Need Advice on Metoprolol

Esme12, ASN, BSN, RN · May 18, 2012

Hind sight is always 20/20. Depending on the amount total of amiodarone and metoprolol given po previously I would have clarified with the MD about the 2200 metoprolol and gotten parameters at the time of the bolus or, I would have called a the time of the 2200 dose..."Dr. Backstabber? I am calling with an update on Mrs Syncope....the ED admit with the rapid AF that required the bolus for hypotension earlier. I see she is due for another dose of metoprolol.......Her vitals are blah, blah, blah. Her rhythm remains blah. She seemed to respond to the fluid bolus and has been doing alright so far....I was wondering if there were any parameters on the metoprolol."

I am big on calling the MD. Especially ones that prove they aren't worthy of my trust. They can yell and scream to their little hearts content about being called. They know they should give parameters. That two faced MD threw you under the bus because she is an incompetent........&%&%$ person. I can't be sued for calling the MD and making sure they are the scapegoat but I can be sued for not calling. I don't give a rats bah two tee whether or not they get upset....WHATEVER.....do your job "DOCTOR".

I cover my own butt. I'm too smart to be anyone's jackass.

Never trust this MD again...you see what her tactics are.....you are her whipping post for her incompetence. She is probably accustom to being spoon fed by competent nurses and can't think for herself. How many times I would call with stuff like this and get the "'Uh Yes sure that's a good idea.....I forgot to write it?"

Forgot my foot...idiots.

I Don't think it was your dose of metoprolol that initially dropped the B/P but I do think it prevented her responding to the bolus. Live and learn. When patients are being dosed heavily po like that it is worth a bit of caution. Technically you did just fine. The vitals were perfectly OK at the time to administer the meds....the caution to me would be that she had already bottomed her pressure and was going to prove to be fragile in this department. The MD was being a jerk.

:hug: I'm sorry there are jerk idiots for MD's. Well, done but always CYA and for my usual lecture behaviour like this is the exact reason I say to get and carry your own malpractice insurance. To give you piece of mind. I'm done now....

#1ME · May 18, 2012

Documentation is key! Did you chart that you informed the MD on Pt's BP, HR and that he/she ordered to administer the Metoprolol still? Did the MD write down any parameters regarding holding these meds?

#1ME · May 18, 2012

Technically you did just fine. The vitals were perfectly OK at the time to administer the meds....the caution to me would be that she had already bottomed her pressure and was going to prove to be fragile in this department. The MD was being a jerk.

^^Agree

RoyalPrince · May 19, 2012

You gave a bolus to increase BP from 80s than gave Lopressor 50mg.......Live and learn

Shay1482 · May 19, 2012

It seems to me this pt had issues..the Lasix could have initially lowered her pressure, I would have questioned the doctor about a dosage change in the lopressor before giving 50mg since the pt had been bolused. Then documented the doctor was notified and what the outcome was of that notification. Seems this pt needed cardizem...was the dopamine started at a renal dose or cardiac dose...you don't want to keep throwing fluid at someone without renal function....not sure why any doctor wouldnt have lowered the dose knowing the pt was in a fib with rvr and was on Lasix and had been admitted s/p fall......and for hypotension.......then she writes you up ???? Hello ????

Anna Flaxis, BSN, RN · May 19, 2012

Yes, the metoprolol certainly could have worked that quickly, but remember that the patient *came in* with hypotension. While I'm sure that the metoprolol probably didn't help her in that department, she needed *something* for rate control. 120s isn't scary, but it's not okay to have her taching away all night like that. She needed to be brought down.

Sounds like the doctor was just being a jerk, throwing you under the bus to cover her own behind. That sucks. If you didn't already, I would always make sure to document that the doctor gave you the order to give the medication despite the previous problems with blood pressure. If you didn't, you can go back and do a late entry.

suanna · May 19, 2012

In my experience- If you didn't give the Lopressor the docs would have had a tantrum. Fluid isn't usualy going to cure beta-blocker induced hypotension. I'm a bit worried about the number of fluid boluses this patient got. Fluid overload is a big cause of AF as it increases atrial streach in he heart failure patients. With 20/20 hindsight I would have asked for input from the doc when you had him on the phone for the last episode of hypotension concerning your 22:00 dose. That aside- I would have given it- your VS were good, the patient is in AF with recent RVR- no choice. I'm not clear- did the doc write YOU up for giving an inapropriate medication, or did he document a adverse medication reaction to metoprolol? Whenever a patient has an unexpected or adverse response to a medication there should be documentation filled out. That isn't punitive, but helps to identify problems wit certain medications in specific populations. Without this kind of documentation we would still be giving promethazine to most of our N/V patients IVP instead of Zofran of IVPB promethazine. This question comes up over and over in acute cardiac care- It depends on the attendings views as to what you would do for each patient.

BelgianRN · May 21, 2012

was the dopamine started at a renal dose

/sadpanda

When will we root out the evil and stop people from using renal doses of dopamine. It doesn't work

I think the second bolus was an indication that you were no longer pushing the heart up on the slope of the Frank Starling curve but were on the counterpoint where your bolus of fluid was actually decreasing the stroke volume/cardiac output by further increasing LVEDP. The third bolus finished the job landing you on the bad side of the FS-curve. The resulting loss of inotropic state due to metoprolol further augmented the low output state.

