Sepsis, hypernatremia, and fluid resuscitation

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jakomo

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Hey all,

Not an EM doc, but I've got a question that I am not able to find a clear answer on. If anyone can provide a guideline/literature that would be great, but even general answers would be appreciated.

So, forgive my very generalized scenario: A 65yo patient is brought into your ED for fevers. On initial assessment, you find him to be diaphoretic, clammy, awake but somewhat confused. Vitals signs are showing mild hypotension, tachycardia, and SPO2 in the high 80's which improves with nasal cannula. You suspect septic shock and begin empiric antibiotics and fluid resuscitation of 30ml/kg after getting initial blood/urine cultures and labs.

Your labs return, and among other derangements, the patient has a sodium level of 160.

My question is two parts-

1) How do you reconcile giving rapid fluid boluses in a patient like this where you might be concerned about rapidly over-correcting her sodium?
2) In the absence of being able to obtain proper history, how do you decide whether this patients confusion is d/t delirium from sepsis, or d/t rapid sodium level changes? (I acknowledge given the bigger picture here, the AMS is likely d/t sepsis, but hear me out :p)

Thanks guys!

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If you’re giving volume resuscitation with isotonic fluids, you’re not going to drop the sodium particularly rapidly. Even if you do, rapid correction of hypernatremia does not seem to be a huge deal in adults (c/w children where it is)

The Na will be contributing significantly to delirium. How much is sepsis vs the sodium is kind of academic.
 
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Hey all,

Not an EM doc, but I've got a question that I am not able to find a clear answer on. If anyone can provide a guideline/literature that would be great, but even general answers would be appreciated.

So, forgive my very generalized scenario: A 65yo patient is brought into your ED for fevers. On initial assessment, you find him to be diaphoretic, clammy, awake but somewhat confused. Vitals signs are showing mild hypotension, tachycardia, and SPO2 in the high 80's which improves with nasal cannula. You suspect septic shock and begin empiric antibiotics and fluid resuscitation of 30ml/kg after getting initial blood/urine cultures and labs.

Your labs return, and among other derangements, the patient has a sodium level of 160.

My question is two parts-

1) How do you reconcile giving rapid fluid boluses in a patient like this where you might be concerned about rapidly over-correcting her sodium?
2) In the absence of being able to obtain proper history, how do you decide whether this patients confusion is d/t delirium from sepsis, or d/t rapid sodium level changes? (I acknowledge given the bigger picture here, the AMS is likely d/t sepsis, but hear me out :p)

Thanks guys!

1) If you're using a relatively hypertonic fluid like NS (154 mEq of Na in 1L) you aren't going to drop the patients sodium *that* much. Furthermore, if they're hypotensive and febrile, it's probably because they're net hypovolemic from sepsis, and their hypernatremia is their body's physiologic response to being volume down.

2) Common things being common, a hypotensive, tachycardic and hypoxic patient is far more likely to be delirious 2/2 their hemodynamic derangements than a sodium of 160. This patient literally isn't perfusing/oxygenating their brain.

This is why frequent reassessments are key. Give an intervention --> look for a response in clinical status. If I give abx, 2L NS and supplemental O2 and they improve, it probably wasn't the Na+. If I do all of that and their vital signs normalize and they're still altered, that's when I'm gonna start looking at other causes for their delirium (metabolic, CNS, tox, etc).
 
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Hey all,

Not an EM doc, but I've got a question that I am not able to find a clear answer on. If anyone can provide a guideline/literature that would be great, but even general answers would be appreciated.

So, forgive my very generalized scenario: A 65yo patient is brought into your ED for fevers. On initial assessment, you find him to be diaphoretic, clammy, awake but somewhat confused. Vitals signs are showing mild hypotension, tachycardia, and SPO2 in the high 80's which improves with nasal cannula. You suspect septic shock and begin empiric antibiotics and fluid resuscitation of 30ml/kg after getting initial blood/urine cultures and labs.

Your labs return, and among other derangements, the patient has a sodium level of 160.

