Saturday, December 14, 2013

HTN emergency: Does it really exist?- An ER physician's perspective

"Level 1 triage coming in to Trauma-B"

Me: "Who's in triage? What are they sending?"

Charge RN: "It's a tachycardic emergency."

Me: "Um, but what is it? What are they here for?"

Charge RN: "I just told you! HR was 146.  EMS gave Lopressor x 2 with no relief."

Me: "..." (head explodes- triaged as a level 3)

Do we HAVE “tachycardic emergencies?” Of course not- it depends what the tachycardia is from, whether it’s physiologic, a primary disorder, a response to stress, pain, fever or hypovolemia, whether it’s sinus or a dysrhythmia, whether it’s causative of other symptoms, in response to those symptoms, or merely coexisting. 

Then WHY do we have hypertensive emergencies?

There have been a number of well reasoned arguments on why hypertensive urgency is a non-entity.  From the time that we stopped using the term "malignant hypertension" we have been moving away from treating a number and bringing therapy back to the symptoms of the patient.  A vague entity like hypertensive urgency is generally indistinguishable from asymptomatic hypertension.

But recently I've had to spend more time discussing hypertensive E-mergency. You'd think I'd be happy about that, wouldn't you?  I mean, Emergency Physician, right? And definitely sicker patients: it's right there in the definition of "end organ damage."  On top of that, it comes with a treatment plan: "25% reduction of MAP within the 1st hour."  Sounds good- ill patients get aggressive care, we save organs, ergo lives, high five and go home.  

Except that the aggressive care of hypertensive emergency may make people worse, not better, and is too often invoked with delusions of benefit.  When I was an intern, there was a tried and true recipe to handle this vital sign when it bothered the nurses.  If the systolic pressure was "too high," the contents of a 25mg nifedipine capsule could be aspirated into a small syringe and delivered sublingually.  The result was a predictable, beautiful lowering of the systolic pressure over the next 30 minutes and at the 1 hour mark we had nearly always achieved the prescribed 25% MAP reduction.  Seen this tried and true method lately?  No, since it was realized that there was a downstream 6% stroke rate. The FDA rejected this use of nifedipine to rapidly lower BP in 1985, but in 1996 it was still a common choice: Today, IV pushes of vasoactive agents for no clinical indication still persist.  I find our collective lack of memory… troubling.  Note the use of the term “pseudoemergency” in the above JAMA abstract and the host of editorial comments that followed.  So what IS hypertensive emergency and what should we do about it then?

Here we go: this one doesn't exist either.  Or rather, it's just as meaningless a definition and entity as urgency.  Try this on for size- Hypertensive emergency isn't a disease.  It is an arbitrary grouping of diseases lumped together so you can remember to treat them similarly.  Oh, except the prescribed treatments are NOT similar and the proposed reduction of MAP should be performed in exactly NONE of those cases.

What, in my book, would be a true hypertensive emergency? Well, it should be a case where the blood pressure is physiologically causing the symptom, and rapid lowering should be associated with pt. benefit.  The first part of that sentence is basically addressing the fact that associating a very elevated blood pressure with a disease and calling it "hypertensive emergency" implies that the pathology is caused BY the blood pressure, as opposed to, "happens to be present." (I came across older articles listing epistaxis as a hypertensive emergency.)

Aortic dissection fits the bill nicely.  Eclampsia can be included as a few end organs including the brain are affected and blood pressure lowering is an indicated therapy.  Acute pulmonary edema (not chronic), when presenting with a very high afterload can be included, and this entity has earned the SCAPE acronym from the venerable Dr. Weingart- Sympathetic Crashing Acute Pulmonary Edema. 

All 3 include rapid BP lowering as part of the treatment. 
None of the 3 uses the same preferred agents. 
None of the 3 has the same target blood pressure goals. 
None of the 3 involve tailoring the MAP to become 25% lower than a previously measured pressure- there are hard targets or clinical targets.

Where else does hypertensive emergency get invoked, in my opinion inappropriately?* 


In association with angina and ACS, the assumption would be that the elevated pressure is causing cardiac ischemia.  Yet our therapy is based primarily on antiplatelet agents and not on goal blood pressure.  Interestingly, thisemedicine review: , lists ACS as an entity in which 20-30% reduction in BP is a clinical goal and states, "Treatment is indicated if the SBP is >160 mm Hg and/or the DBP is >100 mm Hg."  I’d love to hear from anyone who thinks it’s a good idea to push these numbers down in pts. going up to cath.  Scary.


