High Potassium Value

[Chrism611]

Hello, first off i am not a Medical Student. I'm a 17 year old volunteer at a nearby pretty high volume ER.

I have a quick question about some treatment decisions on a patient.

Patient was in his 50s, was sent to ER by his primary care physician for elevated Potassium values.

He was triaged regularly in no rush and then was placed in a room.. I was doing an EKG on the patient when the doctor walked in and looked at me doing it and said for me to go get someone to draw blood as soon as I was done with the EKG. The EKG had abnormalities. The doctor told me to have respiratory paged stat.

I went back into the room to finish getting the patient on the monitor and the doctor was still in there. I wasnt aware of the severity of the situation at the time, but after the doctor informed myself and the RN about to draw blood that the patient could arrest at any second and asked me to get a finger stick blood sugar and if it was low (may have been high I don't really remember) that the nurse needed to give certain medication. The d-stick or accu check showed a blood sugar of 112. The doctor then asked the patient about any symptoms as he denied pain. The doctor asked me to get respiratory again, and by that time the labs were back the potassium was 8.3. The doctor ordered an amp of bicarb and some calcium not sure exactly how much calcium.

When respiratory arrived he ordered I think albuterol. He wanted continuous treatments.
My question is why was the breathing treatment of albuterol (or whatever it was) ordered. His Sat was fine 99% - 100%, all other Vitals were stable as well, no difficulty breathing. Was it to help get the K level down or was it precautionary actions or something?

Maybe I missed something. My dad is a pharmacist and I asked him and he informed me that there is no way that it was for the Potassium. Just wanted some of your answers.

Sorry for this being so lengthy and possibly not informative enough for an answer. I don't know that much but I want to learn as much as I can, so any answers are appreciated.
Thank you for your time.

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[Venko]

Hello, first off i am not a Medical Student. I'm a 17 year old volunteer at a nearby pretty high volume ER.

I have a quick question about some treatment decisions on a patient.

Patient was in his 50s, was sent to ER by his primary care physician for elevated Potassium values.

He was triaged regularly in no rush and then was placed in a room.. I was doing an EKG on the patient when the doctor walked in and looked at me doing it and said for me to go get someone to draw blood as soon as I was done with the EKG. The EKG had abnormalities. The doctor told me to have respiratory paged stat.

I went back into the room to finish getting the patient on the monitor and the doctor was still in there. I wasnt aware of the severity of the situation at the time, but after the doctor informed myself and the RN about to draw blood that the patient could arrest at any second and asked me to get a finger stick blood sugar and if it was low (may have been high I don't really remember) that the nurse needed to give certain medication. The d-stick or accu check showed a blood sugar of 112. The doctor then asked the patient about any symptoms as he denied pain. The doctor asked me to get respiratory again, and by that time the labs were back the potassium was 8.3. The doctor ordered an amp of bicarb and some calcium not sure exactly how much calcium.

When respiratory arrived he ordered I think albuterol. He wanted continuous treatments.
My question is why was the breathing treatment of albuterol (or whatever it was) ordered. His Sat was fine 99% - 100%, all other Vitals were stable as well, no difficulty breathing. Was it to help get the K level down or was it precautionary actions or something?

Maybe I missed something. My dad is a pharmacist and I asked him and he informed me that there is no way that it was for the Potassium. Just wanted some of your answers.

Sorry for this being so lengthy and possibly not informative enough for an answer. I don't know that much but I want to learn as much as I can, so any answers are appreciated.
Thank you for your time.

Great question. I will speak generally about hyperkalemia (elevated potassium) as I don't know the details of the case.

Elevated potassium levels in the blood can certainly if left untreated and at severe levels cause the heart to stop beating effectively and cause death. It can occur for many many reasons, but the treatment algorithm is rather well agreed upon.

An elevated potassium can be false due to "hemolysis" of the blood so the physician is always on guard for spurious results.

Once confirmed to be high, the ECG is important. If there are specific changes on the ECG related to the potassium, the doctor will give calcium to protect the heart from the effects of the potassium.

Next, the goal is to shift potassium out of the blood and into the tissues / cells. This is accomplished through the use of insulin (which may require sugar supplement to prevent the blood sugar from going too low), albuterol, and bicarbonate. All of these three things cause the shift to occur, so most likely in your case the albuterol was for this purpose. It will in fact lower the blood potassium level.

