Wednesday, October 16, 2019

What could this rhythm be? And what is going on after it breaks?

Written by Pendell Meyers, edits by Steve Smith


A man in his 30s with no prior medical history presented with palpitations. His vitals and exam were within normal limits with the exception of his heart rate.

Here is his initial ECG:
What do you think? What is the differential?




This shows a regular narrow complex tachycardia, thus the differential is sinus tach, SVT (including AVNRT most commonly, AVRT [which is SVT in the setting of WPW with an accessory pathway] next most common, then atrial tachycardia, etc.) or atrial flutter.

It it were atrial flutter, and because it is regular at a rate of 210, the flutter would have to be conducting 1:1 to the ventricle. There are no definite atrial waves, although the negative deflections in V1 before the QRS complexes could be atrial in origin, or the entire baseline may appear to have a sawtooth pattern in lead II - it is not clear in my opinion. 1:1 atrial flutter seems unlikely because, as it would have to be 1:1 conduction, the atrial flutter rate would have to be a very slow 210 bpm (normal would be 300). The ventricular rate of roughly 210 bpm makes sinus tachycardia unlikely in a 30 year old (max sinus rate theoretically 190ish according to 220-Age rule of thumb).

Aside: if the atrial flutter rate were 300 bpm, it could not be conducted by the AV node, and the ventricular rate could only be 300 if there were an accessory pathway or a peri-AV node bypass tract that inserts into the bundle of His. In the former case, there would have to be a wide QRS (due to the preexcitation of the delta wave), but in the latter case, the QRS would be narrow.



The REVERT vagal maneuver was performed with a change in rhythm.


A repeat ECG was performed:

What do you think?





There is now a regular rhythm with wider QRS complexes than during the tachycardia above, almost imitating LBBB. There is an extremely short PR interval, such that the wide QRS takes off from the end of the P-wave. The takeoff of the QRS complex is not the most obvious delta wave, but overall this appears consistent with accessory pathway conduction, or WPW.

See these two similar cases:

A 40-something woman with no medical history presented with 2 days of chest pain





Now that we suspect the patient has an accessory pathway, the most likely rhythm responsible for his paroxysmal narrow complex regular tachycardia in the first ECG is orthodromic AVRT, in which the action potential is conducted down the AV node (causing a narrow QRS complex) and then up the bypass tract, and so on.


The patient was referred to EP for an EP study and possible ablation.


Learning Points:

You must easily be able to think through the differential of tachycardias based on the categories of narrow vs. wide QRS and regular vs. irregular rhythm:
 - Narrow & Regular
 - Narrow & Irregular
 - Wide & Regular
 - Wide & Irregular

After conversion from a regular, narrow complex tachycardia, you should always obtain a post-cardioversion ECG to look for the presence of underlying causes of the tachycardia, most commonly WPW syndrome.

WPW can distort the QRS complex and mimic bundle branch blocks or other conduction abnormalities, without showing the classic delta wave into an otherwise normal, narrow QRS complex. The risk in this case is that WPW is missed due to the confusing QRS morphology.

Some bypass tracts are "concealed" meaning they do not conduct during normal sinus rhythm and thus leave no evidence on the resting sinus ECG.



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MY Comment by KEN GRAUER, MD (10/16/2019):
===================================
Excellent case for discussion presented by Drs. Meyers & Smith! I would add the following comments regarding selected concepts of arrhythmia diagnosis and management:

Use a Systematic Approach: There are KEY parameters to assess when confronted with any cardiac arrhythmia. These 6 parameters are:
  • #1) Is the patient hemodynamically stable? This clearly is the 1st thing to assess — since if the patient is not hemodynamically stable because of the arrhythmia — then immediate cardioversion is indicated regardless of whether one is dealing with VT or an SVT.
The Next 5 Parameters constitute what needs to be assessed regarding the arrhythmia itself. I find it easiest to remember these parameters by the saying, Watch your Ps, Qs and the 3 Rs”:
  • Are there P waves? And, if there aren’t clearly identifiable P waves — Is there evidence of atrial activity, such as “fib” or “flutter” waves?
  • Is the QRS complex wide or narrow?
  • What is the Rate?
  • Is the rhythm Regular?
  • If P waves are present — Are they Related” to neighboring QRS complexes?
  • CLICK HERE if interested in more on using the “Ps, Qs & 3Rs” Approach.

