Hypertension and Stroke

In this minicast, The Weingart Strikes Back!

Scott Weingart has some issues with our last episode on managing blood pressure in acute ischemic stroke. But the Swami doesn’t take it lying down and has a few things of his own to say.


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Comments

  1. Pik Mukherji

    Awesome podcast, nice work all. First off thanks to all 3 of you guys for the great resources.

    But you’re all crazy. I will try to be succint instead of ranty but:

    1. “Aggressive treatment” has to do with the # of IV pushes? Drips are more “aggressive?” Who makes this stuff up? Who are these consensus experts? (no really, educate me, maybe there’s lit I just have neglected)

    We need to make the pressure low enough that folks don’t bleed to death in their heads when tpa is dosed. However, there is clear danger to lowering them too much. Ie., too “aggressively.” Lower than 180/100 is the rule if tpa is given. However, too low is no good. Don’t be too aggressive.

    So are you telling me Swami, that if you give Labetalol 10mg x 2 and it fails, anything more is too aggressive? Doses and timing don’t matter? That a drip that can be titrated to exactly the pressure you want and backed off of if the pts. mental status worsens is a BAD thing?

    2. Dr. Weingart is probably better read than most humans on the planet. And I agree with his pro-nicardipine comments. But I can’t follow the decision-making here. If you believe that tpa will harm your pt., feel free to put your body between the tpa and the pt. If you believe that tpa is a controversial call in the 88 year old 4 hours out pt., make this view known and discuss with the Neuro attending and pt.

    But if you think that tpa is controversial and may help some of these stroke pts., and the neuro team in your institution is planning to give it, then I COMPLETELY agree that the worst thing you’d want to do is give them an increased risk of, you know, bleeding to death. Push dosing labetalol just can’t be as controlled as a drip of nicardipine.

    So why does Dr. Weingart claim that it’s ok with him to do 2 pushes hoping that they won’t work as a passive aggressive anti-tpa statement? Because when it works and the tpa is pushed, you just gave your pt. a raw deal. Dude, not ok. Stick with nicardipine or clevidipine if that’s your shop’s agent.

    3. It sucks when you say that something never or always happens. It’s always wrong on the inservice exam. So you know someone’s going to dig up the one case report when you do it. Now Dr. Weingart wanted to endorse nicardipine as a GREAT drug when you’re worried about bradycardia. And he’s right- so you should reach for this stuff when the heart rate is on the low side, not run away from it because you think it will happen.

    Why does this happen? Well Brian Hayes is far better suited than me to answer, but I’ll take a stab at it: Same reason as hydralazine. Well known to be more peripherally acting, much more common to see a reflex tachycardia, but in rapid and high doses has been shown to have a paradoxical bradycardic action, especially when the arterial baroreceptors aren’t functioning, allowing an overpowering vagal response. First time I saw hydralazine cause a HR of 40 I was shocked, then did the lit review and wasn’t too shocked anymore.

    And THAT’s a rant, Scott.

    -pik

    1. Rob Orman

      Hi Pik,
      Here is Scott’s response….

      Pik,

      Agree with all of your comments except for you thinking I advocated giving labetalol at all. I thought I was pretty clear: we don’t use labetalol ever for these pts. If you want to go with Swami and use it as a way to avoid giving tPA, I mentioned that I think that puts you at medicolegal risk if the rest of your house is using nicardipine. My personal practice is nicardipine for any neurocrit care pt who needs an antihypertensive. I think the classification of agents as aggressive is not one I would use. I could give enough labetalol by push to be extremely aggressive. To Swami’s credit, the original studies used piddling doses of anti-hypertensives and then would call pts outside eligibility if they did not work. We don’t have great studies to say whether it is the control of the BP or the propensity for high BP that makes pts more at risk to bleed. So he has a point, just not one I agree with.

      Not sure what raw deal you refer to above. If you gave your pt labetalol and it worked to make the pt tPA eligible I said you should then definitively put the pt on nicardipine. You may be confusing the Swami statements with mine.

    2. Rob Orman

      Here’s the Swami’s response…

      Pik -- great points. I think you touch on the controversy created by the vague language of NINDS. I have no idea what they meant by “aggressive” treatment of blood pressure. As far as I can tell, there aren’t a lot of specifics in the paper. Is a drip more aggressive than push doses? I’m not sure. I think it’s always seemed more aggressive because we push diltiazem and labetalol all the time to control atrial fibrillation but a drip seems to be a step further.