Finally, the potassium needs to be removed from the body and it can be done through a medicine called lasix which causes it to be peed out, kayaxalate which causes it to come out in stool, or dialysis which mechanically removes it from the blood.

Special situations include patients whose potassium is elevated in the setting of toxic levels of a medicine called digoxin, who are usually treated with a medicine called digibind (binds the digoxin medicine) to help the patient.

There are other nuances to this, but overall this is hyperkalemia.

The albuterol is certainly used frequently to lower potassium levels.

Cheers,
TL

 

[Chrism611]

Great question. I will speak generally about hyperkalemia (elevated potassium) as I don't know the details of the case.

Elevated potassium levels in the blood can certainly if left untreated and at severe levels cause the heart to stop beating effectively and cause death. It can occur for many many reasons, but the treatment algorithm is rather well agreed upon.

An elevated potassium can be false due to "hemolysis" of the blood so the physician is always on guard for spurious results.

Once confirmed to be high, the ECG is important. If there are specific changes on the ECG related to the potassium, the doctor will give calcium to protect the heart from the effects of the potassium.

Next, the goal is to shift potassium out of the blood and into the tissues. This is accomplished through the use of insulin (which may require sugar supplement to prevent the blood sugar from going too low), albuterol, and bicarbonate. All of these three things cause the shift to occur, so most likely in your case the albuterol was for this purpose. It will in fact lower the blood potassium level.

Finally, the potassium needs to be removed from the body and it can be done through a medicine called lasix which causes it to be peed out, kayaxalate which causes it to come out in stool, or dialysis which mechanically removes it from the blood.

Special situations include patients whose potassium is elevated in the setting of toxic levels of a medicine called digoxin, who are usually treated with a medicine called digibind (binds the digoxin medicine) to help the patient.

There are other nuances to this, but overall this is hyperkalemia.

The albuterol is certainly used frequently to lower potassium levels.

Cheers,
TL

Thanks a lot. This explained just about everything.

I left out that this patient had previously had a kidney transplant. That was problem an important factor.

I do understand this now though, once again I appreciate it. When you are lowering hyperkalemia, does the speed have anything to do with it? I know you can not lower hypertension too fast, or are not supposed to, as well as body temperature, but are there any guidelines on how fast you can lower it?

Also, will you see a decrease in levels when the potassium is moved from the blood into the tissues or not until laxis?

Thanks again that was a very informative and helpful answer 🙂.

 

[wook]

Thanks a lot. This explained just about everything.

I left out that this patient had previously had a kidney transplant. That was problem an important factor.

I do understand this now though, once again I appreciate it. When you are lowering hyperkalemia, does the speed have anything to do with it? I know you can not lower hypertension too fast, or are not supposed to, as well as body temperature, but are there any guidelines on how fast you can lower it?

Also, will you see a decrease in levels when the potassium is moved from the blood into the tissues or not until laxis?

Thanks again that was a very informative and helpful answer 🙂.

Beta-2 adrenergic agonists (e.g. albuterol) drive potassium into the cells by increasing the activity of the Na-K-ATPase pump in skeletal muscle.

When we lower potassium in the E.D. most are TEMPORIZING measures. They transiently lower the potassium by pushing it into the cells. As you alluded, more permanent measures for lowering the total body potassium need to be implemented to remove the potassium from the body. This can be accomplished through kayexalate (i.e. sodium polystyrene sulfonate), hemodialysis, and lasix (i.e. furosemide) (as discussed by Thyme).

Thanks.


Wook

 

[Venko]

Thanks a lot. This explained just about everything.

I left out that this patient had previously had a kidney transplant. That was problem an important factor.

I do understand this now though, once again I appreciate it. When you are lowering hyperkalemia, does the speed have anything to do with it? I know you can not lower hypertension too fast, or are not supposed to, as well as body temperature, but are there any guidelines on how fast you can lower it?

Also, will you see a decrease in levels when the potassium is moved from the blood into the tissues or not until laxis?

Thanks again that was a very informative and helpful answer 🙂.

My pleasure to help and also an excellent question about the speed of lowering it.

The speed is not as important as the values in potassium, however, there is some suggestion that the speed at which it increased in the blood relates to the likelihood the heart will be affected...for example if it went from normal (4.0) to extremely high (6.0) in 30 minutes, this may cause more heart problems than if the change occurred over 1 year...but I don't know this is proven yet.

