Thursday, August 13, 2020

Chest discomfort, Sinus Tachycardia, Q-waves, ST Elevation, and Intermittent Wide Complex Tachycardia. Activate the Cath Lab?

This ECG was texted to me with no other information:

Computer Diagnosis:
SINUS TACHYCARDIA
INCOMPLETE RIGHT BUNDLE BRANCH BLOCK [90+ ms QRS DURATION,
TERMINAL R IN V1/V2, 40+ ms S IN I/aVL/V4/V5/V6]
LEFT ANTERIOR FASCICULAR BLOCK [QRS AXIS <= -45, QR IN I, RS IN II]
ANTEROSEPTAL MYOCARDIAL INFARCTION , PROBABLY RECENT [40+ ms Q
WAVE IN V1-V4]
***ACUTE MI***

What do you think? Below is my response.

There is sinus tach.  There is an incomplete RBBB and LAFB.  There are QR-waves in aVL and V2, and a QS-wave in V3.  There is ST elevation in V2 and V3, with upright T-waves in V2 and V3.  There is reciprocal ST depression in inferior leads and also in V5 and V6.














This was my response:

If it is the right clinical situation, such as acute chest discomfort, it looks like proximal left anterior descending occlusion with right bundle branch block and left anterior fascicular block. Because of the tachcardia, I would expect her to be very poor left ventricular function and maybe Cardiogenic shock.  
Alternatively, it is someone who has an old myocardial infarction and is now very sick with something else.

Then I looked into the patient's chart and found an old EKG:
This shows a previous QR-wave in V2, diagnostic of old anterior MI.  
It does not show RBBB but does show Left anterior fascicular block.



I wrote back:

"I am looking at his old EKG. It looks like he has an old anterior lateral MI as well.  This suggests that it is not an acute coronary syndrome."

"His previous echo one month prior shows the same thing: “consistent with old infarct in LAD vascular territory, with EF 45%”

"I think there is something else causing his tachycardia which is exaggerating his EKG findings and mimicking an acute myocardial infarction."


Later, I obtained more clinical history.

The patient initially presented with a report of SOB prehospital, but this he denied.  Instead, he complained of left chest "itchiness".  He had a h/o ischemic cardiomyopathy and right MCA stroke.  

At some point, he was seen to be less responsive and have left gaze deviation.

He was brought to the critical care area where these rhythms were seen on the monitor:

Wide complex tachycardia with no apparent P-waves, and very irregular
Consistent with atrial fibrillation with aberrancy

A Regular wide complex tachycardia.  The initial part of the QRS is very narrow, so this is some re-entrant SVT with aberrancy

Irregular again.  Looks like atrial fibrillation.

Still Irregular










Blood pressure during these rhythms was adequate; there was no shock.

The patient spontaneously converted back to sinus tachycardia.

At this point, they recorded the above 12-lead.

The cath lab had been activated and then they sent me the ECG.  The patient was awake at this point, lactate was 7 mEq/L and so seizure was suspected as the etiology of the transient loss of consciousness and gaze deviation.

Cardiology came to assess the patient.

They agreed that the ECG findings were due only to old MI and tachycardia.  Cath lab was cancelled.

Here is the troponin profile (contemporary troponin I, URL = 0.030 ng/mL):
It rose and fell, with one value above the 99th percentile URL.  It is therefore an acute MI, but in this case it is a type 2 MI due to tachycardia supply-demand mismatch.



Learning Points:

1. Old MI with persistent ST Elevation (LV aneurysm morphology) can look like acute MI
2. When there is tachycardia, you should doubt the diagnosis of ACS unless it is:
       a) massive MI with cardiogenic shock and thus poor LV function and poor stroke volume,
       b) in a patient with previous poor LV function
       c) combined with other acute pathology causing tachycardia
3. Not all anterior LV aneurysm has a QS-wave.  When there is RBBB (even if incomplete), what would be a QS-wave of completed old anterior MI will transform into a QS-wave simply because of the conduction abnormality.

For examples of point 3, see the 2 cases at this link.  In the second one, the patient mistakenly received thrombolytics.  Moreover, the ECGs in RBBB and in normal conduction can be compared side by side, as the RBBB was rate-related.

Dyspnea, Right Bundle Branch block, and ST elevation


Here are two more cases where the differential diagnosis is acute OMI vs. LV aneurysm:

Is this acute STEMI? LV Aneurysm? Would you give Thrombolytics?


9 Hours of Chest Pain and Deep Q-waves: Is it too late for Thrombolytics? (Time Window for Reperfusion; Acuteness on the ECG)




===================================
MY Comment by KEN GRAUER, MD (8/13/2020):
===================================
This is a challenging case — which is made all the more difficult by suboptimal quality of the initial 12-lead ECG — and lack of additional simultaneously-recorded leads for the arrhythmia tracings. But sometimes we need to make do with whatever tracings are available ...

