It is estimated that anywhere from 72 to 74 million people in the United States aged 20 or older are affected by hypertension.1 This accounts for approximately 30% of the population over 20 years old.2 Somewhere between 3% and 45% of all adult ED patients will have at least one elevated blood pressure reading during their ED stay.3 Given the ubiquitous nature of the predisposing disease, hypertensive emergencies are commonly encountered by emergency physicians. It behooves the emergency physician to be able to readily identify a true hypertensive emergency, and to know when and how elevations in blood pressure should be treated in the emergency department.
Defining the Problem – Is This an Emergency?
In the modern age of pharmaceuticals, with a plethora of antihypertensive agents available to physicians, the incidence of hypertensive emergencies has declined from 7% to 1% of patients with hypertension.4 Still, this presentation is common enough that emergency physicians must be able to readily identify true hypertensive emergencies, and know when and how to treat them.
The classification of hypertension is periodically reviewed by the Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The most recent guidelines, the JNC 7 report, were released in 20035 and are currently being updated – the JNC 8 is set for release later this year.
The JNC 7 report does not outline specific blood pressure values in defining hypertensive emergency. Rather, the term “hypertensive crisis” is generally applied when one experiences an acute elevation of blood pressure, with a systolic blood pressure over 180 mm Hg or a diastolic blood pressure over 110.6 Per the JNC 7, a hypertensive emergency is a hypertensive crisis in which there is evidence of acute target-organ damage (e.g., encephalopathy, myocardial infarction, unstable angina, pulmonary edema, stroke, life-threatening arterial bleeding, or aortic dissection). Such cases warrant parenteral drug therapy and hospitalization, often to an intensive care setting.5
Though falling out of favor, the term “hypertensive urgency” is still often used to describe hypertensive crises without evidence of target-organ damage. Such cases usually do not require hospitalization, and can often pose a dilemma for emergency physicians who are uncomfortable sending home patients with persistently elevated blood pressure. Per the JNC 7, cases of “hypertensive urgency” should receive immediate combination oral antihypertensive therapy.5 According to ACEP’s Clinical Policy on Asymptomatic Hypertension in the ED, “initiating treatment for asymptomatic hypertension in the ED is not necessary when patients have follow-up.” If ED treatment is initiated, ACEP’s policy recommends that it should be in an attempt to gradually lower blood pressure and clearly states that blood pressure “should not be expected to be normalized during the initial ED visit.”7
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Hypertensive crises are thought to be initiated by humoral vasoconstrictors causing an abrupt increase in systemic vascular resistance, ultimately overwhelming the body’s autoregulatory mechanisms.2 Failure of these mechanisms begins a physiologic cascade: Elevated pressures in proximal capillary beds accompany arteriolar dilation, and ultimately smaller arterioles may rupture or leak, resulting in fibrin deposition into their walls. This fibrinoid necrosis is responsible for end organ damage, resulting in ischemia and further release of vasoactive mediators, effectively activating a cycle of progressively worsening blood pressure elevation and subsequent organ injury.8
The most common presentations of hypertensive emergencies in the ED are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Other important presentations include aortic dissection, intracranial hemorrhage, sympathetic crises (cocaine toxicity/pheochromocytoma), eclampsia, and MI9 (Table 1.)
According to the JNC 7 report, “the initial goal of therapy in hypertensive emergencies is to reduce the mean arterial blood pressure by no more than 25% (within minutes to 1 hour), then, if stable, to 160/100-110 mm Hg within the next 2-6 hours.”5 This general approach is often applicable, but there are also specific guidelines or recommendations that apply to many of the presentations/diagnoses listed in Table 1. Generally, relatively rapid but controlled reduction in blood pressure is indeed warranted. The emergency practitioner must be aware that the elevated blood pressure in many of these patients is often a physiologic response to their acute condition, and aggressive treatment of the hypertension may actually increase morbidity and mortality. This is especially true for patients with acute intracranial events.10
After reading this article, the physician should be able to:
- Define hypertensive emergency.
- Understand the distinction between hypertensive emergency and “hypertensive urgency.”
- Decide when acute elevations in blood pressure should be treated in the ED.
- Avoid the potential pitfalls entailed in overaggressive treatment of elevated blood pressure.
- Discuss the goals of treatment in hypertensive emergencies.
- Understand the options available for treating hypertensive emergencies.
Detailed review of the treatment guidelines and recommendations for each of the hypertensive emergencies listed in Table 1 is beyond the scope of this article, but a brief review of some of the treatment recommendations in this context, particularly those that differ from the aforementioned general recommendations for blood pressure reduction, will serve to further the discussion of when and how elevated blood pressure should be treated in the ED setting.