As for the levels, the level represents the amount of potassium in the blood (more specifically the serum which is the fluid outside of the red blood cells but flowing in the vessels), so if the potassium is shifted into the tissues / cell, then level reported back from the lab will be lower.

Great questions!

TL

 

[wook]

My pleasure to help and also an excellent question about the speed of lowering it.

The speed is not as important as the values in potassium, however, there is some suggestion that the speed at which it increased in the blood relates to the likelihood the heart will be affected...for example if it went from normal (4.0) to extremely high (6.0) in 30 minutes, this may cause more heart problems than if the change occurred over 1 year...but I don't know this is proven yet.

As for the levels, the level represents the amount of potassium in the blood (more specifically the serum which is the fluid outside of the red blood cells but flowing in the vessels), so if the potassium is shifted into the tissues / cell, then level reported back from the lab will be lower.

Great questions!

TL

👍

Hey Thyme...think we could recruit him to go into EM?

Wook

 

[Apollyon]

Your dad misled you (sorry).

There are a few ways to get potassium out of the body: sweat, urine, stool, and blood. Sweat is negligible. Kayexalate (sodium polystyrene sulfate) binds the K+, and it comes out with the poop. People on "loop diuretics" (like Lasix - furosemide) lose potassium through their urine, as do people on thiazide diuretics (like HCTZ - hydrochlorothiazide). That's why some people are on "potassium sparing" diuretics, such as spironolactone. Dialysis on the blood will remove potassium.

The other treatment we have just mobilize the potassium, or move it around. Most potassium in the body is intracellular. Most sodium is extracellular. This creates a gradient, which also imparts an electric charge (fundamentally). This also helps the heart beat - the cells in the heart slowly leak sodium, which starts the heart beating. However, potassium is the next step (and calcium after that). If the potassium is high outside the cell, and high inside the cell, there's no gradient, and the heart can stop (which is exactly what happens with lethal injection - they bolus in potassium chloride). As such, there are a few things we do: calcium IV doesn't move the potassium into the cell, but "moves the goal posts", by raising the blood calcium level. Now, if the potassium is up, and the calcium is up, there's no differential difference between them. (That is, for example, you have 10 oranges and 8 apples; a difference of 2. All of a sudden, 10 more oranges are dropped in. Now, there are 20 oranges and 8 apples - a difference of 12. If you drop in 10 apples, the difference is again 2.)

Other things are glucose and insulin; insulin pushes glucose into cells, and drags potassium with it. Usually, we will give glucose IV with the insulin, to make sure the insulin has substrate with which to work - it's like throwing gas on a fire, so the firefighters have a bigger flame to fight. If the gas wasn't thrown on the fire, the water from the firefighters might put the fire completely out (and, if the glucose is the fire, pushing glucose to zero isn't good). The albuterol causes insulin release (which pushes glucose, with potassium, into the cells), and also stimulates the Na+/K+ pump (as the gradient with potassium high inside and low outside, and sodium high outside and low inside, tends to want to equalize - physics and all that - the body has to pump against the gradient). The sodium potassium pump pumps harder sodium out and potassium in. We also give sodium bicarbonate to alkalinize the blood - this also activate the Na+/K+ pump, by exchanging H+ ions for Na+ ions - H+ out of the cell, and Na+ in. Then, the pump does it's job by pumping that sodium out again, and potassium into the cell.

The reason why the doctor got keyed up after seeing the EKG is he saw something on it worrisome - peaked T waves, or a widened QRS. It is doubtful it had gotten to the sine wave stage.

 

[Apollyon]

Ah, man, as I was composing my learned treatise, you guys got to it ahead of me! Honest, there weren't any responses when I started!

 

[Chrism611]

My pleasure to help and also an excellent question about the speed of lowering it.

The speed is not as important as the values in potassium, however, there is some suggestion that the speed at which it increased in the blood relates to the likelihood the heart will be affected...for example if it went from normal (4.0) to extremely high (6.0) in 30 minutes, this may cause more heart problems than if the change occurred over 1 year...but I don't know this is proven yet.

As for the levels, the level represents the amount of potassium in the blood (more specifically the serum which is the fluid outside of the red blood cells but flowing in the vessels), so if the potassium is shifted into the tissues / cell, then level reported back from the lab will be lower.

Great questions!

