Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Beta vs. Beta Blocker – comment

In the comments to Beta vs. Beta Blocker, Anonymous wrote . . .

Gang, is it time to review pharmacology?


It is almost never a bad time to learn more about pharmacology.

Dopamine acts as a beta agonist, but because it’s not terribly selective, it also acts as an alpha agonist. Metoprolol acts as a beta blocker and, because it’s highly selective, has relatively few alpha effects. So we might expect a patient who received appropriate doses of both dopamine and metoprolol to experience no net change in his beta activity. But his alpha activity would increase. Wouldn’t some peripheral vasoconstriction push our patient’s central blood pressure upwards?

But does the patient need any help with blood pressure?

If we are giving drugs to this patient, why use untested combinations?

I did not find any studies that examined the use of dopamine combined with metoprolol for the pure alpha effects of dopamine. Is there any research to support this?

Dopamine alone probably would have been harmful to TOTWTYTR’s patient. Metoprolol alone might also have been harmful (depending upon the heart’s position on the Starling curve.) But the combination seems potentially useful to me — and well within an emergency physician’s scope of practice to order.

It is interesting that you state that Dopamine alone probably would have been harmful. I agree that it is not a good idea under the circumstances.

TOTWTYTR describes it this way

an 80 year old gentleman complaining of dyspnea and chest pain (6/10). He’s conscious, alert, and oriented. He had “the look”. The one that we know when we see it, but can only describe as “looks like s@#$”. Which, come to think of it should be an official medical term. His skin is 2+ diaphoretic and pale, his respiratory rate is 28, lungs are clear. He is able to speak full sentences without difficulty. His radial pulse is 150, his BP is 68/P. His 12 lead EKG shows ST elevation in V1-4, with reciprocal changes in II, III, AVF.

Those circumstances are –

1. The patient had good radial pulses, even when the blood pressure is measured at 68 by palpation. A palpated pressure tends to run lower than an auscultated pressure, so this is probably a systolic pressure in the 70s.

2. The patient has received ASA (AcetylSalicylic Acid – Aspirin)[1] and oxygen. Since the patient’s lungs are clear, he was given 250 ml of NS (Normal Saline solution), but his 12 lead appears to rule out RVI (Right Ventricular Infarction).[2] We would expect ST elevation in leads II, III, and AVF if this were an RVI. While it is possible that the right ventricle is infarcting, we just do not have anything to support that conclusion.

3. After the 250 ml NS, the blood pressure is measured at 88/palp. So, probably a systolic pressure in the 90s.

Is this rise in pressure because of the fluid? Maybe.

Is this rise in pressure because of the oxygen? Maybe.

Is this rise in pressure because of the ASA? Maybe.

Is this rise in pressure because of placebo effects? Maybe.

Is this rise in pressure because of a homeopathic remedy? Sorry – kidding, I already mentioned placebo effects.

Has the patient’s pressure been labile (bouncing around with a very wide range)? Maybe.

Is this an example of spontaneous resolution of symptoms? Maybe.

Is this some combination of the above? Maybe.

We do not know. We are only guessing.

We only have 2 blood pressure data points to go by. This is not information that any conclusions should be based on. The least harmful interpretation appears to be – fluid helped, so try more fluid. But constantly reassess for signs that this is not the right treatment.

People are biased. We look for signs that we are doing something right, rather than signs we are doing something wrong. This patient appears to be close to dying. He needs for us to not make any mistakes.

Some patients do survive in spite of everything we do to them. We should not count on that.

The more treatments we use, the greater the chance that we will make a mistake. We are already treating this patient with 3 different treatments. I need a very good reason to add treatments at this point. He appears to be improving with the treatments already given. He may be improving in spite of the treatments already given.

Why are we giving the treatments?

Some may only want to get the pressure up so that they may give NTG (NiTroGlycerin, or GTN – Glyceryl TriNitrate in Commonwealth countries).[3] I am not in favor of this approach. Anyone with chest pain and a pressure that is not elevated is behaving abnormally. I am hesitant to throw a potent vasodilator into a patient, who recently had a pressure so low that I felt the need to treat it. My goal is not to see how close to death I can get him and still have him survive, even though that could make for some interesting blog posts.

