The 12 Rhythms of Christmas: Sinus Bradycardia

This article is the second in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It’s a continuation of the theme behind last year’s 12 Leads of Christmas.

We were almost day behind kicking off the series (a peril of posting around the holidays), so I’m going to interrupt my planned order with an easy post to get things back on schedule. The arrhythmia hinted at near the end of the first post will instead be revealed tomorrow.

Last year I posted a nearly identical article titled Don’t let your bradycardic patient D.I.E., but this is an update focused on sinus bradycardia and with a slightly new mnemonic. Our new post should be called, Don’t let the cause of bradycardia H.I.D.E..

Sinus Bradycardia

I’ve told you before that I’m terrible with mnemonics, but there is one I used to find both memorable and useful: the DIE mnemonic for insidious but reversible causes of bradycardia in the emergency medicine and acute care setting. DIE stands for drugs, ischemia, electrolytes. While I love its simplicity, I no longer rely on that exact mnemonic because it leaves out an important cause of bradycardia you do not want to miss—hypothyroidism.

Unlike ischemia, hypothyroidism is not a major concern from a prehospital perspective, and unlike hyperkalemia, it’s not quickly reversible, but given its importance in the trajectory of a patient’s care and how easily it can be overlooked, I think it still deserves a spot in my favorite memory aid.


Yes, there are other causes of bradycardia that should be on your differential, but what makes this list special is that all four have specific emergency treatments, the standard ACLS trio of pacing, atropine, and epi/dopamine/norepi/isoproterenol (depending on preference and what you carry) does little or nothing to address them, and, if missed, patients are unlikely to get better with only supportive care.

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 don’t transport/transfer the patient to a PCI center, there could be serious mobidity or even mortality down the line.

I don’t think you need the EKG to diagnose hypothermia and start warming, 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 and pose an extra threat of sudden death that must be considered.

While the Cushing reflex is an important cause of bradycardia and its care is mostly supportive, the underlying issue (increased ICP) is usually clear. If a patient is unresponsive with decompensated hypothyroidism (myxedema coma), however, supportive care will get them nowhere unless someone decides to check their thyroid function. Since the majority of patients we see with a decreased level of consciousness are experiencing neurological events, sepsis, and/or drug/alcohol intoxication, it requires a high level of suspicion to pick up the more subtle signs of serious hypothyoidism.


While decidedly less common than the other three entities, as discussed above, it is no less important. If hypothyroidism is not suspected as the cause of a patient’s bradycardia during the patient’s initial presentation, it is unlikely it will be picked up down the line. Certainly not all patients with hypothyroidism are bradycardic, but it’s certainly worth considering when the finding is present.

We don’t have time to delve deeper into the diagnosis of severe hypothyroidism and myxedema coma, but the linked articles over at Medscape are a good starting point.

Sinus bradycardia, T-wave inversions, hypothyroidism

Figure 1. This ECG was performed on a patient with severe hypothyroidism whose TSH was 60.12 mcIU/mL (ref 0.36–3.74) and Free T4 0.19 ng/dL (ref 0.76–1.46).



Despite its relatively high prevalence, ischemia is probably (hopefully?) the least missed of the four topics discussed here. Still, even though most STEMI’s present with normal heart rates, subtle ischemia is common and can be accompanied by bradycardia, so it’s good to force yourself to at least consider the possibility in any patient with a low heart rate. Though brady-dysrhythmias (i.e. SA node dysfunction, AV-blocks) are often associated with inferior MI’s due involvement of the SA and AV-nodes, standard sinus bradycardia can be see with STEMI’s of any distribution.

