Sunday, May 1, 2022

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

 Written by Pendell Meyers

A man in his 40s presented for "left sided chest pain sudden onset yesterday when sneezing and coughing that is worsened with inspiration." He also complained of associated SOB, dizziness, jaw pain, and back pain, which he described as "muscle spasms." He has also had rhinorrhea and cough for 1 week. Also, left hand numbness today. 

He went to urgent care for evaluation. An ECG was performed there (unavailable) which reportedly was abnormal, so EMS was called to urgent care to take him to the ED.

On EMS arrival, they noted the patient vomited then became unresponsive. He was reportedly in PEA arrest, so they started chest compressions. After approximately 30 seconds of compressions, before the defibrillator could be applied, the patient started moving and moaning. Vitals then showed bradycardia, hypotension, and hypoexmia. He was then transported to the ED.

EMS recorded an ECG and transmitted it to the ED physicians before arrival:

Here is the same image after PM Cardio app processing:
What do you think?

It's an unusual and terrifying ECG. There is sinus rhythm at a rate of approximately 120 bpm with 2:1 AV block (see lead V1 where the P waves are very clear), resulting in ventricular rate near 60 bpm. The QRS shows RBBB and LAFB. There is concordant STE in V1-V5. The inferior leads have large upright T waves that are likely hyperacute, with reciprocal large volume TWI in aVL (these are more than expected for the LAFB). The T waves in V2-V4 have terminal T wave inversion, but I am not convinced or reassured that there might be meaningful reperfusion; overall it looks like active OMI.

In other words, it is diagnostic for proximal LAD occlusion (or even left main), but with the addition of 2:1 AV block. 

First ECG on ED arrival:

Similar to EMS ECG.

20 min later:

Mostly similar to above.

The cath lab was activated.

Bedside echo showed very poor LV function, diffuse bilateral B lines. The ED physician diagnosed cardiogenic shock from OMI.

The cardiologist cancelled the cath lab activation and presented to bedside. He stated that he would not cath the patient before PE was ruled out by CT angiogram.

Side note: Even without understanding the ECG, PEs do not usually cause acute AV block, and obviously the ED bedside echo is the opposite of RV failure. 

The ED provider was unable to convince him otherwise, so rolled the patient immediately to CT and performed CT angiogram within 20 minutes, and convinced the cardiologist that there was no large proximal PE on the scan.

And so the delay to cath was only about 45 minutes or an hour. At cath, the patient's cardiac index was 1.9 L/min/m2 even on dopamine, and an impella assist device was placed prior to angiogram. He was also intubated around this time.

Angiogram showed acute thrombotic 100% occlusion of the proximal LAD. The report also describes 100% stenoses at the mid and distal LAD. Three stents were placed, in the prox, mid, and distal LAD. In each location, the residual stenosis is listed at 0%. Unfortunately, the post procedure TIMI flow is listed as 2 (instead of 3, which would be normal flow and successful reperfusion). There is no description in the cath report detailing the reasons and attempted interventions for suboptimal flow, unfortunately. I get the sense that, despite best efforts, flow through the culprit LAD was unable to be perfectly restored despite PCI.

Here are some of the cath images:

Pre-intervention. Red arrows show the location of the proximal LAD Occlusion.

Post-intervention. Even after waiting several seconds since contrast infusion to capture the image, you can see the LAD is not fully perfused with contrast even when the other visible vessels are. In video, the contrast creeps very slowly past the original lesion and down the LAD. 

There is no post cath ECG immediately available.

Initial troponin T (older generation, both limit of detection and lowest abnormal value is 0.01 ng/mL; in other words, the assay is either undetectable at less than 0.01 ng/mL, or abnormal at 0.01 or above) returned at 4.52 ng/mL (very high, already higher than the average STEMI in our studies).

Later that night, this occurred (pt intubated, sedated):

Two of the P waves conduct, otherwise this is complete AV block with resultant ventricular asystole.

Transcutaneous pacing ensued, then a transvenous pacemaker was placed (it seems that 2:1 AV block had not been noticed on prior ECGs, and no temporary pacer wire was placed during the cath lab!).

