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Hypertensive emergency, a life-threatening complication of high blood pressure, may signify

a patient's first presentation for hypertension. In patients with severe hypertension, primary
care clinicians must be able to distinguish between hypertensive urgency and true
hypertensive emergency. Can your hypertensive patient be managed on an outpatient basis, or
is admission to the ICU needed? Current treatment recommendations, including those for
specific manifestations of hypertensive emergency, are reviewed here.

An estimated 1% to 2% of patients with chronic hypertension will at some time develop


hypertensive urgency or emergency.1 According to recent data from the National Health and
Nutrition Examination Survey (NHANES) 1999 to 2010,2 the prevalence of hypertension has
remained stable at 30.5% among men and 28.5% among women in the United States;
however, 74% of the hypertensive population is unaware of having this condition.
Furthermore, 71.6% of hypertensive patients are managed for the condition, and in only
46.5% is blood pressure well controlled.2

In 2006, essential hypertension was estimated to account for more than 44 million emergency
department visits in the US. The direct and indirect costs of hypertension totaled $73 billion
in 2009.3,4

CLINICIAN-IQ QUIZ: ACC/AHA Guidelines: Secondary prevention of ASCVD


Treatment & Diagnosis of Nephrology
Drug & Dosing Information

NEW TERMINOLOGY AND CLASSIFICATION

The terms malignant hypertension, hypertensive crisis, and accelerated hypertension have
been replaced by hypertensive urgency or hypertensive emergency. Hypertensive urgency and
emergency are differentiated by the absence or presence of acute end-organ damage,
respectively.

Given the inconsistent terminology used, database searches can be challenging. The Seventh
Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure (JNC7),5,6 published in 2003, is considered the gold standard for
categorizing hypertension in the outpatient setting. The JNC7 authorsclassify normal blood
pressure as < 120/< 80 mm Hg. The document further classifies blood pressure into the stages
shown in Table 1.5,6 Blood pressure higher than 180 mm Hg systolic and/or 120 mm Hg
diastolic is generally considered severe hypertension— a designation that includes
hypertensive urgency and hypertensive emergency.6

What Defines Hypertensive Urgency/Emergency?


Hypertensive urgency is defined as a diastolic blood pressure of 110 mm Hg or greater
without the acute signs of end-organ damage.7 Some sources suggest that a patient must also
have certain risk factors (eg, heart disease, renal disease) to be given this diagnosis.8 The
presence of acute and rapidly evolving end-organ damage with an elevated diastolic blood
pressure, usually greater than 120 mm Hg, establishes a diagnosis of hypertensive
emergency.6,8,9

No specific blood pressure measurement indicates a hypertensive emergency, however;


rather, the defining feature of this diagnosis is the presence of progressive target end-organ
damage.7 This is most commonly manifested in cardiopulmonary, central nervous system,
and/or renal findings; for the specific forms of end-organ damage, see Table 2.5,6,10,11
Preeclampsia and eclampsia are also considered manifestations of hypertensive end-organ
damage but are beyond the scope of this article.5,11

The most common form of organ damage associated with hypertension is ischemic heart
disease, in the form of either heart failure or acute coronary syndrome.12

PATHOPHYSIOLOGY

Blood pressure is calculated by cardiac output (ie, stroke volume multiplied by heart rate)
multiplied by total peripheral resistance. Total peripheral resistance is influenced by a variety
of humoral and neural factors, also known as vasoactive substances (see Figure 13,4). During
an episode of acute hypertension, a failure of autoregulatory function occurs, precipitated by
one or more of a host of potential causes. This failure of autoregulation then leads to
increased systemic vascular resistance. In the setting of end-organ damage, release of
inflammatory markers ensues, which ultimately causes endovascular injury and fibrin
necrosis of arterioles.4,10,11

The renin-angiotensin-aldosterone system also plays a significant role in the cascade of


hypertension, stimulating decreased renal perfusion and lowering tubular sodium
concentration. This in turn stimulates aldosterone to increase blood pressure by maintaining
excess volume through sodium retention and potassium excretion, further potentiating the
cycle of uncontrolled blood pressure.4,13,14
Patients with chronically elevated blood pressures have a compensatory response, lying in the
threshold mechanism, that protects against end-organ damage. Acute changes in blood
pressure are better tolerated in these patients because of their decreased propensity for
hypoperfusion.4 In contrast, normotensive patients who experience precipitous changes in
blood pressure are at increased risk for organ hypoperfusion. The main concern regarding
organ hypoperfusion is that it can lead to ischemia4 (see Figure 23,4).

PATIENT HISTORY

Acute hypertensive urgency or emergency can be triggered by many factors. Systemic


etiologies (including kidney disease) caused by immunologic mediators or renal artery
stenosis can cause or exacerbate hypertension. The patient should be asked about his or her
normal blood pressure range, as this may offer clues to medication compliance. Rebound
hypertension can be seen in patients who abruptly discontinue medications such as clonidine
or β-blockers, as this causes an increase in sympathetic outflow.9,15

All patients should be queried regarding their use of OTC medications and other drug use,
including cocaine, methamphetamines, phencyclidine, and alcohol.1,4,11,16 Patients taking
monoamine oxidase inhibitors (MAOIs) are at increased risk for serious medication
interactions; concomitant administration of MAOIs with other antidepressants can lead to a
hypertensive reaction, but also to serotonin syndrome.1,17 Because MAOIs inhibit the
breakdown of tyramine, patients taking them should avoid tyramine-containing foods and
herbal supplements (including, but not limited to, St. John's wort, ginseng, and
yohimbine).1,15,18

TREATMENT: HYPERTENSIVE URGENCY

The treatment of hypertensive urgency is usually immediate and warrants close follow-up.
Although elevated blood pressures can be alarming to the patient, hypertensive urgency
usually develops over days to weeks.8 In this setting, it is not necessary to lower blood
pressure acutely.12 A rapid decrease in blood pressure can actually cause symptomatic
hypotension, resulting in hypoperfusion to the brain.5,6,8

After ruling out end-organ damage, the next step is to treat according to the guidelines for
hypertensive urgency.5,6 These recommendations include the use of rapid-onset oral
antihypertensive agents, such as clonidine, labetalol, or captopril.23 Use of these agents is
only suggested for gradual, short-term reduction of blood pressure (ie, over 24 to 48 hours)
while the patient is being monitored for potential hypertension-related organ damage, either
in the emergency department or in an observational hospital setting.5,6,23
Once the short-acting agents have adequately reduced blood pressure, long-term agents can
be chosen to prevent rebound hypertension.16 Patients are typically monitored for 24 hours in
the hospital during this transition. Upon discharge, the patient should be scheduled for
follow-up within one to two days.11 Patient education, including a discussion of medication
adherence, weight loss, and reduced dietary salt, is key to prevent recurrences and optimize
overall treatment compliance.