Although I’ll focus my attention on the monitoring lead rhythm strips — it’s important to start with the 12-lead. As per Dr. Smith’s interpretation (above) — despite marked baseline artifact on the initial 12-lead ECG that was texted to him — We can establish that the rhythm is sinus (ie, sinus tach at ~110/minute) — and that the QRS is wide (I measure 0.12 second in a number of leads) — with a marked left axis consistent with LAHB.
  • I think it’s difficult to tell if we are dealing with incomplete RBBB vs some other type of conduction defect (ie, lacking IRBBB features of a terminal s wave in lateral limb leads —  and only intermittent presence of a terminal r’ in lead V1 — all complicated by the prior anterior MI and unusual morphology of the QRS complex in lead V2).
  • That said — what’s important is that we know this patient’s initial ECG in the ED shows a sinus mechanism with QRS widening and predominant negativity in lead II. This information proves invaluable in assessing the rhythm strips to follow.

In all — there are 6 tracings in this case, including the initial 12-lead ECG, a prior 12-lead, and 4 rhythm strips.
  • For clarity — I’ve numbered the tracings in the sequence that they appear above in Dr. Smith’s discussion.
  • NOTE: I do not see clarification if the lower lead in the first 3 rhythm strips is a lead V1 or MCL-1. Both are “right-sided” leads that present similar morphologic characteristics — so for simplicity, I’ve labeled tracings with a lead V1 designation.


QUESTION:
Imagine you are ONLY shown ECG #4, which is the 2nd tracing in the series of rhythm strips shown above. How would you interpret this tracing? (Figure-1).

Figure-1: What if the only tracing you saw was ECG #4? How would you interpret this rhythm? (See text).



My THOUGHTS on Figure-1: IF the initial 12-lead ECG was not available, and the only tracing you were provided with was ECG #4 (which is the 2nd in the series of 4 rhythm strips) — I’d say the following:
  • There is a regular WCT ( = Wide-Complex Tachycardia) rhythm at ~150/minutewithout clear sign of atrial activity. The differential diagnosis consists of VT vs SVT with either preexisting bundle branch block or aberrant conduction. The ventricular rate of ~150/minute could be consistent with: i) VT; ii) Sinus tachycardia (in which sinus P waves are hidden within the preceding ST-T wave); iii) A reentry SVT rhythm (AVNRT or AVRT); oriv) AFlutter.

KEY POINT: Regarding the rhythm we see in Figure-1 — QRS morphology is not helpful in distinguishing between VT vs some form of SVT. This is because:
  • We only have 2 leads to look at ... Use of QRS morphology as a discriminating feature between VT vs SVT is best accomplished when you have a 12-lead ECG, under which appears one or more simultaneously-obtained rhythm strips. We don’t have this here.
  • Although the initial deflection in lead II of ECG #4 looks fairly narrow — it is not “pencil-thin” narrow. One can not rule out VT on the basis of this less-than-pencil-thin initial deflection in a single lead (Even if the initial deflection was pencil thin in this 1 lead — this would not completely rule out the possibility of VT).
  • Although the QR pattern in lead V1 is “consistent” with RBBB conduction — because there is no initial positive deflection (ie, no initial r wave) — QRS morphology in lead V1 of ECG #4 does not discriminate between VT vs supraventricular conduction. Both rhythms are possible when you see a QR morphology in lead V1.

PEARL #1: Attention to QRS morphology can be of invaluable assistance for interpretation of some (not all) wide-complex tachycardias. The most common form of aberrancy is with RBBB-conduction (because in most individuals, the right bundle branch tends to have the longest refractory period).
  • IF you see a wide tachycardia with ECG features of typical RBBB — then this strongly supports a supraventricular etiology. Typical RBBB morphology shows a “terminal delay” in ventricular depolarization — in which it is the last portion of the QRS complex that shows the changes. With typical RBBB, there should be: iAn rsR’ or rSR’ complex in lead V1 (with the S wave descending below the baseline); andii) A wide terminal S wave in lateral leads I and V6.
  • RBBB conduction does not always manifest a “typical” QRS morphology. For example, it is possible to see a QR pattern in lead V1 with RBBB, instead of a typical triphasic rsR'.
  • PEARL #2: Any pattern of a known conduction block can be seen with aberrant conduction (RBBB — or LAHB, LPHB, LBBB; RBBB/LAHB, RBBB/LPHB). Therefore — One of the most helpful aids for recognizing aberrant conduction is that the pattern of QRS widening resembles some form of known conduction block. In contrast — VT most often originates from a site in the ventricles outside of the conduction system — which is why VT rhythms often manifest “uglier” QRS morphologies that do not resemble any known type of conduction block. CAVEAT: While this general rule usually holds true — exceptions do exist either due to types of VT such as Fascicular VT that do resemble known conduction block patterns — and/or the fact that some patients have extremely abnormal QRS morphology in their baseline ECG due to severe underlying heart disease. (This is why finding a baseline tracing in sinus rhythm can sometimes be so helpful in assessing QRS morphology during the wide tachycardia).
BOTTOM LINE Regarding Figure-1: Definitive diagnosis of the regular WCT rhythm in ECG #4 is simply not possible on the basis of this single 2-lead rhythm strip alone.


