PB + Js AF
TLDR
Trying something different this one.
A PRETEST (1-3 min total)
(answers at bottom of this page)
TLDR
Trying something different this one.
A PRETEST (1-3 min total)
(answers at bottom of this page)
Lb for Lb #1 Champ
This ECG pattern is my favorite arrhythmia to teach. Couple reasons why. First it seems to be the pattern medical school forgot to teach us about. Which is a shame because it is pretty damn simple. I expect a resident I teach to know it next time they see it—and they do. A lot of my ecg collection of these is sent by residents. Not many patterns I’d expect the same yield teaching but its pretty easy.
Importantly, these patients are very sick making it high yield— NNT low as my site's followers. The best part? Unlike the STEMI patient who vanishes to the cath lab—we get to fix this ourselves right in the ED. I love it. Commit it to memory and you will have everything you need to rapidly stabilze the next you see —without even waiting for labs or other tests!
So, comin in hot straight outta' triage our first patient today:
Ms. Ida is a 70 yo F c/o feeling like she may faint at any time today against a background of general shittiness and malaise progressive x 1 week.
ECG #1: "Slow AF" (Click to enlarge, Esc key to return. )
Patient #1, Ms. Ida. Quick self quiz:
There are p waves present. (T/F)
There is complete heart block present. (T/F)
You recognize this pattern as _ and your next step is _.
PB and Js AF
Don’t worry if you couldn't answer #3. The goal is to be able to easily answer after reviewing this lesson.
So first of all, the ecg and chief complaint both are singing the same tune here. It seems very likely the heart rhythm here is the explanation for the shitiness and faint feeling she presents for. It'd almost be more suprising if she didn't feel faint.
To plan how to stabilize a bradyarrhythmia we need to pinpoint where in the conduction system is the problem. This involves looking for p waves, rhythm, and wideness of QRS as a basic starting point. Lets start at the top and focus on the p waves—for the diagnosis of a heart block we rely on these lil guys.
Here, the only p waves I can see would require a little imagination. Whenever I catch myself saying something like, “oh I think I see one here maybe” I've learned that I am completely wrong and there just aren't any. It’s kinda like “Yeah I think I feel a pulse.” The act of finding a single clear p wave, like checking a pulse, is not a heavy thinking activity. So if I ever “think I might”—I've learned I probably didn't.
No p waves, not super wide, and irregular, does this ring any bells? Yes, atrial fibrillation it could be, although this is one of the laziest most sluggish I’ve ever seen. This history was Immediately confirmed from patient and family at bedside. In fact, a longstanding history of AF, managaed with amiodarone. So calling it atrial fibrillation, albeit a “scary slow” one isn’t wrong at all. Though, I much prefer writing it out in shorthand form as, “slow AF.” This allows those with a bit of creativity while decoding the abbreviation to actually hear my brain’s verbatim thoughts on first glance of the 12 lead—it's slow as F—-.
Yup, this is stupid slow. IV Diltiazem is definitely *not* the answer here. Let’s never discover any new blanks on the death notes that need our name filled in.
Hmm, AF a little boring of a diagnosis for my favorite bradyarrhythmia. Could there be a darker diagnosis lurking in the tracing?
I have devised a groundbreaking original mnmeonic aid in the diagnosis here. I trust that, with your help, one day it will be well known and relied upon in emergency departments around the world….
Congratulations, if you're still reading you just learned the first half, s AF, which stands for "slow atrial fibrillation"
PB +Js AF
I begin treatment and repeat ecg. The repeat (pictured below) demonstrates dramatic improvement. Even more convienently, it is a great example of the mnemonic's other half, PB&J.
Second ecg, now "junctional rhythm."
(Click to enlarge, Esc key to return. )
The complete lack of recognizable p waves in the setting of a regular bradycardia may bring to mind the diagnosis, which the computer and later cardiologist who confirmed the tracing made— "junctional rhythm. " That’s good it should. The rhythm is clearly more regular compared the first and the QRS remains on the slim side.
Lets recall that junctional rhythms arise when there’s a problem with the first line of our specialized supraventricular pacemakers (SA node and atrial cells). Now, no longer repressed, the slower intrinsic pacemaking ability of other cardiac cells is unmasked (AV node, ventricles) . These cells are now forced to do a job they weren't even specailized for and really never wanted in the first place. The further along the conduction system we find our replacement cells the worse their performance (HR max). This explains how the HR is our first clue to the location of a "block". Who can blame these cells? Our body has spent it's energy educating them in a completely different task. No cell has ever graduated top of their class with dual degree in both inotropy and chronotropy. They specialize just like us.