Figure-1: The 2 ECGs in this case (See text).



Assessing the 6 Parameters in This Case:
For clarity — I’ve put the 2 tracings in this case together in Figure-1. Although there is some angulation of these tracings — measurements are intact.
  • Regarding the 6 Parameters: The patient in this case was symptomatic with “palpitations” — but this man in his 30s was hemodynamically stable with normal vital signs other than a fast heart rate.
  • Normal sinus P waves (ie, upright P waves in lead II) are not seen. There may be 1:1 retrograde activity (RED arrows in ECG #1) — but if these sharper-than-expected deflections do reflect retrograde atrial activity — the RP’ interval would be relatively long (occurring well within the ST segment). RP’ intervals occurring well within the ST segment are too long to be consistent with AVNRT — but could be consistent with anterograde AVRT (since it takes more time for retrograde conduction over an accessory pathway that lies further away, because it is outside of the AV node).
  • The QRS complex is narrow (ie, clearly not more than half a large box in duration in any of the 12 leads in ECG #1).
  • The 3 Rs: The ventricular rhythm is extremely Regular — the Rate is ~210/minute — and although no sinus P waves are present, P waves could be Related” to neighboring QRS complexes by 1:1 retrograde = VA conduction.
CONCLUSION: The patient is hemodynamically stable. The rhythm in ECG #1 is a regular SVT (SupraVentricular Tachycardia) at ~210/minute without clear sign of sinus P waves. As mentioned, there may be 1:1 retrograde atrial conduction — but it is difficult to be certain about this from ECG #1. As per Dr. Meyers — the principal differential diagnosis of a regular SVT without clear sign of sinus P waves includes: i) Sinus Tachycardiaii) Reentry SVT (either AVNRT if the reentry circuit is contained within the normal AV nodal pathway — or AVRT if an accessory pathway is involved)iii) Atrial Tachycardiaor iv) Atrial Flutter.

NOTE: It is worth spending a moment on how we determined the heart Rate — since accurate estimation of rate can sometimes be extremely helpful in determining which of the above diagnostic considerations is the most likely cause of a regular SVT rhythm.
  • When the rhythm is fast and regular — the Every-Other-Beat Method allows rapid and accurate rate estimation. Find a QRS complex that begins on a heavy line. We chose the 2nd beat in lead I (See the 1st vertical RED line under this beat in lead I of ECG #1).
  • The amount of time (ie, the R-R interval) that it takes to record 2 beats (BLUE numbers in lead II) is just under 3 large boxes (RED numbers in lead I). Therefore — HALF the rate is a little faster than 300/3 ~105/minute.
  • The actual rate for the rhythm in ECG #1 is therefore ~105 X 2 = 210/minute.
  • CLICK HERE if interested in brief video review of this Every-Other-Beat Method.

How Heart Rate Helps in SVT Diagnosis:
  • Although the formula for estimating the maximal rate of sinus tachycardia for stress testing (ie, during exercise) is ~ 220 minus Age — in my experience, it is highly unlikely (though not impossible) for sinus tachycardia in a horizontal" adult patient (ie, in a patient you are examining, who has not just been running) to exceed 170/minute. This statement does not hold true for children — as sinus tachycardias over 200/minute are not that uncommon in the pediatric age group. But the rate of 210/minute for the patient in this case essentially rules out sinus tachycardia.
  • The most common ventricular response to untreated AFlutter is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range 250-350/minute— and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. Therefore (as per Dr. Meyers) — the SVT in this case at a rate of ~210/minute is highly unlikely to be AFlutter in this previously healthy man in his 30s, since this would entail a flutter rate of 210 X 2 = 420/minute, which is much faster the atrial rate for flutter. NOTE: This rate range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial (and therefore ventricular) rate for flutter.
  • Finally — Although listed in the above differential diagnosis — ATach is far less common as a cause for a strictly regular SVT as seen in ECG #1 compared to AVNRT or AVRT, especially in a previously healthy younger adult.
  • THEREFORE  By the process of elimination, the most likely cause of the regular SVT at ~210/minute in ECG #1 is a reentry tachycardia. And, if the RED arrows we’ve drawn in ECG #1 do in fact represent retrograde atrial activity with a long RP' interval — then it’s likely this patient has WPW (CLICK HERE for review of the common arrhythmias encountered with WPW).
  • PEARL: From the above, it can be seen that if the regular SVT is at a rate close to 150/minute (ie, 140-160/minute) — that any of the 4 diagnostic entities listed above could be present (sinus tach/AVNRT-AVRT/ATach/AFlutter). It is when the rate of a regular SVT without clear sign of sinus P waves is substantially faster than this — that a reentry SVT (AVNRT/AVRT) becomes by far the most likely diagnosis!

