Drug question - lopressor

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sozme

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So here is the situation:

There is a patient with severe panic disorder and diagnosed OCD by psych. He is a compulsive pulse checker. Arrives at an acute care center off-campus with a HR stable at around 120-130 with fever and signs of dehydration. Given 3000ml NS over a period of 3-4 hours in acute care center along with 1g tylenol & 1mg ativan. Patient was very anxious during his whole stay in acute care ctr and was transferred to the ER on the main campus.

Because of his heart rate concerns (kept asking the doctor I was with as well as the nurse if his HR was in a 'dangerous' zone despite being an otherwise healthy 25y/o normal EKG & recent stress echo), they hit him with 50mg of Lopressor IV although the cardiologist oncall said this was not necessary, he ok'd it given the patients high anxiety at his rapid heart rate. Also administered another milligram of ativan.

His later diagnosis was viral gastroenteritis, probably from bad sour cream he ingested the night earlier.

But anyway, my question is about the Lopressor and this may seem to be a very, very silly question. Now one of the reasons why patients develop tachycardia with many infections is because the microorganism is emitting vasoactive substances, so in order to compensate the heart obviously must increase rate to maintain adequate blood pressure.

The dummy question I have is this: If the patients heart rate is elevated in order to maintain adequate pressure/CO, wouldn't giving him a beta blocker only work to exacerbate the problem? You will have to forgive me as I am only a first year med student. I asked the ID doctor and the cardiologist and they said it shouldn't be an issue.

To me if the heart is compensating by increasing HR, it seems dangerous to lower BP further to get rate control. This question probably is quite ridiculous but thanks anyway for your patience.
 
Does a beta blocker control heart rate? Hint: What are beta cells and what happens when they are blocked?

Some HTN meds cause reflex tachycardia and some do not. Those that control the heart rate do not.
 
Lopressor works by relaxing blood vessels and slowing heart rate to improve blood flow and decrease blood pressure. So it's not an issue.
 
So you mentioned his rate being in the 120-130s but you never mentioned what his BP was. That's a pretty important thing to know before giving any antihypertensives. I see where you are coming from when you say that lowering the HR further will decrease BP and further decrease organ perfusion. Metoprolol is a selective beta-1 antagonist, which causes a decrease in HR and contractility, which can possibly lead to decreased perfusion depending on how low exactly the BP is lowered to. You mentioned he was given 3 L of NS.

1. What effect do you think the NS had on his BP?
2. Do you think by him having 3 L, he was better off when he received his dose of metoprolol than if they gave it to him without the fluids first?
3. What do you think of the dose that was used? Is 50 mg IV a relatively high, normal, or low dose? Would 200 mg have been appropriate?
4. If he did develop hypotension requiring immediate reversal, can it be simply done? If so, how would you do it?
5. Why don't we use beta-blockers in patients with cocaine-induced chest pain? Hint: read up on unopposed alpha stimulation. Heck, I'll tell you. Theoretically, blocking beta receptors can lead to more EPI/NE binding to alpha receptors, which can potentially lead to vasoconstriction and raise BP back up in individuals with lots of sympathomimetic activity (perhaps a person with a panic attack?). So it kind of compensates for the decrease in BP.

Think about your answers to these and try to piece together why they didn't see any possible hypotension/bradycardia as significant issues in this case.
 
I'm curious as to why they administered 3L of NS over a 3-4 hr period. I'm assuming this is not common practice. What level of dehydration was the patient? Temp? Na levels? Answers to these questions are pretty much just to satisfy my curiosity.
 
So you mentioned his rate being in the 120-130s but you never mentioned what his BP was. That's a pretty important thing to know before giving any antihypertensives. I see where you are coming from when you say that lowering the HR further will decrease BP and further decrease organ perfusion. Metoprolol is a selective beta-1 antagonist, which causes a decrease in HR and contractility, which can possibly lead to decreased perfusion depending on how low exactly the BP is lowered to. You mentioned he was given 3 L of NS.

1. What effect do you think the NS had on his BP?
2. Do you think by him having 3 L, he was better off when he received his dose of metoprolol than if they gave it to him without the fluids first?
3. What do you think of the dose that was used? Is 50 mg IV a relatively high, normal, or low dose? Would 200 mg have been appropriate?
4. If he did develop hypotension requiring immediate reversal, can it be simply done? If so, how would you do it?
5. Why don't we use beta-blockers in patients with cocaine-induced chest pain? Hint: read up on unopposed alpha stimulation. Heck, I'll tell you. Theoretically, blocking beta receptors can lead to more EPI/NE binding to alpha receptors, which can potentially lead to vasoconstriction and raise BP back up in individuals with lots of sympathomimetic activity (perhaps a person with a panic attack?). So it kind of compensates for the decrease in BP.

