In this episode on Hypertensive Emergencies, Dr. Joel Yaphe, EM residency program director at the University of Toronto & Dr. Clare Atzema, one of Canada’s leading cardiovascular EM researchers will discuss the controversies of how to manage patients who present to the ED with high blood pressure and evidence of end organ damage related to the high blood pressure. Hypertensive emergencies are a grab bag of diagnoses that all need to be treated differently. Hypertensive Encephalopathy, Aortic Dissection, Acute Pulmonary Edema, Pre-eclampsia & Eclampsia, Acute Renal Failure, Subarachnoid Hemorrhage and Intracranial Hemorrhage all need individualized blood pressure management.
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Definition of Hypertensive Emergency
When seeing a patient with high BP, our experts recommend the following questions be used to differentiate true hypertensive emergencies from less urgent presentations:
- is there acute end-organ dysfunction and/or damage?
- is the dysfunction attributable to the elevated blood pressure (or will the elevated BP likely to make the dysfunction worse)?
- is altering the BP necessary to improve the organ dysfunction?
If the answer is “Yes”, this may be a hypertensive emergency. If not, these patients with high BP can be treated on an individualized basis, less aggressively.
The two categories of hypertensive emergencies
- Microvascular disorders (e.g. encephalopathy, pre-eclampsia/eclampsia), which are characterized by small vessel dysregulation, with endothelial damage and local inflammation
- “Macro” vascular disorders (i.e. CHF, aortic dissection, stroke, subarachnoid hemorrhage)
How does Hypertensive Encephalopathy present?
Suspect hypertensive encephalopathy when the patient has severe hypertension (usually >180/110), severe headache +/- vomiting.
Symptoms progress to confusion and altered mental status.
Retinopathy may be present, and seizures can occur.
The diagnosis is confirmed by normal CT plus cerebral function improvement with a decrease in the blood pressure.
The treatment goal is diastolic BP between 100-105 within 2-6 hours. Don’t lower the BP more than 20% in the first hour!
TREATING THE ELEVATED BLOOD PRESSURE
General principles for lowering BP rapidly in the ED
- Blood pressure should almost never be rapidly lowered (except in aortic dissection).
- Lower pressure by no more than 25%, to avoid ischemia in organs auto-regulated to higher BP.
- Therapies that correct the cause (e.g. phentolamine if the BP is elevated by catecholamines) will be most effective.
- Monitor the symptoms to determine whether the BP has been adequately lowered.
IV Drug choices for Hypertensive Emergencies
There are 3 major categories:
1. B-blockers: Labetolol is useful for most hypertensive emergencies. Give a 20mg slow IV push, then double the dose q10 min, up to 300mg. Be cautious in patients with asthma or COPD, and hepatic failure. Esmolol has quicker onset/offset, and may be safer in patients with mildly reactive airways.
2. Vasodilators: Nitroglycerin is great for ACS and pulmonary edema, but arterio-dilates only at high doses. Therefore for CHF patients, use higher doses to produce afterload reduction. Nitroprusside dilates both arteries and veins, but generates cyanide w prolonged use of high doses as it breaks down. Starting dose is 0.3–0.5mcg/min, and max dose is 2 mcg/min (less in renal pts). Hydralazine also dilates arteries, but has less predictable effects, and raises HR. Phentolamine (an a1 blocker) arterio-dilates to counteract catecholamines (i.e. cocaine, pheochromocytoma).
3. Calcium channel blockers: Dihydropyridine CCBs lower blood pressure by vasodilation (i.e. amlodipine, nifedipine, and nicardipine in USA). The phenylalkylamine class of CCBs mainly have negative inotropic and negative chronotropic effects (i.e. diltiazem and verapamil)
Subarachnoid Hemorrhage & Intracranial Hemorrhage Blood Pressure Management
Patients with subarachnoid hemorrhage (SAH) and intracranial hemorrhage (ICH) may rebleed if BP is too high, and may stroke if BP drops too rapidly.
Our experts recommend slow BP reduction only if necessary, and diligent correction of other metabolic disturbances (hyperglycemia, acidosis, fever, etc).
Should INTERACT 2 trial change practice for blood pressure management in subarachnoid hemorrhage?
