Dont let your bradycardic patient D.I.E.

At the risk of plagiarizing myself, I’d like to revisit a topic that I discussed on my personal blog a couple of years ago. The story goes that I am not very good with mnemonics. For me they are almost never useful in clinical practice, and as the patient gets sicker my chances of properly recalling the applicable mnemonic decreases exponentially.

There is, however, one that I never forget, and it’s the DIE mnemonic for bradycardia. I developed this memory aid based off a talk on bradycardia given by the great Dr. Mel Herbert, where he discusses the above differential but in a different order and with no handy catch-phrase.


When the patient in front of you is sick, these are the three common and reversible causes of bradycardia that you need to recognize in the emergency setting. Yes, there are other causes of bradycardia that should be on your differential, but what makes this list special is that all three have specific emergency treatments and the standard ACLS trio of pacing, atropine, and dopamine does little or nothing to address them.

It’s okay to miss Lev’s disease in the emergency setting because the definitive treatment is contained in the usual ACLS algorithm: pacing. If you don’t recognize that your patient is hyperkalemic, however, then all the atropine and transcutaneous pacing in the world isn’t going to lower her potassium. You don’t even need to have heard of sick sinus syndrome to properly treat it, again with pacing. If you miss ischemia though, and bring the patient to a non-PCI center, then there could be trouble down the line. I don’t think you need the EKG to diagnose hypothermia, but you’d better be considering medication effects in every significantly bradycardic EKG you see. Beta blockers and calcium channel blockers can easily sneak past your differential, while the QT-prolonging effects of other anti-arrhythmics can be magnified by a slow heart rate pose an extra threat of sudden death that must be considered.

If there’s one entity missing from the mnemonic, it’s ‘H’ for hypothyroid or ‘M’ for myxedema coma (let’s just pretend they’re one in the same). Really though, who wants to remember DIME or HIDE when DIE sticks in the mind so well? Use one of the others if you’d like, but I think DIE is just too easy and memorable to make the longer forms worthwhile.

So let’s get into the three major players…


It’s fitting that this is the first item in the mnemonic because it is also the culprit I am most likely to overlook. The overdose can be intentional or accidental, and things like decreased renal function can lead to the latter without the patient even taking a single extra pill. I throw around the term “overdose,” but what we’re really talking about is any supratherapeutic levels of drugs or medications the patient may have taken. The culprits I worry about most in the undifferentiated bradycardic patient are calcium channel blockers, beta blockers, and digoxin, but there’s a whole host of medications — lots of anti-arrhythmics — that cause marked bradycardia in excessive doses. Enjoy some examples, and ponder whether you would have considered “overdose” as a possibility when seeing these ECG’s.

Metoprolol and Diltiazem OD

Junctional bradycardia in a patient on both metoprolol and diltiazem. Bradycardia resolved and returned to normal sinus rhythm 24 hrs after discontinuing both medications.

Digoxin toxicity

Junctional bradycardia in a patient with a digoxin level of 4.4 ng/mL (ref 0.8 – 2.0 ng/mL), later treated with digoxin immune fab.

Dig toxicity

Junctional bradycardia in a patient with a digoxin level of 2.9 ng/mL (ref 0.8 – 2.0 ng/mL). The QRS morphology matches his baseline EKG.

TCP in dig toxicity

Transcutaneous pacing was attempted in the prior patient with unrecognized failure to obtain electrical capture at 50mA.

Sinus bradycardia and a prolonged QT-interval in a patient with sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.

Sinus bradycardia and prolonged QT-interval following sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.



Despite its relatively high prevalence, ischemia is probably (hopefully?) the least missed of the three topics discussed here. Still it happens, and it’s good to force yourself to at least consider the possibility in any patient with bradycardia. We most commonly discuss ischemia causing bradycardia in the setting of inferior STEMI, especially larger and more obvious infarctions, but it can sometimes present subtly or in unexpected coronary distributions. The often bizarre atrial arrhythmias and various levels of AV-block seen with inferior MI are thought to be due to ischemia of the SA and AV nodes, but the Bezold-Jarisch reflex could also play a role as well. Thankfully, most brady-arrhythmias seen with inferior STEMI’s resolve with reperfusion and time, but those associated with anterior STEMI tend to be more malignant and portend a worse outcome.

Sinus brady, inferior STEMI

Marked sinus bradycardia in a patient with obvious inferior STEMI.

Sinus brady, subtle inferior STEMI

Sinus bradycardia in a patient with somewhat subtle infero-posterior STEMI.

Complete heart block, inferior STEMI

Complete heart block in a patient with an extensive infero-posterior STEMI and cardiogenic shock. The patient experienced PEA arrest and expired shortly after this ECG was acquired.

AV-dissociation, inferior STEMI

AV-dissociation (probably CHB) in a patient with a large inferior STEMI.

Atrial bradycardia, global MI

Uncertain and irregular atrial bradycardia in a patient who presented with vague epigastric discomfort and hypotension. Echo showed near-global LV dysfunction, troponin-I (ref < 0.04 ng/mL) peaked at almost 100 ng/mL!



In terms of overall numbers, I believe that electrolyte disturbances are certainly the most missed cause of bradycardia. It’s unusual to miss ischemia significant enough to cause bradycardia, and drug toxicity is a fairly uncommon presentation, but electrolyte abnormalities are an everyday event in most emergency departments.