My question is two parts-

1) How do you reconcile giving rapid fluid boluses in a patient like this where you might be concerned about rapidly over-correcting her sodium?
2) In the absence of being able to obtain proper history, how do you decide whether this patients confusion is d/t delirium from sepsis, or d/t rapid sodium level changes? (I acknowledge given the bigger picture here, the AMS is likely d/t sepsis, but hear me out :p)

Thanks guys!


The only sodium levels I’ve seen that high are in nonverbal nursing home patients. Although I did find these case reports interesting.

 
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Agree that rapidly lowering hypernatremia doesn’t seem to be a problem. I would be fine giving them multiple liters of LR and then upstairs can give them free water later
 
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Is the OP a NPP or something? As an EM doc, here're my answers:

1) Don't care.
2) Moot point
They're an FM doc.


Kinda underscores why EM should be practiced by EM trained people...
 
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okay fine, I'll bite:

1) Given that fluid resusciatation will be performed w/ isotonic crystalloid, you really don't need to worry about overly rapid correction of the hypernatremia. Moreover, perfusion takes precedence over theoretical concerns about overcorrection of electrolyte disturbance.

2) You really don't need to 'decide' on the etiology of encephalopathy in a case like this--it's safe to assume it's multifactorial. Sepsis severe enough to cause hypotension will commonly lead to a metabolic encephalopathy. Hypernatremia will reinforce this. However, people with access to water and the physical and cognitive capabilities to drink will not develop severe hypernatremia, so the primary issue was probably either septic encephalopathy, poor fluid management at the nursing home, or pre-existing dementia. One thing to keep in mind, however, that the presence of one (or several) causes of encephalopthy do not preclude alternative etiologies. Patients like this often merit a head CT to r/o a SDH as well. (Chronic subdural-->aspiration pneumonia+dehydration)
 
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OP's post history says that they're freshly graduated, so cut them some slack.

But yeah; fix the hypoperfusion first. One bag of NS isn't going to tank the Na.
We need more of these threads... ones that discuss "the medicine".
 
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1) If you're using a relatively hypertonic fluid like NS (154 mEq of Na in 1L) you aren't going to drop the patients sodium *that* much. Furthermore, if they're hypotensive and febrile, it's probably because they're net hypovolemic from sepsis, and their hypernatremia is their body's physiologic response to being volume down.

2) Common things being common, a hypotensive, tachycardic and hypoxic patient is far more likely to be delirious 2/2 their hemodynamic derangements than a sodium of 160. This patient literally isn't perfusing/oxygenating their brain.

This is why frequent reassessments are key. Give an intervention --> look for a response in clinical status. If I give abx, 2L NS and supplemental O2 and they improve, it probably wasn't the Na+. If I do all of that and their vital signs normalize and they're still altered, that's when I'm gonna start looking at other causes for their delirium (metabolic, CNS, tox, etc).

All very good points, but I bet someone with a sodium of 160 would be profoundly altered. We all get thirsty when our Na goes to 145. Imagine how they feel. I've never seen a walking, talking person with a Na of 160. I have seen walking and talking people with an Na of 120.
 
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Rule #4 in EM. Always correct the thing that will kill the patient first. You can, if you wish, follow the ABCs.
A: make sure there is nothing obstructing air getting into the lungs
B: he is hypoxic so put on O2
C: he is hypotensive so raise his blood pressure.

It ain't ANBC. or NABC. It's ABC!!
 
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All very good points, but I bet someone with a sodium of 160 would be profoundly altered. We all get thirsty when our Na goes to 145. Imagine how they feel. I've never seen a walking, talking person with a Na of 160. I have seen walking and talking people with an Na of 120.

Very true. Old women on booze and SSRIs defy their sodium levels all the time.
Or, as its known here in Florida... "Tuesday".
 
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I don't want to know what's "Friday" for the old boozy FL women.

Correct.