TL

So this patient's Potassium had probably been increasing over a long period of time?

And that is a good thing to know about the lab work. So the Potassium in the tissues is less dangerous than the potassium in the blood?
And is the use of laxis or other drugs (excluding dialysis) used in the ER or after patient admission usually?

To Wook, thanks for your answers as well. They were helpful especially with the specific use of the albuterol. The same question I asked Thyme I guess would be that when it is moved from the blood, is it still as dangerous even though the values are lower? So it will continue to be dangerous until dialyzed or use of laxis or kayexalate?


And to your last post Wook, ive been involved with Emergency Medicine for a year now. I love every second of it. I've learned tons, and want to know more 😛. I can read read or understand basic rhythms like afib, sinus, vfib, v-tach, and know about a few emergency drugs. It never gets old. Every day we get something significant its different. Ive seen everything from amputated limbs from crush injuries, to GSW to the chest and a thoracocotomy to many ODs and full arrests. There soo much.

the day we had this particular patient, I also learned from a patient with pulmonary hypertension that they can not be airlifted due to altitude levels and such. So I really enjoy the field, its what I want to do. I spend almost every day in the summer volunteering and during the past school year every Friday night and holiday I got.

A lot of people don't appreciate what you guys do. I'm amazed by it. Thanks for your helpful answers and all and for what you do for everyone.

 

[Chrism611]

Your dad misled you (sorry).

There are a few ways to get potassium out of the body: sweat, urine, stool, and blood. Sweat is negligible. Kayexalate (sodium polystyrene sulfate) binds the K+, and it comes out with the poop. People on "loop diuretics" (like Lasix - furosemide) lose potassium through their urine, as do people on thiazide diuretics (like HCTZ - hydrochlorothiazide). That's why some people are on "potassium sparing" diuretics, such as spironolactone. Dialysis on the blood will remove potassium.

The other treatment we have just mobilize the potassium, or move it around. Most potassium in the body is intracellular. Most sodium is extracellular. This creates a gradient, which also imparts an electric charge (fundamentally). This also helps the heart beat - the cells in the heart slowly leak sodium, which starts the heart beating. However, potassium is the next step (and calcium after that). If the potassium is high outside the cell, and high inside the cell, there's no gradient, and the heart can stop (which is exactly what happens with lethal injection - they bolus in potassium chloride). As such, there are a few things we do: calcium IV doesn't move the potassium into the cell, but "moves the goal posts", by raising the blood calcium level. Now, if the potassium is up, and the calcium is up, there's no differential difference between them. (That is, for example, you have 10 oranges and 8 apples; a difference of 2. All of a sudden, 10 more oranges are dropped in. Now, there are 20 oranges and 8 apples - a difference of 12. If you drop in 10 apples, the difference is again 2.)

Other things are glucose and insulin; insulin pushes glucose into cells, and drags potassium with it. Usually, we will give glucose IV with the insulin, to make sure the insulin has substrate with which to work - it's like throwing gas on a fire, so the firefighters have a bigger flame to fight. If the gas wasn't thrown on the fire, the water from the firefighters might put the fire completely out (and, if the glucose is the fire, pushing glucose to zero isn't good). The albuterol causes insulin release (which pushes glucose, with potassium, into the cells), and also stimulates the Na+/K+ pump (as the gradient with potassium high inside and low outside, and sodium high outside and low inside, tends to want to equalize - physics and all that - the body has to pump against the gradient). The sodium potassium pump pumps harder sodium out and potassium in. We also give sodium bicarbonate to alkalinize the blood - this also activate the Na+/K+ pump, by exchanging H+ ions for Na+ ions - H+ out of the cell, and Na+ in. Then, the pump does it's job by pumping that sodium out again, and potassium into the cell.

The reason why the doctor got keyed up after seeing the EKG is he saw something on it worrisome - peaked T waves, or a widened QRS. It is doubtful it had gotten to the sine wave stage.

Thanks for your reply as well. All of you touched on the same thing using different methods making it understandable. And I'm not offended by my dad being wrong 😛, just wanted to make sure I was correct with what I remember.
I also enjoyed the analogies you used making these understandable.
Thanks again. 🙂

 

[Apollyon]

I also enjoyed the analogies you used making these understandable.

Very little of medicine is per se difficult - it's just so much to know. It's like someone giving you a million dollars - in pennies.

