Rapid A-Fib, Calcium or Beta Blocker?

[678 Responding]

Well, I was in the ER the other night doing a clinical rotation, and we had a 80 Y.O. lady come in with a rapid a-fib around 130-150, occasional PVC's and abbarent beats, asymptomatic, BP around 130/90. She does have a hx of a-fib. The reason why she came into the ER was because she said her BGL had been above 500 for the past few days and can't seem to get it to go down. So I do an accucheck and its 486. Confirmed. So, the resident does his evail, orders 5 Units of Insulin IV, and 5mg of Lopressor IV. I was a little taken back, since we were always taught to use a calcium channel blocker first for an uncontrolled a-fibb rather than a beta blocker, as also states our pre-hospital protocols. So the 5mg is pushed, and it doesn't even touch her. Her rate is still the same, and BP is untouched, se he tries it a second and a third time. Still nothing. He eventually stops trying, and her rate is around 120-130 now, BP still the same. I asked the resident why he used Lopressor instead of Cardizem for this patient, and he couldn't give me a straight answer. He tried to say something about "other underlying pathological conditions" etc etc. but I wasn't buying it. I still feel this lady should have been given Cardizem instead of the Lopressor. Does anyone else have a possible reason why he did this, what are your protocols for this, and whether or not I would have been wrong for giving Cardizem if this were my pt. in the field. Do you feel the calcium channel blocker would have had much of a different effect than the beta blocker in this case? Thanks!!

[Doczilla]

Both cardizem and lopressor will slow conduction across the AV node in a similar manner and are indicated for rapid a-fib. If she had other conditions, such as coronary artery disease, then the beta blocker may have additional benefits. In the presence of acute ischemia, the beta blocker will reduce morbidity and mortality, attenuate deleterious remodelling of the heart, and reduce the emergence of a more serious arrhythmia. Additionally, if she's already on a beta blocker, the doc may have been wary of giving a CCB, which may have deleterious adverse effects. Lopressor is a fine choice for treating the rapid a-fib. 15mg is also not that big a dose, particularly in 5mg aliquots. Considering also that her BGL has been above 500 for a few days, dehydration may have been contributing to her rapid heart rate. The elevated heart rate may not have been the cause, but the symptom, of her underlying problem. Therefore aggressive treatment with antiarrhythmics might do more harm than good. The doc was right not to get too focused on treating the number, especially since she was not symptomatic.

Based on the information you've given us, this is not someone that you should push cardizem on in the field.

'zilla

[AZCEP]

Good example of treating a symptom, not the problem. A rate that varies that widely tends to be caused by something other than a true tachydysrythmia. I'd agree with Doczilla's assessment of possible dehydration for this patient.

True, controlling the rate will increase cardiac output to a point, but the tank is empty. There is probably little fluid for her heart to pump. Giving this patient with this history a calcium channel blocker is a good way to cause a refractory hypotension. Pretreatment with some calcium chloride can limit this, but why would you want to use it in the first place?

[OVeractiveBrain]

Unrelated to the patient, but particularly of interest your question about why Beta blockers:

In my EMS system our protocols are designed towards rate control, not rhythm conversion. In our tachycardia protocol (including rapid afib) if the patient is ALREADY on beta blockers, we are to give Lopressor 5mg q 5min max 15mg (all we carry) IVP until the rate is controlled. Only if they are not already on BEta Blockers should we look towards cardizem or verapamil (sometimes we have both, sometimes just cardizem, why Im not so sure) to control the rate. Our dosages are the 10mg prefilled birsto-jets and not the 0.25mg/kg followed by 5-15mg / hr recommended by ACLS. Our system has two major level I teaching hospitals within 5 minutes of one another, and never a transport time more than 20 minutes, so the goal is to control rate, rather than convert rhythm. I, too, was taken aback by the protocol for Beta Blockers rather than Cardizem, but eh, whatcha gonna do?

We obviously treat underlying causes first, but if there is a tachydisrhythmia, do as above.

