Tuesday, November 30, 2021

ECG Blog #265 (73) — VT or Something Else?


The patient whose ECG is shown in Figure-1 was admitted for carbon monoxide poisoning. The computer interpreted the rhythm in this tracing as VT (Ventricular Tachycardia).

 

QUESTION:

  • Do you agree with the computer interpretation?
  • If not — How would YOU interpret the ECG in Figure-1? 

 

Figure-1: Initial ECG in the ED from a patient admitted with carbon monoxide poisoning.

 

=======================================

NOTE: Some readers may prefer at this point to listen to the 5:40-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on these tracings (that appear below ECG MP-73).

=======================================


Today's ECG Media PEARL #73 (5:40 minutes Audio) — Reviews the concept of "Shark Fin" Selevation and depression as a sign of extensive acute infarction.

 

 

 

MY Approach to the ECG in Figure-1:

As always — I favor a Systematic Approach for interpretation of every ECG that I encounter (This Systematic Approach is reviewed in ECG Blog 205).

  • Rate & Rhythm: The computerized interpretation of the rhythm is wrong. This is not VT. Instead, the mechanism of the rhythm is sinus — as determined by the presence of regular upright P waves in lead II (as per the RED arrow in lead II of Figure-2). Sinus P waves are also seen in lead V1 (RED arrow in this lead in Figure-2) — as well as in a number of other leads. Overall, QRS complexes are regular at a rate of ~110/minute — therefore the rhythm is sinus tachycardia.
  • Intervals: The principle teaching point for this tracing lies with assessment of QRS duration. I initially thought the QRS complex was wide. On closer inspection — I realized that the QRS is not wide — but that instead, there was "Shark Fin" ST segment elevation in multiple leads, making it appear that the QRS was wide!


Figure-2: I've labeled key findings from Figure-1 (See text).


What is Shark Fin Morphology?

It's important to be aware of the pattern of "Shark Fin" ST segment elevation — in which the QRS complex looks wide, because it blends in with ST segments that show extreme ST elevation in multiple leads. As a result — the boundary between the end of the QRS complex and the ST segment becomes indistinguishable in those leads showing marked ST elevation or depression.

  • As discussed in detail in today's Audio Pearl (above) — "Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion. Consideration of prompt cardiac cath is essential for clarifying the anatomy — since in many (most) cases, prognosis is likely to be poor unless there is prompt reperfusion.
  • The KEY for confirming that "Shark Fin" morphology is the cause of the striking ECG picture this produces — is to find 1 or 2 leads in which you can clearly define the limits (end point) of the QRS complex. The most helpful lead for doing this in today's case is lead V1 — in which I've drawn in a RED line parallel to the heavy ECG grid line in simultaneously-recorded leads V1,V2,V3. Note that I've extended this line down to the corresponding complex in the long lead II rhythm strip (Figure-2).
  • The reason for continuing the RED line all the way down to the corresponding beat in the long lead II rhythm strip — is that this tells you where the QRS complex ends and the ST segment begins in the long lead II rhythm strip.
  • Knowing this landmark for the complexes in the long lead II rhythm strip — allows us to draw in and extend upward the PINK lines parallel to the heavy ECG grid line in the other 3 sets of simultaneously-recorded leads (PINK lines in Figure-2).
  • Putting IAll Together: The ECG in Figure-2 shows sinus tachycardia at ~110/minute with massive (ie, "Shark Fin" morphology) ST elevation in leads I, II, aVF — and in leads V2-thru-V6. A lesser degree of ST elevation is seen in leads III and aVL. Marked (ie, "Shark Fin" morphology) ST depression is seen in lead aVR, with a lesser degree of ST depression in lead V1.

 

Technical Points about this Tracing:

Unfortunately — the ECG in today's case is significantly angled. Presumably, this occurred because a picture of this ECG was taken and sent via smart phone, in the hope of expediting a 2nd opinion on this case.

  • It's important to appreciate the effect that an angled tracing may have in distorting ECG measurements. That said — one can compensate for this angling by drawing in your reference line for assessing simultaneously-occurring events parallel to the ECG heavy grid line in whatever lead(s) you are looking at (as was done with the RED and PINK lines in Figure-2).
  • NOTE: The reason I deviated from my Systematic Approach (as outlined in ECG Blog #205) — was my concern about QRS widening. This is because parameters for Axis, Chamber Enlargement and assessment of ST-T wave changes all depend on determining the reason for QRS widening. Figuring out that the cause of the unusual ECG picture in today's case was "Shark Fin" morphology with a normal QRS duration completely changed my assessment of this tracing.

 

  

Back to the HISTORY in Today's Case:

We were told that the patient in today's case was admitted for carbon monoxide poisoning. 