In most patients with stroke, elevated blood pressure is the physiologic response to the stroke, as opposed to the cause. Approximately 85% of strokes are nonhemorrhagic. Patients with nonhemorrhagic strokes often have moderate hypertension that actually portends a better prognosis. Rapid reduction of blood pressure can compromise cerebral blood flow and cause increased ischemia.11 The Intravenous Nimodipine West European Trial for acute stroke was stopped because of increased negative neurologic outcomes in the treatment group, which were attributed to effects of blood pressure reduction.2,12
From the latest American Heart Association (AHA) guidelines for the management of stroke, we have the following: Although severe hypertension may be considered an indication for treatment, there are no data that define the levels of hypertension that require emergency management. However, data do suggest that the systolic blood pressure level that would prompt treatment would be over 180 mm Hg. A systolic blood pressure over 185 mm Hg or a diastolic blood pressure over 110 mm Hg is a contraindication to intravenous administration of rtPA.13
Still, it is not clear whether those values should be the threshold for starting emergency treatment outside the setting of administration of rtPA.
In the absence of other organ dysfunction necessitating rapid reduction in blood pressure or in the setting of thrombolytic therapy, there is little scientific evidence and no clinically established benefit for rapid lowering of blood pressure among persons with acute ischemic stroke.13 The current AHA guidelines recommend the use of labetalol or nicardipine as the initial vasoactive medications if blood pressure does indeed need to be reduced in a patient with ischemic stroke.13
Table 1. Causes of Hypertensive Emergencies
After reading this article, the physician should be able to:
- Aortic dissection
- Cerebral infarction
- Congestive heart failure
- Flash pulmonary edema
- Hypertensive encephalopathy
- Intracranial hemorrhage
- Myocardial infarction
- Sympathetic crises (cocaine toxicity/pheochromocytoma)
Patients with intracerebral hemorrhage (ICH) often have marked elevations in blood pressure. Several physiologic mechanisms likely contribute to this, including stress activation of the neuro-endocrine system and increased intracranial pressure causing reflex systemic hypertension. Several studies have shown that systolic blood pressures over 140-150 mm Hg within 12 hours of the onset of ICH are associated with more than double the risk of death or dependency.14 The INTERACT and ATACH trials are both relatively large clinical trials that support the safety and efficacy of rapid blood pressure lowering in ICH.
Still, per the latest guidelines on the management of intracerebral hemorrhage, the issue of blood pressure management remains a controversial one. Although studies have shown that intensive blood pressure lowering is clinically feasible and potentially safe, the blood pressure target, duration of therapy, and whether such treatment improves clinical outcomes remain unclear.15 Emergency physicians should make decisions regarding blood pressure management in ICH in close consultation with a neurosurgeon. When blood pressure reduction is indicated, nicardipine is recommended as a drug of choice.
Persistent elevation of blood pressure in cases of aortic dissection serves to increase the shearing force across the interface of the intimal flap and can cause further propagation or extension of the dissection.2 Rapid blood pressure reduction, often beyond the general goal of a reduction in mean arterial pressure (MAP) of about 25%, is recommended for acute aortic dissection. The goal of blood pressure reduction is for the systolic blood pressure to be reduced to a level between 100 and 120 mm Hg. A drug of choice for this scenario is labetalol. Alternatively, a combination of a beta-blocker and vasodilator can be used.16 Blood pressure management decisions should be made in close consultation with a vascular surgeon.
Hypertension complicates more than 10% of pregnancies and is responsible for as many as 13% of maternal deaths in the United States.17 Though delivery is the definitive treatment for severe pre-eclampsia and eclampsia, ED management usually entails administration of magnesium sulfate for seizure prophylaxis and aggressive blood pressure control. Systolic blood pressure over 160 mm Hg has been shown to be the most important factor associated with a cerebrovascular accident in patients with pre-eclampsia.2,18 ED management focuses on aggressively reducing blood pressure to a systolic blood pressure less than 160 mm Hg and/or a diastolic blood pressure under 110. Traditionally, a drug of choice for use in this particular hypertensive emergency has been hydralazine. Recent evidence shows that hydralazine should likely not be used as a first-line agent in pre-eclamptic or eclamptic patients. Hydralazine’s latent period of 5-15 minutes is usually followed by a progressive, unpredictable, and often precipitous fall in blood pressure that can last up to 12 hours. Labetalol and nicardipine have been shown to be equally efficacious and ultimately preferable drugs for this population.1,2
The modern-day emergency physician has a vast armamentarium of antihypertensive medications at their disposal for hypertensive emergency. Accumulating evidence has resulted in older mainstays like hydralazine and nitroprusside largely falling out of favor except in cases that fail to respond to other therapies. A review of the basic properties and indications for use of some of the most commonly utilized medications can be found in Table 2.
One or a combination of the listed medications is often used for blood pressure reduction in patients who present to the emergency department with acutely elevated blood pressure. Historically, many patients with asymptomatic hypertension – that is, elevated blood pressures without any evidence of end organ involvement (“hypertensive urgency”) – have also been treated with such antihypertensive agents in the ED.
