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/QT)-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:

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!

Tuesday, May 8, 2018

Palpitations of unusual etiology

Written by Pendell Meyers, with edits by Steve Smith

A male in his 60s with history of HTN and previous complaint of palpitations but with a negative holter monitor workup, presented to our ED with palpitations for the past hour, associated with lightheadedness and presyncope.

He was hemodynamically stable and well appearing, but was symptomatic with palpitations and lightheadedness.

Here is his 12-lead on arrival:
What do you think?

There is a regular, seemingly wide complex tachycardia at 224 beats per minute. The computer QRS duration is calculated at 178ms, but I believe the true QRS duration is much shorter, and in most leads no greater than 100ms. The QRS morphology is similar to RBBB with LPFB. However, the RBBB morphology in V1 is not the classic rSR' [first wave (r-wave) smaller than the second (R'-wave)]. Instead, the first R-wave in V1 is taller than the second (the R'-wave).  This "sign" has been described as an indicator of ventricular origin. However, the initial deflection of the QRS complex has undeniably rapid and organized (steep slope) conduction, strongly suggesting that the conduction pattern is utilizing the intrinsic conduction system of the Purkinje fibers.

For a QRS complex to have narrow QRS duration, organized initial conduction, and morphology consistent with RBBB + LPFB, it must either:

1) be supraventricular with RBBB and LPFB


2) originate in the left anterior fascicle itself

The differential at this point includes SVT with RBBB and LPFB, anterior fascicular VT, and good old regular VT, all plus or minus hyperkalemia to be safe.

Here are some helpful ECG core content diagrams for review of the differential of a wide complex QRS, as well as tachycardias in general:

Back to the case:

The treating physicians recognized the morphology as likely fascicular VT, and suspected that it may be one of the verapamil sensitive variants. As a review, posterior fascicle VT is thought to be fairly consistently responsive to verapamil; anterior fascicle VT is thought to be a similar entity to posterior fascicle VT but it seems less consistently responsive to verapamil. The working diagnosis of anterior fascicle VT thus prompted consideration of verapamil. Vagal maneuvers and/or trial of adenosine also would have been acceptable choices at this point.

The team first confirmed good LV function with bedside US (this is important before giving verapamil, as it is contraindicated by our guidelines in the setting of structural heart disease and heart failure). They then gave 10 mg verapamil IV. There was no response. They they tried 12 mg adenosine with no response. The patient was then sedated with etomidate and cardioverted with 200J, with immediate return to sinus rhythm.

Here is the post-cardioversion ECG:

This shows sinus rhythm with RBBB. There is no LPFB present on this ECG. So the RBBB seen on the presentation ECG is already present at baseline, however the LPFB was not. This feature does not help distinguish between SVT with RBBB and LPFB vs. fascicular VT originating in the left anterior fascicle, because it is still possible to have a rate-related LPFB in the setting of SVT with preexisting RBBB.

The patient underwent an electrophysiology study, during which Bundle Branch Reentrant Ventricular Tachycardia (BBRVT) was reproduced and successfully ablated. He received an AICD, also underwent a cath showing non obstructive disease and cardiac MRI without abnormalities.

Bundle Branch Reentrant Ventricular Tachycardia is a rare arrhythmia involving components of the infra-His conduction system (including the three fascicles themselves) as necessary components of a reentrant pathway. As you would expect, there are different ways to combine these circuit limbs, all of which would create different reentrant loops and different QRS morphologies.

Tchou and Mehdirad have been credited with describing three categories of BBRVT (see diagram below). Because our patient's QRS morphology includes RBBB and LPFB, this may be consistent with Type B, which appears to use one of the LBB fascicles anterogradely and the other retrogradely to comprise the reentry loop. If the circuit were to progress anterogradely down the LAF and retrogradely up the LPF, it would theoretically have the appearance of RBBB with LPFB, matching our patient.

There are other matching possibilities, however, including Type C with additional rate-related LPFB. At some point, enumerating these possibilities becomes purely academic because they do not have implications for prospective clinical management.

If these reentrant tachycardias are particularly sensitive to any medications, I am not yet aware of it. I cannot find any evidence stating that BBRVTs typically respond to any particular medication with any reliability. The few publications that do comment on pharmacologic therapy in the acute arrhythmic phase seem to agree that pharmacologic therapy is usually ineffective. Because they exist in the conduction system below the AV node, I would not expect that they should respond to AV nodal blockade such as adenosine.