Headache is not end organ damage.  That should end the discussion, but let’s go on.  The causal connection is poorly established, and the presence or absence of headache pain correlates poorly with blood pressures.  Studies on the topic are mixed at best.  I recall reading in my dog-eared copy of Tintinalli that this entity classically presents as occipital headache, but only in the presence of diastolics greater than 130.  Hypertension causing headache, if it actually exists, is thought to be uncommon, occurring less than 15% of the time.  Consider that pain may elevate hypertensive pts. blood pressure.  Yet pts and doctors make this connection commonly, prescribing anti-hypertensives when pain control often does the job quite a bit better and more safely.  For an even more complicating point, consider that when the symptom of HA is concerning for SAH, THEN the lack of HTN would be a low risk factor as per Perry’s 2008 BMJ review.  But a benign symptom remains a benign symptom when a pt. with known HTN has an elevated pressure while they are in pain.  Reglan, please.

Now for actual end organ damage:  In association with CVA and brain hemorrhage, there is clear end organ damage related to chronic HTN.  But is the damage caused by the acutely elevated pressure?  Or is that a reactive phenomenon happening after the infarct?  It’s become clear that rapid reduction of MAP may harm these pts. more than help.  From ACEP's Focus on Hypertensive Emergency: "there is little scientific evidence and no clinically established benefit for rapid lowering of blood pressure among persons with acute ischemic stroke."  The 2013 Stroke Guidelines suggest: "the recommendation not to lower the blood pressure during the initial 24 hours of acute ischemic stroke unless the blood pressure is >220/120 mmHg or there is a concomitant specific medical condition that would benefit from blood pressure lowering remains reasonable."  See that really high number there?  No, that’s not my threshold to start IV meds – it’s a suggestion that your pt. should be lower than that at the end of day 1.  Is your guy still in the ED at that point?  Your therapy can be accessed in a committee meeting on hospital boarding, not in your nurse’s PYXIS.

Check out -, and if you actually look at this, look at the entry: Induced Hypertension for the Management of Acute Ischemic Stroke.   That’s right, we sometimes push the pressure higher in response to an acute CVA.

Ah, but what if it's a hemorrhagic CVA?  Or if they're getting lytic therapy? (No, I'm not going there.**)  Then it's a different story, and we think BP should be addressed and may improve hematoma size, possibly even outcome.  And we will still ignore the 25% rule, instead opting for a hard goal of treatment.  SBP of <185 is suggested for lytics but you can also check out INTERACT, ATACH or INTERACT 2*** for a treatment discussion of hemorrhage.)  


Chronic changes can happen.  No IV meds for you.  Sudden bleeds can happen. That ship has sailed. No IV meds for you.  In the rare setting of “malignant” hypertension (yes, the texts still use that word), with acute vision loss and papilledema, ophthalmology textbooks recommend treatment.  They suggest “blood pressure should be lowered in a slow, deliberate, controlled fashion” to - wait for it – prevent end organ damage.****  No IV meds for you.


Renal failure related to blood pressure is exceedingly common in our practice. It is also rarely an acute entity related to sudden elevation in blood pressure.  I'd wager that when we rattle off the list of the 4 end organs we include kidney reflexively and rarely try to describe what that would look like.  Elevated blood pressure? Of course we see very elevated pressures in patients on multiple medications with suffering kidneys.  But this is a chicken and the egg problem akin to the classic "My HTN is causing my H/A" complaint.  Could this be a hypertensive emergency?  I suppose if:

The Cr. was recently better than the current value;
AND there is protein AND blood in the urine;
AND the BP is persistently and impressively elevated despite my earnest attempts to ignore and repeat it.  ("I've tried doin' nothing, and I'm all out of ideas..."*****)

Even then, I'm likely to go the oral medications route than treat with IV medications aggressively as would be prescribed by the "hypertensive emergency" label.  See the above eye discussion for slow, deliberate and controlled.  Oral meds will be just fine here, thank you.

...aaand we're done.  In no medical circumstance that I have encountered has there been an indication to lower MAP by 25% within an hour with powerful IV medication.  When you reach for those meds, you tend to have a hard target defined by the disease you are treating.  The phrase "hypertensive emergency" should join its equally painful brother, "hypertensive urgency" in that place labelled, "stuff we used to say," along with "female hysteria treated with therapeutic internal massage."

P. Mukherji, MD
ER physician at NSLIJ

*Not included: Possible appropriate uses of the term in entities like hypertensive encephalopathy, PRES syndrome, and  IMO especially aneurysmal SAH.  Gimme a break, it’s a rant, not a reference material.

**But if you want to go there, a pithy anti-tPA summation exists at LITFL, here:

*** Especially if you like not having patient oriented outcomes, or your pt. is a Chinese male and you're giving urapidil. I recommend we look out for ATACH2 where IV nicardipine is used while looking at death and disability outcomes.  I might be able to generalize that one to my patients.

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