Think about your answers to these and try to piece together why they didn't see any possible hypotension/bradycardia as significant issues in this case.

Sorry the pt was normotensive, I cannot remember specific numbers.

I was actually wondering if the metoprolol would cause his pressure to plummet and his HR to increase. I am thinking based only on 1st year microbiology, vasoactives released by a variety of different bugs, etc. I know little to nothing about pharmacology, just curious.

50mg is the lowest available dose so far as I know. I also know these drugs can be used as anxiolytics.
 
Sorry the pt was normotensive, I cannot remember specific numbers.

I was actually wondering if the metoprolol would cause his pressure to plummet and his HR to increase. I am thinking based only on 1st year microbiology, vasoactives released by a variety of different bugs, etc. I know little to nothing about pharmacology, just curious.

50mg is the lowest available dose so far as I know. I also know these drugs can be used as anxiolytics.


The Lopressor blocks the beta receptors in the heart that helps to regulate HR. Based on its MOA, increased HR should not be an issue. Hypotension can sometimes be an issue but I don't think it would apply to this patient. Just a lowly P1 so maybe some of the others can elaborate.
 
I just want to re-state his question again to make sure we are all on the same page. The patient's viral infection is a factor in causing peripheral vasodilation which leads to a decrease in blood pressure, so to compensate for this BP drop, his heart is speeding up. So by giving metoprolol, wouldn't this slow his heart down, thus eliminating the compensation and put him back at having hypotension again? (but it would be even worse because now he has the viral infection causing vasodilation, plus the metoprolol causing a decrease in BP)

So to answer the question of whether or not its a significant issue, I would have to say no in this specific case. But it could be significant in other cases. There are a lot of factors. First and foremost, he was given fluids for dehydration, but they also increase BP by increasing circulatory volume (similar to patients who go into shock and get hypotension). Secondly, the dose of metoprolol isn't anything to be too concerned about in this case. A single dose of 50 mg is closer to the lower end of the dosage range and wouldn't be as concerning as if they ordered 200 mg, relatively speaking. Thirdly, if the metoprolol *did* exacerbate the patient's state and put him into severe hypotension due to counteracting the heart's tachycardia, it can be easily reversed with a fluid bolus. And lastly, like I said, there is the possibility of unopposed alpha stimulation. If you're blocking the beta receptors, you're freeing up EPI and NE to go elsewhere. The body will naturally restore BP by alpha-1 stimulation.

So with all of that being said, I agree with the attendings and I don't think that a single dose of metoprolol would've caused life-threatening hypotension or shock. Its just one of the things you do and monitor the BP afterward just to be safe. Now the situation would be different if his BP was 90/65. Hope I helped. It's too late for me so I probably didn't do the best job of explaining it and I'm kinda starting to think I misinterpreted your question lol oh well.
 
Oh I think I understand now. So you said if they give metoprolol, it will lower his BP which will cause his heart to compensate by speeding up even more? Is that your rationale?

Metoprolol lowers blood pressure by directly slowing the heart down, and also by reducing its force of contraction (just like everyone else already said). So there's no way the heart can speed up. That *is* the mechanism of how it lowers BP, is its effects directly on the heart. It has absolutely no direct effect on peripheral vascular resistance or peripheral blood vessels. Sorry for the long winded answers earlier, I think I was reading to far into it your case.
 
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I'm curious as to why they administered 3L of NS over a 3-4 hr period. I'm assuming this is not common practice. What level of dehydration was the patient? Temp? Na levels? Answers to these questions are pretty much just to satisfy my curiosity.

go read up on SIRS and sepsis. Fluid resuscitation is key.
 
Yeah, Lopressor is gonna have a pretty significant parasympathetic action, and I doubt the effect on the patients blood pressure would be significant enough to induce any sort of background reflex tachycardia.
 
I didn't know you could get viral enteritis from a soured dairy product

Also, I really doubt a self limiting enteritis is causeing his tachy. Is probably because he's a psych pt that is in a panic attack requiring repeat Ativan doses. He is a compulsive hr checker that has tachy and is getting worked up. Hell, I'm pretty mellow and I can't get worked up a over something enough to get my hr at 100+
 
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Because of his heart rate concerns (kept asking the doctor I was with as well as the nurse if his HR was in a 'dangerous' zone despite being an otherwise healthy 25y/o normal EKG & recent stress echo), they hit him with 50mg of Lopressor IV although the cardiologist oncall said this was not necessary, he ok'd it given the patients high anxiety at his rapid heart rate. Also administered another milligram of ativan.

