Hypertensive Emergencies

Ok, in the context of the thread it implied that was the protocol for hypertension, which seemed odd. Still, I don't think IV BBs are really indicated in STEMI there either but to each their own.
 
β-Blockers

Indications (Apply to all β-blockers)
  • Administration to all patients with suspected myocardial infarction and unstable angina in the absense of contraindication. These are effective antianginal agents and can reduce incidence of VF.
  • Useful as an adjunctive agent with fibrinolytic therapy. May reduce nonfatal reinfarction and recurrent ischemia.
  • To convert to normal sinus rhythm or to slow ventricular response (or both) in supraventricular tachyarrhythmias (reentry SVT, atrial fibrillation, or atrial flutter). β-Blockers are second-line agents after adenosine.
  • To reduce myocardial ischemia and damage in AMI patients with elevated heart rate, blood pressure, or both.
  • Labetolol recommended for emergency antihyptertensive therapy for hemorrhagic and acute ischemic stroke.

Precautions/Contraindications (Apply to all β-blockers unless noted)
  • Early aggressive β-blockade may be hazardous in hemodynamically unstable patients.
  • Do not give to patients with STEMI if any of the following are presents:
    - Signs of heart failure.
    - Low cardiac output.
    - Increased risk for cardiogenic shock.
  • Relative conraindication includes PR interval >0.24 second, second- or third-degree heart block, active asthma, reactive airway disease, severe bradycardia, SBP <100 mm Hg.
  • Concurrent IV administration with IV calcium channel blocking agents like verapamil or diltiazem can cause severe hypotension and bradycardia/heart block.
  • Monitor cardiac and pulmonary status during administration.
  • Propanolol is contraindicated and other β-blockers relatively contraindicated in cocaine-induced ACS.
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Hazinski, M., Samson, R. and Schexnayder, S. 2010. 2010 handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: American Heart Association.

Wouldn't the same rationale apply to administering a class II/beta blocker as administering nitroglycerin to patients experiencing a myocardial infarction?

By the way, it mentions both labetolol for intracranial hemorrhage or ischemia, and beta blockers for STEMI with tachycardia and hypertension.

I think most of us were thinking that this isn't isolated hypertension. I personally was thinking about intracranial hemorrhage, ischemia, edema, etc.
 
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Merck said:
Still, I don't think IV BBs are really indicated in STEMI there either but to each their own.
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In the setting of STEMI and lacking any contraindications, oral BB's are an AHA class I recommendation and IV BB's are class IIa recommendation.

I know that there have been studies that have called into question the necessity or efficacy of this practice, though.

What I was taught by my medical directors early in my career (and what I think the protocol's intent is) was that BB's should be used as an adjunctive therapy to reduce MV02 if the patient remained tachycardic after NTG and opioid administration.

In actual practice, I don't see BB's used for STEMI that much in the EMS or ED setting; I suspect it's because EMS just doesn't usually get around to it, and the the ED the patient is usually sent to the CL quickly.

When I have seen BB's used, it often seems to be in very small doses as part of a rigid protocol where they give ASA-PLAVIX-NTG-MS-BB in rapid-fire fashion without really giving the opioids time to work (peak affect of MS is like 25 min) or really assessing for the need for BB's.


Class I
  • Definitely recommended. Definitive, excellent evidence provides support.
  • Definition:

    - Class I interventions are always acceptable, unquestionably safe, and definitely useful.
    - Proven in both efficacy and effectiveness.
    - Must be used in the intended manner for proper clinical indications​
  • Required Evidence
    - One or more Level 1 studies are present (with rare exceptions).
    - Study results are consistently positive and compelling.​


    Class IIa and IIb​
  • Acceptable and useful
  • Definition
    - Both Class IIa and IIb interventions are acceptable, safe, and considered efficacious, but true clinical effectiveness is not yet confirmed definitively.
    - Must be used in the intended manner for proper clinical indications.​
  • Required Evidence
    - Available evidence, in general, is positive.
    - Level 1 studies are absent, inconsistent, or lack power.
    - Classes IIa and IIb are distinguished by levels of available evidence and consistency of results.
    - No evidence of harm.​


    Class IIa
  • Acceptable and useful. Very good evidence provides support.
  • Definition
    - Class IIa interventions are acceptable, safe, and useful in clinical practice.
    - Considered interventions of choice.​
  • Required Evidence
    - Generally higher levels of evidence.
    - Results are consistently positive.​
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Thank Halothane, that was my point. We don't use IV beta blockers unless there is some outside indication for it. Of course oral beta blockers are indicated within 24 hours, and usually given sooner.

As to the original metoprolol is not the best choice for a hypertensive emergency.
 
Why hasn't anybody discussed the BGL. Couldn't that level presented be the cause of the HTN?
 
Mickster said:
Why hasn't anybody discussed the BGL. Couldn't that level presented be the cause of the HTN?
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I brought it up earlier.

