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Student Case: "The Precordial Thump"


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Great, thank you!

 

She possibly decided to sputter out at that inopportune moment due to her tachycardia induced cardiomyopathy

-her sx likely related to her heart have been going on for quite some time and she had been holding up till now

-I would lean more towards the initiation of the diltiazem with possible secondary insult due to the extra fluids she's received as the culprit

(I believe CCB should be avoided in patients with HF? although unknown at the time. I believe BB are first line for rate control for AFib/Flutter?)

 

-also could still be ischemia related, perhaps her one set of troponins were on the tail end of a non stemi a few days ago?

 

 

In hindsight:

-perhaps better to go with metoprolol for the initial rate controlling agent?

-more judicious oversight over the fluid administration?

 

If she needs additional hemodynamic support to boost her CO, (I don't think it'd be initiated in the ED, but)

-could place a temporary VAD? IABP or an impella device??

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Great, thank you!   On the money again with your post below

 

She possibly decided to sputter out at that inopportune moment due to her tachycardia induced cardiomyopathy

-her sx likely related to her heart have been going on for quite some time and she had been holding up till now    -  nice catch

-I would lean more towards the initiation of the diltiazem with possible secondary insult due to the extra fluids she's received as the culprit   - precisely

(I believe CCB should be avoided in patients with HF? although unknown at the time. I believe BB are first line for rate control for AFib/Flutter?)  

 

-also could still be ischemia related, perhaps her one set of troponins were on the tail end of a non stemi a few days ago?  Always should be high on the ddx with patients with new diagnosis of cardiomyopathy.  

 

 

In hindsight:

-perhaps better to go with metoprolol for the initial rate controlling agent?  Certainly better than a CCB, but still probably not the best choice in this scenario.  

-more judicious oversight over the fluid administration?    We actually didn't give any fluids aside from the small drip bag prior to her becoming hypotensive.  

 

If she needs additional hemodynamic support to boost her CO, (I don't think it'd be initiated in the ED, but)

-could place a temporary VAD? IABP or an impella device??   Definitely a good thought in this case where we are assuming that this is a temporary insult we just have to ride out.  

 

 

 

 

So, what happened exactly?  Why is this patient in cardiogenic shock?  

 

After her MI, this patient probably had undiagnosed ischemic cardiomyopathy (though did not arrive in overt clinical "congestive heart failure" - remember the difference between CM and CHF!) and when we gave the cardizem her already bad EF tanked, pushing her until acute decompensate CHF and cardiogenic shock.  Calcium channel blockers are harmful in patients with a cardiomyopathy.  Beta blockers are beneficial in patients with cardiomyopathy over the long term to prevent maladaptive remodeling, but should only be added when the patient is very stable and very compensated cardiomyopathy.  In this case with a tachyarrhythmia and very borderline EF to start, I'm not convinced she had much of any reserve, and IV BBs may very well have pushed her into decompensated CHF as well.  

 

http://www.heartonline.org.au/media/DRL/Potentially_harmful_drugs_to_avoid_in_heart_failure.pdf

 

So, what agents would have been ideal (in consultation with a cardiologist), to provide rate control without decreasing CO... as UGoLong said, digoxin would probably have been a good choice, just be aware that it does take a long time to work.  Amio is another potential choice, but in addition to its rate control it has rhythm control effects (would convert her to NSR), which as we said above is a bad idea in a stable patient before ruling out a clot.  

 

 

Can we offer a more targeted therapy in addition to the empiric therapy / inotropes?  

 

So, the problem was the calcium channel blockers.  Switching off the cardizem drip ASAP was a critical intervention (nice job), but we know there are "antidotes" in CCB overdose as well, namely calcium (makes sense right?), glucagon, and insulin (crazy high doses of it) + glucose.  I had an interesting discussion with our cardiologist and with our CCU pharmacist about this case and whether or not there would be a role for the antidotes, since this case isn't really an "overdose" situation but a "normal dose".  They weren't entirely sure, but said that they would throw every thing we have at the patient if she didn't turn around with supportive care.  

 

So, we did our best supportive care we could muster and she did just fine.  We supported the respiratory system w/ bipap which quickly improved her pulmonary edema / hypoxia, we supported cardiovascular system with dobutamine and that maintained her pressures without issue.  If the dobutamine had not worked and she was still in aflutter and in shock, we would have cardioverted her to optimize her heart function regardless of the risk of thromboembolism... also could have considered impella.  She ended up doing fine, regained her baseline mental status rather quickly.  Repeat echo the next day in CCU showed an EF of 30% from the 10% EF we saw in the ED... so the CCB really hit that EF hard!!.  

 

 

Was there a mistake made, and if so, what could we have done to avoid it?

 

We see a ton of patients with a fib/aflutter, and 90% of the time, cardizem will work like a champ.  We just have to be careful to look out for cardiomyopathy.  Having learned from this case, I am now going to do a really good history and exam looking for sign of heart failure.  I'm going to chart check for an echo and might even call to the neighboring hospital to get a verbal on what their last EF was.  If I have a high suspicion but am not able to get the data I need, I might even quickly throw the ultrasound probe to look at the EF... it would take all of 3 minutes to figure this out.  In this case, we may have caught on before giving the diltiazem and could have avoided everything.  I would have just called the cardiologists and deferred to them to handle it any way they'd like, be it digoxin or admit for TEE then cardioversion, it doesn't really matter because the patient was relatively stable enough to wait for several hours before being definitively treated.  

