Beta Blockers!

[Halaljello]

Can Someone please tell me why Beta blockers must be used in extreme caution in diabetics? are there beta 2 receptors in the pancreas? They really didnt explain this too well in class.

Also, how can beta blockers exacerbate periph. vascular disease?
he said somthing about alpha override vasoconstriction but im still kinda confused.

thanks for ur help!

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[ckent]

beta blockers are not contraindicated in diabetics, but they should be used with caution because beta blockers can block patients from sensing that they are hypoglycemic (hypoglycemia--> increase epinephrine and norepinephrine, catecholamines to start sweating, feel funny, anxious, helps diabetics know that they need to eat some sugar). Beta blockers are also very dangerous in patients who use cocaine, because then you have block the beta effect which can be to dilate some vessels, and have unopposed alpha constriction with blockage of NE reuptake. Not sure of the exact concern with PVD, would be interested in learning if there is some danger in using betas with those patients too.

 

[rxfudd]

Also, the liver has B2 receptors that initiate gluconeogenesis and glycogenolysis. A non-specific B-blocker (like propranolol) will block B2, thus exacerbating hypoglycemia in an insulin-dependent diabetic.

 

[praying4MD]

i think where beta blockers are most definitely contraindicated would be congestive heart failure because the heart needs all the catecholamines/NE, etc. and all the energy and "oommpf" it can get to pump blood out systemically, so if you inhibit the contractility via beta blockers, or inhibit the actual force of contraction you can exacerbate the congestive heart failure---> more pulmonary edema, more backflow, and pretty soon, not only left heart failure but also right heart--> peripheral edema, etc. or even precipitate CHF.

 

[Mossjoh]

rxfudd is correct!

In a hypoglycemic episode, the beta-2 receptors on the liver are blocked and you can't breakdown glycogen or produce glucagon in response.

This leads to a severe hypoglycemia.

Also, for you information. don't use beta-blockers in people with asthma. The Beta-2 receptors on the bronchioles cause brochodilation when stimulated. With beta-blockers you maintain the brochoconstriction and this can precipitate and asthma attack.

Mossjoh

 

[jed2023]

Beta blockers are especially dangerous in diabetics that inject insulin because episodes of hypoglycemia resulting from their insulin usage cannot be adequately compensated for by adrenal secretion of epinephrine. (I don't know if they would be that dangerous in the typical non-insulin dependent diabetic that actually has elevated glucose levels continually.) As has been mentioned in the above posts, epi stimulates beta-2 receptors on the liver, which cause glycogenolysis (and enhanced gluconeogenesis). Even in normal people, though, beta blockers will cause a blunted response of the liver to hypoglycemia. For these reasons, beta-1 specific antagonists are often favored over the cruder non-selective beta blockers. Specific examples include atenolol (a beta-1 antagonist) and acebutalol (actually a partial agonist, but with antagonist properties).

 

[ckent]

Originally posted by praying4MD
i think where beta blockers are most definitely contraindicated would be congestive heart failure because the heart needs all the catecholamines/NE, etc. and all the energy and "oommpf" it can get to pump blood out systemically, so if you inhibit the contractility via beta blockers, or inhibit the actual force of contraction you can exacerbate the congestive heart failure---> more pulmonary edema, more backflow, and pretty soon, not only left heart failure but also right heart--> peripheral edema, etc. or even precipitate CHF.

Ironically, beta blockers are actually indicated for CHF (all CHF patients should be on beta blockers). It's been shown to decrease morbidity and mortality, mainly by preventing some of the deleterious remodeling of the heart with heart failure. If you have an acute exacerbation of heart failure, then you might try tapering back the beta blocker temporarily for the reasons that you mentioned; but in general, all of your heart patients should be on beta blockers.

 

[babinski bob]

ckent is correct about the use of B-blockers in CHF. 20 years ago everyone thought that B-blockers would be the last drug on the planet to use in the case of CHF. One would think that in CHF, CO should be maintained/increased to eliminate pulmonary congestion that is be occurring. However, more recent studies have supported the use of very specific B-blockers for the treatment of CHF. These include carvedilol > labetalol, metoprolol, bisprolol. B-blockers apparently decrease some of the deleterious effects resulting from diffuse activation of the sympathetic NS that occurs in CHF including: a) the activation of proapototic proteins in the myocardium and b) renin release and the subsequent elaboration of Angiotension II which exerts potent mitogenic effects on heart. In the case of acute heart failure in the hospital, you would want to give dobutamine or LOW doses of dopamine.

