To continue on the ranty but too lengthy exposition of IV blood pressure lowering… Where else does hypertensive emergency get invoked, in my opinion, inappropriately?
Let’s continue and go through our top 4 sources of end organ damage so we can see what therapies are indicated:
Heart!
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, this emedicine review: http://emedicine.medscape.com/article/1952052-overview#a30, 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.
Brain!
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 a hypertensive patient’s 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 ischemic CVA, 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 –http://stroke.ahajournals.org/content/early/2013/01/31/STR.0b013e318284056a.full – 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. IMO, we are leaning towards treatment but the prescription of INTERACT2, that BP should be normalized, is premature.)
Eye!
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.
Kidney!
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’ nothin, 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.”
Pik
P. Mukherji
@ercowboy
*But if you want to go there, a pithy anti-tPA summation exists at LITFL, here: http://lifeinthefastlane.com/using-clot-busting-drugs-to-treat-acute-strokes/
** Especially if 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.
*** From Opthalmology, by Myron Yanoff and Jay S. Duker. In my head, they’re the Rosen and Tintinalli of eye stuff.
****Simpsons quote. This is for all you residents who have never seen the Simpsons, Princess Bride or heard of SNL. I’m Gumby, dammit.
Other references:
Stewart IMG. Headache and hypertension. Aust N Z J Med. 1976;6:492-497. for an interesting insight on the role of suggestion biasing this association,
http://www.acep.org/Education/Continuing-Medical-Education-(CME)/Focus-On/Focus-On–Hypertensive-Emergency/ which I’ve quoted from here, and
Martin JN, Thigpen BD, Moore RC, et al. Stroke and Severe Pre-Eclampsia and Eclampsia: a Paradigm Shift Focusing on Systolic Blood Pressure. Obstetrics Gynecology. 2005; 105:237-238, which gives a decent guideline of goal SBP <160, which I was previously unaware of
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