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One final point that I'd say cases like this have helped me learn as a new PA in emergency medicine is to further grasp the significance and application of "Primum Non nocere".  

 

Medicine encompasses an overwhelming amount of information to learn, as all of you students are starting to see I am sure!  I always struggled with trying to figure out which things to focus on, because we simply can't learn it all.  I can understand that as a student most of your focus will be on passing the test and surviving through clinicals.  I'd just say, let "first do no harm" also help you focus your learning, because I think its probably the most important principle in medicine.  

 

One of my favorite old school attendings said it best... "If you see 1000 patients this year, 900 of them will be just fine no matter what you do.  Of the remaining 100 that you do manage to impact, you will hurt 90 of them.  Of the remaining 10, you will save 9 of their lives, and will end up killing 1 of your patients."  

 

Clearly this isn't meant to be an evidence based statistical breakdown, but it is meaningful to me because it shows that the vast majority of the time, if we do nothing at all, the patient will turn out just fine.  Yet, if we end up trying to meddle with things, we have a real chance of hurting, possibly even killing our patients.  That's why its so important to remember "First, do no harm".  Not only is it about not intentionally hurting your patients (clearly), its about knowing inside and out the potential consequences of everything you do for your patients, and knowing how to deal with them if the sh*t hits the fan. We have to know the class D medications, what contraindications to always look out for, the potentially lethal adverse effects, the toxicities, the complications etc.  

 

Of the massive amount of information to learn out there, these are the things I now find myself focusing on more than anything.  I am not stressing out about learning the diagnostic criteria for a canker sore, the benign side effects of prozac, exact dosages, half lives, home care instructions, etc ... these are all things I can look up as needed.  

 

As a new PA, learning in this fashion is perhaps the best way to ease the (incredibly high) stress and anxiety that comes when you are first thrown out into practice.  Even if you don't know what exactly is going on in a situation, as long as you know that the patient won't be harmed, you can sleep at night.  

 

Just some food for thought to wrap up the case....

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This is great!  I stumbled upon this during a study break....and I'm so glad that I did.  What a great review of some cardiology, ACLS, and types of shock and how to distinguish between them.

I'm in my 4th semester of didactic and am really itching to begin rotations.  And reeeaallly nervous about these types of high-stakes situations.

 

I do have a few questions that I'm hoping someone can answer:

 

What is bedside BGL?  And TEE?

 

Can bedside ultrasound be used to 'rule out' underlying cardiomyopathy?  In other words, would you have been able to see her low EF before giving her the calcium channel blocker?

 

A follow-up to the above question, what methods are there (besides the physical exam and CXR, which you did) to address the question of underlying systolic heart failure in a person with her risk factors for heart failure?  Does simply having unexplained, slight pitting edema "count?" 

 

I hope these questions aren't too naive...we're in a safe space I guess :)

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This is great!  I stumbled upon this during a study break....and I'm so glad that I did.  What a great review of some cardiology, ACLS, and types of shock and how to distinguish between them.   I'm glad you liked it!

 

I'm in my 4th semester of didactic and am really itching to begin rotations.  And reeeaallly nervous about these types of high-stakes situations.  Don't worry... as a student you won't be the one everyone looks to when the patients start to decompensate, BUT you should pretend you are and think about what  exactly you would do in that situation.  

 

I do have a few questions that I'm hoping someone can answer:

 

What is bedside BGL?  Blood glucose level.  And TEE? Trans-esophageal echo (vs TTE trans thoracic echo)

 

 

Can bedside ultrasound be used to 'rule out' underlying cardiomyopathy?  In other words, would you have been able to see her low EF before giving her the calcium channel blocker?   You can definitely use bedside echo to determine EF (after some practice you can tell just by guestimating, or you can just use the EPSS that I talked about above) and it definitely would have been sufficient to avoid the above situation.  I would not say that right now my bedside echo is good enough to rule out all cardiomyopathies, like a diastolic cardiomyopathy, HOCM, the rarer/genetic cardiomyopathies, etc, and I doubt that most emergency physicians could do this either.  That's why its important to always keep in mind the limitations of bedside ultrasound.  It is not the end-all answer to everything.  It is a tool that we can use to answer very specific and targeted clinical questions (i.e. is there an effusion?  is the EF <30%? etc)

 

 

 

A follow-up to the above question, what methods are there (besides the physical exam and CXR, which you did) to address the question of underlying systolic heart failure in a person with her risk factors for heart failure?  Does simply having unexplained, slight pitting edema "count?"   What are the variety of ways to be able to rule out systolic heart failure without physical exam or CXR?  I suppose the answer to that would be bedside echo.  There are lab tests like BNP but these will have low sensitivity to rule out a systolic heart failure if the patient is euvolemic and compensated.  In general, I think the most important thing would be having a high suspicion and taking the whole picture into account.  You have to specifically seek out signs and symptoms of heart failure clinically (dyspnea on exertion, orthopnea, PND, leg swelling, risk factors, etc), and lab tests (BNP, troponin), CXR.  But, it definitely isn't easy to tell sometimes without the echo!  

 

I hope these questions aren't too naive...we're in a safe space I guess :)   Not at all.  Great questions.  

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