While INTERACT 1 showed lowering BP slows hematoma growth, INTERACT 2 (full pdf) showed no benefit.
INTERACT 2 study suggested blood pressure may be safely reduced to systolic of 140, but no benefit was shown for re-bleeding.
Therefore, our experts suggest using AHA guidelines, (see below) which suggest at target systolic BP of 160.
If you decide to lower the BP, avoid nitroprusside, because it causes a relative decrease in cerebral perfusion pressure, due to a peripheral shunt effect.
Each patient should be approached individually.
Use labetolol or nifedipine, go slowly, and monitor closely.
Patients with ICH are at high risk for ischemia with BP reduction. The AHA guidelines divide patients into 3 groups:
- For SBP >200 or MAP >150 —consider lowering BP by IV infusion under close monitoring
- ICH with suspected raised ICP and high BP — get ICP monitoring first, before lowering BP
- SBP >180 or MAP >130 but no suspicion of high ICP — consider a slower, more modest BP reduction using IV medications
Does the choice of antihypertensive drug affect mortality and morbidity?
According to a Cochrane review of 15 RCTs (869 pts), there was no evidence that any class of IV antihypertensive drugs reduces mortality/morbidity, and no superiority was found among drug classes.
The CLUE trial has since shown advantages of nicardipine (less hypotension, bradycardia and AV blocking were observed) over labetolol for treatment of acute hypertension with end organ damage.
Drug of choice for hypertensive encephalopathy, aortic dissection & eclampsia?
Dr. Yaphe recommended labetolol for most situations (see above for dose).
Our experts recommend using the drug you are most familiar with, if the clinical context is appropriate.
How to manage patients with high BP and impaired renal function
If creatinine is high, check urine for proteinuria or active sediment, and the CBC and retinas for other indications of acute renal failure.
It may be impossible to tell if renal failure is acute if no recent bloodwork is available.
For these patients, our experts recommend very close followup with an internist, or hospital admission for further workup.
Use caution and an individualized approach.
Management of Elevated Blood Pressure in Congestive Heart Failure (CHF)
Start with high doses of nitroglycerine (see above for explanation) to achieve arterial dilatation.
Give up to 6 sublingual doses while IV drip is being prepared.
Non-invasive positive pressure (NIPPV) ventilation is also key to managing the pulmonary edema. see Episode 4 on Acute Congestive Heart Failure
Tips for a true Hypertensive Emergency – Aortic Dissection
BP can be very high, so verify and monitor by an arterial line in the right radial artery.
If target HR of 60 and systolic BP of
Use diltiazem if a B-blocker cannot be used.
Pearl: if aortic root is involved (check for a new murmur!) avoid B-blockers, as tamponade may be imminent.
*note nicardipine is an option in aortic dissection, however it is not available in Canada
Blood Pressure Management in Eclamplia & Pre-eclampsia
Pre-eclampsia is BP >160 /110, along with proteinuria (or low platelets, elevated LFT or Cr) or pulmonary, liver, cerebral or visual symptoms, in a patient >20 weeks pregnant.
Eclampsia is the same, but with seizures.
Labetolol is best for BP reduction along with Mg+, although hydralazine (5mg IV slow push over 1-2 minutes, repeat 5-10mg prn) can be used as a second line (*note that hydralazine has an unpredictable effect on blood pressure and should not be used as a first line medication)
Give 2g/hr IV Mg+ for seizure prophylaxis.
Goal is still only 25% BP reduction, and consult OB as delivery is the definitive Rx!
Now Test Your Knowledge
To learn more about hypertension on EM Cases:
Episode 40: Asymptomatic Hypertension
Rapid Reviews Video – Asymptomatic Hypertension
Dr. Helman, Dr. Yaphe and Dr. Atzema have no conflicts of interest to declare.
Hiratzka LF et al. Circulation 2010; 121:1544. www.ncbi.nlm.nih.gov/pubmed/20233780
Peacock WF et al. Crit Care 2011;15:R157. www.ncbi.nlm.nih.gov/pubmed/?term=Peacock+WF+et+…
Perez MI and Musini VM. Cochrane Database Syst Rev. 2008;CD003653. www.ncbi.nlm.nih.gov/pubmed/18254026
Anderson CS et al. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage. NEJM 2013;368:2355. full pdf
Connolly ES Jr et al. Stroke. 2012;43:1711. www.ncbi.nlm.nih.gov/pubmed/?term=Connolly+ES+Jr…
Hi, thanks for this excellent podcast !!