FOLLOW-UP: As per Dr. Meyers — ECG #2 was obtained after the vagal maneuver. I’ve drawn BLUE arrows to highlight those leads in which delta waves are seen — which confirms the diagnosis of WPW.

Should This Patient be Ablated?
The patient in this case was a previously healthy man in his 30s, who presented with “palpitations”. There is no mention of prior episodes of SVT. There is no mention of drug therapy — only that the REVERT vagal maneuver was performed and was successful. Is EP referral for ablation the optimal course of treatment for this patient? In my opinion — the answer is not a yes — but rather, Idepends” ...
  • Clearly the approach to treatment of numerous cardiac arrhythmias has changed in recent years, with ever increasing expertise in the exciting field of cardiac electrophysiology. But even in the best of centers with the most experienced of EP cardiologists — ablation IS a procedure, and there IS potential for adverse effect.
  • If I was a previously healthy 30-year old man with a 1st episode of a hemodynamically tolerated SVT that was easily resolved by simple vagal maneuver (without even need for antiarrhythmic medication) — I would not opt for an invasive procedure with potential for significant side effects as my 1st intervention (despite VERY high likelihood for “cure” of this arrhythmia with very low chance of adverse effect). “Low risk” is not the same as “NO risk” — and if I was the patient, I'd prefer to start with a far less invasive intervention.
  • That said — there is notYes-or-No answer to this question. I’m simply suggesting that rather than automatically referring this patient to EP cardiology for ablation of his accessory pathway at this point — that an appropriate alternative course might be diligent follow-up while teaching this patient vagal maneuvers that he can perform at home on his own (ie, Valsalva), perhaps with a prn antiarrhythmic “cocktail” (ie, a single dose of beta-blocker or diltiazem or verapamil) that can be tried if this hemodynamically stable SVT recurs. Recurrence of this SVT might be infrequent (if it recurs at all), and it might again be easily managed — possibly even without need for daily antiarrhythmic therapy.
  • NOTE: ED referral of this patient for follow-up care IS of course indicated! — but such follow-up need not necessarily be to an EP cardiologist (or even necessarily to a cardiologist). Of course — IF repeated episodes occurred despite appropriate antiarrhythmic medication — that would be a different story (in which case, referral to your friendly EP cardiologist becomes the optimal management approach). Along the way to guiding optimal decision-making for this case — informed patient consent and patient preference are critical.
  • CLICK HERE for more on “My Take” on How to Advise the Patient with WPW.

Our THANKS to Drs. Meyers and Smith for presenting this case!




Thursday, October 10, 2019

Do you understand these T-wave inversions?

Case submitted and written by Alex Bracey, with edits by Pendell Meyers

A man in his 50s without prior medical history was sent to the emergency department from an urgent care facility for concern of an "abnormal ECG" after he had complained of chest pain earlier in the day. He was symptom free at the time of arrival.

Here is the triage ECG at the Emergency Department (we did not immediately have access to the urgent care ECG just yet):

ED ECG#1
What do you think? What do you think his urgent care ECG (done during pain) will show?






This ECG shows sinus bradycardia with terminal ST depressions in II, III, aVF, V3-V6, with reciprocal changes in aVL and I. These findings indicate reperfusion of the inferior and lateral walls, implying that an ECG during active symptoms would likely show OMI.


Note: This is the same pathophysiology and electrophysiology involved in Wellens syndrome, which is simply the name given to reperfusion of anterior wall OMI when the patient is in the pain free state of reperfusion and has not yet lost the anterior wall (requires persistent R-waves to be classic Wellens syndrome). This pattern occurs in any wall of the heart, whichever wall is currently reperfused from a prior occlusion.