I hope no one gave the patient that dose.

Lol pharmacy students. All your comments above selective beta-1 antagonism activity and you missed the deadly dose on order verification. A code was called and the patient had to be rescued by the stat cart. You will have a meeting with the director in the morning.
 
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50mg is the lowest available dose so far as I know. I also know these drugs can be used as anxiolytics.

No, that dose is not the lowest available dose, not orally; and definetly not intravenous.

A single dose of 50 mg is closer to the lower end of the dosage range and wouldn't be as concerning as if they ordered 200 mg, relatively speaking.

Please verify route of medication in OP.
 
Amen! Dose conversion from IV to PO metoprolol is not 1:1. Giving 5-10mg IVP is the usual IV dose.....
 
No, that dose is not the lowest available dose, not orally; and definetly not intravenous.



Please verify route of medication in OP.

Amen! Dose conversion from IV to PO metoprolol is not 1:1. Giving 5-10mg IVP is the usual IV dose.....

Yes 5mg is correct. He went home with a prescription for 50mg tabs if it happened again. I got confused. Thanks for the reply 007.
 
Also, I really doubt a self limiting enteritis is causeing his tachy. Is probably because he's a psych pt that is in a panic attack requiring repeat Ativan doses. He is a compulsive hr checker that has tachy and is getting worked up.

a panic attack isn't going to give someone a sustained heart rate as high as 130 for more than a brief period (10 mins or so).
 
Amen! Dose conversion from IV to PO metoprolol is not 1:1. Giving 5-10mg IVP is the usual IV dose.....

Oh I see. Oral metoprolol is 100% absorbed BUT 50% of the dose gets metabolized before entering systemic circulation. I didn't catch that initially. Excellent point and thanks for pointing out the conversion ratio and usual intravenous dose to us students who are still in school and learning.
 
Oh I see. Oral metoprolol is 100% absorbed BUT 50% of the dose gets metabolized before entering systemic circulation. I didn't catch that initially. Excellent point and thanks for pointing out the conversion ratio and usual intravenous dose to us students who are still in school and learning.

It seems that everyone has missed the OP original question, although I could be the one seriously confused.

What you seem to be concerned about is that they are giving lopressor to treat the tachycardia, but the reason the patient is tachycardic is the compensatory mechanism to keep the patient normatensive. So if the patient is normatensive because of the tachycardia, and we give lopressor will the patient's blood pressure bottom out and should we be concerned about that? Am I making a correct assumption regarding your question or your original concern?

If this is the case, which I think it is, there is little to be concerned about. As previous poster stated, the patient was given 3 liters increasing blood volume and subsequently BP and then the unopposed alpha stimulation would also help to compensate for drops in BP.
 
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I hope no one gave the patient that dose.

Lol pharmacy students. All your comments above selective beta-1 antagonism activity and you missed the deadly dose on order verification. A code was called and the patient had to be rescued by the stat cart. You will have a meeting with the director in the morning.

Heh, sure thing. I just assumed typo, as it was checked by pt's cardiologist.

Technically, this dude is refrac, so 15 migs would be in order, no?
 
It seems that everyone has missed the OP original question, although I could be the one seriously confused.

What you seem to be concerned about is that they are giving lopressor to treat the tachycardia, but the reason the patient is tachycardic is the compensatory mechanism to keep the patient normatensive. So if the patient is normatensive because of the tachycardia, and we give lopressor will the patient's blood pressure bottom out and should we be concerned about that? Am I making a correct assumption regarding your question or your original concern?

If this is the case, which I think it is, there is little to be concerned about. As previous poster stated, the patient was given 3 liters increasing blood volume and subsequently BP and then the unopposed alpha stimulation would also help to compensate for drops in BP.

Yes, thank you.

Would there have been a better option aside from lopressor to get his HR down? After 2 mg of Ativan (and the patient took 0.5mg of Klonopin BID so apparently the ativan dose was a much higher dose equivalent) his HR was still pretty elevated.
 
Yes, thank you.

Would there have been a better option aside from lopressor to get his HR down? After 2 mg of Ativan (and the patient took 0.5mg of Klonopin BID so apparently the ativan dose was a much higher dose equivalent) his HR was still pretty elevated.