As far as B-blockers exacerbating peripheral vascular disease, all i can think of is that the alpha effect of peripheral vasoconstriction will predominate, thereby worsening any PVD that may be present. Alpha blockers (like phenoxybenzamide) are the standard therapy for PVD like Raynaud's phenomenon.

 

[praying4MD]

wow. how weird. it's all over our syllabus about beta blockers being contraindicated in CHF. thanks for the new info guys. i will take it up with our cardiology lecturer soon after i do a little more research on it on my own. yikes. sorry for dispensing wrong information in that case-- it was totally unintentional and i will try to be more careful in the future.

thanks again guys.

 

[omores]

Praying: please do educate your cardiology lecturer! You should be able to find plenty of data (I'm on a hopelessly slow dial-up right now, so I can't do any good research for you), but there were some MAJOR studies published in the few years.

In fact, one of the "quality of care" indices that's often cited is the percentage of CHF patients who are placed on beta blockers by their docs, since there's such good evidence to back up their use.

 

[ckent]

Originally posted by omores
Praying: please do educate your cardiology lecturer! You should be able to find plenty of data (I'm on a hopelessly slow dial-up right now, so I can't do any good research for you), but there were some MAJOR studies published in the few years.

In fact, one of the "quality of care" indices that's often cited is the percentage of CHF patients who are placed on beta blockers by their docs, since there's such good evidence to back up their use.

I disagree. I think that the syllabus is long overdue for an update, it's not like this research just came out last year, there have been cardiologists at my school pushing for beta blocking CHF patients for the past 50 yrs based on their own research. It's not a really big deal because it's not like anyone is going to let you guys as med students take their CHF patient off beta blockers, but it's just kind of silly that it hasn't been updated yet.

 

[AJM]

Originally posted by ckent
I disagree. I think that the syllabus is long overdue for an update, it's not like this research just came out last year, there have been cardiologists at my school pushing for beta blocking CHF patients for the past 50 yrs based on their own research. It's not a really big deal because it's not like anyone is going to let you guys as med students take their CHF patient off beta blockers, but it's just kind of silly that it hasn't been updated yet.

That's true. Beta-blockers as a treatment for CHF have been used for years. It is not a new therapy by any means, and is one of the few medications we have that actually reduces mortality in CHF. Praying -- your syllabus doesn't just need an update, but it probably needs to be completely rewritten. Who knows what else is out of date in it?

 

[AJM]

Originally posted by Mossjoh
Also, for you information. don't use beta-blockers in people with asthma. The Beta-2 receptors on the bronchioles cause brochodilation when stimulated. With beta-blockers you maintain the brochoconstriction and this can precipitate and asthma attack.

Actually, beta-blockers are fine to use in patients with controlled asthma/COPD. Chronic beta-blocker use has never been shown to increase mortality in asthmatics or COPDers. As long as you start with a low dose, and ramp up slowly, they are very well tolerated. The typical beta-blockers we use these days are more beta-1 selective anyway, so have decreased effects on the beta-2 receptors in the airway. The only time you want to avoid starting beta blockers in these patients is if they are actively wheezing or having an exacerbation.

 

[praying4MD]

Ok. I trust what everyone is saying for sure [even though I feel like a complete idiot right now since this is supposed to be so bleeding obvious, and something I should totally know...] so maybe you can help me here. Here are direct quotes from my syllabus:

"Beta Blockers (i.e metoprolol) also [in addition ito ACE Inhibitors] reduce mortality in heart failure patients treated with an ACEI but they SHOULD BE CAUTIOUSLY USED IN CHF because they may WORSEN CHF symptoms!!!"

[the bold, caps, etc is also directly copied from the syllabus, not my own.]

the following is a chart listing preferred anti-hypertensive drug therapy also from my syllabus:

Medical Condition..........Preferred AntiHTN Drugs
-------------------------------------------------------------
Diabetes or CHF............ACEI or ARB [prevents diabetic nephropathy]

CAD or Angina...............CCB or BB
Old MI...........................BB [obviously only those without intrinsic sympathomimetic activity are cardioprotective-- Beta Blockers with ISA do not improve survival in patients recovering from MI and are NOT recommended as Cardioprotective Drugs]
Isolated Systolic HTN in subjects > 60 yrs. old............ Diuretic or CCB

Other quotes which are now causing me much muddled confusion:

"Calcium channel blockers, unlike beta blockers, are effective in patients who have variant or vasospastic angina, whereas beta blockers are used for exertional angina."