You've heard those stories on the news about "Gertrude McCarthy" who was arrested when she drove thru the front of a restaurant and was piss-drunk? Yeah; that's Friday. I've taken care of my share of those.
 
Oh, he's an FM intern? Ok I apologize for my snark.

I think he's (she's?) PGY-3.
But still - the spirit of the thing (wants to do the right thing by not causing another problem while fixing one) is there.
I wouldn't know grass from astroturf about clinic lyfe, and I'm PGY-11.

Hey OP: What's one of the more common errors/pitfalls that you encounter in clinic? I'd like to send a patient back to his PMD and have the PMD not shake his head in frustration about "what the ER doc did".
 
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I think he's (she's?) PGY-3.
But still - the spirit of the thing (wants to do the right thing by not causing another problem while fixing one) is there.
I wouldn't know grass from astroturf about clinic lyfe, and I'm PGY-11.

Hey OP: What's one of the more common errors/pitfalls that you encounter in clinic? I'd like to send a patient back to his PMD and have the PMD not shake his head in frustration about "what the ER doc did".
Nah, attending. Their last post (which they deleted) mentioned something about them working in the ER.

This job market's got me a bit crispy
 
Nah, attending. Their last post (which they deleted) mentioned something about them working in the ER.

This job market's got me a bit crispy

Thanks all. I recognize this is just a social forum and I'm not treating this as medical literature. I'm just trying to learn the jist of management of a problem that I am not well versed in. D/t privacy, I can't just go reading through people's charts for fun to see how others manage things, so sometimes when I overhear staff talking about a case, I can't help but ponder what your train of thought is when you're managing conflicting problems.

My last post was deleted by admins for a snarky response to the original snark directed towards me for asking said question.

To clarify - I am a new graduate from Family Medicine residency. I am living in Canada, and whether we like it or not, population density forces FM docs to step up to bat or leave swaths of land without physicians at all. I agree that EM docs should be in the ED and respect that. I recognize limitations to my experience and skillset when it comes to EM, and thus work fast track only.

RustedFox: I try to keep me feelings in check when it comes to medical care from various services. Fresh out of residency and rotating with various services - every specialty always complains about others, but ALL work hard. EM guys get pissed with consultants. Surgeons get pissed with EM guys. FM guys and specialists mutually get pissed at each other. End of the day, none of us know it all, and all have limitations to what we were taught or know. I'd like to believe we all have the patients best interest in mind. To answer your question though - nothing really! I recognize your job is to treat critical and life threatening conditions. My job is to treat the basics from birth on, chronic disease, and use my sneaky communication skills to treat microchips, ghosts, and toxins all without giving a single med :)

I'm not trying to be an EM doctor. I'm trying to be an overall better doctor. Cheers guys, and thank you.
 
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Thanks all. I recognize this is just a social forum and I'm not treating this as medical literature. I'm just trying to learn the jist of management of a problem that I am not well versed in. D/t privacy, I can't just go reading through people's charts for fun to see how others manage things, so sometimes when I overhear staff talking about a case, I can't help but ponder what your train of thought is when you're managing conflicting problems.

My last post was deleted by admins for a snarky response to the original snark directed towards me for asking said question.

To clarify - I am a new graduate from Family Medicine residency. I am living in Canada, and whether we like it or not, population density forces FM docs to step up to bat or leave swaths of land without physicians at all. I agree that EM docs should be in the ED and respect that. I recognize limitations to my experience and skillset when it comes to EM, and thus work fast track only.

RustedFox: I try to keep me feelings in check when it comes to medical care from various services. Fresh out of residency and rotating with various services - every specialty always complains about others, but ALL work hard. EM guys get pissed with consultants. Surgeons get pissed with EM guys. FM guys and specialists mutually get pissed at each other. End of the day, none of us know it all, and all have limitations to what we were taught or know. I'd like to believe we all have the patients best interest in mind. To answer your question though - nothing really! I recognize your job is to treat critical and life threatening conditions. My job is to treat the basics from birth on, chronic disease, and use my sneaky communication skills to treat microchips, ghosts, and toxins all without giving a single med :)

I'm not trying to be an EM doctor. I'm trying to be an overall better doctor. Cheers guys, and thank you.