If this is an RVI, then the approach is quite different. I am dumping as much fluid into the patient as I can. Part of the reason is to keep the pressure from dropping too much when I give NTG. RVI is different from the other heart attacks. RVI combined with another area of infarction is even more uncommon. Not having a V4R or MCR4 lead to look at, we cannot rule out RVI, even then we cannot be certain, but it seems very unlikely. On the other hand, the response to fluid is consistent with RVI. Could leads have been misplaced? Always a possibility, but unlikely to produce this result. My goal is to get the patient to the hospital in the best condition for him to survive. That does not mean the best looking vital signs. Although I am more comfortable looking at normal looking vital signs, I do not make them my goal. Vital signs are only some of the indicators of the patient’s condition. Their meaning is open to interpretation. There is still the possibility that this is an SVT (SupraVentricular Tachycardia), but I do not consider that likely, based on what TOTWTYTR wrote.

What might metoprolol (Labetolol)[4] do to this patient? Slow the heart rate and lower the blood pressure; Slow the heart rate and raise the blood pressure;[5] Or something else?

But the combination seems potentially useful to me — and well within an emergency physician’s scope of practice to order.

Now, the last sentence. With this patient, I am more worried about potentially harmful, than potentially useful. Where is the research to support this type of treatment? The theoretical and possibly illusory benefit does not make me feel comfortable with the many significant risks. The risks are all of the risks of metoprolol, all of the risks of dopamine, and any other risks that may result from combining these medications. I do agree that this should be within the emergency physician’s scope of practice to order. I am continually amazed at EMS protocols that place limits on the dosages or combination of drugs that may be ordered by a physician. Usually these limitations are on drugs that are dosed by titration – the initial dose should be estimated based on the weight, age, health, . . . of the patient. All subsequent doses should be based on the apparent response of the patient to the previous doses.

Opioids and benzodiazepines are the medications usually treated with these artificial limitations on the ability of the physician to give appropriate orders. If anything tells you that a treatment is poorly understood, it would be EMS protocols that do not allow physicians to give an order for that treatment, or EMS protocols that limit the orders the physician may give. Opioids and benzodiazepines are safe when given by competent paramedics – not paramedics with tons of experience, just competent paramedics. Why do these physicians prevent competent paramedics from giving these drugs? Because they know that they allow incompetent paramedics to work in their system. Such reckless physicians should not have anything to do with EMS.

Unfortunately, EMS is poorly understood. It is as much like the emergency department as the emergency department is like the ICU. On the other hand, things do appear to be improving. Is it hard to get paramedic students experience pushing benzodiazepines and opioids? If you are an emergency physician, you probably gave orders for both in your last shift. How hard is it to get a paramedic student some supervision and experience pushing these, reassessing, and finding out where the paramedic student’s assessment is leading him? That would be in a back woods EMS system. If you are near a burn center (even a trauma center), there are far more opportunities to give repeated and large doses of these medications. Repeated doses require reassessment, but so does the individual dose – otherwise, how do you know when it is it appropriate to stop, or pause, administering these medications? They should be given slowly, the patient should be reassessed, and they should be repeated until there is a reason to stop, or pause. The only time to stop at a maximum dose, would be because you have run out of the medication. The only way to determine too much/enough/not enough is by reassessments.

So, that is one view of the problem of protocols limiting physician orders. This is a different case. Medicine is a combination of Art and Science. A scientifically practiced art may apply more to EMS. Physicians should be aiming for something a bit higher – artfully practiced science. Too many do not get this. Some ignore the art and the science, in favor of a discipline in which they are not trained – law.

What I want to know, for this patient, who is looking better and has only a 4 minute ride to the hospital, is why mess with that? There is little reason to believe that this will help and a lot of reason to believe it will hurt. Where is the research to show that the dopamine/metoprolol combination is effective in the hospital? Where is the research to show that the dopamine/metoprolol combination is effective when used in EMS?

Surely TOTWTYTR knows his medical command physician better than we do; perhaps he’s a numbskull, perhaps not. We could second-guess the appropriateness of hanging a drip only 4 minutes from the ED. But on its face, the physician’s order does not seem utterly unreasonable to me.

The difference between a good idea and utterly unreasonable, to me, is whether it is supported by research. Theories are nice, but lead us into traps of overconfidence. CAST (the Cardiac Arrhythmia Suppression Trial) gave us a great example of that. The theory was that since, after a heart attack, people with PVCs tend to drop dead more often than those without PVCs. Therefore, getting rid of the PVCs will keep a lot of those people from dying. The opinion of the experts in cardiology was that this was going to save a lot of lives. The results of the trial were –

During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5).[6]

Those taking encainide and flecainide were about 3 1/2 times more likely to die of arrhythmia. The drugs were supposed to have the opposite effect. The drugs were supposed to prevent death from arrhythmia. Since then, prophylactic use of antiarrhythmic drugs has pretty steadily decreased. Except for the thrall over amiodarone.

