SSmith-DRAFT- Anaphylaxis-CP-ST elev in aVR (2-12.21-2023)-I_AM_DONE

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

Comment by KEN GRAUER, MD (2/13/2023):

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

Today's case by Dr. Meyers serves as a reminder of the important clinical entity known as diffuse subendocardial ischemia. The initial ECG (which I've reproduced in Figure-1) — is classic for this entity, as it shows marked ST depression in no less than 9/12 leads — with ST elevation in lead aVR.

• In addition to ST elevation in lead aVR — a lesser amount of ST elevation may also be seen in lead V1 with diffuse subendocardial ischemia (and sometimes also — as occurs in today's case, some ST elevation in lead aVL). 
• The relative amount of ST elevation in lead aVR with diffuse subendocardial ischemia — tends to be comparable to the amount of ST depression seen in many of the leads.
• ST depression will not always be present in 9/12 leads — as is seen in Figure-1. Instead, diffuse subendocardial ischemia may be present with ST depression in only 7 leads.
• Finally — It is well to remember that the amount of ST segment deviation in ECG #1 is extreme! Much of the time — the amount of ST depression (and the amount of reciprocal ST elevation in lead aVR) will not be nearly as marked.

The KEY (as emphasized by Dr. Meyers) — is to think of diffuse subendocardial ischemia whenever you see diffuse ST depression (in ≥7 leads) with ST elevation in lead aVR. This ECG picture should immediately prompt the following diagnostic considerations:

• Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• Subendocardial Ischemia from another Cause (ie, sustained tachycardia — sinus or from some other arrhythmia; shock/profound hypotension; GI bleeding; anemia; etc.).

PEARL #1: It's important to remember that there are frequently no wall motion abnormalities when there is diffuse subendocardial ischemia. This is because: i) The epicardium remains functional, since it is only the endocardium that is ischemic; and, ii) By definition — subendocardial ischemia is diffuse — and therefore does not localize to any particular myocardial region.

PEARL #2: Based on the initial ECG that was shown in today' case ( = ECG #1 in Figure-1) — We should also think of other potential causes of ST depression. These might include: i) Low serum K+ and/or low Mg++; ii) Tachycardia (The rhythm is sinus tach at ~110-115/minute — and that rate is fast enough to produce some ST depression); and, iii) LVH with LV "strain" (Suggested by the deep S wave in lead V1 — and the shape of the ST-T wave depression in inferior and lateral leads). That said — the diffuseness and amount of ST depression in Figure-1 is so marked, that regardless of potential contribution from these other factors — diffuse subendocardial ischemia should be presumed until proven otherwise.

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Application to Today's Case:

As per Dr. Meyers — No definitive explanation for the marked ST segment deviation seen in ECG #1 was determined. That said — management in this case was excellent, in that the patient's severe allergic reaction was promptly treated (with steroids, diphenhydramine and epinephrine) — and — underlying coronary disease was ruled out by Echo and Coronary CT Angiogram.

• BOTTOM Line: The "good news" — is that health care providers in today's case promptly recognized the ECG picture as indication of diffuse subendocardial ischemia (and not of acute MI). And, after resolution of the acute allergic reaction — underlying coronary disease was appropriately ruled out before discharge.

====================== 

LINKS to My Comments on Subendocardial Ischemia:

SSmith — My Comment from May 13, 2020

https://hqmeded-ecg.blogspot.com/2020/05/what-do-you-think-echocardiogram-shows.html

SSmith — My Comment from March 9, 2020

https://hqmeded-ecg.blogspot.com/2020/03/does-ste-in-avr-indicate-acute-coronary.html

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

Comment by KEN GRAUER, MD (2/11/2023):

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

XXX

• 
  

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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

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

MY Comment by KEN GRAUER, MD (5/13/2020):

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

It’s good to periodically review the differential diagnosis of the diffuse subendocardial ischemia. Recognition of this ECG pattern should be an automatic REFLEX for the emergency care provider — As soon as one sees diffuse ST segment depression (usually present in at least 7-8 leads) + ST elevation in lead aVR — one should consider:

• Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; shock/profound hypotension; GI bleeding; anemia; etc.).

The initial tracing in this case illustrates an extreme example of this phenomenon — in which all leads except for aVR and V1 manifest profound ST segment depression (Figure-1).