Good response.
But for real; I want to learn from you as well. Give me something to think about. Is it that ER docs reflexively use clonidine or [insert med here] when there are generally better options ? Go ahead.

We need more non-EM folks on here to keep it lively and provide some different points of view. Posters like gutonc and VA HopefulDoc.
Stick around.
 
All very good points, but I bet someone with a sodium of 160 would be profoundly altered. We all get thirsty when our Na goes to 145. Imagine how they feel. I've never seen a walking, talking person with a Na of 160. I have seen walking and talking people with an Na of 120.

Eh, not really. I see it in the unit pretty frequently.
If someone came in with a sodium if 160, I wouldn’t think twice about it. High 160s and I start to attention.
 
Good response.
But for real; I want to learn from you as well. Give me something to think about. Is it that ER docs reflexively use clonidine or [insert med here] when there are generally better options ? Go ahead.

We need more non-EM folks on here to keep it lively and provide some different points of view. Posters like gutonc and VA HopefulDoc.
Stick around.
I bet that very few PCP uses clonidine these days (unless they are treating resistant HTN). Clonidine has a tendency to cause rebound HTN once one stops taking it... If the BP is not outrageous SBP >190 and/or DBP>100, you should just simply restart that person on his/her home regimen and send back to see PCP in less than a week.

I don't see people use Labetalol that much in my program, but I have used with great success. Then again, I am an internist who do not like outpatient medicine. @VA Hopeful Dr probably can chime in.
 
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I bet that very few PCP uses clonidine these days (unless they are treating resistant HTN). Clonidine has a tendency to cause rebound HTN once one stops taking it... If the BP is not outrageous SBP >190 and/or DBP>100, you should just simply restart that person on his/her home regimen and send back to see PCP in less than a week.

I don't see people use Labetalol that much in my program, but I have used with great success. Then again, I am an internist who does not like outpatient medicine. @VA Hopeful Dr probably can chime in.

You must be in a better educated part of the country. I see so much single agent metoprolol, clonidine, etc for first line essential hypertension. I'm just assuming it's the noctors screwing it up since it's like medicine 101.
 
You must be in a better educated part of the country. I see so much single agent metoprolol, clonidine, etc for first line essential hypertension. I'm just assuming it's the noctors screwing it up since it's like medicine 101.
I saw one crazy thing from a noctor... Propranolol for BP as a single agent.

I also saw Minoxidil but it was a nursing home patient. I d/c'ed it. I hope it was not prescribed by a doc. Even said to myself that I should get the topical form to treat my baldness. Lol
 
I bet that very few PCP uses clonidine these days (unless they are treating resistant HTN). Clonidine has a tendency to cause rebound HTN once one stops taking it... If the BP is not outrageous SBP >190 and/or DBP>100, you should just simply restart that person on his/her home regimen and send back to see PCP in less than a week.

I don't see people use Labetalol that much in my program, but I have used with great success. Then again, I am an internist who do not like outpatient medicine. @VA Hopeful Dr probably can chime in.
The amount of first line clonidine I see from PCPs despite free HCTZ and amlodipine at the supermarkets makes me support MOC.
 
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Hey all,

Not an EM doc, but I've got a question that I am not able to find a clear answer on. If anyone can provide a guideline/literature that would be great, but even general answers would be appreciated.

So, forgive my very generalized scenario: A 65yo patient is brought into your ED for fevers. On initial assessment, you find him to be diaphoretic, clammy, awake but somewhat confused. Vitals signs are showing mild hypotension, tachycardia, and SPO2 in the high 80's which improves with nasal cannula. You suspect septic shock and begin empiric antibiotics and fluid resuscitation of 30ml/kg after getting initial blood/urine cultures and labs.

Your labs return, and among other derangements, the patient has a sodium level of 160.