The evaluation for end organ ischemia and appropriate referral for subsequent care occurs in a minority of patients with elevated blood pressure in most EDs.19,20 This is particularly unfortunate given that it is unnecessary to treat the blood pressure of such patients in an emergency department setting, and doing so may actually increase the risk of adverse events.7,21
The general approach to treating hypertensive emergencies entails a rapid, controlled reduction of blood pressure. As in a few of the cases discussed, it is occasionally necessary for emergency physicians to rapidly reduce a patient’s blood pressure even beyond the general recommendation of a 25% drop in mean arterial pressure.
Focused treatment of patients suffering from specific hypertensive emergencies should follow the guidelines and recommendations pertinent to their particular diagnosis. The emergency physician must take care to not undertake overaggressive treatment of simple blood pressure elevations without any evidence of target-organ damage.
Provided adequate follow-up, most patients who have elevated blood pressure in the emergency department can be safely discharged home without any intervention for their blood pressure. If the emergency physician is to intervene, initiation of treatment with an appropriate oral antihypertensive to gradually reduce the patient’s blood pressure over 24-48 hours and securing prompt outpatient follow-up for further management of hypertension is the recommended approach, as it allows for appropriate management while avoiding unintended side effects.
After reading this article, the physician should be able to:
Dr. Phull is a fourth-year emergency medicine resident at Northwestern Memorial Hospital, Chicago. Dr. Aldeen is an Assistant Professor in the Department of Emergency Medicine at Northwestern University Feinberg School of Medicine, Chicago, and Director of the Chicago Cardiac Arrest Resuscitation Education Service. Dr. Robert Solomon is Medical Editor of ACEP News and editor of the Focus On series, core faculty in the emergency medicine residency at Allegheny General Hospital, Pittsburgh, and Assistant Professor in the Department of Emergency Medicine at Temple University School of Medicine, Philadelphia.
Dr. Phull, Dr. Aldeen, and Dr. Solomon have disclosed that they have no significant relationships with or financial interests in any commercial companies that pertain to this article.
ACEP makes every effort to ensure that contributors to College-sponsored programs are knowledgeable authorities in their fields. Participants are nevertheless advised that the statements and opinions expressed in this article are provided as guidelines and should not be construed as College policy. The material contained herein is not intended to establish policy, procedure, or a standard of care. The views expressed in this article are those of the contributors and not necessarily the opinion or recommendation of ACEP. The College disclaims any liability or responsibility for the consequences of any actions taken in reliance on those statements or opinions.
- Varon J. Treatment of acute severe hypertension. Drugs 2008;68(3):283-97.
- Marik PE, et al. Hypertensive crises: Challenges and management. Chest 2007;131:1949-62.
- Slovis CM. Increased blood pressure without evidence of acute end organ damage. Ann. Emerg. Med. 2008;51:S7-9.
- Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. Ann. Emerg. Med. 2003;41(4):513-29.
- Chobanian AV, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-52.
- Aggarwal M, Khan IA. Hypertensive crisis: Hypertensive emergencies and urgencies. Cardiol. Clin. 2006;24(1):135-46.
- Decker WW, et al. Clinical policy: Critical issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department. Ann. Emerg. Med. 2006;47:237-49.
- Ault MJ, Ellrodt AG. Pathophysiological events leading to the end-organ effects of acute hypertension. Am. J. Emerg. Med. 1985;3:10-5.
- Zampaglione B, et al. Hypertensive urgencies and emergencies: Prevalence and clinical presentation. Hypertension 1996;27(1):144-7.
- Barry DI. Cerebrovascular aspects of antihypertensive treatment. Am. J. Cardiol. 1989;63:14C-18C.
- Semplicini A, et al. Hypertension in acute ischemic stroke: A compensatory mechanism or an additional damaging factor? Arch. Intern. Med. 2003;163:211-6.
- Ahmed N, et al. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke 2000;31:1250-5.
- Harold PA, et al. Guidelines for the early management of adults with ischemic stroke. Stroke 2007;38:1655-711.
- Willmot M, et al. High blood pressure in acute stroke and subsequent outcome: A systematic review. Hypertension 2004;43:18-24.
- Lewis BM, et al. Guidelines for the management of spontaneous intracerebral hemorrhage. Stroke 2010;41:2108-29.
- Cheun AT, Hobson RW. Hypertension in vascular surgery. Ann. Emerg. Med. 2008;51(3 suppl):S28-33.
- Pregnancy-related mortality surveillance – United States. MMWR Feb. 21, 2003;52(SS02):1-8.
- Martin JN, et al. Stroke and severe pre-eclampsia and eclampsia. Obstet. Gynecol. 2005;105:237-8.
- Karras DJ. Evaluation and treatment of patients with severely elevated blood pressure in academic EDs. Ann. Emerg. Med. 2006;47:230-6.
- Lehrmann JF, et al. Knowledge translation of the American College of Emergency Physicians’ clinical policy on hypertension. Acad. Emerg. Med. 2007;14:1090-6.
- Zeller KR, Von Kuhnert L. Rapid reduction of severe asymptomatic hypertension. Arch. Intern. Med. 1989;149:2186-9.