Here is the ECG after TVP:

Ventricular paced rhythm. Use the modified Sgarbossa criteria and tell me: is there evidence of downstream reperfusion after PCI?

Here are a few leads blown up:

Here they are annotated for the ST/S ratios we use in the modified Sgarbossa criteria:

As you can see, the ECG is positive for the modified Sgarbossa criteria, suggesting ongoing evolution of OMI. The inferior leads also look concerning. Notice that the ECG is falsely negative for OMI by the original Sgarbossa criteria, as there is no lead with 5mm of discordant STE.

Sadly, this is worrisome for no-reflow phenomenon. Despite the intervention improving angiographic flow, the myocardium does not show signs of meaningful reperfusion. Instead, the ECG is playing out as a full thickness completed MI.

Echo the next morning showed EF 24% with severe hypokinesis of the anterior, anterolateral, mid inferior, basal anterior septum, mid inferior septum, and the entire apex. There was also severe swirling of contrast in the LV apex consistent with low flow state. There was a very tiny thin mobile echodensity seen attached to the apical lateral wall, which may represent LV thrombus.

Troponin T peaked at 8.43 ng/mL (very high, terrible MI and long term outcome).

Days later:

RBBB with anterior LV aneurysm morphology. 

[There are QR-waves with shallow T-wave inversion -- LV aneurysm usually has QS-waves, but QS-waves become QR-waves in the setting of RBBB].  
See this post: Dyspnea, Right Bundle Branch block, and ST elevation

The patient apparently survived to discharge, but long term follow up is obviously bleak.

Learning Points:

Acute ACS with new RBBB and LAFB is a very high risk sign of proximal LAD OMI, with very high rates of cardiogenic shock and death even before emergent intervention.

PE doesn't cause AV block.

Use the modified Sgarbossa criteria as the best available approach to finding OMI in ventricular paced rhythm.

No reflow phenomenon occurs when microvascular reperfusion fails despite epicardial coronary intervention. It cannot be predicted before attempting intervention as far as I know.

Other cases of LAD OMI with RBBB/LAFB:

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

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 (5/1/2022):


Highly instructive case presented by Dr. Meyers — with a series of lessons to remember. I focus my comments on the processed PM Cardio app version of the initial EMS tracing, that I’ve reproduced in Figure-1.

As per Dr. Meyers — this ECG is highly suggestive of acute proximal LAD occlusion. It does not suggest acute PE.
  • There is bifascicular block (RBBB/LAHB) — which is a common accompaniment of large proximal LAD occlusions.
  • The usual initial positive deflection (r wave) of RBBB has been replaced by large initial Q waves in leads V1 and V2 (confirming the large anteroseptal infarction). The extra fragmentation (notching) in lead V2, and especially in leads V3,V4 — provides additional evidence of “scar”.
  • Support that the LAD occlusion begins proximally — is forthcoming from the finding that ST elevation begins immediately with lead V1. ST elevation appears to be maximal in leads V3,V4 — and continues through to lead V5.

PEARL #1: Normally with complete RBBB — there will be a certain amount of ST-T wave depression in this lead, reflecting the oppositely-directed repolarization change expected with RBBB. The fact that despite this, there still is some ST elevation in lead V1 suggests that were it not for this conduction defect — the relative amount of ST elevation in lead V1 would have been significantly greater.

  • NOTE: Concern was voiced by Cardiology regarding the possibility of a large acute PE. While anterior T wave inversion with a long QTc are findings that suggest acute RV “strain” —  the rest of the 12-lead (as per Dr. Meyers), is not suggestive of acute PE because: i) The presence of AV block (See below); ii) The ST elevation that is seen in leads V1-thru-V5 (which is not expected with acute PE); andiii) An ST-T wave appearance in the inferior leads that is the complete opposite of what should be expected with a large acute PE (ie, hypervoluminous, hyperacute-appearing T waves in the inferior leads — instead of the T wave inversion of RV strain).