[scope2776]

so i'm a little confused about your patient....

Our protocols focus on ventricular rate control to bring decrease cardiac output and therefore decrease BP. So I know with a-fib w/RVR I would consider a calcium channel blocker, but you described abbarent conduction - so does this mean conductions that did not go through the AV node? If this is the case, as in a Kent or James fiber, I would not consider calcium channel blockers because I would be shutting off the hearts only way to regulate rhythm and possibly send my pt in v-tach. We have no protocols for beta-blocker use in this case.

Overall she seems like she has a pretty poopy heart, without a very, and i mean very, through eval. on my part i won't even consider pushing verapamil in the field, even if she is showing some unstable signs. And your darn sure I would call med control.

I could be all confused about this....

[p3medic]

With the info provided i would agree this is most likely a symptom rather than a cause, i.e hyperglycemic diabetic on the dry side, with an appropriate sympathetic response to same. I'd give a fluid challenge and see were that gets me. As for cch v.s beta blocker, I tend to use the same class of drug they are taking, assuming they are on one or the other, otherwise look at the pts hx and make the appropriate choice....both drugs have there place.

[678 Responding]

She was dehydrated, so they started a fluid bolis on her. This didnt seem to change the heart rate all. We dont focus on conversion either, only rate control. Calcium channel blockers are great for rate control, as they affect the slow conduction, and are very close to Beta channels, so they have the same effect. Less force of contraction and slower heart rate. We dont use verapakill anymore, its not as cardiac specific, as cardizem is a much better choice for rate control. The patient would thow an abbarant beat every once in a while, so it hardly effects the rate and BP at all. Now that I look back at the picture, I think she might have been dehydrated, the heart tries to compensate, and in being in a chronic a-fibb, went into a RVR. I wasnt there long enough to see what happened to her or what the final result was. I do know that she was admitted though for the high BGL. I was just curious as to why some people prefer a Beta channel blocker for A-fibb/flutter with RVR over a Calcium blocker, as we are being taught to use drugs like Cardizem for this type of patient rather than Lopressor. Thanks everyone for your input.

[AZCEP]

Using terms like "verapakill" shows a misunderstanding of the utility of the drug. Yes, it is not quite as good as Cardizem for the rate control of AF/Aflutter. It is however very effective when it is used. As I already mentioned, a little pre-dosing with some calcium chloride would limit some of it's vasoactive effects for the patient that is significantly dehydrated. I don't blame you for coming up with the term, but the educational system that you are working in.

I've used Calan numerous times, and have never been anywhere near experiencing this, ahem, side effect. It works great, and you don't have to worry about re-dosing if you are within 30 minutes of a facility.

Most beta blockers are "kinder/gentler" rate control agents. The trouble with most is they are not as rapid in their onset as the calcium channel blockers. Perhaps more correctly, the effects of the drug aren't as obvious to the provider that is using them.

I think I may be missing something in the translation of this:

Calcium channel blockers are great for rate control, as they affect the slow conduction, and are very close to Beta channels, so they have the same effect. Less force of contraction and slower heart rate.

There isn't a beta channel on the myocardial cell wall. It is a beta receptor. It's activation allows the cell to break down stored energy and release it through contraction, and/or electrical stimulation. The calcium channel, in this instance the slow calcium channel, slows the inward flow of the calcium cation into and out of the cell. This inhibition prolongs phase 2 of the action potential. Lengthen the AP, slow the heart rate. The slower the rate, the greater the amount of fiber stretch, leading to a greater force related to Starling's law. The calcium channel blockers do reduce contractility, but some of this effect is balanced with the slower rate.

[678 Responding]

AZCEP, thanks for the response.

They arent advocating much use of Verapamil here anymore, and I hear that term "Verapakill" quite often from the medics as it can have some pretty nasty side effects. Nothing from my school. just street talk. As for the Beta blockers, I meant to say Receptor, not channel. Had a long day. hehehe. Thanks again for the input!