Focus On: Hypertensive Emergency

Contributors
Amit Phull, MD and Amer Z. Aldeen, MD. Dr. Phull is a 3rd year Emergency Medicine resident at Northwestern Memorial Hospital of Chicago, Illinois. 

Disclosures
In accordance with the Accreditation Council for Continuing Medical Education (ACCME) Standards and American College of Emergency Physicians policy, all individuals in control of content must disclose to the program audience the existence of significant financial interests in or relationships with manufacturers of commercial products that might have a direct interest in the subject matter.

Dr. Phull and Dr. Aldeen have disclosed that they have no significant relationships with or financial interests in any commercial companies that pertain to this article. 

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"Focus On: Hypertensive Emergency" is approved by the American College of Emergency Physicians for one ACEP Category I credit.

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Introduction
It is estimated that anywhere from 72 to 74 million peoplein the United States aged 20 or older are affected byhypertension.⁽¹⁸⁾ This accounts for approximately 30% ofthe population over 20 years old.⁽¹²⁾ Somewhere between3 and 45% of all adult ED patients will have at least one elevatedblood pressure reading during their ED stay.⁽¹⁷⁾ Given the ubiquitous nature of the predisposing disease,hypertensive emergencies are very commonly encountered by emergencyphysicians. It behooves the emergency physician to be able toreadily identify a true hypertensive emergency, and to know whenand how elevations in blood pressure should be treated in theemergency department.

Defining the Problem - Isthis an Emergency?
In the modern age of pharmaceuticals, with a plethora ofanti-hypertensives available to physicians, the incidence ofhypertensive emergencies has declined from 7% to 1% of patientswith hypertension.⁽¹⁶⁾ Still, this presentation iscommon enough that emergency physicians must be able to readilyidentify true hypertensive emergencies, and know when and how totreat them.

The classification of hypertensionis periodically reviewed by the Joint National Committee (JNC) onPrevention, Detection, Evaluation, and Treatment of High BloodPressure. The most recent guidelines, the JNC 7 report, werereleased in 2003 and are currently being updated - the JNC 8 is setfor release later on this year. 

The JNC 7 Report does not outlinespecific blood pressure values in defining hypertensive emergency.Rather, the term "hypertensive crisis" is generally applied whenone experiences an acute elevation of blood pressure, with asystolic blood pressure > 180, or a diastolic blood pressure> 110.⁽¹⁾ Per the JNC 7, a hypertensive emergency isa hypertensive crisis in which there is evidence of acutetarget-organ damage (e.g. encephalopathy, myocardial infarction,unstable angina, pulmonary edema, stroke, life-threatening arterialbleeding, or aortic dissection). Such cases warrant parenteral drugtherapy and hospitalization, often to an intensive caresetting.⁽⁶⁾

Though falling out of favor, theterm "hypertensive urgency" is still commonly used to describehypertensive crises without evidence of target-organ damage. Suchcases usually do not require hospitalization, and can often pose adilemma for emergency physicians that are uncomfortable sendinghome patients with persistently elevated blood pressures. Per theJNC 7, cases of "hypertensive urgency" should receive immediatecombination oral antihypertensive therapy.⁽⁶⁾ Accordingto ACEP's Clinical Policy on Asymptomatic Hypertension in the ED,"initiating treatment for asymptomatic hypertension in the ED isnot necessary when patients have follow-up".  If ED treatmentis initiated, ACEP's policy recommends that it should be in anattempt to gradually lower blood pressure and clearly states thatblood pressure "should not be expected to be normalized during theinitial ED visit".⁽⁷⁾

HypertensiveEmergencies
Hypertensive crises are thought to be initiated by humoralvasoconstrictors causing an abrupt increase in systemic vascularresistance, ultimately overwhelming the body's auto-regulatorymechanisms.⁽¹²⁾ Failure of these mechanisms begins aphysiological cascade: elevated pressures in proximal capillarybeds accompany arteriolar dilation and ultimately smallerarterioles may rupture or leak, resulting in fibrin deposition intotheir walls. This fibrinoid necrosis is responsible for end-organdamage, resulting in ischemia and further release of vasoactivemediators, effectively activating a cycle of progressivelyworsening blood pressure elevation and subsequent organinjury.⁽³⁾