My question is two parts-

1) How do you reconcile giving rapid fluid boluses in a patient like this where you might be concerned about rapidly over-correcting her sodium?
2) In the absence of being able to obtain proper history, how do you decide whether this patients confusion is d/t delirium from sepsis, or d/t rapid sodium level changes? (I acknowledge given the bigger picture here, the AMS is likely d/t sepsis, but hear me out :p)

Thanks guys!
1. It doesn't matter. If someone is septic and you sit on them waiting to get a sodium level back because you're worried about a metabolic electrolyte derangement, that's malpractice. In general isotonic fluids should not lead to rapid correction. Even if it does it is unlikely to lead to any issues.
2. It doesn't matter for the purposes of a EM physician. They'll be on a ward for several days/weeks with a hospitalist figuring that out; you aren't going to completely treat someone's sepsis/hypernatremia in the ER. As for how the hospitalist figures it out, they treat the sepsis then the hypernatremia and decide from there.
 
I bet that very few PCP uses clonidine these days (unless they are treating resistant HTN). Clonidine has a tendency to cause rebound HTN once one stops taking it... If the BP is not outrageous SBP >190 and/or DBP>100, you should just simply restart that person on his/her home regimen and send back to see PCP in less than a week.

I don't see people use Labetalol that much in my program, but I have used with great success. Then again, I am an internist who do not like outpatient medicine. @VA Hopeful Dr probably can chime in.
Barring other comorbitidies, labetalol is my go to BB for hypertension (4th line med). I've found it especially good for resistant cases.

But like you it was hardly ever used in my residency program.

The only time I've started clonidine for BP in the last 3 years was as a prn med to get the nursing home to quit bugging me when the 97 year old's BP went above 140.
 
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The amount of first line clonidine I see from PCPs despite free HCTZ and amlodipine at the supermarkets makes me support MOC.
I probably have never seen it as a first line agent in the part of the country I'm at...
 
Any thoughts on using diltiazem for first line BP management? I do it not infrequently in our free clinic or for county site patients who will be able to follow up just not for a few months due to county BS.

My thinking is it’s cheap, few side effects, and I don’t need to check a K like I would with lisinopril. But I’ve never had any formal education in this subject beyond some vague recollections from my FM rotation.
 
Any thoughts on using diltiazem for first line BP management? I do it not infrequently in our free clinic or for county site patients who will be able to follow up just not for a few months due to county BS.

My thinking is it’s cheap, few side effects, and I don’t need to check a K like I would with lisinopril. But I’ve never had any formal education in this subject beyond some vague recollections from my FM rotation.
Not a fan. If you're going with a CCB why not pick amlodipine or nifedipine? Same benefits but you don't mess with heart rate. But the data says similar efficacy so its mostly a person preference.

Also formulation matters. Short-acting diltiazem actually increases morbidity in hypertension so make sure you're using the 12 or 24 hour ones.
 
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Not a fan. If you're going with a CCB why not pick amlodipine or nifedipine? Same benefits but you don't mess with heart rate. But the data says similar efficacy so its mostly a person preference.

Also formulation matters. Short-acting diltiazem actually increases morbidity in hypertension so make sure you're using the 12 or 24 hour ones.
Interesting. I like the idea of nifedipine...I should read up.

It’s a bummer because a lot of these patients would really benefit from a skilled internist managing their meds, but the reality is I’m probably the only physician they’ll see this year, especially in the free clinic.
 
I saw one crazy thing from a noctor... Propranolol for BP as a single agent.

I also saw Minoxidil but it was a nursing home patient. I d/c'ed it. I hope it was not prescribed by a doc. Even said to myself that I should get the topical form to treat my baldness. Lol

I've seen this precise situation work in the very anxious patient (family member).
 
Interesting. I like the idea of nifedipine...I should read up.

It’s a bummer because a lot of these patients would really benefit from a skilled internist managing their meds, but the reality is I’m probably the only physician they’ll see this year, especially in the free clinic.
It's a good medicine, the only reason I don't use it more is that in my neck of the woods amlodipine is significantly cheaper.