BACK to Today's Case: The reason I liked this case — is that putting together all information we have allows the high-likelihood diagnosis arrived at by Dr. Smith above.
  • Today’s patient developed the series of 4 tachyarrhythmias shown above in the critical care area of the ED. The patient remained hemodynamically stable throughout the time he was in these tachyarrhythmias!
  • I’ve reproduced in Figure-2 the first 3 of the above 4 tachyarrhythmias. Now that you do have access to the initial 12-lead ECG — HOW WOULD YOU interpret the rhythms in ECGs #3, #4 and #5?

Figure-2: The first 3 of the 4 tachyarrhythmias in this case (See text).



My THOUGHTS on Figure-2: The “good news” — is that since this patient remained hemodynamically stable throughout — there was never a need for immediate cardioversion.
  • Looking first in Figure-2 at ECG #3 — the rhythm is rapid and irregularly irregular without clear sign of atrial activity. As per Dr. Smith — this suggests that despite QRS widening, the rhythm in ECG #3 is AFib with a rapid ventricular response.
  • QRS widening in ECG #3 is not new — since we know from assessment of the initial 12-lead ECG that the baseline QRS is wide (with predominant negativity in lead II that shows a similar morphology to many of the beats seen in the upper lead in ECG #3).
  • Many of the beats in ECG #3 show extra widening. This is easiest to see in lead V1 for beats #1,2, 4,5, 7, 9, 11, and 13-thru-22. In further support that this rhythm is AFib and not VT are the findings that: i) The rhythm maintains the same irregular irregularity throughout regardless of whether the QRS shows additional widening or not; andii) The initial negative deflection in the narrower beats in ECG #3 is similar in shape to the initial part of the QRS for the wider beats. This is easiest to see in lead V1. The essential difference in QRS morphology between narrower and wider beats is a terminal delay (tall R wave) — and this is consistent with RBBB aberration.

Look next at ECG #5:
  • This rhythm is again irregularly irregular without evidence of atrial activity — so the rhythm is again AFib with a rapid ventricular response.
  • Lead V1 in ECG #5 is especially diagnostic. Notice how each of the 19 beats in lead V1 begins with an almost identical negative deflection. Added on to this negative deflection almost every-other-beat is a terminal delay producing a tall terminal R wave in beats #1, 3, 5, 7, 9, 11, 13, 15 and 19. This identical initial deflection in lead V1 with terminal delay establishes RBBB aberration as the cause of additional QRS widening.

Finally — Take another look at ECG #4Unlike ECGs #3 and #5 — the rhythm in ECG #4 is quite regular. We discussed earlier that IF all you had to look at was ECG #4 — it would not be possible to distinguish VT from SVT from this single regular wide tachycardia rhythm strip alone. But in the context of the initial 12-lead ECG and the 2 additional rhythm strips shown in Figure-2 — We can confirm a supraventricular etiology in ECG #4.
  • Doesn’t the shape of the QRS complex in lead II of ECG #4 look very similar to the shape of the QRS complex in the long lead II rhythm strip at the bottom of the initial 12-lead ECG?
  • Doesn’t the shape of the QRS complex in lead V1 of ECG #4 look very similar to the shape of the QRS complex for beats #1, 3, 5, 7, 9, 11, 13, 15 and 19 in ECG #5, that we established as being conducted with RBBB aberration?

BOTTOM LINE: Interpretation of the tachyarrhythmias in this case is complex. Hopefully, at least some of the points suggested above will be enough to suspect a supraventricular etiology for each of these tachyarrhythmias.
  • Given that the patient was asymptomatic from these arrhythmias — there was time to contemplate additional measures. Spontaneous conversion back to a sinus mechanism in this case obviated the need for further intervention.
  • FINAL PEARL #3: When AFib is fast — the rhythm may at first glance look like it is regular. However, careful observation (and caliper measurement) reveal there is an irregular irregularity in ECG #5 which essentially confirms that this rhythm is rapid AFib.
  • P.S.: For another example of intermittent RBBB conduction, in which a similar initial deflection with terminal delay facilitated recognition of RBBB Conduction — Please SEE the June 25, 2020 post in Dr. Smith's Blog.


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