Also, i think we should clarify which beta blockers we are all referring to-- that might make things easier [nonselective, cardioselective, those with ISA, etc.] I don't know whether that would make a difference or not, but maybe it would clear things up a little.

Maybe what the lecturer is alluding to is that many different conditions could PRESENT as CHF??? [as in dilated cardiomyopathy, IHSS, and restrictive cardiomyopathy all presenting as CHF) but you would treat the underlying condistion in a different way, depending on what the underlying cause is??? I don't know anymore. Now I'm lost.

Somebody help.

 

[praying4MD]

Originally posted by AJM
Actually, beta-blockers are fine to use in patients with controlled asthma/COPD. Chronic beta-blocker use has never been shown to increase mortality in asthmatics or COPDers. As long as you start with a low dose, and ramp up slowly, they are very well tolerated. The typical beta-blockers we use these days are more beta-1 selective anyway, so have decreased effects on the beta-2 receptors in the airway. The only time you want to avoid starting beta blockers in these patients is if they are actively wheezing or having an exacerbation.

Ok, yea, we should definitely start clarifying which beta blockers we are talking about at this point because all this is confusing me now.

 

[ItsGavinC]

Originally posted by AJM
Actually, beta-blockers are fine to use in patients with controlled asthma/COPD. Chronic beta-blocker use has never been shown to increase mortality in asthmatics or COPDers. As long as you start with a low dose, and ramp up slowly, they are very well tolerated. The typical beta-blockers we use these days are more beta-1 selective anyway, so have decreased effects on the beta-2 receptors in the airway. The only time you want to avoid starting beta blockers in these patients is if they are actively wheezing or having an exacerbation.

So in general, administering esmolol (Brevibloc) would not prove problematic in individuals with asthma unless they are actively wheezing?

 

[AJM]

Praying4MD --

Your syllabus is correct. Beta-blockers should be used cautiously in CHF, but the long-term use of them also has shown decreased mortality in CHF.

If you start a beta blocker during an acute CHF exacerbation, it can make the exacerbation worse (just like if you start one during an asthma exacerbation). You also don't want to start at too high of a dose so that the patient becomes immediately symptomatic from their CHF. This is why they must be used with caution, particularly when starting treatment. The way we usually initiate beta-blockers in heart failure patients is to kind of creep up on them. When patients are pretty asymptomatic, we start at a very low dose, and every week or so, slowly increase the dose to the maximum that they can tolerate. This is exactly how you start beta blockers on asthmatics as well. The trick is that the patient can't be in an acute exacerbation.

The different types of beta blockers do not really add too much to this current discussion. I think you should first spend some time understanding the use of beta blockers in general, and then pay attention to which ones are primarily beta-1, beta-2, or nonselective. (remember, there is really no "pure" beta-1 or beta-2 antagonist).

hope that helps!

 

[praying4MD]

AWESOME! thanks ever so much for your excellent and clear explanation of the use of beta blockers. it certainly clears things up for me much more now.

in appreciation,
Praying_That_I_Don't_Kill_Patients

 

[ckent]

Originally posted by praying4MD

Other quotes which are now causing me much muddled confusion:

"Calcium channel blockers, unlike beta blockers, are effective in patients who have variant or vasospastic angina, whereas beta blockers are used for exertional angina."

