Digoxin strikes again! Job well done. You nailed it. Let’s discuss.
ECGAFib @ 90’s, normal axis, QRS/ST segments c/w Digoxin Effect
How Does Digoxin Work?
As you may remember, digoxin inhibits our old friend the Na+/K+ ATPase that creates the sodium gradient for the Na+/Ca++ exchanger. This leads to build-up of calcium inside the cardiac myocytes. And if you’re really astute, you may remember that it also increases vagal tone, leading to a slowed ventricular rate with accelerated atrial ones. That’ll change your ECG
ECG Changes
Generally think increased automaticity and decreased AV conduction (fast atria and slow ventricles); specifically: AFib with slow ventricular response, bidirectional VT, accelerated junctional rhythms, atrial tachycardia with AV Block, atrial fibrillation with complete AV block (regularized atrial fibrillation)
A Little Culture
No talk would be complete without mention of Salvador Dali, that Spanish surrealist with the trademark mustache. Some say he is the original Brooklyn Hipster. Let’s just say that he did it before it was cool. Check it out below:
“Dig”ing Deeper (Effect vs. Toxicity)
Our ECG is a good example of the Digitalis Effect (short QT, prolonged PR, the above QRS / ST segment abnormality). The astute practitioner realizes this merely indicates the patient is taking digoxin. It should be distinguished from true Digoxin Toxicity characterized by GI distress (vagal) and life-threatening dysrhythmias from hyperK+ (Na+/K+ ATPase).
Managing Digoxin Toxicity
Initial tests include an ECG, BMP, VBG as well as digoxin levels. In acute toxicity, Digibind (Dig Fab) is indicated if (1) K+ > 5, (2) ingestions >10 mg (adult), >5 mg (child), (3) levels >15 nM, or in (4) life-threatening dysrhythmias or cardiac arrest. Concerns for “Stone Heart” should not stop you from giving calcium to life-threatening hyperkalemia (Levine, 2011). You should consider charcoal for acute ingestions (<1 hr) and consider dialysis for chronic toxicity, as renal failure is often a precipitant of chronic toxicity. Lastly, manage the complications that arise (bradycardia, tachycardia, AV Blocks, etc) as you normally would in the ED.
How About Our Patient?
Clinically, our patient has an ECG showing the Digoxin Effect and no symptoms of Digoxin Toxicity. Prior to discharge, a quick check of her K+ and a digoxin level were performed, and they were within normal limits. The patient discharged to follow-up with a PMD and cardiologist after a discussion about headaches, hypertension, and organizing her medication.
Job well done bloggers!
P.S. I mustache for more puns in future posts…
References:
Jon B. Cole and David J. Roberts. Cardiovascular Drugs. Rosen’s Emergency Medicine, Chapter 152, 1982-1993.e2
Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med. 2011 Jan;40(1):41-6. doi: 10.1016/j.jemermed.2008.09.027.
Life in the Fast Lane. http://lifeinthefastlane.com/ecg-library/basics/digoxin-toxicity/
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1 Comment
ablumenberg · December 6, 2016 at 9:53 am
Awesome post!!
I would be weary of hemodyalisis as a treatment for dig toxicity — the Vd is relatively high (4-10 L/Kg) and HD is unlikely to remove much of the drug. As far as hyperkalemia of digoxin toxicity, the total body potassium shouldn’t be elevated (unless there is a second concommintant process) but rather caused by extracellular shift. Removing potassium from the body with HD or diuresis is potentially dangerous because when the digitalis wears off the patient may be hypokalemic.
There is a lot of culture with digitalis! Some think Van Gogh’s work is influenced by the visual changes associated with digitalis toxicity.
https://en.wikipedia.org/wiki/The_Starry_Night#/media/File:Van_Gogh_-_Starry_Night_-_Google_Art_Project.jpg
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071623/