 

[wook]

Ah, man, as I was composing my learned treatise, you guys got to it ahead of me! Honest, there weren't any responses when I started!

Punchbuggy! You're it!


Wook

 

[Dwindlin]

I'm glad this came up. Something has been bothering me for a while and I have as of yet been unsuccessful in finding a good explanation.

I understand that Calcium stabilizes the membrane. I don't understand how. HyperK causes depolarization right? Wouldn't increasing Ca also depolarize the membrane? How does that help things?

 

[wook]

I'm glad this came up. Something has been bothering me for a while and I have as of yet been unsuccessful in finding a good explanation.

I understand that Calcium stabilizes the membrane. I don't understand how. HyperK causes depolarization right? Wouldn't increasing Ca also depolarize the membrane? How does that help things?

"...Calcium directly antagonizes the membrane actions of hyperkalemia, while hypocalcemia increase the cardiotoxicity of hyperkalemia. Hyperkalemia-induced depolarization of the resting membrane potential leads to inactivation of sodium channels and decreased membrane excitability. Calcium antagonizes this membrane effect, although how this is achieved is not well understood.."

The above is an explanation from UpToDate (i.e. I can't claim credit for the above explanation).


Thanks.


Wook

 

[Dwindlin]

"...Calcium directly antagonizes the membrane actions of hyperkalemia, while hypocalcemia increase the cardiotoxicity of hyperkalemia. Hyperkalemia-induced depolarization of the resting membrane potential leads to inactivation of sodium channels and decreased membrane excitability. Calcium antagonizes this membrane effect, although how this is achieved is not well understood.."

The above is an explanation from UpToDate (i.e. I can't claim credit for the above explanation).


Thanks.


Wook

Thanks, I don't have access to uptodate. And maybe the bolded is why I've been struggling to find an answer.

 

[Venko]

So this patient's Potassium had probably been increasing over a long period of time?

And that is a good thing to know about the lab work. So the Potassium in the tissues is less dangerous than the potassium in the blood?
And is the use of laxis or other drugs (excluding dialysis) used in the ER or after patient admission usually?

To Wook, thanks for your answers as well. They were helpful especially with the specific use of the albuterol. The same question I asked Thyme I guess would be that when it is moved from the blood, is it still as dangerous even though the values are lower? So it will continue to be dangerous until dialyzed or use of laxis or kayexalate?


And to your last post Wook, ive been involved with Emergency Medicine for a year now. I love every second of it. I've learned tons, and want to know more 😛. I can read read or understand basic rhythms like afib, sinus, vfib, v-tach, and know about a few emergency drugs. It never gets old. Every day we get something significant its different. Ive seen everything from amputated limbs from crush injuries, to GSW to the chest and a thoracocotomy to many ODs and full arrests. There soo much.

the day we had this particular patient, I also learned from a patient with pulmonary hypertension that they can not be airlifted due to altitude levels and such. So I really enjoy the field, its what I want to do. I spend almost every day in the summer volunteering and during the past school year every Friday night and holiday I got.

A lot of people don't appreciate what you guys do. I'm amazed by it. Thanks for your helpful answers and all and for what you do for everyone.

It is our pleasure to help out! You are asking very insightful questions especially given your age (though your experience seems to exceed your age😉. I hope you continue to enjoy learning and good luck in whatever specialty you choose when the time comes...if it happens to be EM....well the better for us all!

 

[Venko]

Thanks, I don't have access to uptodate. And maybe the bolded is why I've been struggling to find an answer.

I don't remember the details anymore, but I remember it made sense when I was on toxicology and they were going over the pathophysiology of digoxin toxicity...maybe check that out for an answer?

I'm sorry I don't remember anymore though...

 

[AzEMMD]

You get to do EKGs and blood draws as a high school EM volunteer? Jeez, when I volunteered in high school all they'd let me do was stock shelves and clean beds 😉 I'm surprised a pharmacist wouldn't know about how albuterol works to lower potassium, this kind of thing seems pretty straight forward and would be right up their alley.

 

[Venko]

You get to do EKGs and blood draws as a high school EM volunteer? Jeez, when I volunteered in high school all they'd let me do was stock shelves and clean beds 😉 I'm surprised a pharmacist wouldn't know about how albuterol works to lower potassium, this kind of thing seems pretty straight forward and would be right up their alley.

