Hypertension with acute stroke : what to do?
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This document discusses guidelines for treating hypertension in patients presenting with acute stroke. It recommends the following: 1) For patients within 72 hours of an acute ischemic stroke, extremely high blood pressure (systolic >220 mmHg, diastolic >120 mmHg) should be lowered gradually by 15-25% over 24 hours to avoid exacerbating ischemia. 2) After the acute phase, blood pressure should be reduced in all stroke and TIA patients, targeting levels under 140/90 mmHg, preferably using an ACE inhibitor or diuretic. 3) Gentle lowering of blood pressure appears to be well tolerated in many acute stroke patients, though more data is still needed on safe levels during the
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Hypertension with acute stroke : what to do?
- 1. Hypertension with acute stroke: when to treat and when not? BY Ashraf Reda, MD,FESC Prof and head of card. Dep., Menofiya University President of WGLVA Chairman of EGYBAC
- 2. VIII. Treatment of Hypertension in Association With Stroke Acute Stroke: Onset to 72 Hours Acute ischemic Stroke Treat extreme BP elevation (systolic > 220 mmHg, diastolic > 120 mmHg) by 15-25% over the first 24 hour with gradual reduction after. •If eligible for thrombolytic therapy treat very high BP (>185/110 mmHg) Avoid excessive lowering of BP which can exacerbate ischemia
- 3. VIII. Treatment of Hypertension in Association With Stroke Acute Stroke: Onset to 72 Hours Strongly consider blood pressure reduction in all patients after the acute phase of stroke or TIA . Stroke TIA Target BP < 140/90 mmHg An ACEI / diuretic combination is preferred Combinations of an ACEI with an ARB are not recommended
- 4. Is it harmful to lower BP in acute stroke? • Yes----No---we really don’t know • --you can easily reduce the BP in the acute stroke and change simple hemiparesis into established hemiplegia • Clearly, lowering blood pressure too low is harmful, but the question is, how low can you go before it is harmful?
- 5. No enough data to answer all questions
- 6. Impaired autoregulation • Most patients have RF and already impaired auto regulation • Reduction of bl flow to the affected areae occurs whether it is acute Hgic or ischemic stroke ---how? • So perfusion and flow is mainly dependent on MBP
- 8. However there is always the other side of the coin
- 9. Rationale for treating HTN in AIS • Not all patients have defective autoregulation • Penumbra (peri-infarction tissue at risk) is not present in all cases • Clinical data suggest that many pt tolerate gentle BP lowering • natural history studies demonstrate no deleterious effect in the vast majority of patients when the BP falls spontaneously.
- 10. The GAIN study
- 11. Spontaneous BP fall without deleterious effects
- 16. SO…….. • high blood pressure may be deleterious in some stroke patients, particularly those receiving lytic agents • gentle lowering of BP appears to be well tolerated in many patients • the real issue is what is going on in that first 3 to 6 hours when the tissue is hemodynamically unstable, and that is where we need more data
- 17. Let us complicate the subject! With a 2-mm Hg elevation in the mean pressure, you get these rather dramatic increase s in MCA velocities in cerebral perfusion because it is passively dependent on blood pressure.
- 18. The main target is to resume the flow in the ischemic areas withinn3-6 hours And the big Q is what to do with BP in this early hours
- 19. So……….. • Not all acute ischemic stroke share the same brain hemodynamics • T-PA treated need some BP control • Without T-PA some patient need a relatively high BP especially in the first 3-6 hours ( significant stenosis in a big artery, multiple occlusions) • Splitting patents and tailoring therapy • Brain tissue perfusion monitoring studies are needed
- 20. Autoregulation maintains cerebral blood flow relatively constant between 50 and 150 mm Hg mean arterial pressure. Ruland S , and Aiyagari V Hypertension 2007;49:977-978 Copyright © American Heart Association
- 21. BP lowering agents in acute stroke • ACEI is theoretically the best in normalising autoregulation • Labetalol followed by Nicardipine are widely accepted and used whenever drud therapy is needed • Nitrates could be used occasionally especially with CAD but may increase ICP • IV enalapril • Na nitroprusside is rarely used (BP >240) • Shift to oral within 24-48 hrs
- 22. BP targets in AIS • Previously HTN: up to180/100 • Previously normotensive: 160-180/90-100 • Not t-PA illegible: – Up to 220/120 just observe except: • • • • Aortic dissection Acute pulmonary edema AMI Hypert.encephalopathy
Editor's Notes
- There are a few data on this topic, but vanishingly little. In fact, the Cochrane analysis, when looking at blood pressure in acute stroke, said that there were not enough data to do an analysis. That was their conclusion. Here are some of the data that suggest lowering blood pressure is harmful in acute stroke. In the tissue plasminogen activator (t-PA) arm of the National Institute of Neurological Disorders and Stroke (NINDS) t-PA trial, patients who received blood pressure medication had a worse outcome. They couldn't say that was directly related to the blood pressure because there weren't enough patients. It was an observation. In the International Stroke Trial (IST), early death increased about 18% for every 10-mm Hg drop in systolic blood pressure below 150, and it was one of the first studies to report a U-shaped curve. This U-shaped curve has also been noted in the GAIN (Glycine Antagonist [Gavestinel] in Neuroprotection) study and other studies, so lowering blood pressuretoo low is bad, and raising it too high is bad. The truth is somewhere in the middle, it seemsHere is a study that suggests a 2-fold increased risk of poor outcome for every 10% decrease in systolic blood pressure in the first 24 hours. To sum this up, here is another study, "Should hypertension be treated after acute stroke?" It was published in the Archives of Neurology. Notice the year -- 1993. I am quoting studies that are almost 15 years old now. It concluded that decreasing mean blood pressure >16% below baseline impairs cerebral perfusion, regardless of the drug used
