Rhythm Nation – February 2020

Ah, February. The month of hearts of all types – the ones that move too fast, the ones that don’t move fast enough, and the ones that just can’t seem to make up their minds. 

Thank you to Dr. Sharland Johnson for submitting this ECG! 

A 31-year-old female with PMH of HTN on amlodipine, presents to the Critical Care and Trauma area for circumferential, pleuritic chest pain that is worse with movement and started upon awakening this morning. Her pain initially was 6-7/10 and is currently 4-5/10. She states that she has had a pretty boring life, spending most of her time working in a busy ED, and thus has no time to use cocaine or take long flights or do any of the things she knows you’re going to ask her. She quit OCP use last year after she broke up with her partner on Valentine’s Day. 

Exam:

Vitals: BP 100/70 mm Hg, HR 60/min, RR 18/min T 98, SpO2 98% room air

Gen: mildly uncomfortable appearing but calm, speaking full sentences, AAOx3

Neck: No JVD. Supple.

CV: RRR, S1S2. No murmurs.

Resp: CTAB. Pain elicited on deep breathing and movement. No chest wall tenderness.

Abd: soft, mild epigastric tenderness, non-distended, normal bowel sounds

Ext: No peripheral edema.

Just as you wonder what this patient is doing in the critical care area, your attending waves her triage ECG in front of you:

Her prior ECG is below:

baseline

What myocardial territories do you suspect are involved? What pathology should you consider given this patient’s demographic? Post your answers in the comments below! As usual, the answer will be released next week. 

 

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5 Comments

Stacey Frisch · February 5, 2020 at 5:42 pm

One possibility to consider: Diaphragmatic irritation 2/2 subdiaphragmatic pathology, especially considering pt is low risk for ACS. This would also go along with pt’s pleuritic quality of pain and epigastric ttp. Could be from acute pancreatitis or biliary pathology. Acute pancreatitis presents with EKG changes in more than half of cases, known to mimic usually inferior MI in many cases.

Suspected pathophysiology of EKG changes in acute pancreatitis include:
1. Electrolyte abnormalities such as hypokalemia, hypomagnesemia, hypocalcemia, and hyponatremia. Hypomagnesemia in particular can cause coronary vasospasm and stunning of the myocardium to resemble ischemic-appearing ECG changes
2. Direct damage of myocytes secondary to release of proteolytic enzymes (ex. trypsin).
3. Vasovagal stimulus secondary to the acute intra-abdominal disease can cause a cardiobiliary reflex and can present as bradycardia, AV block, hypotension, and syncope

Maybe the patient had a few too many post-night shift boozy breakfasts 😉

References:
Yu ES, Lange JJ, Broor A, Kutty K. Acute Pancreatitis Masquerading as Inferior Wall Myocardial Infarction: A Review. Case Reports in Gastroenterology. 2019;13(2):321-335.
Rubio-Tapia A et al. Electrocardiographic Abnormalities in Patients With Acute Pancreatitis. Journal of Clinical Gastroenterology. 2005;39(9):815-818.

    deSouza · February 6, 2020 at 1:37 am

    Nice comment, Frisch. Thanks for participating.

Jane Belyavskaya · February 7, 2020 at 6:58 am

In a patient with no contributory medical history and new EKG changes with a history of a “stressful event”, what about Takotsubo Cardiomyopathy? Although it classically occurs in post-menopausal women, it is usually due to emotional stress associated with a cathecholamine surge which may result in microvascular spasm and sympathetic nervous system activation.
In the ED, takotsubo is indistinguishable from a STEMI and can present with ST elevations or new TWI inversions.
So maybe she just has a broken heart?

Akashi YJ, Goldstein DS, Barbaro G, Ueyama T.Takotsubo cardiomyopathy: a new form of acute, reversible heart failure.Circulation. 2008 Dec 16;118(25):2754-62.PMID: 19106400
Abdulla I, Ward MR.Tako-tsubo cardiomyopathy: how stress can mimic acute coronary occlusion.Med J Aust. 2007 Sep 17;187(6):357-60. PMID: 17874985

Molly Kentarou Yamazaki · June 28, 2020 at 6:38 pm

As Jane said it could definitely be Takotsubo Cardiomyopathy purely because of the TWI inversions

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