Its cool, maybe they don't work in a setting where albuterol is used like that....

 

[Rendar5]

just to add some fire to the fray, i'm not sure kayexalate actually does anything, except cause diarrhea due to the sorbitol in the mixture. It may just be one of the biggest medical myths in current existence, or so I hear.
<_<
>_>

 

[Chrism611]

You get to do EKGs and blood draws as a high school EM volunteer? Jeez, when I volunteered in high school all they'd let me do was stock shelves and clean beds 😉 I'm surprised a pharmacist wouldn't know about how albuterol works to lower potassium, this kind of thing seems pretty straight forward and would be right up their alley.

Yeah, they all like me pretty much, always let me see everything. I've done CPR, bagged patients, and do probably at least 15 EKGs a day ( we see a lot of patients) . Hook people up to monitors administer O2. I don't draw blood, I just do finger sticks. Its basically an ER techs job. I'm the only volunteer in the ER though.

And I know 😛. My dad however works at the hospital I volunteer at. He worked that night so I asked him about it on the way home. Not sure why he didn't know, now that I've found out and to specifics I can let him know 😛.

 

[xaelia]

just to add some fire to the fray, i'm not sure kayexalate actually does anything, except cause diarrhea due to the sorbitol in the mixture. It may just be one of the biggest medical myths in current existence, or so I hear.
<_<
>_>

Correct.

SPS-sorbitol will only bind the K+ free in the gut and does not affect serum levels except indirectly. Additionally, it has been linked to intestinal necrosis and is certainly harmful to a subset of uremic and critically ill patients.

That being said, it is otherwise mostly harmless.

I usually don't do anything heroic about hyperK unless there are EKG changes; every intervention has the potential to cause harm.

 

[wook]

just to add some fire to the fray, i'm not sure kayexalate actually does anything, except cause diarrhea due to the sorbitol in the mixture. It may just be one of the biggest medical myths in current existence, or so I hear.
<_<
>_>

"...Studies demonstrating efficacy with sodium polystyrene sulfonate documented a potassium-lowering effect after multiple doses were given over one to five days; single doses are not very effective. In two of the original studies, the serum potassium fell by at least 0.4 meq/L in the first 24 hours in 23 of 30 patients and all seven patients treated with three daily doses of sodium polystyrene sulfonate in sorbitol had a gradual and steady decrease in serum potassium over five days; concomitant therapy with high doses of glucose and low dietary potassium intake may have contributed to the hypokalemic response..."

"....The association between sodium polystyrene sulfonate and sorbitol with intestinal necrosis led the Food and Drug Administration to issue a recommendation in September 2009 that sodium polystyrene sulfonate should no longer be administered in sorbitol. However, many hospitals and pharmacies only stock sodium polystyrene sulfonate premixed in sorbitol. Sodium polystyrene sulfonate alone is not always available and, when available, comes as a powder that must be reconstituted.

Sodium polystyrene sulfonate in sorbitol can also injure the esophagus and stomach when given orally, possibly resulting in manifestations such as bleeding and esophageal necrosis. Other complications of sodium polystyrene sulfonate in sorbitol include hypocalcemia, volume overload, and hypokalemia..."

Glad you brought this up...I didn't know about the Sorbitol issue. The quoted part is from UpToDate....what can I say, it's easier to cut and paste then type.


Thanks.

Wook

 

[wook]

Correct.

SPS-sorbitol will only bind the K+ free in the gut and does not affect serum levels except indirectly. Additionally, it has been linked to intestinal necrosis and is certainly harmful to a subset of uremic and critically ill patients.

That being said, it is otherwise mostly harmless.

I usually don't do anything heroic about hyperK unless there are EKG changes; every intervention has the potential to cause harm.

Dang....I was typing (actually cutting pasting) when you posted this. Punchbuggy!


Thanks.


Wook

 

[njac]

When respiratory arrived he ordered I think albuterol. He wanted continuous treatments.
My question is why was the breathing treatment of albuterol (or whatever it was) ordered. His Sat was fine 99% - 100%, all other Vitals were stable as well, no difficulty breathing. Was it to help get the K level down or was it precautionary actions or something?

Maybe I missed something. My dad is a pharmacist and I asked him and he informed me that there is no way that it was for the Potassium. Just wanted some of your answers.

Your dad needs to go review some pharmacology and mechanism of the beta agonists.