Next time this MD orders a third bolus, resist and write him/her up and slap a FS-curve in his/her face. Seems to me the MDs were trying to use rhythm control via amiodarone and some rate contol via a beta blocker and then were confused that when she converted she was bradycardic.

I do think the dose of metoprolol was a bit high considering the recent fragile blood pressure and the poor response to fluids, and it contributed to the low inotropic state of the heart. But it are the fluids the MD ordered that pushed this heart over the edge in my humble opinion. If only he/she would have been wise beyond his years and ordered a little bit of lasix again it might have helped get you back.

Only thing that works against overdosage of beta blockers are inotropes, too bad they are so pro aritmogenic that they tend to send the heart back in Afib.

Esme12, ASN, BSN, RN · May 22, 2012

Yeah.....I agree Belgian. However, this still has popularity in non acedemic centers in the US and on step down units so they can have the titrated drip on the floor where the nurse has 6 patients or more and not have to come in to assess the patient tomove them to ICU. :cool:

Candyn · May 22, 2012

Hi all,

I am a new grad and I am really interested in this topic. I am trying to learn here so if someone do not mind, please explain further.

1. A patient can be hypotensive but fluid overload? If he or she is not in ICU where you have all the invasive lines, how do you tell if patient is hypotensive but fluid overload or deficit?

2. BelgianRN made this statement "I think the second bolus was an indication that you were no longer pushing the heart up on the slope of the Frank Starling curve but were on the counterpoint where your bolus of fluid was actually decreasing the stroke volume/cardiac output by further increasing LVEDP." So when you give too much fluid, it does not help with preload and it will increase LVEDP and stretchh the heart muscle too much and decrease contraction? that is why better to give lasix?

3. BelgianRN also made this statement "Only thing that works against overdosage of beta blockers are inotropes, too bad they are so pro aritmogenic that they tend to send the heart back in Afib." I know beta blockers work on Rate (???) so if we lower the rate, we use inotropes (strength) to work against? What do you mean they are so pro aritmogenic that tend to send heart back in afib?

thank lot:)

BelgianRN · May 22, 2012

Hey Candyn,

I'll try to answer your 1, 2 and 3.

1) Yes you can certainly be fluid overloaded and hypotensive. If your left ventricle is failing to pump out enough blood due to volume overload that caused the left ventricle to become overstretched so it doesn't contract properly, you'll have a decreased BP. At the same time you'll have stacking of blood in the pulmonary vasculature because it doesn't get moved forward by the left ventricle. This causes pulmonary edema. And this is the hallmark sign of cardiogenic shock.

Even when you are in the ICU try to look at the patient not the monitor (aside: today during ACLS training we decided to switch off the monitor and test their [our fellow ICU nurses] assessment skills during codes. It was true shock how disoriented they became without a monitor).

In a patient you'll notice one to all signs of shock: decreased urine output, change in LOC, diaphoreses, palor, distended neck veins, orthopnea, dyspnea, pink frothy secretions, hypotension, crepitations on lung auscultation, decreased pulse pressure... etc. Depending on the acuity and the extend of the shock it ranges from benign symptoms to a near death patient.

Fluid deficits are not always easy to spot clinically. Of course dehydrated patients have dry mucous membranes, loss of skin turgor, etc. But it is perfectly possible for someone to have edema build up but still be volume depleted in the vasculature. In general a rule of thumb we use is if you raise the legs of the patient and his BP increases you are still volume depleted intravascularly. If you add external fluids or try to recruit fluid from edema in the body that's up to your MD and yourself.

2) to keep it simple would be to compare the ventricle of the heart to a rubber band. You want your rubber band to shoot further away you stretch it more, but if you stretch it too much it breaks or deforms and it won't shoot at all. The same with the heart as long as you are on the uphill slope of the FS-curve more fluid equals higher LVEDP equals more stroke volume thus better cardiac output (your rubber band shoots further). If you go over the top your left ventricle becomes overstretched and can't contract properly you start to loose stroke volume even though your LVEDP is higher than before and your cardiac output goes down (you stretched your rubber band too much).

3) beta blockers are not only active on the heart rate (negative chronotropy) but have other effects as well. It has a negative inotropy as it decreases the contractility of your heart muscles and it decreases conduction time through the heart and the AV node in particular. Apart from that it has calming effects so it is sometimes used against anxiety, and in asthmatics it can induce bronchoconstriction due to blocking of the beta 2 receptors that cause bronchodilation in the lungs.

As beneficial as beta blockers are in reducing the oxygen consumption of the heart. When the dosage is too high for a particular patient/situation the negative effects take over. In this case as I presume the patient had decreased stroke volume due to the frank starling mechanism being on the downhill slope. The beta blocker will add a decreased heart rate and decreased contractility in the balance which would contribute to decreased cardiac output and thus hypotension.

So in order to treat this you administer something that has a positive inotrope action. Preferably something that doesn't cause increased hypotension. In this case dopamine. The problem with most/all positive inotropes is that they are also a positive chronotrope and cause increases in heart rate. And most/all positive inotropes are pro-aritmogenic which means they can in turn cause rhythm issues and Afib is a likely candidate because the patient's heart is already keen on going into Afib.

If you experience negative effects due to beta blockers, just increasing the heart rate isn't always the answer. Generally the loss of contractility of the heart is the black sheep that is causing all these problems and it is what needs to be addressed.

Sorry for the longwinded explanation. I just spent the entire day telling our ICU staff that yes atropine is outdated during CPR and so is standard bicarb. Old habits die hard :)