      It’s clear that patients with higher blood pressure are at increased risk of intracranial hemorrhage. It’s also clear that lowering them too much will hypoperfuse the penumbra and that’s also bad. So where is the sweet spot and how do we get there? After listening to Scott, I would consider giving nicardipine in bolus dose followed by a drip if the bolus doses got them under 185/100 instead of using labetalol. Even with this intervention, each of us has to decide how aggressive we are willing to be. If you do the bolus, how many doses before you call it? If you start a drip, how high are you willing to titrate the drip? NINDS gives us no guidance on these points. We have to assume that at some point, being too aggressive with blood pressure management (i.e. multiple bolus doses or a high drip to get to 180/100) will harm the patient and each of us has to decide where that line is.

      Since I believe that we don’t know which patients should get tPA, I am easily persuaded that it’s the wrong drug when patients have relative contraindications. If they come in with a sky high blood pressure and we get it down with an anxiolytic (if indicated) and a push of labetalol, I start them on a labetalol drip. Why? Because it worked for that patient. Then they get the tPA as per the neuro team. I’ve done this before and haven’t seen any problem with it but we’re talking about a small n (around 10 or so).

      Lastly, this might not have been clear but I agree with Pik as far as getting between the patient and tPA if I think it’s the wrong drug for them. I’ve done this on many cases and made it clear that I didn’t think the patient was a tPA candidate based on multiple relative contraindications or other factors. Unfortunately, being in a stroke center, the patient tends to be more apt to listen to the junior resident who has the word “neurologist” in their title as opposed to the more seasoned EP. If I think the patient is getting a one-sided version of the story during consent, I make it clear that the drug has a downside and that we don’t know if they’ll get better or get worse. I make it clear to the neuro team that I think tPA is the wrong drug. Then, it’s up to the patient.

      Thanks again for the rant. I have to say that I though this question would be less controversial than the others (the 4.5 hour window, age cutoffs for tPA and improving symptoms) but it’s welcome nonetheless. I hope we keep the controversy going on this topic and others.

  2. Manrique Umaña

    Hi Rob. As always, great podcast! First time in your blog since I get all of your podcasts downloaded directly to my iphone and hear them when going to work and back.
    It’s always interesting to me when you have on your show multiple guests as you can get different views on the subject being addressed.
    This time, as I was listening to the discussion on whether nicardipine or labetalol is a better choice for treating very high blood pressure in the setting of the acute ischemic stroke patient who is being considered for thombolytic therapy, I was thinking to myself: you lucky guys!
    Why is that? Easy. For many of us working in developing counties, we still have to deal in that same clinical scenario with treating this patients with sodium nitroprusside.
    We all know it’s a crappy drug but it also is the only titratable intravenous antihypertensive medication many of us have available for treating the hypertensive emergencies we see.
    For many of us, the debate is whether NTP or hydralazine is the least poor choice for the treatment of these patients. And if the patient also has renal insuficiency, the choice is a very easy one.
    I’m pretty sure many of your listeners worldwide would appreciate that from time to time there’s a mention on the show about the opinion of the expert on what to do when you have to make a diagnostic or treatment choice in places with less than ideal conditions.
    Again, keep up the good work podcasting! Love the show!
    Regards, Manrique.

  3. rabbott47

    The discussion focuses on efficacy and titratability -- as if the titratable issue was related primarily to the efficacy of reaching the goal pressure> But, there are 2 subsets of the titratable issue that weren’t touched on: overshoot and duration.

    Using labetolol, I have (even using a low dose -- 10 mg) attained pressures far in excess of my goal (i.e. 110 rather than 140 in ICH).

    And, in the second issue, sometimes even the goal BP turns out to be counterproductive -- i.e. the flow dependent ischemic stroke who has a full-on hemispheric stroke syndrome when, using nicardipine, I achieve my goal SBP of 180, but has minimal symptoms when I turn off the nicardipine and in 5 minutes am back up to 195. Being able to get back to 195 within 5 minutes by turning off the nicardipine (as was the case) rather than in 3-4 hours, a potential with labetolol (wouldn’t it make a cool M&M to discuss using phenylephrine to bring the BP back up after labetolol? -- bet Scotty has done something like that sometime in his career, eh?), just seems preferable. After the brief dip, even though with profound neuro deficits, the DWI the following day just showed a few small patches (“just a few small patches” in describing a patient sounds good. But, if describing my own MRI, would sound awful.) of watershed infarction -- I wonder if the MRI would have been so benign if we had achieved the same goal BP with the same profound neuro deficits, but with a longer duration using labetolol -- and if the clinical neuro outcome would have been as good? Just wondering. Don’t want to do the trial to find out.

    BTW, I bet that there are few folks out there old enough to remember the olden days of diazoxide -- blast in 300 mg, and no matter what the starting pressure, within milliseconds you were at 110-120 and stayed there for hours or days. Pretty cool drug for teaching interns (like me) to recognize a variety of different watershed stroke syndromes.

Awesome article, I know - please share your erudite thoughts...