I think it was a perfectly reasonable decision. Although some might argue whether it was necessary at all in a stable patient with a normal ECG ( aside from tachycardia of course ). I think if the attending would have just let it ride the patient would have returned to normal on their own. Now, if the patient wasn't responding to the benzos it makes sense to give the lopressor.

I would imagine that in a patient with a case of severe anxiety/panic disorder, the feeling of their heart racing in their chest would likely cause a sensory positive feedback loop only furthering the patient's anxiety.

Good question though. We need some more Med Students over here asking us Pharmers questions like this. It helps keep us sharp and its nice to see a Med Student respecting the Pharmacist's knowledge.
 
Good question though. We need some more Med Students over here asking us Pharmers questions like this. It helps keep us sharp and its nice to see a Med Student respecting the Pharmacist's knowledge.

I was just thinking the same thing. How nice it is to have therapy discussions and sharing knowledge. 👍

And being reminded to always check dose/route, 😳
 
My thoughts as I work in the ER.

1. Lopressor 5mg IV is NOT a smart move for anyone you are concerned to be near septic shock. Even on a 25yo. Yes, he's probably healthy and has a 95% shot of starting normotensive prior to IV lopressor and staying normotensive after IV lopressor... but you have NO leg to stand on if poop hits the fan.

2. To lower his HR, I would've given the guy Ativan 2mg IV x1 (more cardiac stable than the other BZ). Then I would've flooded the guy with a max of 4L 0.9NS and then 2L 0.45NS.

3. I would seriously re-consider treating the HR just to appease the guy. This is just going down the wrong path. This is not a guy with a fib w/ RVR, this is a guy who meets criteria for SIRS/sepsis. By blocking the body's ability to compensate for a possible decrease in CO, you are setting yourself up for some chaotic consequences.

My guess is the guy did fine.... but the methods of getting there was not based on EBM. You guys were playing with fire.
 
I hope no one gave the patient that dose.

Lol pharmacy students. All your comments above selective beta-1 antagonism activity and you missed the deadly dose on order verification. A code was called and the patient had to be rescued by the stat cart. You will have a meeting with the director in the morning.

It took a bunch of pharmacists/pharmacy students that long to figure this out. Ugh

I didn't know you could get viral enteritis from a soured dairy product

Also, I really doubt a self limiting enteritis is causeing his tachy. Is probably because he's a psych pt that is in a panic attack requiring repeat Ativan doses. He is a compulsive hr checker that has tachy and is getting worked up. Hell, I'm pretty mellow and I can't get worked up a over something enough to get my hr at 100+

You didn't know you could culture viruses?

My thoughts as I work in the ER.

1. Lopressor 5mg IV is NOT a smart move for anyone you are concerned to be near septic shock. Even on a 25yo. Yes, he's probably healthy and has a 95% shot of starting normotensive prior to IV lopressor and staying normotensive after IV lopressor... but you have NO leg to stand on if poop hits the fan.

2. To lower his HR, I would've given the guy Ativan 2mg IV x1 (more cardiac stable than the other BZ). Then I would've flooded the guy with a max of 4L 0.9NS and then 2L 0.45NS.

3. I would seriously re-consider treating the HR just to appease the guy. This is just going down the wrong path. This is not a guy with a fib w/ RVR, this is a guy who meets criteria for SIRS/sepsis. By blocking the body's ability to compensate for a possible decrease in CO, you are setting yourself up for some chaotic consequences.

My guess is the guy did fine.... but the methods of getting there was not based on EBM. You guys were playing with fire.
This.
 
Can someone explain the "cardiac stability" of benzodiazepines that the previous person posted? Does that mean lorazepam has less bradycardic effects on the heart as opposed to say clonazepam? I was never taught about how each BZD compares with regards to cardiac effects so I could use a quick and dirty lesson here.
 
My thoughts as I work in the ER.

1. Lopressor 5mg IV is NOT a smart move for anyone you are concerned to be near septic shock. Even on a 25yo. Yes, he's probably healthy and has a 95% shot of starting normotensive prior to IV lopressor and staying normotensive after IV lopressor... but you have NO leg to stand on if poop hits the fan.

2. To lower his HR, I would've given the guy Ativan 2mg IV x1 (more cardiac stable than the other BZ). Then I would've flooded the guy with a max of 4L 0.9NS and then 2L 0.45NS.

3. I would seriously re-consider treating the HR just to appease the guy. This is just going down the wrong path. This is not a guy with a fib w/ RVR, this is a guy who meets criteria for SIRS/sepsis. By blocking the body's ability to compensate for a possible decrease in CO, you are setting yourself up for some chaotic consequences.

