Friday, November 11, 2022

An elderly woman with acute vomiting, presyncope, and hypotension, and a wide QRS complex

 Written by Pendell Meyers

Family of an elderly woman with many comorbidities called EMS when she suddenly experienced shortness of breath, nausea, vomiting, and near syncope. She was alert and oriented and hypotensive with initial BP 70/50. A 12 lead ECG was obtained by EMS and is shown below:

What do you think?

There is sinus tachycardia (do not be fooled into thinking this is VT or another wide complex tachycardia!) The ECG is diagnostic of LAD occlusion (or even left main occlusion possibly), with the classic pattern of RBBB and LAFB with huge concordant STE in V1-V2, I, and aVL, with reciprocal depression in most other leads (and/or a component of subendocardial ischemia pattern). This is "shark fin" morphology. With so much STD in leftward and inferior leads V4-V6, II, III, and aVF, of course there must be STE in aVR. 

This one of the highest risk OMI patterns possible to see on an ECG. This pattern is essentially always accompanied by cardiogenic shock and high rates of VT/VF arrest, etc.

The patient arrived to the ED in cardiogenic shock but awake.

Code STEMI was activated.

A repeat ECG was performed:

An interesting mix of subendocardial ischemia pattern AND precordial swirl LAD OMI pattern. It is similar to the first ECG but the RBBB has temporarily resolved.

For some combination of reasons likely including age and prognosis, the cardiologist did not want to take the patient to the cath lab. No angiogram was done, and no thrombolytics were given.

The initial troponin I was 87 ng/L. Four hours after arrival the level was 17,823 ng/L, and none further were measured.

A stat echo showed EF 25% with global hypokinesis and anteroapical akinesis.

She was made comfort care and expired within 8 hours of onset.

Learning Points:

Acute LAD or left main OMI causing RBBB and LAFB with concordant STE in anterolateral leads is a terribly high risk OMI pattern. You must understand the QRS pattern and how to find the J point in order to recognize this pattern.

OMI and subendocardial ischemia patterns can both be present at the same time. Aslanger's pattern, for example, is inferior OMI with simultaneous subendocardial ischemia pattern. 

Other cases of LAD OMI with RBBB/LAFB:

A man in his 40s who really needs you to understand his ECG

Cardiac Arrest at the airport, with an easy but important ECG for everyone to recognize

A woman in her 60s with 6 hours of chest pain, dyspnea, tachycardia, and hypoxemia

Reproduced info from prior post about acute RBBB and LAFB in anterolateral OMI

Some of the most severe LAD or left main occlusions present with acute RBBB and LAFB, and these findings carry the highest risk for acute ventricular fibrillation, acute cardiogenic shock, and highest in-hospital mortality when studied by Widimsky et al. (in-hospital mortality was 18.8% for AMI with new RBBB alone). Additionally, the RBBB and LAFB make the recognition of the J-point and STE more difficult and more likely to be misinterpreted. Upon successful and timely reperfusion, the patient may regain function of the previously ischemic or stunned fascicles.

Widimsky PW, Rohác F, Stásek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86–95.

MY Comment by KEN GRAUER, MD (11/11/2020):
As per Dr. Meyers — today's case involves an important ECG pattern in need of prompt recognition. From an academic standpoint — I found several subtle ECG findings from the 2 tracings in this case to be especially interesting.
  • For clarity — I've put the 2 tracings from today's case together in Figure-1. I've labeled the features I highlight in this figure.

  • To Emphasize: My comments do not alter the diagnostic considerations discussed above in excellent detail by Dr. Meyers. Instead — I focus on several advanced concepts in ECG interpretation, awareness of which may serve useful in other cases.

  • What is the rhythm in ECG #1?

  • Both tracings provide a long lead II rhythm strip below the 12-lead. But is the system for recording the long lead rhythm strip the same in ECG #1 and ECG #2?
  • HINT: Look at how the vertical dark BLUE lines and the light BLUE line in ECG #1 do (or do not) line up with QRS complexes in leads III and aVF.

  • How wide is the QRS in ECG #1?

  • WHY do beats #6 and #10 in the long lead II rhythm strip of ECG #2 look different than the 15 other beats in this long lead rhythm strip?
  • Still in ECG #2 — Look at how different beat #10 looks in leads V1,V2,V3 — compared to the other beats in these simultaneously-recorded leads (ie, compared to beats #9, 11, 12, 13 in leads V1,V2,V3). WHY is this so?

NOTE: My reason for focusing on these challenging questions — is that they bring out a number of important points regarding optimal use of simultaneously-recorded leads. While not important for decision-making in today's case — these points may prove invaluable for diagnosis of tachyarrhythmias and/or problematic ST-T wave deviations in selected case.

Figure-1: I've labeled the 2 tracings in today's case to highlight a number of KEY advanced features of ECG interpretation.

What is the Rhythm in ECG #1?
As per Dr. Meyers — despite what appears to be marked QRS widening, the rhythm in ECG #1 is not VT. Instead — RED arrows indicate sinus P waves in both tracings.
  • The amplitude of P waves in both tracings is small. In addition — there are artifactual undulations in the baseline of limb leads in ECG #1. As a result — I was not at all certain I was seeing sinus P waves when I first looked at lead II.
  • That said — careful scrutiny of other leads in ECG #1 confirmed that the rhythm in this tracing was indeed sinus tachycardia (ie, In addition to the small-but-present negative deflection before each QRS in lead V1 — sinus P waves are also seen in leads V4,V5,V6).