- That gives you an idea that lowering the BP more than 10% to 20% might not be a good idea. Now, what is the problem? The problem is, as we've already heard mentioned in the first presentations, that brain autoregulation is impaired. First of all, it is impaired because these patients have risk factors -- diabetes, hypertension -- so in most of these people, the autoregulatory curve is shifted to the right already. Then, ischemia further impairs cerebral autoregulation within the area of infarct, so when most acute stroke patients come in, they are over here on their autoregulatory curve, and slight drops in the mean arterial pressure can result in profound drops in brain perfusion. The problem is that this is all theory, because we have no practical way right now to measure autoregulatory curves in acute stroke
- This was the GAIN study that Dr. Furlan referred to, in 2003. They enrolled more than 1400 patients with acute ischemic stroke. The blood pressure treatment was at the discretion of the principal investigator, and then they looked at outcomes.
- What they found was that the blood pressure fell on its own without any obvious deleterious effect in most patients. These are the mean systolic and diastolic curves, and this is hours after stroke onset, so during the first few hours, the BP fell fairly dramatically and all of these patients did fine.
- What about blood pressure and outcome in the TOAST (Trial of ORG 10172 in Acute Stroke Treatment) study? This was published in 2006. This was Harold Adams's study of heparinoid. They looked at more than 1200 patients and looked at their BP over the first 7 days. They found that the average MAP correlated with good outcome, as judged by a Glasgow Outcome Scale score of 1 or 2 at 90 days. Here you can see that the lower MAP equaled a better outcome. The odds of having a good outcome decreased by 11% to 16% for every 10-mm Hg increase in the MAP, which translates to saying that the lower the blood pressure, the better the patients did in the TOAST study. So now we have 2 studies indicating that lower blood pressures are better
- this is a slide that he kindly provided to me about the Cleveland Health Quality Choice. Among t-PA protocol violators, high blood pressure was a very common reason for protocol violation, with a rate of almost 13%.What was interesting in that study and in this study, from the Connecticut Community Hospitals, is that blood pressure not monitored per recommendations was very common. It was seen in 79% of patients, and in those patients in whom BP was not monitored, ie, it was too high and not treated properly, the rate of intracranial hemorrhage was an astounding 15% to 16%. Again, high blood pressure was associated with more complications in patients who received t-PA
- We also have good data from the ACCESS (Acute Candesartan Cilexetil Therapy in Stroke Survivors) trial. This was published in Stroke in 2003. This was a study of acute candesartan treatment in patients with acute ischemic stroke, one of the best prospective, randomized trials of acute intervention with a blood pressure-lowering agent. They randomized 342 patients and treated with a modest dose of candesartan, 4-16 mg/day, for hypertension. The trial was actually stopped early because of overwhelming efficacy in the group that got candesartan vs placebo
- As you see from these graphs, whether you look at the candesartan group or the placebo group, over the first few days BP fell either spontaneously or with candesartan, but fell by similar degrees. Again, the group that received candesartan did much better over the long run
- Let's talk a little bit about hemodynamic manipulation in acute stroke, raising the blood pressure to help patients with acute stroke. There are actually some data on this; for example, there are animal data in a rabbit infarct model that if you raise the BP within the first hour -- again, very early -- it reduces infarct volume. And then there are some clinical data from 2002 on the effects of induced hypertension on intracranial pressure and flow velocities in the middle cerebral artery (MCA). In this study, by Schwarz, they raised the mean pressure only 2 mm Hg, and it increased MCA velocity by 25 cm/second without increasing ICP. Unfortunately, this was a technical study without any clinical correlate. Did it matter? We can't say from this study. I am just showing you the literature
- This is the kind of patient in whom we might be thinking about perfusion therapy. They've got large-vessel multiple occlusions, they've got an infarct, and they are not getting enough blood to their brain. The name of the game in the first 6 hours is to get more blood to the brain. Of course, we use thrombolytic agents to do that, but there may be other ways we can manipulate the BP if we have a way to measure the effect of our mean pressure manipulations on cerebral perfusion. That is what we need, and again, we need studies in those 3- to 6-hour patients. With new imaging like CT perfusion with the mobile CT scanner, you can do these things as many times as you want, right in the neuro-ICU. Now the technology may be there to start to study some of these things, and we're moving into what I call the physiological era of stroke management. No more using just NIH Stroke Scales, but tissue perfusion monitoring and, I think, blood pressure.