The most common presentations ofhypertensive emergencies to the ED are cerebral infarction (24.5%),pulmonary edema (22.5%), hypertensive encephalopathy (16.3%) andcongestive heart failure (12%). Other very important presentationsinclude aortic dissection, intracranial hemorrhage, sympatheticcrises (cocaine toxicity / pheochromocytoma), eclampsia, andmyocardial infarction.⁽²⁰⁾  [Refer to Table 1 -list of these presentations]

According to the JNC 7 Report, "theinitial goal of therapy in hypertensive emergencies is to reducethe mean arterial blood pressure by no more than 25% (withinminutes to 1 hour) then, if stable, to 160/100-110 mm Hg within thenext 2-6 hours".⁽⁶⁾ This general approach is oftenapplicable, but there are also specific guidelines orrecommendations that apply to many of the presentations/diagnosesin Table 1. Generally, relatively rapid, but controlled, reductionin blood pressure is indeed warranted. The emergency practicionermust be aware that the elevated blood pressure in many of thesepatients is often a physiologic response to their acute conditionthough, and aggressive treatment of the hypertension may actuallyincrease morbidity and mortality. This is especially true forpatients with acute intracranial events.⁽⁴⁾

Treatment Guidelines
Detailed review of the treatment guidelines andrecommendations for each of the hypertensive emergencies listed inTable 1 is beyond the scope of this article, but a brief review ofsome of the treatment recommendations in this context, particularlythose that differ from the aforementioned general recommendationsfor blood pressure reduction, will serve to further the discussionof when and how elevated blood pressures should be treated in theED setting.

Ischemic Strokes
In most patients with stroke, elevated blood pressure isthe physiologic response to the stroke as opposed to thecause.  Approximately 85% of strokes are non-hemorrhagic.Patients with non-hemorrhagic strokes often have moderatehypertension that actually portends a better prognosis. Rapidreduction of blood pressure can actually compromise cerebral bloodflow and cause increased ischemia.⁽¹⁵⁾ The IntravenousNimodipine West European Trial for acute stroke was actuallystopped because of increased negative neurologic outcomes in thetreatment group, which were attributed to effects of blood pressurereduction.^(2,12)

From the latest AHA guidelines forthe management of stroke, we have the following: although severehypertension may be considered an indication for treatment, thereis no data that defines the levels of hypertension that requireemergency management.  However, data does suggest that thesystolic blood pressure level that would prompt treatment would be> 180 mm Hg. A systolic blood pressure > 185 mm Hg or adiastolic blood pressure > 110 mm Hg is a contraindication tointravenous administration of rtPA.

Still, it is not clear whether thosevalues should be the threshold for starting emergency treatmentoutside the setting of administration of rtPA.

Although no definitive data fromcontrolled trials are available, in the absence of other organdysfunction necessitating rapid reduction in blood pressure or inthe setting of thrombolytic therapy, there is little scientificevidence and no clinically established benefit for rapid loweringof blood pressure among persons with acute ischemicstroke.⁽⁸⁾ The current AHA guidelines recommend the useof labetalol or nicardipine as the initial vasoactive medicationsof choice if the blood pressure does indeed need to be reduced in apatient with ischemic stroke.

IntracerebralHemorrhage
In patients with ICH, there are often marked elevations inblood pressure. Several physiologic mechanisms likely contribute tothis, including stress activation of the neuro-endocrine system,and increased intracranial pressure causing reflex systemichypertension.  Several studies have shown that systolic bloodpressures > 140-150 within 12 hours of the onset of ICH areassociated with more than double the risk of death ordependency.⁽¹⁹⁾ The INTERACT and ATACH trials are bothrelatively large clinical trials that support the safety andefficacy of rapid blood pressure lowering in ICH.

Still, per the latest guidelines onthe management of intracerebral hemorrhage, the issue of bloodpressure management remains a controversial one: although studieshave shown that intensive blood pressure lowering is clinicallyfeasible and potentially safe, the blood pressure pressure target,duration of therapy, and whether such treatment improves clinicaloutcomes remain unclear.⁽¹¹⁾ Emergency physicians shouldmake decisions regarding blood pressure management in ICH in veryclose consultation with a neurosurgeon. When blood pressurereduction is indicated, nicardipine is recommended as a drug ofchoice.