I could be mistaken, but i believe that your prof was referring to how ccb's can help patients with pritzmel's (sp?) angina, a vasospasive disorder that causes chest pain (oftentimes at rest). Beta blockers are given to most patients who are admitted with a good history of new onset chest pain or exertional angina, usually in the ER, since they have been shown to decrease mortality in patients with acute MI's. I don't agree with your prof's assertion that CCB's are first line agents in any patients though, except perhaps those with pritzmel's, raynaud's phenomenon, or pulmonary htn. In general, I think that physicians should attempt to try patients either on an ACE, beta blocker, or hctz for most patients who are otherwise "asymptomatic" depending on their risk factors for developing certain diseases (eg obese-->pre-diabetic--> ACE; without health insurance or otherwise healthy-->hctz, family hx of cad-->beta blocker). If you think about htn, you are essentially trying to prevent a disease from occuring, and while ccb's have been shown to decrease htn and prevent some of the complications associated with htn, just about all of the other htn agents have added benefits to them that go beyond lowering bp in terms of preventing diseases associated with htn. The most popular ccb's aren't even generic yet (unlike hctz, which I think costs 8 dollars a month), and there was actually a recent study (this year) that suggested that hctz is associated fewer pt's developing chf who were previously "assymptomatic" compared to ccb's. Even the drug rep at my school who pushes norvasc ( a ccb, amlodopine) doesn't ask any of us to use his product as a first line agent but rather he asks us to consider it for use along side the other anti-htn agents that have been shown to be superior to his product.

 

[babinski bob]

ItsGavinC quote:
--------------------------------------------------------------------------------
Originally posted by AJM
Actually, beta-blockers are fine to use in patients with controlled asthma/COPD. Chronic beta-blocker use has never been shown to increase mortality in asthmatics or COPDers. As long as you start with a low dose, and ramp up slowly, they are very well tolerated. The typical beta-blockers we use these days are more beta-1 selective anyway, so have decreased effects on the beta-2 receptors in the airway. The only time you want to avoid starting beta blockers in these patients is if they are actively wheezing or having an exacerbation.
--------------------------------------------------------------------------------



So in general, administering esmolol (Brevibloc) would not prove problematic in individuals with asthma unless they are actively wheezing?



Actually, esmolol is used as an antiarrhythmic... Specifically, it's a class II antiarrhythmic. It has a fast onset of action, short duration. It's the drug of choice for treating arrhythmias that occur during surgery. It's NOT really used much for the tx of CHF. Moreover, esmolol is a cardioselective B-blocker and should not cause much wheezing, as bronchoconstriction is a B2 effect. But in general, the consensus is to avoid B-blocker use in asthmatics simply because while a cardioselective B-blocker may have higher affinity for B1 receptors, there is still going to be some interaction w/ B2 receptors which might precipitate an asthma attack.

 

[babinski bob]

praying4MD quote:
--------------------------------------------------------------------------------
Originally posted by AJM
Actually, beta-blockers are fine to use in patients with controlled asthma/COPD. Chronic beta-blocker use has never been shown to increase mortality in asthmatics or COPDers. As long as you start with a low dose, and ramp up slowly, they are very well tolerated. The typical beta-blockers we use these days are more beta-1 selective anyway, so have decreased effects on the beta-2 receptors in the airway. The only time you want to avoid starting beta blockers in these patients is if they are actively wheezing or having an exacerbation.
--------------------------------------------------------------------------------

Ok, yea, we should definitely start clarifying which beta blockers we are talking about at this point because all this is confusing me now.



The specific B-blockers which are approved for CHF in the USA include carvedilol & labetalol (nonspecific B blocker w/ A1 blocking effect), & metoprolol (cardioselective B blocker). These are going to be administered chronically and aren't going to prove much use in the case of an acute CHF attack as previous people have mentioned. The tx of ACUTE CHF is usually handled by the administration of dobutamine (B1 agonist) or LOW levels of dopamine (activates prejunctional D2 receptors --> dec NE release --> peripheral vasodilation; activates renal D1 receptors --> ensure renal perfusion; causes NE release at myocardium <--mechanism unknown). Hope this clarifies the drug-specifics...

 

[ItsGavinC]

Originally posted by babinski bob
Actually, esmolol is used as an antiarrhythmic... Specifically, it's a class II antiarrhythmic. It has a fast onset of action, short duration. It's the drug of choice for treating arrhythmias that occur during surgery. It's NOT really used much for the tx of CHF. Moreover, esmolol is a cardioselective B-blocker and should not cause much wheezing, as bronchoconstriction is a B2 effect. But in general, the consensus is to avoid B-blocker use in asthmatics simply because while a cardioselective B-blocker may have higher affinity for B1 receptors, there is still going to be some interaction w/ B2 receptors which might precipitate an asthma attack.

Thanks for the prompt answer!