My guess is the guy did fine.... but the methods of getting there was not based on EBM. You guys were playing with fire.


You are right if the patient meets the criteria for SIRS, but does this patient meet the SIRS criteria. I dont think we even have enough data to make that assumption. Increased HR in a patient with Severe Anxiety/Panic disorder. We dont have RR, Blood Gases, or CBC. I think it would be hard to peg this person with SIRS without any of those values.
I dont think it was an unreasonable decision based on the information we received in the original post.

To reduce the HR just to appease the patient would not be appropriate, but in the absence of SIRS I dont think it was unreasonable since he was refractory to benzo's.

Great Discussion BTW, this is how we all get better.
 
You are right if the patient meets the criteria for SIRS, but does this patient meet the SIRS criteria. I dont think we even have enough data to make that assumption. Increased HR in a patient with Severe Anxiety/Panic disorder. We dont have RR, Blood Gases, or CBC. I think it would be hard to peg this person with SIRS without any of those values.
I dont think it was an unreasonable decision based on the information we received in the original post.

To reduce the HR just to appease the patient would not be appropriate, but in the absence of SIRS I dont think it was unreasonable since he was refractory to benzo's.

Great Discussion BTW, this is how we all get better.

His RR was normal. CBC did not point to sepsis/SIRS.
 
I love how an ambulatory psych pt having a panic attack secondary to acute enteritis from rotavirus infected sour cream has turned into Sepsis case
 
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Can someone explain the "cardiac stability" of benzodiazepines that the previous person posted? Does that mean lorazepam has less bradycardic effects on the heart as opposed to say clonazepam? I was never taught about how each BZD compares with regards to cardiac effects so I could use a quick and dirty lesson here.

by "cardiac stability" he means likelihood of precipitating hypotension. Clonazepam is not available IV so doesn't usually come up in this discussion - the injectable benzos, Lorazepam, Midazolam and Diazepam.
 
You are right if the patient meets the criteria for SIRS, but does this patient meet the SIRS criteria. I dont think we even have enough data to make that assumption. Increased HR in a patient with Severe Anxiety/Panic disorder. We dont have RR, Blood Gases, or CBC. I think it would be hard to peg this person with SIRS without any of those values.
I dont think it was an unreasonable decision based on the information we received in the original post.

What are the components SIRS criteria? At what number do we get concerned? Do we immediately get blood gases in patients when concerned for sepsis?
 
O rly?

I just feel bad for the kid.

Refuses to take SSRIs apparently bc he is so scared of the potential side effects.

Was still surprised to see his HR that elevated just due to anxiety until I learned he was dehydrated and had a fever. Now that I think about it my own HR is pretty elevated even when I have a fever. Anyways.

TheMoreYouKnow_480x340.jpg

That's sirs right there. I don't need criteria to tell me what I'm worried about in the ER.

You are right if the patient meets the criteria for SIRS, but does this patient meet the SIRS criteria. I dont think we even have enough data to make that assumption. Increased HR in a patient with Severe Anxiety/Panic disorder. We dont have RR, Blood Gases, or CBC. I think it would be hard to peg this person with SIRS without any of those values.
I dont think it was an unreasonable decision based on the information we received in the original post.

To reduce the HR just to appease the patient would not be appropriate, but in the absence of SIRS I dont think it was unreasonable since he was refractory to benzo's.

Great Discussion BTW, this is how we all get better.

His RR was normal. CBC did not point to sepsis/SIRS.
 
SSRI for this patient and strong CBT

Are you planning on making the patient wait 3-4 weeks to feel the effects of the SSRI? Is CBT going to hold its own til then? And is an SSRI the best option for an anxiety attack anyways?
 
Are you planning on making the patient wait 3-4 weeks to feel the effects of the SSRI? Is CBT going to hold its own til then? And is an SSRI the best option for an anxiety attack anyways?

This patient definitely needs those things...but if he won't take the SSRI, then he won't. Best tx for anxiety is a BDZ anyways. I would have given him lorazepam or diazepam in house (probably diazepam d/t rapid onset) and then 0.5 mg alprazolam QD + 0.5 mg PRN. Hopefully that helps and he can come back for f/u and talk about starting an SSRI then.

IMO, the best anxiety SSRI/SNRI are citalopram/escitalopram or venlafaxine. Those would be my recommendation.
 
I love lurking these threads because I feel like I'm learning so much.

