Scoop or Droop

What interesting findings do you note on this ECG?

Click to enlarge. Go ahead, click it.  It won't hurt.

It is slow atrial fibrillation (some would even call it fib-flutter) at a rate between 40 and 60-ish with normal axis.  There is also T wave flattening, a short QTc (the top part that I cropped off says 0.402), U waves, and sagging inferior/lateral ST segments. 

What does all that mean?  Digoxin.

Digoxin is a cardiac glycoside commonly extracted from the foxglove plant:

Digitalis lanata in the Jardin des Plantes, Paris. Public domain.
Photo credit.

 It is used most often for rate control in atrial fibrillation and to increase contractility in congestive heart failure.  There are three main effects:

• It slows conduction through the AV node, which helps slow atrial fibrillation
• It increases cardiac automaticity (the ability of heart cells to initiate depolarization without external stimuli)
• It increases myocardial contractility, which helps in congestive heart failure

There are four main ECG findings that you see in patients with therapeutic levels of digoxin.  The first are T wave changes, such as flattening, inversion, terminal peaking, and such.  Second, the QT interval shortens due to decreased ventricular repolarization time.  In addition, U waves are commonly seen.  Finally, the ST segments sag – usually referred to as the “dig scoop.”  This is especially visible in leads with tall R waves (inferior and lateral leads).  Take a minute to look at the ECG above and pick out each of those findings.

This leads me to a brief and unimportant rant: Everyone has heard the term “Dig scoop.”  I think it looks less like a scooped ST segment than it does a sagging or drooping ST segment.  It isn’t scooped like someone grabbed some baseline-flavored ice cream.  The ST segments sag, like they’re tired.  So I like the term “dig droop.”  I think it is slightly more accurate, plus it has the double-D alliteration.

They are drooping, not scooped! Also, note the U waves.
Photo credit (Public domain)

Toxic levels of dig can result from chronic or acute processes.  Chronic toxicity presents with nonspecific complaints like weakness and malaise (unhelpful complaints in the older population, huh?).  Visual disturbances like light halos are actually pretty rare, but can occur.  On top of the digitalis toxicity, CHF patients can have jumbled electrolyte levels from diuretic use that complicates the clinical picture.

The signs of acute poisoning revolve around the main effects of digoxin: slowed conduction through the AV node and increased automaticity.  Physical complaints usually involve nausea and vomiting.  Electrocardiographic effects include essentially any dysrhythmia (outside of bundle branch blocks and rapid AFib).  The increase in automaticity can result in PVCs – uniform, multiform, bigeminy, trigeminy, and such. The decreased AV conduction results in heart blocks, from first to third degree.* 

Three main dysrhythmias that should make you immediately consider digoxin toxicity are atrial tach (usually with a block), junctional tach, and ventricular tachycardia.  VTach can be nutty too, with stuff like bidirectional and alternating VTachs.(1)  Those are good to remember, but anytime your brain recoils from the weirdness of a rhythm on the monitor – think of digoxin.  When the ECG looks like two people holding hands, think of dig.  In my experience, digoxin makes for weird rhythms that need plenty of work and calipers to work through.

The management of dig-toxic patients depends on whether they are stable or not.  Stable patients usually just get to skip a few doses of digoxin to lower their levels.  Unstable patients are more complex.  Dysrhythmias are treated per ACLS, with pacemakers, ventricular antiarrhythmics, and such.  Electrolyte levels are corrected, and severely toxic patients can be given digoxin-specific Fab fragments (Digibind) as a kind of antidote.  Prehospital providers can’t screw with electrolyte levels and Digibind isn’t in my formulary.  So I guess it’s lucky that we’re good at ACLS in the field, isn’t it?  That is essentially all we are left with. 

If you want to get deeper into dig and how it works, you’re on your own.  Make sure to check out the article cited below by Gene Ma et al., and Life in the Fast Lane, ECGpedia, UpToDate, and other websites have good information.  Enjoy.

*If you want a real headache, heart blocks can result in (sort of) regular AFib: A complete heart block with slow, regular junctional escape. How’s that for fun?

1. Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: Digitalis toxicity. J Emerg Med 2001;20(2):145-52.