 

[HiddenTruth]

So i still dont udnerstand why you you WOULD use beta blockers in a person with CHF? How is it beneficiary? And with asthma same thing, i udnerstand that most betal blockers are beta 1 selective but again a some of the other posts have said that you still might stimulate the beta 2 rec and exacerbate an asthamatic response. I udnerstnad that in acute conditions you do not sue them, but how does that differ in terms of tx whether the person is symptomatic or asymp? I just dont understand that how are they beneficiary, because whether acute or not they still are acting the same way to reduce contractility thus causing backflow, pulm edema leading to rite sided heart failure, etc...please explain. thanks.

 

[babinski bob]

HiddenTruth So i still dont udnerstand why you you WOULD use beta blockers in a person with CHF? How is it beneficiary? And with asthma same thing, i udnerstand that most betal blockers are beta 1 selective but again a some of the other posts have said that you still might stimulate the beta 2 rec and exacerbate an asthamatic response. I udnerstnad that in acute conditions you do not sue them, but how does that differ in terms of tx whether the person is symptomatic or asymp? I just dont understand that how are they beneficiary, because whether acute or not they still are acting the same way to reduce contractility thus causing backflow, pulm edema leading to rite sided heart failure, etc...please explain. thanks.


The reason why they are beneficial is because in CHF, one of the deleterious effects that takes place is cardiac remodeling. Initially, it's beneficial because the heart hypertrophies to maintain wall stress (wall stress = [P x R]/thickness) and maintain cardiac output. But over time, it becomes so darn thick that ventricular filling is impaired and myocardial O2 delivery becomes impaired. When this happens, you get end stage heart failure and the patient is in deep ****. Now what causes this remodeling to occur? The answer: angiotensin II. Remember, AT-II is formed thru the renin-angiotensin cascade which is highly upregulated in individuals with CHF.

B-blockers DAMPEN the response of the sympathetic NS so that NOT AS MUCH AT-II is formed. There is still some AT-II being generated but not as much. Clearly, SOME hypertrophy is beneficial. Therefore, by giving a B-blocker, cardiac remodeling is maintained within normal physiologic limits. This is one reason why B-blockers are useful in CHF.

Another reason why B-blockers are used is because persistent sympathetic stimulation activates pro-apoptotic myocardial genes which results in ...... apoptosis!!! Apoptosis (or death) to the myocardium clearly cannot be a good thing!!! B-blockers BLOCK the activation of these proapototic proteins.

Now the reason for using B-blockers in asymptomatic individuals is to BLOCK all of these deleterious effects from occuring over time. This is why you use it when the patients are asymptomatic... to block the aforementioned progression of events.

During ACUTE CHF, the heart can no longer pump out the 5L/min that it is supposed to because the damn heart is worn out, it's hypertrophied like a mo-fo, isn't being perfused very well cuz it's so damn thick, isn't filling well because it's walls are so thick and noncompliant. As a result, pulmonary congestion ensues and this is when the patient returns to the hospital and is drowning in their lungs (ie severe pulmonary congestion). So what are we going to do?

We give a powerful B1 agonist like dobutamine to increase myocardial contractility and hopefully alleviate some of the pulmonary congestion. We're obviously going to use other drugs like a diuretic and vasodilator to help improve the sxs. But in the case of end stage CHF, there isn't much you can do except to try and alleviate the symptoms because the patient is pretty much down for the count.

Now as you mentioned, we definetely do NOT want to give a B-blocker in ACUTE CHF because it'll do the opposite of what we want.

Remember, for people with CHF that are asymptomatic, B-Blockers are NOT the only drug they're receiving. They're definetely going to be on a diuretic (Fursemide, hydrochlorothiazide) to reduce total volume and decrease afterload. They're also likely going to be on an ACE inhibitor for the same reasons. By giving this COMBINATION of drugs, the hope is that we will have relieved some of the pressure in the pulmonary system such that no congestion is occuring.

 

[HiddenTruth]

yo UMN bob....very well done...awesome explanation..thanks a million dude...i think i am ready for step one now...

 

[ERMudPhud]

I can recall one other instance when beta blockers are indicated in acute CHF-though its a bit of a zebra. Years ago I used to see this patient in the ED who had critical mitral stenosis and would some times present in flash pulmonary edema. The key to her treatment was to slow her heart rate so that the left atrium had time to empty. The more you pounded her with lasix, nitrates the faster her heart would go and the worse she would get. After she got intubated a couple of times her cardiologist trained her to come into any ED screaming "esmolol, give me esmolol" We all just kept wishing she would get her valve fixed but she never did.