This is in contrast to posterior fascicular VT, which is verapamil responsive, and to right ventricular outflow tract VT, which is responsive to adenosine.

Apparently BBRVT is highly associated with structural heart disease and cardiomyopathy in most cases, but more rarely has been described in the absence of structural heart disease (which our patient seems to fall into, except for his baseline RBBB). This further highlights the importance of considering bedside US for LV function before considering verapamil in these cases.

Image obtained from:

See these other cases of fascicular VT to compare and contrast with this case:

Posterior Fascicle VT
Another Posterior Fascicle VT
Originating in the posterior fascicle, therefore shows morphology of RBBB + LAFB
Usually verapamil sensitive

Anterior Fascicle VT
Originating in the anterior fascicle, therefore shows morphology of RBBB + LPFB
Sometimes verapamil sensitive, somewhat less so than posterior fascicle VT

Right Ventricular Outflow Tract VT
Originating in the RV outflow tract, therefore shows morphology similar to LBBB with inferior frontal plan axis (positive QRS complexes in inferior leads)
Usually adenosine responsive

Unfortunately, as EM physicians we rarely know the exact electrophysiologic diagnosis prospectively. What we can see prospectively is whether the QRS morphology matches one of the established patterns:

RBBB + LAFB Morphology: 
DDx includes classic VT vs. SVT+RBBB+LAFB vs. posterior fascicle VT vs. BBRVT vs. (probably other even more rare and obscure rhythms); if you believe it is one of the ventricular causes but not classic VT, then posterior fascicle VT seems to be one of the most common, and it is typically verapamil sensitive. Electricity works.

RBBB + LPFB Morphology: 
DDx includes classic VT vs. SVT+RBBB+LPFB vs. anterior fascicle VT vs. BBRVT vs. (who knows what else); if you believe it is one of the ventricular causes but not classic VT, then anterior fascicle VT is possible and may be verapamil sensitive, but it may not be; the pharmacologic solutions are unknown in this category. Electricity works.

LBBB + inferior axis (positive in inferior leads) Morphology: 
DDx includes classic VT vs. SVT+LBBB vs. RVOT VT vs. BBRVT vs. (probably others). If you believe it is one of the ventricular causes but not classic VT, then RVOT VT is possible and is typically adenosine sensitive (and adenosine is already indicated for a stable patient with monomorphic wide complex tachycardia). Electricity works.


Bundle Branch Re-entry Ventricular Tachycardia Storm During the Recovery Phase of Transient Complete Heart Block 

Bundle branch reentry ventricular tachycardia.     1995 Jul;18(7):1427-37. 

Learning Points:

For learners, please remember that one should assume classic VT until proven otherwise by a combination of clinical experience with ECG and clinical findings.

With experience and training, one can recognize wide QRS complexes which are likely to represent VT originating within the conduction system itself. Unfortunately, this category still includes a wide variety of arrhythmias which differ in their mechanisms and effective medications. Perhaps the only universal truth is that they are all susceptible to electrical cardioversion.

Posterior fascicle VT is typically thought to respond to verapamil.

Anterior fascicle VT may respond to verapamil, but seems less responsive than posterior fascicle VT.

RVOT is typically thought to respond to adenosine.

BBRVT is a rare arrhythmia which originates inside the ventricular conduction system and acts similarly to other fascicular VTs we have discussed on this blog. However, there do not appear to be any clear patterns of response to pharmacologic therapy.

Sunday, May 6, 2018

Is There a Delayed Activation Wave???

This 50-something otherwise healthy male presented with one hour of epigastric and lower chest pain.

Here is his initial ECG:
What do you think?
The QRS is 90 ms and the QTc is 400 ms.

There is ST Elevation (STE) in II, III, aVF, with reciprocal ST depression in aVL.  There is also ST depression in V2 and V3.  V2 and V3 almost always have some amount of normal ST elevation, and since posterior MI is associated with inferior MI, you must make notice of this and think it is probably an inferior posterior MI.

However, II, III, and aVF have what appear to be J-waves at the end of the QRS.  If these are J-waves, then couldn't the inferior ST elevation be due to early repol?

1. When there is ST depression in aVL, early repol as a cause of inferior STE is VERY unlikely
2.  These do NOT appear to be J-waves.

Instead, these are spikes at the end of the QRS in II, III, and aVF.  There is also an unusual wave at the end of the QRS in I and V6 .