• ST depression attains up to 5 mm in several leads!
• A comparable amount of reciprocal ST elevation is seen in lead aVR.
• As is seen in ECG #1 — a lesser amount of ST elevation is sometimes seen in lead V1.

Figure-1: The initial ECG in this case, done in the field by the EMS team (See text).

In the March 9, 2020 post of Dr. Smith’s ECG Blog — Dr. Smith presented results from a 2019 article by Harhash et al, that confirm how the ECG pattern shown in Figure-1 does not represent acute LMain occlusion — but rather the differential diagnosis that I show above.

• The case I presented in My Comment to that March 9, 2020 post showed a patient with this pattern — who on cath had no more than minimal coronary disease.
• Dr. Smith also referenced an article by Knotts et al, showing that even when diffuse subendocardial ischemia is due to coronary disease — that only a minority of patients had severe LMain coronary disease as the cause.

Today’s Post by Dr. Smith adds to our knowledge of this syndrome. 

For as helpful as POCUS Echo can be in the diagnosis of acute coronary occlusion — we need to remember that there are frequently no wall motion abnormalities when there is diffuse subendocardial ischemia — because (as emphasized by Dr. Smith): i) The epicardium remains functional, since it is only the endocardium that is ischemic; and, ii) Subendocardial ischemia is diffuse — and therefore does not localize to any particular myocardial region.

P.S.: 

Much of the time — the amount of ST depression (and the amount of reciprocal ST elevation in lead aVR) will not be as extreme as it is in Figure-1. Nevertheless, this ECG pattern of subendocardial ischemia needs to be instantly recognized — so that optimal decision-making based on the clinical scenario can promptly begin (See the October 31, 2018 post on Dr. Smith’s Blog).

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

Pendell DRAFT as of 2-2.1-2023:

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

 Sent by anonymous, written by Pendell Meyers

A man in his late 40s presented to the ED with concern for allergic reaction after accidentally eating a potential allergen, then developing an itchy full body rash and diarrhea. In the ED he received methylprednisolone, diphenhydramine, and epinephrine for possible anaphylaxis. Shortly after receiving epinephrine, the patient developed new leg cramps and chest pain. The chest pain was described as sharp and radiated to both arms.

During active chest pain an ECG was recorded:

Meyers ECG interpretation: Sinus tachycardia, normal QRS complex, STD in V2-V6, I, II, III and aVF. Reciprocal STE in aVR, and a touch in V1 (closest lead to aVR). The precordial STD persists in severity from V4-V6, rather than being maximal in V1-V4 (as in posterior OMI), and so the ECG overall best fits the subendocardial ischemia pattern (diffuse supply/demand mismatch). This pattern occurs regardless of whether the cause is ACS (decreased supply) or any other cause of decreased supply or increased demand. There is a tiny hint of STE in aVL, but overall I do not think this looks like high lateral OMI.

A "STEMI alert" was called and soon cancelled. His vitals are unfortunately unavailable during the chest pain episode.

Pain lasted for approximately 45 minutes.

Initial high sensitivity troponin I returned within normal limits at 10 ng/L (less than 20 is reference range for men for this assay).

After pain had resolved, another ECG was performed:

Almost resolved compared to ECG above.

Given the ECG changes, he was admitted for further workup.

Repeat troponins were:

94 ng/L

190 ng/L

(none further were ordered)

Formal cardiac echo showed:

EF 73%, normal systolic and diastolic function, normal LV cavity size and wall thickness

No valvular stenosis of regurgitation

Coronary CT Angiogram: 

Mid LAD with less than 25% stenosis

All other arteries with no noted stenosis of plaque

Interpreted as "mild, nonobstructive coronary atherosclerosis"

The patient was discharged.

It is unclear to me whether this case could represent 1) simple supply/demand mismatch due to increased demand from epinephrine, 2) Kounis syndrome (usually described as mast cell mediated coronary vasospasm during allergic reaction), 3) brief autolysed left main or LAD ACS with no findings on later echo and CT coronary angio, or 4) something else.

Learning Points:

You must learn and recognize the ECG patterns of OMI and subendocardial ischemia to best understand the ECG in acute care medicine.

Subendocardial ischemia manifests as diffuse ST depression in downward and leftward leads, with maximal precordial STD in V5-V6 and lead II, and reciprocal STE in aVR. You must understand that this pattern does not differentiate ACS from other causes of supply/demand mismatch.