 

[omores]

When I was on the medicine service, we (very cautiously) used BB in acute CHF decompensations for similar reasons. For example, we had a patient with class 4 CHF who would become very tachycardic during her exacerbations. This was her body's way of trying to maintain cardiac output (stroke volume x heart rate!), but in her case it was maladaptive -- the very rapid heart rate would make her heart even less efficient than it already was.

A wee dose of beta blocker actually helped her out as we diuresed her.

 

[Halcyon440]

While you're on the topic I wanted to bring up my own situation.

I'm 29 and was put on Toprol about 6 months ago for sinus tachychardia. I'm on 100mg now.

At the very beginning I experienced some lethargy, but am now tolerating it well. My doctor said it was ok for me to keep exercising and so I am doing martial arts. Sometimes during class my heart does still speed up but never like before where it went over 200 after minimal effort. What I have noticed is that it's sometimes hard for me to catch my breath during class. In general I feel that I am breathing more shallowly now. Sometimes I do pilates and some of the exercise positions make me feel as though I am suffocating.

During my monthly checkups the doctor always asks if I have issues with breathing but I had been saying no because I figured that maybe I am just out of shape. I didn't want him to think I was a hypochondriac or something. But now that I read all this I am wondering if I should be concerned.

What do you think? Thanks!

 

[omores]

What beta blockers provoke -- if anything -- is bronchospasm. This feels quite different from simply being "short of breath": your lungs will actually feel constricted, and the air feels like it's just not moving very well. In severe cases, it's been described (acurately, in my opinion), as the equivalent of drinking a thick milkshake through a tiny straw.

I have asthma, though it's kind of a non-issue now, and take atenolol for sinus tach as well (though I'm off it now because I'm pregnant.) Never had the least bit of a problem with bronchospasm, though when I'm having lung problems due to a cold or something, I stay off it.

Beta blockers, because they reduce your maximal heart rate, can result in exercise intolerance for some folks. Generally this manifests itself as a feeling of tiredness or sluggishness rather than breathlessness, but different people may respond in different ways. It's not something I've had a problem with myself. On atenolol, my maximal heart rate is much lower than without, but I seem to be able to do the same amount of exercise.

Both bronchospasm and excercise intolerance should not be dependent on your position. If you're noticing this intermittently during Pilates, it's likely because certain positions are restricting the movement of your ribcage and diaphragm while you're in them, so you may well feel suffocated. As long as it resolves when you change position, I don't think it's from the beta blockers.

 

[Chubbie]

I have been searching for articles about acute heart failure exacerbation. I do find that you should not start Bblocker in patients who has just experienced acute heart failure exacerbation within 1 month because it can precipitate exacerbation. However, none of the articles I found explain how it can worsens the sx. Is it because of the alpha effect and the bronchospasm. What if the patient was taking beta-blocker while he has acute heart failure exacerbation, do we continue because we want to avoid b-blocker withdrawal effect.

 

[theshellyb]

I have been searching for articles about acute heart failure exacerbation. I do find that you should not start Bblocker in patients who has just experienced acute heart failure exacerbation within 1 month because it can precipitate exacerbation. However, none of the articles I found explain how it can worsens the sx. Is it because of the alpha effect and the bronchospasm. What if the patient was taking beta-blocker while he has acute heart failure exacerbation, do we continue because we want to avoid b-blocker withdrawal effect.

In theory, you don't want a patient on Beta blockers during an acute CHF exacerbation because beta blockers decrease the heart's contractility when it blocks the B1 receptors.

However I'm not sure how this plays out in practice and it looks like the data just isn't there to apply an all-or-none rule: https://www.clevelandclinicmeded.com/medicalpubs/ccjm/june06/fares.htm

 

[evilbooyaa]

In relation to the post that necrobumped a 10 year thread.... if a pt w/ CHF has pulmonary edema d/t impaired contractility, giving beta blockers in the short term will exacerbate their symptoms (by decreasing cardiac contractility and therefore SV). Therefore, if a patient is symptomatic and has pulmonary edema/pleural effusion on a CXR, then you diurese them first before you start them on a beta-blocker. However, if they are already ON a beta blocker, then I believe you keep them on it during their admission.