Aprz said:
Do you guys think that his blood glucose level (BGL) would have anything to do with his hypertension? I kinda doubt that his BGL would be the primary reason that they had hypertension even though it's kinda high. It's just not really that high. Glucose draws fluid from tissues and cells and into the intravascular space where the glucose is at; it's hyperosmolar. That's why it's necrotic when extravasation occurs.
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A BGL of 267 shouldn't make you hyperosmolar enough to have a significant effect on B/P. In otherwise healthy patients the kidneys do a good enough job of controlling water balance to avoid hypertension.
 
I would stay a way from treating hypertension in the field. For one you do not know why the patient is hypertensive to begin with, they could be having a bleed and the pressure is stopping it from bleeding to much. I know that in the most recent NC protocols t doesn't give a treatment for hypertension for the reason of not knowing what the cause is.
 
NCmedic42 said:
I would stay a way from treating hypertension in the field. For one you do not know why the patient is hypertensive to begin with, they could be having a bleed and the pressure is stopping it from bleeding to much. I know that in the most recent NC protocols t doesn't give a treatment for hypertension for the reason of not knowing what the cause is.
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Wait what?

That's not why patients with intracranial bleeds are hypertensive. Hypertension in the presence of increased intracranial pressure is a compensatory mechanism in attempt to provide adequate cerebral perfusion pressure. Not to "stop it from bleeding too much". The body increases blood pressure, particularly systolic blood pressure, to attempt to overcome the increased pressure in the brain in order to deliver oxygenated blood as well as transport waste products out (ie CO2). It's a vicious cycle though the HTN increases ICP as well...

In response to this increase in blood pressure the baroreceptors slow the heart trying to reduce the blood pressure.

Irregular respirations come from direct pressure on the brainstem causing respiratory dysfunction.

Hence Cushing's Triad.

I agree you need to be cautious treating hypertension in the field but that's been discussed pretty well earlier in this thread.
 
Hypertension in the setting of stroke or bleed is a common finding but very nonspecific. It could be chronic hypertension (and may have been a contributing or at least concomitant factor in the stroke), acute hypertension from numerous causes including anxiety about stroke symptoms, or as Rob said the result of Cushing's reflex.

A neuro-interventionalist who our CCT service brings patients who failed tPA would start them on nicardipine if they where hypertensive. I don't know if this was therapeutic for the stroke itself or if lowering BP was necessary before he brought the patient to the cath lab.
 
I was not trying to say that the bleed is the reason they are hypertensive. I was merely trying to point out that with someone who is having a brain bleed and is hypertensive is that the hypertension could be helping out. If you have a bleed or leak and apply pressure to the source it will slow down with enough pressure. So if you give something like nitro and reduce the pressure the bleed could get a lot worse.
 
NCmedic42 said:
I was not trying to say that the bleed is the reason they are hypertensive. I was merely trying to point out that with someone who is having a brain bleed and is hypertensive is that the hypertension could be helping out. If you have a bleed or leak and apply pressure to the source it will slow down with enough pressure. So if you give something like nitro and reduce the pressure the bleed could get a lot worse.
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Picture you have a hose with a small hole in it. The higher you turn up the water pressure, the faster the water leaks out of the hole. The lower you turn down the water pressure, the slower it leaks out the hole. Now, think of the blood vessels in your brain as small hoses. If one of those vessels is leaking, lowering the BP will slow the leak.

However, lowering the BP will also reduce the amount of blood that will be delivered to the brain tissue, which can cause problems even faster than the bleed itself will, because when pressure in the cranium is increased, your brain NEEDS the higher blood pressure in order to get the blood that it needs. That is why we don't try to lower the BP of hypertensive patients who may have a bleed.

You are right that at a certain point, the ICP will have increased enough that it will tamponade the bleeding, and that in a bad bleed, lowering the BP may actually make the bleed even worse. However, your body can increase MAP (and in turn ICP) far, far higher than what it takes to cause fatal brainstem compression, so if the bleed is bad, we can't rely on increasing ICP to tamponade the bleed. In other words, your brain tissue can only be exposed to so much pressure before it becomes fatal, and if it is a bad bleed, the "tamponade pressure" will probably be well above the "fatal pressure".

Bleed + hypertension = very bad. These patients need to have scans done and be seen by a neurosurgeon yesterday. All that can be done in the field is supportive care.

The Brain Trauma Foundation has some good stuff on this, including educational materials and EMS protocols that are evidence-based. Traumatic and non-traumatic bleeds are different, but the general principles surrounding them are the same.
 
NCmedic42 said:
I was not trying to say that the bleed is the reason they are hypertensive. I was merely trying to point out that with someone who is having a brain bleed and is hypertensive is that the hypertension could be helping out. If you have a bleed or leak and apply pressure to the source it will slow down with enough pressure. So if you give something like nitro and reduce the pressure the bleed could get a lot worse.
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Eh, your general concept is correct but not quite now it works from a pathophysiology stand point.

Edit: Halothane nailed it for me
 
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