ECG Blog #296 — Shark Fin Infarction — or Not?

An elderly man presented to the ED (Emergency Department) — with a 1-day history of abdominal pain and the ECG shown in Figure-1.

QUESTION:

• Despite the history of abdominal pain (and not chest pain) — Should the cath lab be activated?
• What is "Shark Fin" ST elevation?

Figure-1: Initial ECG in the ED — obtained from an older man with a 1-day history of abdominal pain. Should the cath lab be activated?

MY Initial Thoughts on ECG #1:

The entity of "Silent" MI (ie, infarction without a history of chest pain) — is more common than is generally appreciated, especially among older individuals (See ECG Blog #228 for more on "Silent" MI). My awareness of this entity led me to rapidly consider the need to activate the cath lab for the ECG shown in Figure-1 despite the lack of chest pain.

• I fully admit that my attention was instantly captured by the "eye-catching" abnormal complexes in the anterior leads V1, V2 and V3 of ECG #1! Could this represent "Shark Fin" ST elevation from a huge acute STEMI in a patient with need of prompt reperfusion?

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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 the illustrative case in ECG Blog #265 — "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 (See Figure-2 below):

Figure-2: I've labeled today's ECG from Figure-1 — to facilitate recognition of "Shark Fin" ST elevation in the anterior leads (See text).

Taking a Closer Look at ECG #1:

Assessing today's tracing systematically:

• The rhythm is sinus tachycardia at ~115/minute (RED arrow in lead II of Figure-2 highlighting the upright sinus P wave in this lead). Regarding "Intervals" — the PR interval is not prolonged. Assessing the QTc is difficult with this degree of tachycardia — though I thought the QTc at most to be no more than slightly prolonged. It was assessment of QRS duration that posed the greatest difficulty!

The QRS complex clearly looks wide in leads V1 and V2 — but not so much in other leads. This was initially confusing to me.

• Leads V1, V2 and V3 were recorded simultaneously with the corresponding portion of the long lead II rhythm strip below the 12-lead. I thought lead V3 was KEY to assessment of QRS duration — as we can clearly see the end point of the QRS complex in this lead. I therefore drew a dotted BLUE line parallel to the heavy ECG grid line in Figure-2, corresponding to the end of the QRS complex. This suggests that the QRS complex is actually no more than minimally prolonged (ie, ~0.10-0.11 second).
• Taking the vertical dotted BLUE line as the end point of the QRS complex  in Figure-2 suggests: i) That the QRS complex is slightly widened and upright in leads V1,V2; and, ii) That there is extreme ST segment elevation in leads V1,V2,V3 (with the point marking the amount of ST elevation beginning just to the right of this dotted BLUE line in these 3 leads). This dramatic amount of ST elevation then descends into deeply inverted T waves in each of these 3 anterior leads.

My "Bottom Line" Impression of ECG #1:

I was left with uncertainty as to the cause of the highly unusual appearance of the QRST complexes in anterior leads V1, V2 and V3.

• QRS morphology is clearly abnormal — in that the QRS is slightly (but not markedly) widened — and the QRS is all positive in leads V1 and V2 (and still predominantly positive in lead V3). In association with wide terminal S waves in lateral leads I and V6 — this picture is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• My initial impression regarding the dramatic amount of "Shark Fin" ST elevation in the 3 anterior leads — was acute LAD (Left Anterior Descending) coronary artery occlusion, causing acute antero-septal STEMI with the bifascicular block (RBBB/LAHB) that is so commonly seen in association with acute proximal LAD occlusion. That said, if this was the cause of the unusual anterior lead appearance — I would not have expected to already see such deep anterior T wave inversion.
• Then I thought that perhaps we are seeing a Brugada-1 ECG pattern (See ECG Blog #238 on Brugada Phenocopy) — that is superimposed on IRBBB/LAHB in a patient with acute LAD occlusion, with deWinter-like T waves in lateral chest leads V4-thru-V6 (ie, Note J-point ST depression that ascends to form prominently peaked T waves — as reviewed in ECG Blog #183). 
• Finally — There are deep, wide Q waves in each of the inferior leads, indicative of inferior MI of uncertain age (with or without associated LAHB).