On this note, "type A" and "type B" Wellens are useless distinctions that arose before we realized that reperfusion is a progression of findings starting with terminal T-wave inversions ("type A") and progressing to full T-wave inversions ("type B"). My analogy for this misunderstanding of Wellens syndrome that I tell my residents is this: "Imagine you were an alien looking through a microscope and you discovered Earth. You zoom in to a city and look at a single street and you see humans, which happens to be a woman walking with her small child. You watch them for a few hours and then report your findings to your fellow aliens: you declare that there are two types of humans: type A (smaller, helpless ones) and type B (large, smarter ones). If they simply had more knowledge and experience with humans, it would be easy to understand that type A and type B are not different types at all, rather different points along the same progression. If you only look at individual snapshots in time, they appear to be different types, however if you follow them for the full course of their progression the pattern becomes clear.

To make type A and B even more useless, they are misnomers applied by someone who had not carefully read Wellens' papers. They called terminal T-wave inversion type B and deep inversion type A. Wellens called terminal T-wave inversion "Pattern A" and deep "Pattern B."


He reports that today while sitting outside he developed sudden onset bilateral arm “burning” and an “odd feeling” though he was not able to further describe it. He had no chest pain, heaviness, or discomfort at any point and was never short of breath during today’s events. When pressed, he recalls that last week he traveled to Denver where he experienced dyspnea on exertion, though he attributed it to the altitude.

He was alarmed by these symptoms today and presented to an urgent care where this ECG was recorded:

Urgent Care ECG (this was done before arrival to ED, during active symptoms):



STE in II, III, and aVF (which probably barely does meet STEMI critiera) with hyperacute T waves in II, IIII, aVF and reciprocal negative hyperacute T-wave in aVL, with STD in V1-V2
Small R waves in II, III, aVF

This is diagnostic of inferoposterior OMI. The most likely culprit vessel would be the RCA.


Back to the present, in the ED, asymptomatic:

Given that the patient was now asymptomatic in the ED with ED ECG#1, I asked for serial ECGs to be recorded every 30 minutes and for any acute changes in discomfort or clinical condition.

At our facility we have a process to promptly evaluate patients for urgent or emergent PCI that present with ECGs concerning for acute coronary occlusions that do not meet STEMI critieria (OMI) called Heart Alert. We activated this process and the cardiology fellow presented to the bedside.

A third ECG was record at this time with no change, persistent reperfusion pattern.

During this time I received a call from the interventional cardiologist. I discussed the case with him as he reviewed the ECG. We agreed that there were dynamic changes; however, he did not feel that it could represent acute coronary syndrome as the patient did not have chest pain at any time during his prior symptoms. 

This is clearly false.

The patient then reported another episode of diaphoresis. An ECG at this time was recorded:




Redemonstration of small STE in II, III, aVF (not meeting criteria in this ECG) and reciprocal changes in aVL, V2. This ECG demonstrates reocclusion of the affected coronary vessel.

At this time the cardiology fellow again contacted the interventionist who agreed to take the patient for urgent PCI at this time. 

His initial troponin T was 0.02 ng/mL.

Here is what they found on cath:

100% mRCA with TIMI 0 flow


Post DES RCA with TIMI 3 flow


His formal echo performed the next day revealed an EF of 50% and Septal, lateral, and apical wall motion abnormalities.

His troponin T continued to climb over the next day with a peak of 1.4 ng/mL.



He had an uncomplicated post-PCI course and was discharged 3 days later.

Teaching Points:


We must understand the ECG patterns of occlusion and reperfusion because they are not currently taught or understood in the classic STEMI paradigm.

Serial ECGs greatly increase the chances of finding diagnostic features of OMI on ECG.


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MY Comment, by KEN GRAUER, MD (10/10/2019):
===================================
Highly insightful case! Drs. Bracey and Meyers have intentionally changed the time sequence in which the tracings in this case were recorded in order to make a number of important points.
  • I limit my comments to discussion of the 1st ECG shown above. This is the initial ECG that was done at the time the patient arrived in the ED.
  • I will offer a different perspective on the interpretation of ECG #1. For clarity — I have reproduced and labeled this ECG in Figure-1.
Figure-1: The initial ECG done in the ED (See text).