Figure-1: The processed PM Cardio app version of the initial EMS tracing.

What About the Rhythm in Figure-1?
It would be easy to misdiagnose the rhythm in Figure-1 as sinus. This is because the long lead II rhythm strip that appears at the bottom of the 12-lead “looks like” a simple sinus rhythm at a seemingly reasonable rate just under 60/minute. But as Dr. Meyers points out — instead of sinus rhythm, there is 2:1 AV block.

  • Note first that the long lead II rhythm strip in this EMS tracing is not simultaneously recorded with the rest of the ECG. Recognition of this fact is important — because it means that we can not correlate the timing of certain deflections that we see in other leads with what is happening in the long lead II rhythm strip.
  • In general, the best lead for identifying P waves in, is standard lead II. Lead II provides the extra advantage of verifying a sinus mechanism if the P wave in this lead is upright. In my experience — the 2nd-best lead for identifying P waves in is lead V1. The interesting feature about the rhythm in this initial EMS tracing — is that the hypervoluminous T wave in lead II is “hiding” the extra P wave (PINK arrows in the long lead II). This would have been extremely to miss if the search for atrial activity only included a look at lead II.

Lead V1 provides the answer — with RED arrows in this lead highlighting 2:1 AV conduction. Support that the “extra deflection” within the R-R interval in lead V1 is truly an extra P wave (and not artifact or some unusual form of T wave notching) — is forthcoming from: i) The unique biphasic (positive-then-negative) shape of the deflections under the RED arrows; ii) The almost-equal distance between these deflections (ie, PACs would not be so equi-distantly placed); andiii) The fact that we can see a similarly placed extra deflection in simultaneously-recorded leads V2 and V3 (although the extra P waves are even more subtle in those leads).
  • I believe the reason the 2:1 block in this tracing is so challenging to recognize, is due to a combination of: factors. These include: i) The rapid atrial rate (ie, ~115-120/minute) — which results in the extra T wave occurring so early in the cardiac cycle; ii) The hypervoluminous inferior lead T waves (as a result of the acute OMI) which facilitate the “hiding” of the extra P wave; andiii) The “ventriculophasic” sinus arrhythmia. 

PEARL #2: Be aware that ventriculophasic sinus arrhythmia is commonly seen with 2nd- and 3rd-degree AV blocks. In its typical form — it is the P-P interval that “sandwiches” a QRS complex that measures slightly less than the P-P interval without any QRS within it, as is seen in Figure-1 (ie, 510 msec. compared to 530 msec.). 

  • It is thought that the reason for slight shortening of the P-P interval for P waves that sandwich a QRS — is that mechanical (ventricular) contraction follows soon after electrical activity (ie, the QRS) — and this results in slightly improved blood flow (therefore, slight shortening of the P-P interval).

PEARL #3: How NOT to Miss AV Block:
As emphasized — the 2:1 AV block in today’s initial tracing is challenging to recognize! That said — there are some easy things to do that will minimize the chance of overlooking subtle arrhythmias like this one.

  • Increase your index of suspicion for a rhythm disorder when you encounter a predisposing clinical setting. The patient in today’s case had just survived a cardiac arrest. His initial ECG showed bifascicular block (presumably new) — in association with acute ST-T wave changes suggestive of LAD occlusion. In this setting — I would not have expected a simple sinus rhythm at a rate slightly below 60/minute as the cardiac rhythm.
  • When looking for occult 2:1 AV conduction (be this from 2:1 AV block — or from atrial flutter with 2:1 AV conduction) — calipers facilitate the process. Simply set your calipers at HALF the R-R interval — and then look in all 12 leads to see if an “extra deflection” can be found at this distance in any of the leads.
  • Look especially carefully at lead V1 when searching for extra atrial activity — as it is not uncommon for this to be the only lead in which you clearly see extra atrial activity. 
  • If your patient is stable (and you have thee luxury of an extra moment of time) — Consider the use of additional lead systems (ie, a Lewis Lead — See the November 12, 2019 post in Dr. Smith’s ECG Blog)

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