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 yearâ€™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..
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 missâ€”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.
Itâ€™s okay to miss Levâ€™s disease in the emergency setting because the definitive treatment is contained in the usual ACLS algorithm: pacing. If you donâ€™t recognize that your patient is hyperkalemic, however, then all the atropine and transcutaneous pacing in the world isnâ€™t going to lower her potassium.
You donâ€™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 donâ€™t think you need the EKG to diagnose hypothermia and start warming, but youâ€™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.
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 itâ€™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.
I’m going to throw around the terms “drugs” and â€œoverdose,â€ but what weâ€™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. TheÂ culprits I worry about most in the undifferentiated bradycardic patient are calcium channel blockers, beta blockers, and digoxin, but thereâ€™s a whole host of medicationsâ€”lots of them anti-arrhythmicsâ€”that cause marked bradycardia in excessive doses.
In terms of overall numbers, I believe that electrolyte disturbances are certainly the most missed cause of bradycardia. Itâ€™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 itâ€™s huge role in cardiac action potentials, serum sodium levels actually have little effect on the surface ECG (though sodium channel blockers doâ€¦). Similarly, though magnesium plays a role in some arrhythmias, there are no direct EKG signs of hyper/hypo magnesemia. Itâ€™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 Iâ€™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, itâ€™s worth keeping in mind.
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 bpmâ€”while likely benignâ€”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 tachycardiaâ€”which I find to be very useful in my patient assessmentsâ€”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)!