These are what J-waves look like:
This is inferior and lateral early repolarization.
The waves in II, V5, and V6 are typical J-waves.
There is typical slurring of the J-point (end of QRS, beginning of ST segment) in lead III
Note absence of ST depression anywhere.
Note that there is some ST elevation in V2 and V3, which is normal (ST depression in these leads is very abnormal)

So the above first ECG is nearly diagnostic of inferior and posterior MI.

One of our fine interns, Daniel Lee, who is also an ECG whiz, found this paper from 2013 and brought it to my attention:
The delayed activation wave in non-ST-elevation myocardial infarction.  
He also wrote about it in this post:

In this paper, they describe a new "N-wave" in NonSTEMI that helps in determining the infarct artery.   When present, the infarct artery is more likely to be the circumflex.  They do not study whether this wave differentiates between MI and non-MI, between STEMI and NonSTEMI, or between OMI and NOMI.

The N-wave was defined as:
(1) a notch or deflection in the terminal QRS complex of the surface ECG
(2) the height of notch or deflection is at least 2 mm (the point of deflection was measured with reference to the PR segment);
(3) a continuous change of the notch (the point of deflection shifted at least 2 mm with
reference to the PR segment in at least 2 leads within 24 hours, even disappeared or merged with the S-wave) 
(4) with a prolongation of QRS duration in these leads.

Here is an ECG with N-waves, from the article:

Are these N-waves in our ECG?  They do not appear to be wide enough, but they still might be.

Case continued:

The first troponin I returned at 0.087 ng/mL (elevated).  Another ECG was recorded:
Hardly any changed, though the computer now measures the QRS at 116 ms.

Approximately 45 minutes after this, the patient's pain became much worse.  Another ECG was recorded:
Obvious inferior, posterior, lateral STEMI
What is the infarct artery?
This is hard to tell.
Of all inferior STEMI, 85% are due to RCA.
When there is ST depression in lead I, that percentage is higher.

When there is no STE in I, the percentage is lower, maybe 65% (such that the % of circumflex is higher at about 35% rather than 15%)

If these spikes are indeed delayed activation waves, then this feature would further favor the circumflex artery.

The cath lab was activated.

A 100% occlusion on of the circumflex, proximal to the first obtuse marginal, was found, opened, and stented.

This case produces more questions than answers

1. Are "Delayed Activation Waves" a real phenomenon?
2. If so, were the waves in this case actually "Delayed Activation Waves" (N-waves)??
3. Can delayed activation waves be used to differentiate non-ischemic ST elevation from ischemic ST elevation?
4. Can they be used to differentiate OMI from NOMI?

Friday, May 4, 2018

Look at these "T"-waves

An alcoholic presented with confusion.  He had this ECG recorded:
What do you think?
Computer measures the QT at 505 ms, and QTc at 533 ms
The measure appears to be correct.

V3 reminds me of this ECG:

Are These Wellens' Waves??

What is going on?

These waves which you think are T-wave are really very large U-waves.  

The clues are:
1) the down-up morphology
2) the apparent very long QT

The K returned at 2.1 ng/mL.
The pH was 7.55 and bicarb was 47, with chloride less than 68.  The patient has a severe hypokalemic metabolic alkalosis from vomiting.

(By the way, the pCO2 was 55.  An appropriate compensation for metabolic alkalosis is 0.9 x bicarb + 15.  So 47 x 0.9 = 43.  Add 15 and you get an expected pCO2 of 58.  A pCO2 of 55 is just a bit below predicted.) 

The importance of this is:
Anything that increases ventilation (hypoxia, agitation, anxiety) can lead to dangerous alkalemia.  
If the pCO2 were to be lowered to normal (= 40), then the pH would rise to 7.70 (very dangerous).

Here are subsequent ECGs:

This one at K = 2.4
The down up morphology remains
The computer measures the QT at 565 ms, QTc at 591 ms
This measurment also appears to be correct
(except that now we know it is measuring the QU-interval, not the QT)

Large U-waves, with long QU-interval, also puts patients at high risk of polymorphic VT

And 6 hours later at K = 2.6 mEq/L:
Now the apparent T-waves are really T-waves (not U-waves), and the QT is 479, QTc 500

Learning Points:

1. When the QT interval is impossibly long, the "T-waves" are probably U-waves.  In this case, the QT was long, but not impossibly so.  Nevertheless, one should think of U-waves.

2.  When there are down up T-waves, and the apparent QT is long, they are probably U-waves.

3.  Large U-waves are associated with a high risk of VT.  (I will write more on this later)

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