  • NOTE: Although it seems like the 1st beat with each lead change in ECG #1 occurs early — there are no PACs in this tracing! (See below).

The System for Recording the Long Lead II is Different!
LOVE using simultaneously-recorded leads. This feature is invaluable for assessing QRS morphology with wide tachycardias in the differentiation between SVT vs VT rhythms.
  • In my opinion — the optimal system for correlating simultaneously-recorded leads with the 12-lead tracing — is the system used in ECG #2. A total of 17 beats are seen in the long lead II rhythm strip from this tracing. These same 17 beats are seen in the 12-lead — with the advantage that we see the first 4 beats in 3 simultaneously-recorded leads (ie, leads I,II,III).
  • We then see beats #5-thru-8 in 4 simultaneously-recorded leads (ie, leads aVR,L,F; and the long lead II) — beats #9-thru-13 in leads V1,2,3 and II — and beats #14-thru-17 in leads V4,5,6 and II.

Did YOU Notice that the system for recording is different in ECG #1? 
  • There are a total of 19 beats in the long lead rhythm strip of ECG #1 — but we only get to see QRS morphology for the first 5 beats in the tracing!
  • These same first 5 beats are then repeated in each set of simultaneously-recorded leads.
  • Although it looks as if the 1st beat after each lead change occurs "early" (the light BLUE number 1 in leads aVR,L,F — in V1,2,3 — in V4,5,6) — there are no early beats (ie, no PACs) in ECG #1.
  • The advantage of this system of monitoring — is that you get to see what the first 5 beats look like in all 12 leads! But the decided disadvantage — is that you have no idea of what the other 14 beats from the long lead II rhythm strip look like in the other 11 leads. 
  • To Emphasize: When the rhythm is regular, it does not matter which rhythm recording system you are using. But IF you are dealing with wide beats or a wide tachycardia that only begins after the first lead change — then you have no idea of QRS morphology for those wide beats in the other 11 leads.

  • Take-Home POINT: Not all rhythm recording systems are the same. There are other variations than the 2 that are used in today's case. Awareness of these differences helps to understand why each beat in the long lead II rhythm strip in ECG #1 is not directly under all beats in the 12-lead above it.

How Wide is the QRS in ECG #1?
As we have shown in multiple cases of "Shark Fin" morphology in Dr. Smith's ECG Blog (ie, See My Comment at the bottom of the page in the May 19, 2020 post as just one example) — defining the limits of the QRS complex (and distinguishing the QRS from marked ST elevation or depression) can sometimes be extremely challenging. So it is in today's tracing.
  • To quote Drs. Meyers & Smith — "When the QRS is wide, the J-point will hide. So, your next step is to Trace it down, and Copy it over". I have done this with vertical RED lines in ECG #1 — and with vertical PURPLE lines in ECG #2.
  • Using these vertical lines as the end point of the QRS — reveals how dramatic the ST elevation is in leads aVR, aVL and V1,V2 of ECG #1. Equally dramatic reciprocal ST depression is seen in the inferior and lateral chest leads.
  • The vertical RED line in leads V1,V2 of ECG #1 also reveals a tall, terminal R' deflection in these leads, consistent with RBBB. So, the QRS complex is wide in ECG #1 — but not nearly as wide as one might think given the QRS limits defined by these vertical lines.

Why Beats #6 and #10 Look Different in ECG #2:
In ECG #2 — Note how different QRS morphology looks for beat #6 in leads aVR,L,F and in the long lead II (compared to QRS morphology for beats #5,7,8 in these leads). Similarly, in ECG #2 — Note how different QRS morphology is for beat #10 in leads V1,2,3 and in the long lead II (compared to QRS morphology for beats #9,11,12,13 in these leads).
  • The rhythm in ECG #2 is sinus. Looking at the long lead II rhythm strip — Note that beats #6 and #10 occur slightly earlier-than-expectedWHY? These beats are not preceded by premature P waves. Are these beats PVCs?

  • Predominant negativity of the QRS for beat #6 in lead aVF and in the long lead II suggests LAHB conduction. Other than beats #6 and 10 in the long lead II — none of the other 15 beats manifest LAHB conduction.
  • The terminal, tall R' in leads V1,V2 for beat #10 suggests RBBB conduction. In contrast — beats #9,11,12,13 in leads V1,V2 do not manifest RBBB conduction.

  • Now compare QRS and ST-T wave morphology for beats #6 and #10 (contained within the dotted LIGHT BLUE rectangles in ECG #2) — with QRS and ST-T wave morphology in these same leads in ECG #1Isn't morphology for the complexes within the light BLUE rectangles of ECG #2 virtually the same as morphology of all beats in these leads of ECG #1?

  • Putting It All Together: The RBBB/LAHB seen in ECG #1 is no longer present in ECG #2 — except for beats #6 and #10. Both of these slightly early-occurring beats are PJCs that conduct with RBBB/LAHB aberration. The rate of the sinus tachycardia in ECG #1 is slightly faster than the rate of the sinus tach in ECG #2 — so I suspect there is a component of rate-related aberration in ECG #1. I thought it fascinating that the same dramatic ST elevation in leads aVR, V1 and V2 that was seen for all beats in ECG #1 — is seen in these PJCs. 
  • Take-Home POINT: Tachycardia is a potential cause of ST elevation that may significantly decrease once heart rate slows.

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