Edit: stupid auto correct
 
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Any thoughts on using diltiazem for first line BP management? I do it not infrequently in our free clinic or for county site patients who will be able to follow up just not for a few months due to county BS.

My thinking is it’s cheap, few side effects, and I don’t need to check a K like I would with lisinopril. But I’ve never had any formal education in this subject beyond some vague recollections from my FM rotation.

Definitely not. Agreed with Norvasc being a good zero thought option to default to
 
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Maybe that was the reason behind it; have not come across the literature yet for that.

Pretty sure you're right. After all, it makes sense: "Nonselective B-blocker in anxious patient may lower anxiety and a BP that's not too far out of line in one swipe"

I'm sure that situation is much more common in the outpatient world than we realize.
 
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Maybe that was the reason behind it; have not come across the literature yet for that.

@VA Hopeful Dr
I used that rational in residency in people I thought had anxiety that was either causing or worsening hypertension. It not only didn't work all that well but as I'm sure you've noticed, patients HATE beta blockers.

These days, if the BP is high but not dangerously so and I think its anxiety I'll just treat the anxiety and keep an eye on the BP. If its high enough that I don't want to let it ride for a few months, I'll treat both and stop the BP med later if their BP settles out once the anxiety is treated.
 
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okay fine, I'll bite:

1) Given that fluid resusciatation will be performed w/ isotonic crystalloid, you really don't need to worry about overly rapid correction of the hypernatremia. Moreover, perfusion takes precedence over theoretical concerns about overcorrection of electrolyte disturbance.

Agree with turkeyjerky, if the patient is volume depleted you need to fluid resuscitate them first, that takes precedence over sodium concerns. Furthermore, in this case of acute volume depletion (as evinced by the shock with tachycardia and hypotension), the patient is not at risk of harm from over correction. This is different than a patient with very chronic hypernatremia without acute volume loss. You would first correct the volume status and then see where you are at vis-a-vis sodium.
 
Any thoughts on using diltiazem for first line BP management? I do it not infrequently in our free clinic or for county site patients who will be able to follow up just not for a few months due to county BS.

My thinking is it’s cheap, few side effects, and I don’t need to check a K like I would with lisinopril. But I’ve never had any formal education in this subject beyond some vague recollections from my FM rotation.

This isn't my wheelhouse, but diltiazem has more effect on rate than pressure correct? Seems like a fairly ineffective BP med. Also the standard preparation is QID dosing correct? (I know there is an XR, but I'm not sure if that is in your free sample supply). QID dosing generally trends with very poor compliance (even short term like treatment with keflex for an acute infection).

I tend to only see diltiazem used for patients who have rate issues as well such as A fib. I think for pure pressure control other CCBs such as amlodipine would be better choices.

Again not my area, but the BP med you choose needs to take into account other existing cardiac disease (i.e. known CHF, BB such as coreg/metorpolol and ACEi are first line).
 
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This isn't my wheelhouse, but diltiazem has more effect on rate than pressure correct? Seems like a fairly ineffective BP med. Also the standard preparation is QID dosing correct? (I know there is an XR, but I'm not sure if that is in your free sample supply). QID dosing generally trends with very poor compliance (even short term like treatment with keflex for an acute infection).

I tend to only see diltiazem used for patients who have rate issues as well such as A fib. I think for pure pressure control other CCBs such as amlodipine would be better choices.

Again not my area, but the BP med you choose needs to take into account other existing cardiac disease (i.e. known CHF, BB such as coreg/metorpolol and ACEi are first line).
This is pretty much accurate, but it would take a decent bit of learning to master the ins and outs of optimal BP management. If you're got the time, energy, and aren't sacrificing any EM reading to do so, go nuts. Heck, I'd be happy to find some good review articles to help if there's interest.
 