I can't wait to be able to explain which and why certain drugs are used. =D
 
This patient definitely needs those things...but if he won't take the SSRI, then he won't. Best tx for anxiety is a BDZ anyways. I would have given him lorazepam or diazepam in house (probably diazepam d/t rapid onset) and then 0.5 mg alprazolam QD + 0.5 mg PRN. Hopefully that helps and he can come back for f/u and talk about starting an SSRI then.

IMO, the best anxiety SSRI/SNRI are citalopram/escitalopram or venlafaxine. Those would be my recommendation.

alprazolam is a horrid drug, and most psychiatrists are far more comfortable with clonazepam (longer acting) as a short term (i.e. 3-4 weeks max) treatment for panic disorder and at low doses (0.25-0.50mg BID)
 
Are you planning on making the patient wait 3-4 weeks to feel the effects of the SSRI? Is CBT going to hold its own til then? And is an SSRI the best option for an anxiety attack anyways?

It seems like the best option. Perhaps a drug like klonopin can be used on a short-term basis while an SSRI is started. CBT will definitely have to be apart of the equation, especially if the patient can afford a good private CBT therapist.
 
O rly?



That's sirs right there. I don't need criteria to tell me what I'm worried about in the ER.

You are right about that. Being "the" MD in that situation you are responsible so worry about what you want. However, I think that after you have been practicing as long as the attending that made the original decision, you will probably be a little less cautious, because your clinical experience would tell you otherwise.

I guess in this case you could say it was an unreasonable decision for you, but you can't say it was unreasonable for the physician who made the call, because they have a lot more information about the case and are able to make a better clinical judgement in the present.

By all means, if I were in your shoes, I would be practicing just as cautiously.
 
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You are right about that. Being "the" MD in that situation you are responsible so worry about what you want. However, I think that after you have been practicing as long as the attending that made the original decision, you will probably be a little less cautious, because your clinical experience would tell you otherwise.

I guess in this case you could say it was an unreasonable decision for you, but you can't say it was unreasonable for the physician who made the call, because they have a lot more information about the case and are able to make a better clinical judgement in the present.

By all means, if I were in your shoes, I would be practicing just as cautiously.

I'll play devil's advocate here.

I wasn't there but here's the deal - a 25yo kid who comes in that tachycardic is sick. There's something going on. Anxiety does not raise your HR that high, there's something else that's plaguing the kid.

How many 25yo have I admitted as a 4th year resident - not a lot. Why? Because these guys are resilient and never that sick.

There is a big red flag to this case:
1. He was admitted - which means he was sick.

He started spiking fevers as an inpatient - there's something there that we should just not brush off as anxiety requiring benzos or anxiety requiring beta blockers. Those are mistakes that any good ED physician should not make.

This is my management for the kid if I personally saw him:

DDX: dysrhythmia (ekg), infectious (cxr and UA vs viral), drug hx (overdose vs withdrawal i.e. opiate, cocaine, vs ssri overdose, tca overdose), PE, metabolic/endocrine (hyperthyroid), if nothing pans out - does this guy have some underlying malignancy like lymphoma vs others?

W/UP: CBC, UA, Urine drug screen (though likely useless), TFT (thyroid), LFT/Lipase, EKG, CXR, rule out for PE (ddimer vs CT chest). I would also personally do a quick echo of his heart - r/o effusions and show a good EF and large endocarditis lesions (if I could see it). I would also send blood cultures if he spikes.

TX: Flood the guy w/ fluid (up to 6L), give the guy some anxiolytics (BZ), low threshold for starting antibiotics if he starts to spike a fever.

Dispo: I would not send the 25yo home if he is persistently tachycardic despite a negative work up. I would obs him just to see if anything manifests itself overnight. There's something wrong here and my sensors are going berserk here.

Bottomline: I would not give the guy lopressor. That is just wrong.

And I am NOT being overly conservative. You want to be a cowboy doctor? Send the kid home w/ some beta blockers or start beta blockers in the ER.

Once you get a subpoena for a malpractice suit because the kid you gave lopressor to became septic in house and died or had significant morbidity - then you are DOOMED.
 
alprazolam is a horrid drug, and most psychiatrists are far more comfortable with clonazepam (longer acting) as a short term (i.e. 3-4 weeks max) treatment for panic disorder and at low doses (0.25-0.50mg BID)

lol@med student talking drugs.
 
I'll play devil's advocate here.

I wasn't there but here's the deal - a 25yo kid who comes in that tachycardic is sick. There's something going on. Anxiety does not raise your HR that high, there's something else that's plaguing the kid.

