Critical care questions: Hypotensive A Fib
I got a bunch of critical care questions for the Weingart-Mallemat interview for the last podcast. Of course, I did not have time to get them all answered, and I felt some of them were already well answered elsewhere. So I’m going to answer a few of them with my references for good resources already out there, starting with this question:
“I have a situation that’s come up a few times recently and I haven’t been able to find a good answer to it in my lit search. Patient with a fib and in CHF. Slightly hypotensive (SBP 100-110), but not unstable or warranting cardioversion. 2 different attendings have recommended giving calcium gluconate prior to the Ca-channel blocker to “blunt the hypotensive effect”. The best explanation I’ve gotten was that it allows AV nodal blockade to occur, but the calcium influx to the peripheral vascular system prevents vasodilation.
So: What is the pharmacokinetics for giving calcium prior to CCB in the a fib patient and is there an alternative (besides electricity) in the hypotensive patient?
In terms of the alternative to electricity and treating the crashing a fibber, I will refer you to the EMCrit Podcast, Episode 20. As usual, Weingart has a great approach to these patients. The problem is (and I hate to break this to all the electricity-heads out there): cardioversion does not work in these really sick a fib patients. These are not the younger paroxysmal a fibbers who come in for their monthly cardioversion. They are usually chronic a fib patients, and have irritable hearts and you get a few minutes of sinus rhythm, at best, before you have them flip right back into a fib with RVR. So this will take some medical finesse. Listen to his podcast, he has a fantastic approach. Make sure if there is an obvious reason they are in a fib (like being floridly sceptic), treat that source. Make sure they have a good preload (US their IVC). When the heart is beating that fast, it does not fill so you want your preload optimized. Don’t be afraid to give them fluid.
Then comes rate control and the calcium question. Many times, in the patient with borderline pressures, reducing their heart rate will actually increase their pressure (more cardiac filling time). But does calcium prevent hypotension with dilt?
The pharmacology of CCB’s is nicely reviewed here. Where people are getting this idea is actually from studies on verapamil (see this and this). There has been one RCT looking at Ca pretreatment with Diltiazem and it could not detect any statistically significant blunting of the BP drop with Ca administration. This is partially because few actually got hypotensive in the study. It is also interesting because pharmacologically, diltiazem should actually have more peripheral effect than Verapamil (Verapamil is supposed to be more cardioselective. Dilt can be used for BP but has more cardiac effects than the dihydropyridines). Yet the study did not really pan this possibility out.
My take: Ca is a safe drug to administer, and as Weingart said on his blog, it has some good inotropic/pressor activity in its own, so why not try it? Optimizing electrolytes in irritable hearts is a goal anyway. Try lower doses of dilt, and repeat. Weingart has a link to a slow infusion he sets up in the above post. I haven’t tried this, but same principle: lower and slower to slowly control HR and not tank BP. I have also used digoxin loading in a few patients (0.25 mg initial dose). Digoxin decreases chronotropy, and this does take up to 6 hours, but it also causes vasoconstriction and increased isotropy. Reliable pharmacists have told me this can be within the first hour, and anecdotally I can say I’ve seen the patients who failed low slow dilt and needed digoxin did get better within the first hour. Not fully better, but any better is good in this population.
In a related post, check out my previous post of diltiazem versus metoprolol in rate control for rapid a fib. Hope this helps, and we’ll be answering more of the left out questions as time goes on.
Diltiazem or metoprolol?
I remember this coming up frequently during my residency, and the answer widely varied based on which attending I was working with. It came up the other day as well during a shift.
One of the questions I get asked frequently is if you should avoid diltiazem if a patient is on beta blockers at home, and vice versa. From what I have seen, there is no evidence to support this case. Obviously, these are both AV nodal blocking agents, and the concern would be for complete AV nodal blockade. However, if they come in in rapid ventricular response, clearly their metoprolol is not cutting it. So I have not found any evidence that you have to match the IV med to their home meds. Use what you are comfortable with.
So if that doesn’t have any impact on your choice, is one better than the other at rate control? An article in the Emergency Medicine Journal in 2005 showed that both were safe and effective at rate control for rapid a fib. Diltiazem, however, did achieve rate control faster, and had a higher percentage decrease in ventricular rate (1). From my standpoint, diltiazem has the advantage here, although you can make the argument that the diltiazem had about a 20 minute advantage, which is of questionable clinical significance.
There are two specific cases where I would say beta blockade has the definite leg up, and this is patients in whom acute coronary syndrome is suspected, or in the treatment of a fib related to thyrotoxicosis. For thyrotoxic patients, consider an esmolol drip. Stay AWAY from beta blockers in your COPD patients as it can cause bronchospasm.
This does not really scratch the surface for a fib, as there is still the topic of cardioversion, instability, digoxin’s role, and the topic of who to anti coagulate. More to come in future posts and a planned a fib podcast.
1. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Demircan C, et al. Emerg Med J 2005; 22: 411-414.
2. Acute Management of Atrial fibrillation. Khoo CW, Lip GYH. Chest 2009; 135(3): 849-859.