When we talk about electrolytes and brady-arrhythmias, we mean potassium. And, by far, the most common bradycardia-producing electrolyte abnormality is hyperkalemia. While calcium can affect your ST/T-waves, it is typically not a direct cause of bradycardia. Despite it’s huge role in cardiac action potentials, serum sodium levels actually have little effect on the surface ECG (though sodium channel blockers do…). Similarly, though magnesium plays a role in some arrhythmias, there are no direct EKG signs of hyper/hypo magnesemia. It’s an even less exciting story for the rest of the electrolytes.

While emergency care providers know to look for peaked T-waves and wide QRS rhythms, it is constantly sobering just how subtle the signs of hyperkalemia can present on the EKG. Below are just a handful of the subtle hyperkalemia cases I’ve encountered. Importantly, hypokalemia can also present with bradycardia in rare cases, but it is much more often associated with a normal or tachycardic rate. Still, it’s worth keeping in mind.

Hyperkalemia K+ 6.5

Severe sinus bradycardia in a patient with a serum K+ level of 6.5 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.6

Junctional bradycardia in a patient with a K+ of 6.6 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.7

Complete heart block in a patient with a K+ of 6.7 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.9

Sinus brady with slight QRS widening (compared to baseline) in a patient with a K+ of 6.9 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 7.2

Junctional bradycardia (with artifact) in a patient with a K+ of 7.2 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 7.7

Junctional bradycardia in a patient with a K+ of 7.7 mEq/L (ref 3.6 – 5.1 mEq/L). Note that exceedingly normal appearance of the T-waves without even a hint of peaking despite the very high potassium level.

Hyperkalemia K+ 8.1

Wide complex bradycardia of uncertain origin (RBBB+LAFB morphology) and “sharp” but small T-waves from a patient with a K+ of 8.1 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 8.7

Irregular, fairly-narrow-complex bradycardia with small but only slightly pointed T-waves. Amazingly, this subtle EKG was from a patient with a K+ of 8.7 mEq/L (ref 3.6 – 5.1 mEq/L)!

Hypokalemia K+ 2.0

Severe sinus bradycardia in a patient with a K+ of 2.0 mEq/L (ref 3.6 – 5.1 mEq/L) and an Mg++ of 2.2 mEq/L (ref 1.7 – 2.2 mg/dL). While hypokalemia typically presents with a normal or tachycardic rate, on rare occasions severe hypokalemia can present with marked bradycardia.


Final Notes

I’d like to make it a final point to always remember that the sick bradycardic patient is free to combine any two (or even all three!) of the above inciting factors. Just because you think you’ve identified hyperkalemia doesn’t mean the patient hasn’t also reached supratherapeutic digoxin levels with renal failure as the root of both issues.

Digoxin toxicity 4.1 Hyperkamleia K+ 6.9

Junctional bradycardia with “scooped” ST-degments and peaked T-waves in a patient with a digoxin level of 4.1 ng/mL (ref 0.8 – 2.0 ng/mL) and a K+ of 6.9 mEq/L (ref 3.6 – 5.1 mEq/L).

Digoxin toxicity 2.6 Hyperkamleia K+ 7.1

Junctional bradycardia with “scooped” ST-segments and slightly peaked T-waves in a patient with a digoxin level of 2.6 ng/mL (ref 0.8 – 2.0ng/mL) and a K+ of 7.1 mEq/L (ref 3.6 – 5.1 mEq/L).


With that I wish you the best, and remember, “Don’t let your bradycardic patient D.I.E.”






  • Peter says:

    Excellent thanks for sharing

  • Carrie says:

    Great article. I wonder though, where you have stated there is no hint of T wave peaking – in relation to the QRS the T waves can actually be considered to be quite tall (particularly in Lead II)

    • @Carrie
      Thank! I agree that they might be a little taller than expected in the limb leads, but doing a casual skim of my 4,000+ EKG collection right now, without even trying I found ten similar looking EKG’s from patients with no related pathology. While slightly taller than the patient’s old EKG’s (the ones I have at least), their slow HR could also be playing a factor. Calling proportion with T-waves takes a highly experiences eye, and also factors in other things like ST-sloping, the area under the T-wave, QRS distortion, and other nuances that suggest the final diagnosis, which in turn affects whether the T-wave is qualitatively “tall.” In this case I’d say they’re within the realm of normal despite being objectively taller than some of the limb QRS complexes.

      If I were to note anything abnormal about the T-waves though, it would be that they are unusually symmetric. This is almost certainly due to the hyperK+, and one might well claim that this symmetry is actually a hint of peaking, negating my statement. To defend my position I’d say that they lack any of the “sharpness” that defines peaked T-waves, and thus don’t qualify, but I’d secretly agree that there is at least a hint that they want to peak.

  • Jonathan Britton says:

    Great review! Thank you!

  • Rod Bair says:

    Consider renal failure as the source for drug toxicity as well, esp beta and calcium channel blockers. Have flown several patients for emergent pacer placement with an elevated creatinine, just needed to go to dialysis. Thanks for a great article

  • Walter Fusco says:

    It’s fitting that this is the first item in the mnemonic because it is also the culprit I am most likely to overlook — I laughed because I can relate!

  • jamshid says:

    Hi VinceDiGulio.
    Your articles are really amazing and we are constantly learning from you. Please write the article on estimation of ST segment axis,the one you promised on EKG club facebook page.
    Thanks again for all the teachings..

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