Acute inferior STEMI with sinus bradycardia

Figure 2. Acute inferior STEMI with sinus bradycardia

Acute anterior STEMI with sinus bradycardia

Figure 3. Acute anterior STEMI with sinus bradycardia

Early acute anterior STEMI with sinus bradycardia

Figure 4. Early acute anterior STEMI with sinus bradycardia

Acute inferior STEMI with sinus bradycardia

Figure 5. Acute inferior STEMI with sinus bradycardia

Inferior STEMI with sinus bradycardia and a PAC

Figure 6. Late inferior STEMI with sinus bradycardia and a PAC

Figure 7. Acute inferior STEMI with sinus bradycardia

Figure 7. Acute inferior STEMI with sinus bradycardia

Acute anterior STEMI with marked sinus bradycardia

Figure 8. Acute anterior STEMI with marked sinus bradycardia



I’m going to throw around the terms “drugs” and “overdose,” but what we’re really talking about is any supratherapeutic levels of an illicit drug or prescribed medication the patient may have taken. 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. 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 them anti-arrhythmics—that cause marked bradycardia in excessive doses.

Sinus bradycardia, prolonged QT, sotalol overdose

Figure 9. Sinus bradycardia and a prolonged QT-interval in a patient with supratherapeutic sotalol levels

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

Figure 10. Sinus bradycardia and a prolonged QT in a patient with sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.



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 and hypothyroidisn are relatively uncommon presentations of bradycardia, but electrolyte abnormalities are an everyday event in most emergency departments.

When we talk about electrolytes in reference to brady-arrhythmias, what we really mean is the serum potassium level, and Hyperkalemia is by far the most common bradycardia-producing electrolyte abnormality. 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 complexes, it is constantly sobering just how subtle the signs of hyperkalemia can present on the EKG. Below are just a couple of the subtle hyperkalemia cases I’ve encountered with sinus bradycardia. 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.


Figure 11. Sinus bradycardia and mild QRS prolongation in a patient with potassium and a K+ of 6.9 mEq/L.

Subtle hyperkalemia with peaked T-waves

Figure 12. Sinus bradycardia and subtly peaked T-waves in a patient with mild hyperkalemia and a K+ of 5.8 mEq/L.

Severe sinus bradycardia with hyperkalemia

Figure 13. Severe sinus bradycardia in a patient with hyperkalemia and a potassium of 6.5 mEq/L.

Severe sinus bradycardia in hypokalemia

Figure 14. Severe sinus bradycardia in a patient with hypokalemia and a potassium of 1.9 mEq/L.


Let’s discuss rate (again)

While we expounded on the rate bounds of sinus tachycardia yesterday, we should also touch on the definition of sinus bradycardia (in less detail). And, same as before, I don’t agree with most of the published numbers…

Just like we stated that there is no strict upper limit for the rate of sinus tachycardia, there is no lower limit for sinus bradycardia. If the sinus node is firing 10 times a minute, then that is sinus brady all the same (although marked or extreme; see Fig. 13 and Fig. 14).

What about the upper limit for sinus bradycardia? Most folks say it’s 60 bpm; I say it’s 55 bpm. Some people even choose 50 bpm as their definition, but I like 55 because a heart rate of 52 bpm—while likely benign—is still something I believe is worth commenting on. The reason I think 60 bpm is too high is that a lot of patients are on medications to control their heart rates, while those that aren’t tend to be more fit, with the result being that it’s exceedingly common to see rates in the 55-60 bpm range. Additionally, unlike subtle tachycardia—which I find to be very useful in my patient assessments—a heart rate of 57 bpm doesn’t really alert me to anything worthwhile (except in rare cases), so I don’t get anything out of defining it as “abnormal.”


Check out the rest of The 12 Rhythms of Christmas (updated as new posts come out)!

The 12 Rhythms of Christmas: Sinus Tachycardia
The 12 Rhythms of Christmas: Atrial Flutter
The 12 Rhythms of Christmas: First Degree AV-Block
The 12 Rhythms of Christmas: Type I AV-Block

1 Comment

  • Scott Michael says:

    I would to add another possible cause of profound Sinus Bradycardia. I worked on a vascular surgery floor for years and a few of our carotid endarterectomies and our carotid stent placements would come back, Sinus Brady, in the 20’s and 30’s due to baroreceptor reflex triggered by pressure on the carotid sinus, from swelling or trauma due to surgery. The patients, quite surprisingly, were fairly asymptomatic. It was very intriguing, the first time I witnessed a patient in the 20’s that was not in an escape rhythm.

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