This is pretty much accurate, but it would take a decent bit of learning to master the ins and outs of optimal BP management. If you're got the time, energy, and aren't sacrificing any EM reading to do so, go nuts. Heck, I'd be happy to find some good review articles to help if there's interest.
Even managing BP can be somewhat tricky... I just don't understand how NP can practice medicine after doing 500-800 hrs. In all honesty, PA are not that much better. They are better because they are smarter as a whole. And having their rotations done at academic centers alongside physicians/residents, make them aware that medicine is complicated.
 
This is pretty much accurate, but it would take a decent bit of learning to master the ins and outs of optimal BP management. If you're got the time, energy, and aren't sacrificing any EM reading to do so, go nuts. Heck, I'd be happy to find some good review articles to help if there's interest.

Agreed, there's a lot of nuance to it, which is the point I'm trying to make to the poster above (more to it than just giving whatever samples you have available).

I fairly rarely initiate BP meds for the first time, as my standard approach is just to refer expeditiously to a primary physician because as noted above, it is more complicated than it first appears.

That being said, sometimes I do initiate treatment (patient unable to access primary care expeditiously) so I would be interested in some review on the topic.
 
I wasn't aware. Tell me more.
Erectile dysfunction in men, decreased exercise tolerance, depression, fatigue. Most BP meds can do that of course but BBs seem to be worse. Makes sense since most others don't decrease heart rate.

Anecdotally I've found that the ones with alpha activity tend to do this less, part of the reason I prefer labetalol and carvedilol.
 
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I'm sure you've noticed, patients HATE beta blockers.

Back in my brief foray into academic medicine, I had a friend who was a physician with the University Health Service. He always had patients who were in art majors come and ask for beta blockers. He imagined whispered backstage at the Creative Arts Center was "Hey, go see Dr. Smith; He has the good stuff."

Of course very different populations and uses.
 
Back in my brief foray into academic medicine, I had a friend who was a physician with the University Health Service. He always had patients who were in art majors come and ask for beta blockers. He imagined whispered backstage at the Creative Arts Center was "Hey, go see Dr. Smith; He has the good stuff."

Of course very different populations and uses.

Pro golfers are known to use beta-blockers to "calm the yips" and smooth their swings, especially when putting.
 
Pretty sure you're right. After all, it makes sense: "Nonselective B-blocker in anxious patient may lower anxiety and a BP that's not too far out of line in one swipe"

I'm sure that situation is much more common in the outpatient world than we realize.
I'm coming to think that it's far more common at my community site than I first realized. Had not really thought about the use of propranolol in this situation, it might be a great choice in a patient who fits this bill.

The problem with us EM docs starting these meds is that we'll never see the patient again, and if we give them something that we think is called for in their particular situation then the next doc who sees them is going to wonder what the heck we were thinking (myself included, most likely). If they were "our" patient, then we'd know how worked and no one else would be there to question our reasoning. It's one of the things that keeps us pretty conservative in general.
 
Back in my brief foray into academic medicine, I had a friend who was a physician with the University Health Service. He always had patients who were in art majors come and ask for beta blockers. He imagined whispered backstage at the Creative Arts Center was "Hey, go see Dr. Smith; He has the good stuff."

Of course very different populations and uses.
Yeah I've heard that the ophthalmologists will use super low doses to steady their hands for surgery at times
 
I've seen angioedema and coughs with ACE inhibitors, but never hyperkalemia. I've seen Pts on an Ace and spironolactone, which you probably shouldn't mix. Lisinopril and amlodipine are free here.
 
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I've seen angioedema and coughs with ACE inhibitors, but never hyperkalemia. I've seen Pts on an Ace and spironolactone, which you probably shouldn't mix. Lisinopril and amlodipine are free here.
Its rare in monotherapy assuming functioning kidneys. The trouble, as you point out, is mixing multiple meds that can do it. I have a fair number of CHF patients on Entresto (both components of which can cause hyperK) and sprinolactone that run potassiums in the low 5s pretty much all the time. Then if someone isn't paying attention and gives them bactrim for their UTI...
 
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