The cells normally furthest from the SA node can't hide their distain for the job when tasked with pacemaking. Not only are they the least fit for the job and provide the slowest HR but they make zero attempt to cover up for our supraventricular cells and leave a big fat wide QRS. We use this to wide QRS to our advantage, as a clue, when trying to locate the level of a block.
As I am sure any technical reader may correctly point out "junctional," refers to a specific location of a block, conviently at, well, the anatomic junction of our conducting system. In other words, it is intended to refer to the specific situation of a block only at the level of AV node/His and not lower down. For example, an exceptionally slow "junctional bradycardia" showing a wide QRS has a more accurate callsign than "junctional". But, I really really think I'm losing readers already with this vocabulary lesson and is better to get back on track and steer away from further terminology. Lets keep to the forest and not the trees. I'll end this with a quick breakdown of each member of the junctional family— the correct name with the associated rate. We don't need to dwell on it just FYI.
Junctional Tachycardia: >100
Accelerated Junctional rhythm: 60-100
Junctional (escape) rhythm: 40-60
Junctional bradycardia: <40
What is more important is the general concept that in the patient with: 1) no P waves 2) Bradyarrhythmia and crazy slow 3) Junctional or Atrial Fibrillation, unless otherwise explained, should get the tenative diagnosis and treatment that we are about to go over.
First if it wasn't clear already—the soon-to-be award winning mnemonic for diagnosis is fully unlocked:
PB + Js AF
P wave (missing)
Bradycardia
Junctional rhythms
Slow AF (slow as f*&k/atrial fibrillation)
(Suspect ______ when you find a combination of these on 12 lead)
To fill in the blank we need the final part of the memory aid, the treatment. Please answer me this? What do we reach for alongside our delicious PB & J sammy? Hint: It does the body good. Promise full reveal next ecg.
ECG# 3: Ms. Billy, 64 yo presenting w/ n/v and diarrhea x 7 d. Generalized weawkness to point no longer can ambulate.
(Click to enlarge, Esc key to return. )
ECG #4 A prior ecg for comparison, confirmed to be recent baseline past couple of visits. Labels are correct—cardiologist who confirmed these flagged her ecg previously as "?abnormal" but not the ecg in question today (pictured above and labeled "new ecg" #3). No clue. I think "new ecg" is very deserving of the flag in my book.
(Click to enlarge, Esc key to return. )
Milk. It does a body good.
Next time you are staring face to face with a scary bradycardia double check that ecg. If it looks all PB and Js AF—-I'll tell you right now, it'll go down a lot easier with a cold glass of milk AKA "IV Calcium".
Lets just appreciate the beauty of these perfect pairs:
PB & Js AF / Milk = (Probable Critical Hyperkalemia) / (Begin immediate treatment w/ IV Calcium)
In each of the above cases labs were not needed for diagnosis and treatment was started following ecg. No cases were dialysis patients, rather each had an acute kidney injury. Every patient had some form of beta blockade, making these great examples of the specific hyperkalemia situation, BRASH. In the first case it was by way of amiodarone and the remaining via beta blocker. Stay tuned for a deeper dive into BRASH soon.
My rationale for treatment based only on gestalt and ecg pattern is reinforced by the most important treatment, IV calcium, being super safe for nearly every patient in this situation encountered. Don't just do a gram of gluconate and wait for labs. Go hard, your confirmation of diagnosis will be immediate right in front of your eyes and faster than any lab result. Shoutout to NYC residents—the nearby code cart should be stocked up and you don't have to rely on anyone to get if running into delays.
Respective K levels for each patient:
Ms. Ida: 7.4 (mild hemolysis), Ms. Billy 9.2 (no hemolysis)
Table above from the following article. Great read and link is full text.
mic drop
You know how long those crazy high K levels can take depending on a hospital's lab, "hmm this can't be correct lets run it a fifth time or maybe should we ask for a recollect."
The above case w/ > 9 K was sent to me by a great resident (early PGY2) whom learned this pattern from me during a lecture. I was told she walked over immediately treating and stabilizing patient in front of an attending struggling. I promise you just eat an uncrustable tonight and this will be all you need to be a damn boss and do the same showing up your next attending on shift. Just please pay it forward and teach after a quick bask in glory. This is what I consider a diagnosis for ED only. One of those restricted to XYZ specialty I always am hearing about. We own this one. Should never be seen or encountered by any other service (i.e. renal, cardiology) if ED is functioning properly.
This was only two patients. I'll share more cases but this pattern is so easy and so high yield. Even just two cases and I know you got this. I have a lot more of these cases I find them to not be rare at all. So we have more to talk about. I hope this was a good primer to BRASH and left you hungry for more.