Expert opinion is important. Unfortunately, if the experts are misinterpreting some of the information, even though it is the state of the art science, at the time, bad treatments can result. Encainide and flecainide did a great job of getting rid of PVCs, but PVCs were not killing the patients. PVCs were just an indication of an injured heart. People with injured hearts and PVCs may have arrhythmic events more frequently than those without PVCs, but getting rid of the PVCs does not cure the heart. It just changes the conduction of electricity in the still injured heart.

So, while the emergency physician is the expert, I am hesitant to treat based on a theory of how things should work. If there is well done research of the effects of a combination of drugs in humans, then I am much more likely to just follow orders.

[Updated 8/11/2019 to correct grammar, spelling, and dead links]


[1] Aspirin

[2] Recognition and treatment of right ventricular myocardial infarction.
Gandy WE.
EMS Mag. 2008 Mar;37(3):69-73, 100.
PMID: 18814636

Free Full Text from EMS World

[3] Nitroglycerin

[4] LABEL: METOPROLOL TARTRATE- metoprolol tartrate injection, solution
FDA Label

[5] Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect, and coincidence.
Chockalingam A, Tejwani L, Aggarwal K, Dellsperger KC.
Circulation. 2007 Jul 31;116(5):e110-3. Review. No abstract available.
PMID: 17664378

Free Full Text from Circulation

[6] Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction.
Cardiac Arrhythmia Suppression Trial (CAST) Investigators.
N Engl J Med. 1989 Aug 10;321(6):406-12.
PMID: 2473403


  1. I’ll add only one comment to the case, which wasn’t mine. In fact it was originally an ED case a friend of mine was involved in. She was the RN and refused to give the Lopressor on the order of cardiologist. She drew it up and handed it to the doctor so he could give it if he wished. Which he did. With the effect that my friend feared based on her experience and her knowledge of pharmacology.

  2. An interventional cardiologist to your “non interventional paramedic”?

    I’m not a fan of cocktails. Concoctions add too many variables to an already less-than-certain situation.

    I will give doses of some medications that will make the occasional doctor apoplectic. The safety factor for me is that I generally limit myself to only one or two medications. The second one is often oxygen. And how hard is it to continually reassess?

    In the hospital, positive STEMI, but between the door and the balloon it gets just a little too complicated?


  3. We would expect ST elevation in leads II, III, and AVF if this were an RVI. While it is possible that the right ventricle is infarcting, we just do not have anything to support that conclusion.

    Right-side 12-lead?

  4. Thank god I don’t have the pressure’s of being a paramedic yet…all I can do in that case is consider my location verses getting als to meet me en-route but in any case snatch and grab. place on O2 call medical direction monitor closely and pray…take my chewing from nurse ratchet for being a basic truck. and my vitals better match hers like what are the odds of that? grrrr

  5. Nice bit of point/counterpoint there, Rogue.If you haven’t already heard, Dr. Ben and a few Lankenau cardiologists are holding a seminar on pre-hospital STEMI care on November 9th.Call Ben if you’re interested.

  6. Brendan,

    Yes, a right sided lead V4R, specifically, or all of the right sided leads would be helpful. The 2nd hand or 3rd hand telling of this did not include that information.

    Any time I am suspicious of anything right ventricular, I look at V4R or MCR4.


  7. Life of an EMT,

    That is the biggest difference between being a basic EMT and being a paramedic, in my opinion. The decisions. Those who don’t make it as medics, but not because of the book work, seem to have trouble making the appropriate decisions. Being yelled at does nothing for me. I find that quiet satire/sarcasm is the best revenge. As long as I maintain good manners and don’t say anything untrue/slanderous . . . .

    I wasn’t yelling. Everybody else in the ED heard the nurse yelling. My suggestion that the Don Rickles School of Nursing should focus a bit more on patient care is only supported by the nurse’s misbehavior.


  8. Trekmedic251,

    Thank you. I will try to arrange my schedule to attend. I’ll have to ask them when they are starting the dopamine/metoprolol protocol.

    :-)They’ll love me there.

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