The CASE Continues:

Clinical follow-up in today's case was very surprising! (See Figure-3).

• Serum K+ = 5.3 mmol/L (ie, no more than minimally elevated).
• Serial Troponins were normal!
• Serial ECGs over the course of the next day failed to show any significant evolution.
• Echo revealed normal systolic and diastolic function without regional wall motion abnormality.
• It turned out that the cause of the patient's acute illness was a right inguinal hernia which led to bowel obstruction with perforation. On operation — intestinal perforation was found with multiple necrotic patches spread throughout the ileum (Figure-3).
• Throughout the patient's course — he never developed chest pain.
• Given no positive findings for an acute cardiac event — cardiac catheterization was not deemed necessary.

Figure-3: Clinical follow-up findings in today's case. Chest X-ray (upper Left) — showed greatly distended intestine, suggestive of bowel obstruction. CT scan and intra-operative photograph revealed right inguinal hernia with bowel obstruction and perforation (with multiple necrotic patches throughout the ileum).

Acute Abdomen as a Cause of Pseudo-Infarction on ECG:

There is a literature documenting a number of cases in which an acute abdomen resulted in an ECG picture suggestive of an acute cardiac event — but for which clinical follow-up revealed no infarction (ie, Pseudo-Infarction ECG patterns).

• Cattermole and McKay (Emerg Med J 23:e48, 2006) — reviewed the literature and reported on an older woman with a rectus sheath hematoma — whose ECG was mistaken for acute inferior MI.
• Herath et al (BMC Cardiovascular Disorders 16:245, 2016) — reported a case of intestinal obstruction with gastric distension, that resulted in dynamic ECG changes mimicking an evolving anterior MI. Of interest — ECG changes resolved promptly following gastric decompression.
• Mixon and Houck (Tex Heart Inst  30:155-157, 2003) — reported a case of intestinal obstruction which altered the anatomy, resulting in actual compression of the right ventricle (and the ECG finding of marked anterior lead ST elevation).
• Other acute abdominal conditions (including cholecystitis and pancreatitis) — have also been shown to produce pseudo-infarction ECG patterns.

NOTE: The mechanism responsible for producing pseudo-infarction patterns in association with acute abdominal conditions is uncertain. Among the mechanisms postulated include:

• Catecholamine surge — secondary to pain and/or the acute abdominal condition itself (perhaps via a similar mechanism to the catecholamine surge associated with Takotsubo Cardiomyopathy).
• Change in the anatomic position of the heart (and/or direct compression of a portion of the heart) — that might be caused by physical contact from gastric and/or intestinal obstruction.
• Increased vagal tone from pain — causing coronary artery spasm or other reflex mechanism that results in ECG changes.
• Variant (Pinzmetal) angina with coronary vasospasm — perhaps precipitated by increased sympathetic tone associated with an acute abdomen.

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Acknowledgment: My appreciation to 陳俊宏 (Chun-Hung Chen from Taichung City, Taiwan) for the case and this tracing.

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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).

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• ECG Blog #228 — reviews the entity of "Silent" MI with an illustrative case (the Audio Pearl in this post reviews How Often Silent MIs occur).
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• ECG Blog #265 — which reviews in detail a case of "Shark Fin" ST elevation due to ischemia/infarction from CO poisoning.
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• ECG Blog #238 — which reviews in detail the entity of Brugada Phenocopy (including an ECG Video Pearl on the essentials of Brugada Syndrome).
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• ECG Blog #183 — reviews the ECG pattern of deWinter-like T-waves (with variations of this pattern discussed in the accompanying Audio Pearl).
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• 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 11, 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.