Regarding this statement ” if aortic root is involved (check for a new murmur!) avoid B-blockers, as tamponade may be imminent”, can you explain more ? Did you mean diltiazem should be fine ? Could you give me any reference to support the statement?
Thanks, you guys are doing a great job
Great question! Should have clarified. With aortic root involvement, pericardial tamponade may be imminent as the dissection progresses. The use of B-blockers in this setting would be dangerous as tamponade will drop the BP and the added insult of B-blockers may result in a ‘clean kill’. It’s a ‘Catch 22’: while we would like to prevent further dissection by using B-blockers, if the patient progresses to pericardial tamponade, we don’t want B-blockers on board. No reference for this.
When dealing with the SAH and ICH hypertensive patients and considering blood pressure reduction, is there any reason to not go with esmolol over labetalol? You mentioned it previously as being good for its rapid offset of action when ceased, just strikes me as an ideal situation in case of accidentally reducing BP too far and causing a decrease in cerebral perfusion pressure.
Thanks heaps for all your work,
Thanks for you comment. I think Esmolol would be perfectly reasonable in the setting you describe and agree that an immediate ‘off’ effect with cessation would be a valuable feature. In Canada, most ED docs are familiar with Labetolol, it’s titration etc. and so this is why it was recommended in the podcast. Many Canadian EDs do not carry Esmolol (although they should!)
Great talk as usual! Here in the US pre-eclampsia BP threshold is 140/90. Does that differ in Canada??
Thanks for your question Ankush. The Canadian 2014 guidelines on Diagnosis, Evaluation, and Management
of the Hypertensive Disorders of Pregnancy define hypertension in pregnancy as “Hypertension in pregnancy should be defined as an systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg, based on the average of at least 2 measurements, taken at least 15 minutes apart, using the same arm. (II-2B).” For patients with BP < 160/110 without comorbid conditions "antihypertensive drug therapy may be used to keep systolic blood pressure at 130 to 155 mmHg and diastolic blood pressure at 80–105 mmHg. (I-B)" For patients with comorbid conditions "For women with comorbid conditions,antihypertensive drug therapy should be used to keep systolic blood pressure at < 140 mmHg and diastolic blood pressure at < 90 mmHg. (III-C)." Here's the link to the guideilines: http://sogc.org/wp-content/uploads/2014/05/gui307CPG1405E1.pdf
I was wondering why in the section of IV Drug choices for Hypertensive Emergencies you referred to nicardipine in USA for the Calcium channel blockers ?
Is this something that should be considered with special access ? What are the advantages of this products vs other options ?
would like to hear everyone’s thoughts on troponin elevation as a marker of end organ damage. If the pt has markedly elevated bp would that alone constitute evidence of end organ damage making it a hypertensive emergency ?
Great talk! Agree with everything totally. Thanks for the awesome work.
however, i wish to have an episode about treatment of HIGH blood pressure in office base..
i had a patient with readings were creeping up to 200/110 over a period of 1 month, i tried few options on office base until he reached one day with a reading of 210/80 with no symptoms at all..
i opt to admit him, his CTS head , as well as urine and kidney function showed no deterioration over all the month…
currently hes on labetalol-hydraazine-and carder and still showing readings of 160s/80s
ive referred him back to nephrologist..
his adrenal CT also was N, as well as echo.
With normal work-up for secondary causes of hypertension I’d consider alcohol dependence as a cause.
I believe that a portion of your post could be misleading for some readers.
INTERACT1 and 2 did not look at SAHs (they studied intraparenchymal hemorrhage) so I would change the phrasing “Should INTERACT 2 trial change practice for blood pressure management in subarachnoid hemorrhage?” for “Should INTERACT 2 trial change practice for blood pressure management in intracerebral hemorrhage?”
Also, the target BP of 160 is indeed for SAH according to guidelines, but I find it confusing in your post since it follows 2 sentences on ICH… For ICH, guidelines state it’s probable safe to go as low as 140 of SBP, as you mention somewhere else in the text.