Aortic Dissection
Persistent elevation of blood pressure in cases of aorticdissection serves to increase the shearing force across theinterface of the intimal flap and can cause further propagation orextension of the dissection.⁽¹²⁾ Rapid blood pressurereduction, often beyond the general goal of a reduction in MAP of~25% is recommended for acute aortic dissection. The goal of bloodpressure reduction is for the systolic blood pressure to be reducedto a level between 100 and 120 mm Hg. A drug of choice for thisscenario is labetalol.  Alternatively, a combination of abeta-blocker and vasodilator can be used.⁽⁵⁾ Bloodpressure management decisions should be made in close consultationwith a vascular surgeon.

Eclampsia
Hypertension complicates > 10% of pregnancies and isresponsible for as many as 13% of maternal deaths in the UnitedStates.⁽¹⁴⁾ Though delivery is the definitive treatmentfor severe pre-eclampsia and eclampsia, emergency departmentmanagement usually entails administration of magnesium sulfate forseizure prophylaxis and aggressive blood pressure control. Systolicblood pressure > 160 has been shown to be the most importantfactor associated with a cerebrovascular accident in patients withpre-eclampsia.^(12,13) ED management focuses onaggressively reducing blood pressure to a systolic blood pressure< 160, and/or a diastolic blood pressure < 110.Traditionally, a drug of choice for use in this particularhypertensive emergency has been hydralazine. Recent evidenceactually shows that hydralazine should likely not be used as afirst-line agent in pre-eclamptic or eclamptic patients.Hydralazine is known to have a latent period of 5-15 minutes thatis usually followed by a progressive, unpredictable and oftenprecipitous fall in blood pressure that can last up to 12 hours.Labetalol and nicardipine have been shown to be equally efficaciousand ultimately preferable drugs for this patientpopulation.^(12,18)

TreatmentOptions/Pitfalls
The modern-day emergency physician has a vastarmamentarium of anti-hypertensive medications at their disposalfor use in the treatment of the patient presenting with ahypertensive emergency. Accumulating evidence has resulted in oldermainstays like hydralazine and nitroprusside largely falling out offavor except in cases that fail to respond to other therapies. Areview of the basic properties and indications for use of some themost commonly utilized medications can be found in Table2. 

One or a combination of the listedmedications is often used for blood pressure reduction in patientswho present to the emergency department with acutely elevated bloodpressure. Historically, many patients with asymptomatichypertension, that is elevated blood pressures without any evidenceof end-organ involvement ("hypertensive urgency"), have also beentreated with such antihypertensive agents in the ED.

The evaluation for end-organischemia and appropriate referral for subsequent care occurs in aminority of patients with elevated blood pressures in mostemergency departments.^(9,10)  This is particularlyunfortunate given that it is unnecessary to treat the bloodpressure of such patients in an emergency department setting, anddoing so may actually increase the risk of adverseevents.^(7,21)

Summary
The general approach to treating hypertensive emergenciesentails a rapid, controlled reduction of blood pressure. As in afew of the cases discussed, it is occasionally necessary foremergency physicians to rapidly reduce a patient's blood pressureeven beyond the general recommendation of a 25% drop in meanarterial pressure.

Focused treatment of patientssuffering from specific hypertensive emergencies should follow theguidelines and recommendations pertinent to their particulardiagnosis. The emergency physician must take care to not overaggressively treat simple blood pressure elevations without anyevidence of target-organ damage.

Provided adequate follow-up, mostpatients who have elevated blood pressures in the emergencydepartment can be safely discharged home without any interventionon their blood pressure at all. If the emergency physician is tointervene, initiation of treatment with an appropriate oralanti-hypertensive to gradually reduce the patient's blood pressureover 24-48 hours and securing prompt outpatient follow-up forfurther management of hypertension is the recommended approach asit allows for appropriate management while avoiding unintended sideeffects.

Table 1

Table 2

References

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