Given that ECG findings are such a crucial predictor of badness why not focus on the worst first? Why is we give these the least attention? Go ahead and argue with me but PB & J findings are more important than the pointed changes of the t wave.
A very quick recap of ecg changes in hyperkalemia. I find it is best described as imagining each end of the tracing being pulled apart as if attached to a string on each end. This causes widening of QRS and difficulty seeing—or complete loss of p waves.
It is a shame medical education really puts the most emphasis on the two extremes of hyperk changes—the sharp peaked t wave and the late stage sine wave. In the first case, these t wave changes are one of the least informative in terms of prognostication and the risk of progression to emergent arrhythmia. Then the second case, the sine wave, is what I would describe as an almost purely academic finding in a pulseless patient receiving CPR that needed earlier or more aggressive treatment.
Without fail, when I ask a physician in training to tell me the progression of hyperkalemic ecg changes it echos my medical education. They nail each end of the spectrum but only at best, if forced out, vaguely describe the middle more important changes. The tragedy here is that the middle is the sweet spot. The PB and Js AF spot.This is where we can best predict badness and make the most timely impact. Sine wave? Are you kidding me? That's an arrested patient, you are already behind when you recognize that.
So often I am hearing someone talk about hyperk like it is some magical forest gremlin that defies accurate description. To hunt it is futile it can masquerade and pose as "anything" on an ecg making a reliable diagnosis and study on the topic futile if withou those pointy t waves. Bullshit. This pattern is a piece of cake and my money is on hyperk next time it's seen. Please please make my day if you find next time you see one.
PRETEST ANSWER:
The rhythm depicted in the first ecg and used in the pre-test is actually a sinus rhythm!!!
This is an example of sinoventricular conduction. The narrow QRS is showing us that despite the HR the pacemaker cells are higher than the ventricles. The fact that there are no p waves present is due to the atrium of the heart rendered incapable of contraction due to the hyperkalemia. However, internodal tracts, carry the pacemaker impulses along the conduction system nonetheless. These internodal cells, as far as I have read, have never been definitively identified but are hypothesized to exist due to this hyperkalemia phenomenon.
Read more about sinoventricular conduction and message me if I am leaving some good stuff out or got anything wrong I am by no means an expert here !
Comments
PB + Js AF
TLDR
Trying something different this one.
A PRETEST (1-3 min total)
(answers at bottom of this page)
Lb for Lb #1 Champ
This ECG pattern is my favorite arrhythmia to teach. Couple reasons why. First it seems to be the pattern medical school forgot to teach us about. Which is a shame because it is pretty damn simple. I expect a resident I teach to know it next time they see it—and they do. A lot of my ecg collection of these is sent by residents. Not many patterns I’d expect the same yield teaching but its pretty easy.
Importantly, these patients are very sick making it high yield— NNT low as my site's followers. The best part? Unlike the STEMI patient who vanishes to the cath lab—we get to fix this ourselves right in the ED. I love it. Commit it to memory and you will have everything you need to rapidly stabilze the next you see —without even waiting for labs or other tests!
So, comin in hot straight outta' triage our first patient today:
Ms. Ida is a 70 yo F c/o feeling like she may faint at any time today against a background of general shittiness and malaise progressive x 1 week.
ECG #1: "Slow AF" (Click to enlarge, Esc key to return. )
Patient #1, Ms. Ida. Quick self quiz:
There are p waves present. (T/F)
There is complete heart block present. (T/F)
You recognize this pattern as _ and your next step is _.
PB and Js AF
Don’t worry if you couldn't answer #3. The goal is to be able to easily answer after reviewing this lesson.
So first of all, the ecg and chief complaint both are singing the same tune here. It seems very likely the heart rhythm here is the explanation for the shitiness and faint feeling she presents for. It'd almost be more suprising if she didn't feel faint.
To plan how to stabilize a bradyarrhythmia we need to pinpoint where in the conduction system is the problem. This involves looking for p waves, rhythm, and wideness of QRS as a basic starting point. Lets start at the top and focus on the p waves—for the diagnosis of a heart block we rely on these lil guys.
Here, the only p waves I can see would require a little imagination. Whenever I catch myself saying something like, “oh I think I see one here maybe” I've learned that I am completely wrong and there just aren't any. It’s kinda like “Yeah I think I feel a pulse.” The act of finding a single clear p wave, like checking a pulse, is not a heavy thinking activity. So if I ever “think I might”—I've learned I probably didn't.