How many 25yo have I admitted as a 4th year resident - not a lot. Why? Because these guys are resilient and never that sick.

There is a big red flag to this case:
1. He was admitted - which means he was sick.

He started spiking fevers as an inpatient - there's something there that we should just not brush off as anxiety requiring benzos or anxiety requiring beta blockers. Those are mistakes that any good ED physician should not make.

This is my management for the kid if I personally saw him:

DDX: dysrhythmia (ekg), infectious (cxr and UA vs viral), drug hx (overdose vs withdrawal i.e. opiate, cocaine, vs ssri overdose, tca overdose), PE, metabolic/endocrine (hyperthyroid), if nothing pans out - does this guy have some underlying malignancy like lymphoma vs others?

W/UP: CBC, UA, Urine drug screen (though likely useless), TFT (thyroid), LFT/Lipase, EKG, CXR, rule out for PE (ddimer vs CT chest). I would also personally do a quick echo of his heart - r/o effusions and show a good EF and large endocarditis lesions (if I could see it). I would also send blood cultures if he spikes.

TX: Flood the guy w/ fluid (up to 6L), give the guy some anxiolytics (BZ), low threshold for starting antibiotics if he starts to spike a fever.

Dispo: I would not send the 25yo home if he is persistently tachycardic despite a negative work up. I would obs him just to see if anything manifests itself overnight. There's something wrong here and my sensors are going berserk here.

Bottomline: I would not give the guy lopressor. That is just wrong.

And I am NOT being overly conservative. You want to be a cowboy doctor? Send the kid home w/ some beta blockers or start beta blockers in the ER.

Once you get a subpoena for a malpractice suit because the kid you gave lopressor to became septic in house and died or had significant morbidity - then you are DOOMED.

If you are looking for someone to just say you are right, I think you are in the wrong place.

I think the ultimate correct answer in the case would be "It depends".

You can sit there and say all day long that you would have treated this case differently, but you were also not standing there and you weren't dealing with this patient directly. Had you been there you may have a differing opinion, perhaps not, but you cannot say without a doubt. I highly doubt, that the attending physician who made this decision was playing "cowboy" and made the decision based on the clinical picture presented to him/her and there is probably a great deal of variables and/or medical history you are unaware of.

Perhaps the patient you outlined in you above post needs to be manged as you stated. The question at hand in the original post, in a nutshell, was whether or not you should give lopressor to treat tachycardia if the tachycardia is a result of some compensatory mechanism. Would the lopressor significantly lower the pt's blood pressure? I believe the question was answered from a pharmacological perspective. In terms of the patient's total plan of care, we will leave that up to you real Dr.'s.

I will say this discussion is a very good thing. We should have a thread sticky'd in the pharmacy forum "MD Questions for the Pharmacists" and Likewise a thread in the MD forum "Pharmacist's questions for the MDs" I think it would be a very good thing.
 
It seems like the best option. Perhaps a drug like klonopin can be used on a short-term basis while an SSRI is started. CBT will definitely have to be apart of the equation, especially if the patient can afford a good private CBT therapist.

But the fact remains that you have a patient that is having attacks now rather then later. The half life of SSRIs is long. SSRIs are first line therapy if you are willing to wait 4-12 weeks for a response. For a basic PK lesson, it takes approximately 5 half-lifes to reach steady state . This is the magical land where drug in= drug out and you have essentially a steady level of drug circulating. So when an SSRI's half life is days, it takes awhile. This pt obviously cannot deal with these attacks. You should give something in the interim.
 
But the fact remains that you have a patient that is having attacks now rather then later. The half life of SSRIs is long. SSRIs are first line therapy if you are willing to wait 4-12 weeks for a response. For a basic PK lesson, it takes approximately 5 half-lifes to reach steady state . This is the magical land where drug in= drug out and you have essentially a steady level of drug circulating. So when an SSRI's half life is days, it takes awhile. This pt obviously cannot deal with these attacks. You should give something in the interim.

This is where you are a touch off. The fact is that the patient CAN deal with panic attacks - heck everyone can deal with them because they are not dangerous they are just uncomfortable. First line treatment for panic disorder is not medicinal it is exposure and response prevention therapy, maybe a psychologist can weigh in. TO make their life more bearable in the interim a 3 to 4 week course of a long acting benzodiazepine like clonazepam BID could suffice.
 
by "cardiac stability" he means likelihood of precipitating hypotension. Clonazepam is not available IV so doesn't usually come up in this discussion - the injectable benzos, Lorazepam, Midazolam and Diazepam.

