Eastvold Pearl #28 - Lithium Toxicity Masquerading as Wellen's Syndrome

Take-home point: Rule out lithium toxicity in all patients on lithium presenting with cardiac toxicity and/or EKG changes.

[1] The case: 48 yo F with history of bipolar disease and depression presents to ED for evaluation of substernal chest pressure radiating to neck with bilateral arm "numbness."  Mild shortness of breath and ROS only positive for mild gradual onset headache.  Symptoms x 7 hours.  Chest pain non-exertional, non-positional, and non-pleuritic.  No fever, focal neurologic deficits, mental status changes, or abdominal pain.  Chest pain 7/10 upon arrival, and improved with 3/10 with nitrate therapy but continued to have ongoing pain/symptoms.  Serial EKG revealed dynamic change, and concern for proximal LAD lesion and Wellen's syndrome was discussed with cardiology.  Cardiology performed a bedside echo which revealed anterior wall motion abnormality, and to a lesser degree inferior-lateral dyskinesia.  Patient was taken to cath lab for elective cath, with knowledge of an elevated troponin of 0.61 (normal < 0.03),  Cardiac cath revealed completely normal coronaries, and no LV aneurysm  Lithium level came back elevated at 2.3, with no history of acute ingestion.  Quick literature review (articles attached) revealed that lithium can mimic ischemic EKGs, especially in the anterior leads.  Further, chronic lithium toxicity can also cause myocarditis.  See EKGs below illustrating deep anterior T wave inversions and prolonged QTc, both of which resolved after lithium level decreased.

[2] Quick skinny on lithium toxicity and EKGs, attached is are 2 review articles as well.

  • Lithium causes toxicity through several mechanisms including competition with many electrolytes (sodium, potassium, calcium, and magnesium) and ion transporters, which can disrupt many cellular functions.  The cellular membrane of concern here is myocytes (and Purkinje fibers....and most people just closed this email!), and these disruptions manifest as EKG changes.   
  • Common EKG changes include [a] QTs prolongation, [b] nonspecific ST segment and T wave abnormalities, [c] T wave inversions (reference #1), [d] transient ST elevations mimicking acute myocardial infarction (reference #2), [e] Brugada changes with possibility of sudden cardiac death (reference #3), [f] SA nodal dysfunction and heart block, and [g] severe bradycardia.
  • ECG changes are more likely to occur with chronic lithium overdoses than acute overdoses
  • Treatment is beyond the scope of this review but some important things to consider are
    • Make sure you get lithium levels on all patients presenting with cardiac symptoms
    • Know the difference between acute vs chronic toxicity, read attached article
    • Know your criteria for hemodialysis
    • Avoid thiazides and ACE-I, as these will increase lithium levels
    • Avoid NSAIDS, can also worsen toxicity.  Often given for myocarditis, but do not given if you think this is lithium-induced myocarditis
    • Check TSH, can be contributing to lithium toxicity
    • Consult toxicology and nephrology early, especially if cardiology is going to manage primarily

Feedback always welcome (joshua.eastvold@gmail.com),

Also, if anyone is interested in publishing this let me know??



[1] Cases J. 2008 Sep 17;1(1):156. doi: 10.1186/1757-1626-1-156.

[2] J Med Toxicol. 2008 Sep;4(3):170-2.

[3] Circulation. 2010 Aug 10;122(6):e418-9

[4] Toxicol Rev. 2006;25(4):221-30.

[5] J Am Soc Nephrol. 1999 Mar;10(3):666-74

EKG #1 upon arrival to ED

wellens Li1.png

EKG #2 - concerning for anterior ischemic.  QTc 494.  

wellens Li2.png

EKG #3 - worsening QTc prolongation, still getting PO lithium, don't ask

wellens Li3.png

EKG #4 - Courtesy call to cardiology, relayed my thoughts regarding concern for chronic lithium toxicity

-- now after lithium level returned to 1.3, complete resolution of anterior T wave changes and normalization of QTc

wellens Li4.png

Eastvold Pearl #25: Anterior MI w/o reciprocal cahnge

As we reflect on the year 2012, it is important to know what does not "reflect" (corny stretch) in the world of EKGs.  Fifty percent of anterior STEMIs lack reciprocal changes.  This is crazy but a fact.  I will try to summarize why this occurs, but you may want to read the attached article.  

We have all learned that reciprocal changes are important in diagnosing STEMIs, and their presence increases the likelihood that the EKG pattern is secondary to coronary occlusion.  Further this concept of reciprocal changes is the main focus of my "Swans Reflecting Elephants" talk, whereby localized ST depression is invariably secondary to subtle STEMIs.  

But does the absence of reciprocal change rule out MI?  The answer is no.  As stated above, 50% of anterior STEMIs lack reciprocal changes.  

That said,  inferior STEMIs will almost always have STD (albeit may be subtle) in I/AVL or at least new TWI in AVL.  Lateral STEMIs also will have reciprocal change.   

The pathophysiology of inferior ST segment changes in the setting of anterior STEMI is actually pretty cool.  I have read a lot on this, and I think you will like this article I am attaching.  To summarize, in the setting of anterior STEMIs there are 3 patterns of inferior ST segment changes, [a] ST depression, [b] ST elevation, and [c] No ST change.  Group "c" accounts for 50%, quoted many times in the literature.  

Look at Figures 1, 2, and 3 in the paper, as this is the best explanation on this issue that I have found.

-- Anterior STEMI with inferior ST depression occurs because the occlusion is proximal LAD (proximal to D1 or 1st diagonal), with infarction extending to high lateral wall.  Thus the inferior ST depression actually represents true reciprocal change from lateral ischemia.  Anterolateral STEMI.

-- Anterior STEMI with inferior ST elevation occurs the the occlusion is distal to D1 AND wrap-around LAD (a variant) that supplies the inferior wall, thus causing inferior STEMI.

-- Anterior STEMI with no inferior ST changes occur in 2 settings, which is exemplified in example #3 in the paper.  [1] Occlusion distal to D1 with no wrap-around LAD, so no infarction of lateral (distal) or inferior (no wrap-around) regions.  There is NO reciprocal change for true anterior ischemia.   [2] This setting is the cool one.  If you have a proximal LAD lesion to D1 AND a wrap-around LAD, the ST changes counteract each other.