No p waves, not super wide, and irregular, does this ring any bells? Yes, atrial fibrillation it could be, although this is one of the laziest most sluggish I’ve ever seen. This history was Immediately confirmed from patient and family at bedside. In fact, a longstanding history of AF, managaed with amiodarone. So calling it atrial fibrillation, albeit a “scary slow” one isn’t wrong at all. Though, I much prefer writing it out in shorthand form as, “slow AF.” This allows those with a bit of creativity while decoding the abbreviation to actually hear my brain’s verbatim thoughts on first glance of the 12 lead—it's slow as F—-.
Yup, this is stupid slow. IV Diltiazem is definitely *not* the answer here. Let’s never discover any new blanks on the death notes that need our name filled in.
Hmm, AF a little boring of a diagnosis for my favorite bradyarrhythmia. Could there be a darker diagnosis lurking in the tracing?
I have devised a groundbreaking original mnmeonic aid in the diagnosis here. I trust that, with your help, one day it will be well known and relied upon in emergency departments around the world….
Congratulations, if you're still reading you just learned the first half, s AF, which stands for "slow atrial fibrillation"
PB +Js AF
I begin treatment and repeat ecg. The repeat (pictured below) demonstrates dramatic improvement. Even more convienently, it is a great example of the mnemonic's other half, PB&J.
Second ecg, now "junctional rhythm."
(Click to enlarge, Esc key to return. )
The complete lack of recognizable p waves in the setting of a regular bradycardia may bring to mind the diagnosis, which the computer and later cardiologist who confirmed the tracing made— "junctional rhythm. " That’s good it should. The rhythm is clearly more regular compared the first and the QRS remains on the slim side.
Lets recall that junctional rhythms arise when there’s a problem with the first line of our specialized supraventricular pacemakers (SA node and atrial cells). Now, no longer repressed, the slower intrinsic pacemaking ability of other cardiac cells is unmasked (AV node, ventricles) . These cells are now forced to do a job they weren't even specailized for and really never wanted in the first place. The further along the conduction system we find our replacement cells the worse their performance (HR max). This explains how the HR is our first clue to the location of a "block". Who can blame these cells? Our body has spent it's energy educating them in a completely different task. No cell has ever graduated top of their class with dual degree in both inotropy and chronotropy. They specialize just like us.
The cells normally furthest from the SA node can't hide their distain for the job when tasked with pacemaking. Not only are they the least fit for the job and provide the slowest HR but they make zero attempt to cover up for our supraventricular cells and leave a big fat wide QRS. We use this to wide QRS to our advantage, as a clue, when trying to locate the level of a block.
As I am sure any technical reader may correctly point out "junctional," refers to a specific location of a block, conviently at, well, the anatomic junction of our conducting system. In other words, it is intended to refer to the specific situation of a block only at the level of AV node/His and not lower down. For example, an exceptionally slow "junctional bradycardia" showing a wide QRS has a more accurate callsign than "junctional". But, I really really think I'm losing readers already with this vocabulary lesson and is better to get back on track and steer away from further terminology. Lets keep to the forest and not the trees. I'll end this with a quick breakdown of each member of the junctional family— the correct name with the associated rate. We don't need to dwell on it just FYI.
Junctional Tachycardia: >100
Accelerated Junctional rhythm: 60-100
Junctional (escape) rhythm: 40-60
Junctional bradycardia: <40
What is more important is the general concept that in the patient with: 1) no P waves 2) Bradyarrhythmia and crazy slow 3) Junctional or Atrial Fibrillation, unless otherwise explained, should get the tenative diagnosis and treatment that we are about to go over.
First if it wasn't clear already—the soon-to-be award winning mnemonic for diagnosis is fully unlocked:
PB + Js AF
P wave (missing)
Bradycardia
Junctional rhythms
Slow AF (slow as f*&k/atrial fibrillation)
(Suspect ______ when you find a combination of these on 12 lead)
To fill in the blank we need the final part of the memory aid, the treatment. Please answer me this? What do we reach for alongside our delicious PB & J sammy? Hint: It does the body good. Promise full reveal next ecg.
ECG# 3: Ms. Billy, 64 yo presenting w/ n/v and diarrhea x 7 d. Generalized weawkness to point no longer can ambulate.
(Click to enlarge, Esc key to return. )
ECG #4 A prior ecg for comparison, confirmed to be recent baseline past couple of visits. Labels are correct—cardiologist who confirmed these flagged her ecg previously as "?abnormal" but not the ecg in question today (pictured above and labeled "new ecg" #3). No clue. I think "new ecg" is very deserving of the flag in my book.