All of which are on shortage, I believe.
 
This is where you are a touch off. The fact is that the patient CAN deal with panic attacks - heck everyone can deal with them because they are not dangerous they are just uncomfortable. First line treatment for panic disorder is not medicinal it is exposure and response prevention therapy, maybe a psychologist can weigh in. TO make their life more bearable in the interim a 3 to 4 week course of a long acting benzodiazepine like clonazepam BID could suffice.

Your assessment of this is incorrect. Patients with panic attacks are not going to die from the panic attack, but it may precipitate self-harming or negative behaviors including avoidance of the trigger. If the triggers are something like school or work, it could have a major impact on the patient's life. Even if it is not, quality of life is significantly lower for individuals who experience frequent panic attacks. Exposure as treatment? I've never heard of that before for panic.
 
But the fact remains that you have a patient that is having attacks now rather then later. The half life of SSRIs is long. SSRIs are first line therapy if you are willing to wait 4-12 weeks for a response. For a basic PK lesson, it takes approximately 5 half-lifes to reach steady state . This is the magical land where drug in= drug out and you have essentially a steady level of drug circulating. So when an SSRI's half life is days, it takes awhile. This pt obviously cannot deal with these attacks. You should give something in the interim.

Yes...but not all drugs reach full efficacy just because they are at SS. This is one of them...the SSRIs like citalopram have a half life of about one day but are still not effective in six days. Altering brain chemistry takes time.
 
Your assessment of this is incorrect. Patients with panic attacks are not going to die from the panic attack, but it may precipitate self-harming or negative behaviors including avoidance of the trigger. If the triggers are something like school or work, it could have a major impact on the patient's life. Even if it is not, quality of life is significantly lower for individuals who experience frequent panic attacks. Exposure as treatment? I've never heard of that before for panic.

No my assessment is exactly correct.

Patients with PDA (Panic Disorder with Agoraphobia) can be started on a short course of benzodiazepines but this is not a long-term solution for several reasons which I suspect a pharmacy student would understand. In this case, the tranquilizers are used as a way to give the patient enough confidence to undergo cognitive behavioral therapy wherein they are exposed to the things and/or situations that trigger their panic attacks. Through repeated exposure, their level of fear decreases and they stop having panic attacks altogether. There is no long-term medication treatment for someone with primary panic disorder, and in fact long-term treatment (i.e. daily) with benzodiazepines for people with simple anxiety is highly unethical (for reasons which a pharmacy student would or should understand).
 
No my assessment is exactly correct.

Patients with PDA (Panic Disorder with Agoraphobia) can be started on a short course of benzodiazepines but this is not a long-term solution for several reasons which I suspect a pharmacy student would understand. In this case, the tranquilizers are used as a way to give the patient enough confidence to undergo cognitive behavioral therapy wherein they are exposed to the things and/or situations that trigger their panic attacks. Through repeated exposure, their level of fear decreases and they stop having panic attacks altogether. There is no long-term medication treatment for someone with primary panic disorder, and in fact long-term treatment (i.e. daily) with benzodiazepines for people with simple anxiety is highly unethical (for reasons which a pharmacy student would or should understand).

risks dont ALWAYS outweigh benefits, nor is the opposite true of course , but you should know as a med student by now that clinical pictures frequently dont fit squarely within the proven evidence, guidelines, textbooks, etc, and that in some patients, higher risks are justified. What if a person has failed therapy repeatedly, is at risk for serious self harm, will not tolerate inpatient, or has no insurance for psychotherapy , but is at substantial risk if untreated, in such a case , wouldnt you think bzd's would represent a less risky option than no treatment or subpar (ie ssris) treatment? The fact that this is actually a question means that bzd for panic disorder can hardly be called "highly unethical", in such a blanket way. We were taught that bzds while not 'recommended' for long term , are frequently used because they are the least 'bad' of the available options, for the patient's health, particularly when nothing else can be implemented in a practical way.

First thing you learn about drugs is that they all represent some mix between toxicity and efficacy, and that the clinical picture must be considered in each patient in order to weigh risks vs benefits.

The ethics of using any chemical substance in any patient to achieve some physiological changes always depend on the acceptable levels of risk of harm in the patients and provider's eyes compared to the expected/desired level of benefits.

Now if prescribers were treating with chronic bzd's by default, and not disclosing some of the well known risks to their patients, I would call THAT "highly unethical"
 
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