  • QUESTION: How should we interpret the ECG in Figure-2 in light of this history?

 

 

 

ANSWER:

  • Brief review of carbon monoxide poisoning provides insight on how best to clinically interpret the ECG in Figure-2.

  

Cardiac Toxicity from CPoisoning:

The clinical presentation of acute CO (Carbon MonOxide) poisoning can be subtle. The gas is colorless, odorless, tasteless and non-irritating — so it can easily go undetected. Initial symptoms are varied, and often nonspecific (ie, headache, weakness, dizziness, nausea or vomiting, shortness of breath, mental confusion). 

  • The mechanism of CO toxicity stems from its exceedingly high affinity for binding with hemoglobin (~200 times greater than oxygen) — which leads to formation of carboxyhemoglobin, thereby substantially reducing the oxygen-carrying capacity of the blood.
  • Toxic effects from CO poisoning most severely affect the cardiovascular system and central nervous system — because of the increased oxygen demand of tissues in these organ systems. 
  • Cardiac Toxicity from CO poisoning includes an increased incidence of cardiac arrhythmias, conduction defects, myocardial ischemia/injury, and impaired LV (left ventricular) function (Zaky et al — Cardiovasc Regen Med, 2015). Although myocardial infarction may occur — this most often is the result of supply-demand mismatch (ie, "Type II" infarction) and not from acute coronary occlusion. That said — Hsu et al have documented that acute LAD occlusion from CO poisoning can occur (Kaohsiung J Med Sci 26:271-275, 2010).

  

Case CONCLUSION:

Clinical details are lacking in today's case. What is known, is that the patient was intubated (therefore unable to provide any history) — and — in refractory shock at the time the ECG in Figure-2 was obtained. Unfortunately, this leaves us with more questions than answers. That said — My Thoughts are the following:

  • As noted above — most infarctions that occur as a result of carbon monoxide poisoning are not the resut of acute coronary occlusion. Given that the patient in today's case was in refractory shock at the time ECG #1 was obtained — I interpreted the massive ST elevation in multiple leads (with marked ST depression in leads aVR and V1) — as representing diffuse subendocardial ischemia from severe CO poisoning, resulting in markedly impaired LV function.
  • I was then provided with a follow-up ECG on this patient, who unfortunately remained in refractory shock (Figure-3):

 

Figure-3: Comparison of the initial ECG in today's case — with a follow-up tracing (See text).

 

Final THOUGHTS:

The follow-up ECG ( = ECG #2) shows a rapid sinus tachycardia at ~135-140/minute, consistent with the patient's refractory shock state.

  • There is very poor R wave progression in ECG #2 — with no more than a tiny r wave in leads V1, V2 and V3.
  • Although the overall amount of ST segment deviation (elevation and depression) is markedly less in ECG #2 compared to what it was in ECG #1 — 3-4 mm of ST elevation persist in lead V3. The dfference between the 2 tracings in Figure-3 — is that the diffuse ST elevation seen on the initial ECG is now localized in ECG #2, primarily to the anterior leads (ie, leads V2, V3, V4) — with a much lesser degree of ST elevation in selected limb leads (ie, leads I, II, aVL, aVF). This made me wonder if rather than diffuse subendocardial ischemia — there may have been LAD (Left Anterior Descending) coronary artery occlusion at some point during the evolution of this case.

 

 

"Take-Home" PEARL:

Be aware of the entity of "Shark Fin" morphology — which can easily be mistaken for QRS widening.

  • Look closely in all 12 leads for the 1 or 2 leads that allow you to precisely define the limits of the QRS complex (as described in explaining Figure-2).
  • Realize that the massive ST segment elevation (and/or reciprocal ST depression) of "Shark Fin" morphology is most often the result of acute coronary occlusion.

 

==============================

Acknowledgment: My appreciation to Ehab Abdoh Bahgaat (from Hofuf, Saudi Arabia) for the case and this tracing.

==================================

 

Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
  •  
  • The November 22, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was cardiac arrest, ischemic Osborn waves, with massive Shark Fin ST deviation from acute STEMI.
  • The June 12, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB) in addition to Shark Fin ST elevation & depression
  • The January 24, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LAHB) in addition to Shark Fin ST elevation & depression — followed by progressive Low Voltage due to Myocardial Stunning from the huge infarct.

  • The May 13, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews ECG recognition and the differential diagnosis of diffuse subendocardial ischemia.




2 comments:

  1. excelente interpretación! felicidades

    ReplyDelete
    Replies
    1. Gracias. Fue un caso muy interesante — :) (Thanks; it was a very interesting case)

      Delete