(Click to enlarge, Esc key to return. )
Milk. It does a body good.
Next time you are staring face to face with a scary bradycardia double check that ecg. If it looks all PB and Js AF—-I'll tell you right now, it'll go down a lot easier with a cold glass of milk AKA "IV Calcium".
Lets just appreciate the beauty of these perfect pairs:
PB & Js AF / Milk = (Probable Critical Hyperkalemia) / (Begin immediate treatment w/ IV Calcium)
In each of the above cases labs were not needed for diagnosis and treatment was started following ecg. No cases were dialysis patients, rather each had an acute kidney injury. Every patient had some form of beta blockade, making these great examples of the specific hyperkalemia situation, BRASH. In the first case it was by way of amiodarone and the remaining via beta blocker. Stay tuned for a deeper dive into BRASH soon.
My rationale for treatment based only on gestalt and ecg pattern is reinforced by the most important treatment, IV calcium, being super safe for nearly every patient in this situation encountered. Don't just do a gram of gluconate and wait for labs. Go hard, your confirmation of diagnosis will be immediate right in front of your eyes and faster than any lab result. Shoutout to NYC residents—the nearby code cart should be stocked up and you don't have to rely on anyone to get if running into delays.
Respective K levels for each patient:
Ms. Ida: 7.4 (mild hemolysis), Ms. Billy 9.2 (no hemolysis)
Table above from the following article. Great read and link is full text.
mic drop
You know how long those crazy high K levels can take depending on a hospital's lab, "hmm this can't be correct lets run it a fifth time or maybe should we ask for a recollect."
The above case w/ > 9 K was sent to me by a great resident (early PGY2) whom learned this pattern from me during a lecture. I was told she walked over immediately treating and stabilizing patient in front of an attending struggling. I promise you just eat an uncrustable tonight and this will be all you need to be a damn boss and do the same showing up your next attending on shift. Just please pay it forward and teach after a quick bask in glory. This is what I consider a diagnosis for ED only. One of those restricted to XYZ specialty I always am hearing about. We own this one. Should never be seen or encountered by any other service (i.e. renal, cardiology) if ED is functioning properly.
This was only two patients. I'll share more cases but this pattern is so easy and so high yield. Even just two cases and I know you got this. I have a lot more of these cases I find them to not be rare at all. So we have more to talk about. I hope this was a good primer to BRASH and left you hungry for more.
Given that ECG findings are such a crucial predictor of badness why not focus on the worst first? Why is we give these the least attention? Go ahead and argue with me but PB & J findings are more important than the pointed changes of the t wave.
A very quick recap of ecg changes in hyperkalemia. I find it is best described as imagining each end of the tracing being pulled apart as if attached to a string on each end. This causes widening of QRS and difficulty seeing—or complete loss of p waves.
It is a shame medical education really puts the most emphasis on the two extremes of hyperk changes—the sharp peaked t wave and the late stage sine wave. In the first case, these t wave changes are one of the least informative in terms of prognostication and the risk of progression to emergent arrhythmia. Then the second case, the sine wave, is what I would describe as an almost purely academic finding in a pulseless patient receiving CPR that needed earlier or more aggressive treatment.
Without fail, when I ask a physician in training to tell me the progression of hyperkalemic ecg changes it echos my medical education. They nail each end of the spectrum but only at best, if forced out, vaguely describe the middle more important changes. The tragedy here is that the middle is the sweet spot. The PB and Js AF spot.This is where we can best predict badness and make the most timely impact. Sine wave? Are you kidding me? That's an arrested patient, you are already behind when you recognize that.
So often I am hearing someone talk about hyperk like it is some magical forest gremlin that defies accurate description. To hunt it is futile it can masquerade and pose as "anything" on an ecg making a reliable diagnosis and study on the topic futile if withou those pointy t waves. Bullshit. This pattern is a piece of cake and my money is on hyperk next time it's seen. Please please make my day if you find next time you see one.
PRETEST ANSWER:
The rhythm depicted in the first ecg and used in the pre-test is actually a sinus rhythm!!!
This is an example of sinoventricular conduction. The narrow QRS is showing us that despite the HR the pacemaker cells are higher than the ventricles. The fact that there are no p waves present is due to the atrium of the heart rendered incapable of contraction due to the hyperkalemia. However, internodal tracts, carry the pacemaker impulses along the conduction system nonetheless. These internodal cells, as far as I have read, have never been definitively identified but are hypothesized to exist due to this hyperkalemia phenomenon.
Read more about sinoventricular conduction and message me if I am leaving some good stuff out or got anything wrong I am by no means an expert here !
Comments