Signed,
Another Pharmacist.

 

[Venko]

Your dad needs to go review some pharmacology and mechanism of the beta agonists.

Signed,
Another Pharmacist.

Come on, what is the point of this jab at his dad? This kid is clearly wise beyond their years, they ask insightful questions and are inquisitive. They asked their dad a question, and he didn't at the time know the answer, we have all made mistakes, oversights etc....this young person was even so wise as to politely suggest they would address the oversight with their dad, so why not just let it be?

 

[wook]

Come on, what is the point of this jab at his dad? This kid is clearly wise beyond their years, they ask insightful questions and are inquisitive. They asked their dad a question, and he didn't at the time know the answer, we have all made mistakes, oversights etc....this young person was even so wise as to politely suggest they would address the oversight with their dad, so why not just let it be?

👍

 

[Old_Mil]

Hello, first off i am not a Medical Student. I'm a 17 year old volunteer at a nearby pretty high volume ER.

I was doing an EKG on the patient when the doctor walked in and looked at me doing it and said for me to go get someone to draw blood as soon as I was done with the EKG. The EKG had abnormalities. The doctor told me to have respiratory paged stat.

...no offense intended, but as a 17 year old volunteer at a hospital, why are you doing these things? That seems a bit irresponsible on the part of an attending, to me. It really has the potential to leave you in a really bad situation, liking you has nothing to do with it.

 

[link2swim06]

...no offense intended, but as a 17 year old volunteer at a hospital, why are you doing these things? That seems a bit irresponsible on the part of an attending, to me. It really has the potential to leave you in a really bad situation, liking you has nothing to do with it.

Are you trying to say because of his age or him being a volunteer?

There has been 3rd/4th year med students in their late teens and I did similar things while I was a volunteer.

 

[mlw47]

Did anyone else listen to this?

http://emcrit.org/misc/is-kayexalate-useless/


Apparently kayexalate doesn't work.

 

[Chrism611]

...no offense intended, but as a 17 year old volunteer at a hospital, why are you doing these things? That seems a bit irresponsible on the part of an attending, to me. It really has the potential to leave you in a really bad situation, liking you has nothing to do with it.

Most of my EKGs are done with the supervision of an RN and even sometimes a MD in emergency situation. I know how to get a good EKG with no tremors and the doctor lets me know if it needs to be redone.

I do nothing that is not supervised or irresponsible on part of the staff or attending physicians. Some even don't like me, but when we're swamped and there's routine EKG's that need to be done and I am capable of doing them, what's the problem?

I, however, do respect your opinion and concerns. I can assure you that me putting 10 leads on a patient and pressing a button when the rhythm is straight with a RN bedside as well and then having it in the attending's hand within 5 minutes can not do anything to hurt a patient. I can also assure you that the next 5 leads I put on as well as a blood pressure cuff and O2sat probe does not hurt the patient. No offense taken, I just wish to elaborate on my position. I do understand the important of certain situations and how certain situation can end up bad in a matter of minutes or seconds and during those situations, anything I do is supervised.

 

[Old_Mil]

Did anyone else listen to this?

http://emcrit.org/misc/is-kayexalate-useless/


Apparently kayexalate doesn't work.

If kayexalte doesn't work, is it magic potassium fairies that reduce a patient's K after you administer it? I mean, all ebm aside, I have seen it work with my own eyes many times. If it isn't the pharmacology, I'd like to know what metaphysical mechanism of action it has. I'm thinking "placebo effect" is probably a poor explanation for something meant to correct electrolyte abnormalities.

 

[Rendar5]

If kayexalte doesn't work, is it magic potassium fairies that reduce a patient's K after you administer it? I mean, all ebm aside, I have seen it work with my own eyes many times. If it isn't the pharmacology, I'd like to know what metaphysical mechanism of action it has. I'm thinking "placebo effect" is probably a poor explanation for something meant to correct electrolyte abnormalities.

you give kayexelate with absolutely no other therapies? Everytime I've seen it used, it's always in conjunction with other therapies proven to work. I don't know the data and I never tried Kayexalate on its own, so I can't say I know it doesn't work. But I can say that I've never seen great evidence that it's an effective agent, either from experience or from data.