I propose the following additional Teaching Points regarding interpretation of ECG #1, considering the clinical context in which this patient presented:
  • Although I was not surprised by ECG findings on the Urgent Care ECG (which was the 2nd ECG shown above) — I do not think ( = my opinion) that there was any way to be certain there was ongoing acute infero-postero OMI from assessment of ECG #1 alone.
  • From an ECG Learning perspective — Systematic interpretation of ECG #1 should result in recognition of at least 4 additional findings not mentioned above. Admittedly, recognition of these findings does not alter management in this case — but there are times when failure to routinely use a systematic approach will result in overlooking ECG findings that are important (as I have shown on prior posts).

At the time ECG #1 was obtained in the ED — all that the ED physician knew was the HISTORY (a 50s man who was previously healthy, had chest pain earlier that day — but was asymptomatic at the time ECG #1 was done)Systematic Interpretation begins with Descriptive Analysis (I’ve put additional findings that should be recognized in BOLD).
  • Rate & Rhythm — There is sinus bradycardia (rate in the 50s, perhaps with some sinus arrhythmia).
  • Intervals (PR/QRS/QT) — The PR interval is normal. The QRS complex is narrow. The QTc is not prolonged.
  • Axis — There is marked left axis deviation — with a predominantly negative QRS in lead II (ie, the axis is more negative than -40 degrees). This is consistent with LAHB (Left Anterior HemiBlock)We don’t know if this is a new finding ...
  • Chamber Enlargement  There is no atrial enlargement, and no RVH. But criteria for LVH are met! (ie, R in lead aVL≥12 mm).

Q-R-S-T Changes:
  • Q = There are small (normal septal) q waves in leads I and aVL.
  • R = There is something strange about R wave progressionThere may be a tiny q wave in lead V2? Abrupt transition from the negative QRS in lead V1 — to the predominantly positive QRS complex by V2 — with then loss of R wave by V3, just doesn’t make physiologic sense. Note a much more logical progression of QRS and ST-T wave morphology across the chest leads for the other 2 ECGs done in this case. Recognition that placement of lead V2 may be off in ECG #1 is relevant in this case, given the ultimate evolution of acute infarction.
  • ST-T Wave Changes  As emphasized by Drs. Bracey and Meyers, there is terminal T wave inversion in multiple leads in ECG #1 (BLUE arrows highlight this in leads V3 and V4 — but it is also present in leads II, aVF, V5 and V6). As was also emphasized — this ECG finding of a biphasic T wave with terminal T wave inversion (and with frank T wave inversion in lead IIIalerts us in a patient with chest pain earlier that day — to the strong possibility that these findings may reflect reperfusion changes. (PINK — then BLUE arrows, highlight the biphasic nature of these T waves.) That said, there really is no ST elevation, no ST depression, and no non-septal Q waves in ECG #1 — and, in the absence of a prior or subsequent tracings — I don’t think ( = my opinion) that a definitive diagnosis of acute infarction can be made. We simply have NO idea as to when these ECG abnormalities may have developed … These ECG changes could certainly be acute — or, they may have developed days (or longer) before ECG #1 was done.
  • That said — it should be noted that in addition to these biphasic T waves with terminal inversion (and the frank T inversion in lead III) — ST segments just before these T waves are inappropriately flat in multiple leads (short horizontal BLUE lines in Figure-1). This loss of the normal gradual ST segment upslope is a distinctly abnormal ECG finding, especially in a patient with recent chest pain.
BOTTOM LINE: It should be appreciated that other than leads aVR and V1 — the remaining 10 leads in ECG #1 all show abnormal ST-T wave findings. In a previously healthy middle-aged adult who experienced new chest pain earlier in the day — the overall assessment of ECG #1 alone should clearly justify timely cardiac catheterization.
  • Once the earlier ECG from the Urgent Care Center became available — the diagnosis of acute ongoing infero-postero OMI became obvious. But, I thought it important to highlight all of the ECG findings that should be noted on ECG #1 — and, to emphasize that even if no Urgent Care Center ECG had been done, that timely cath would still be indicated.

Our THANKS to Dr. Bracey and Meyers for this insightful case!



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