5 was conducted — on the contrary, NOT only the shorter PR interval, but also the different QRS shape of this beat #5 (compared to beat #6 which IS conducted, and which manifests a shorter R wave) indicates that beat #5 is NOT being conducted. My point was simply that as uncommon as atrial escape rhythm might be in this setting — the change in P wave shape for this last beat (beat #8) in ECG #1, together with this same different (smaller, notched) P wave shape for each of the beats that are conducted in the 2nd tracing to me suggested that in addition to junctional escape — there was also an atrial escape rhythm occurring. As I believe we both believe — more monitoring would be needed to clarify this — and the clinical relevance of what we see will only be determined once we can determine if there is or is not an appropriate response to exercise in this previously healthy 20-year old who did present with exertional symptoms of “lightheadedness”. THANKS as always for your thoughts!

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