 

[Apollyon]

you give kayexelate with absolutely no other therapies? Everytime I've seen it used, it's always in conjunction with other therapies proven to work. I don't know the data and I never tried Kayexalate on its own, so I can't say I know it doesn't work. But I can say that I've never seen great evidence that it's an effective agent, either from experience or from data.

What other therapies remove the K+ from the body, versus just moving it around?

Dialysis, urine, diarrhea, sweat. Oh yeah, and vomiting. Vomit and sweat aren't clinically useful. The Lasix takes care of the urine.

So, you have the stool, and the HD. Unless they are ESRD, I've never sent a patient to emergent dialysis. Then again, since my prelim year in IM, I haven't seen a non-dialysis hyperkalemia. However, for the patients that weren't dialyzed, but got Kayexalate, and their potassium dropped (and didn't go up again after the effects of the mobilizing agents wore off), well, what do you say to that?

 

[Venko]

What other therapies remove the K+ from the body, versus just moving it around?

Dialysis, urine, diarrhea, sweat. Oh yeah, and vomiting. Vomit and sweat aren't clinically useful. The Lasix takes care of the urine.

So, you have the stool, and the HD. Unless they are ESRD, I've never sent a patient to emergent dialysis. Then again, since my prelim year in IM, I haven't seen a non-dialysis hyperkalemia. However, for the patients that weren't dialyzed, but got Kayexalate, and their potassium dropped (and didn't go up again after the effects of the mobilizing agents wore off), well, what do you say to that?

👍 🙂

 

[Rendar5]

What other therapies remove the K+ from the body, versus just moving it around?

Dialysis, urine, diarrhea, sweat. Oh yeah, and vomiting. Vomit and sweat aren't clinically useful. The Lasix takes care of the urine.

So, you have the stool, and the HD. Unless they are ESRD, I've never sent a patient to emergent dialysis. Then again, since my prelim year in IM, I haven't seen a non-dialysis hyperkalemia. However, for the patients that weren't dialyzed, but got Kayexalate, and their potassium dropped (and didn't go up again after the effects of the mobilizing agents wore off), well, what do you say to that?

1. I say they were also given sorbitol that causes diarrhea. Unless you have a source of kayexalate that does not also contain sorbitol.
2. I say that the offending source of the hyperkalemia was also affected. whether that's low potassium diet, cessation of an ACE, use of lasix, etc. Can you mention a cause of hyperkalemia that we don't address in some manner in addition to kayex??

All I can say is that I've never seen plain kayexalate used in isolation to other treatments for hyperkalemia (I doubt any US hospitals even use plain kayexalate), the original studies showing it's use didn't even have controls, and there's RCT's out there that potentially refute kayexalate's effect.

I think that there's a general assumption that you give kayexalate, you see a potassium drop, and you assume that the kayexalate causes it, and you forget about everything else that just happened to the patient.

 

[Venko]

1. I say they were also given sorbitol that causes diarrhea. Unless you have a source of kayexalate that does not also contain sorbitol.
2. I say that the offending source of the hyperkalemia was also affected. whether that's low potassium diet, cessation of an ACE, use of lasix, etc. Can you mention a cause of hyperkalemia that we don't address in some manner in addition to kayex??

All I can say is that I've never seen plain kayexalate used in isolation to other treatments for hyperkalemia (I doubt any US hospitals even use plain kayexalate), the original studies showing it's use didn't even have controls, and there's RCT's out there that potentially refute kayexalate's effect.

I think that there's a general assumption that you give kayexalate, you see a potassium drop, and you assume that the kayexalate causes it, and you forget about everything else that just happened to the patient.

For the record, I have given kayexalate alone before.

I certainly believe it is the stooping that is the portal of exit for potassium. Because we give kayexalate doesn't mean that sorbitol doesn't do the work. Maybe we should start trying just giving sorbitol? I'm cool with it.

To my knowledge there is no solid research to say it doesn't work....just as there is no solid evidence to say it does. This is a similar situation to much of medicine. Are there any residents needing a research project???

 

[Rendar5]

For the record, I have given kayexalate alone before.

without the sorbitol? didn't know it came that way still.

 

[Apollyon]

without the sorbitol? didn't know it came that way still.

Yes, it does. As to "everything else we do" for K+, again, the only effective things to get it out are the diuretics and dialysis, along with the sodium polystyrene sulfate. Again, "everything else" just moves it around, but, as is prone to occur with physics, that gradient will tend to resolve, and return to pre-treatment states.