1,3 Hypertensive emergencies are associated with acutely progressive
secondary organ damage (e.g., stroke or myocardial infarction [MI]). Hypertensive
urgency is not an immediately life-threatening situation; a reduction in BP to a safe
level can occur more slowly in the next 24 to 48 hours.
Acute, potentially life-threatening elevations of BP can occur in previously
normotensive individuals with acute glomerulonephritis, head injury, or severe
burns; during pregnancy (eclampsia); and with the use of recreational drugs such as
cocaine. Other causes include abrupt medication withdrawal or medication
nonadherence, drug–drug interactions (including herbal medications), erythropoietin
administration, or drug–food interactions (i.e., patients receiving monoamine oxidase
inhibitors who ingest foods rich in tyramine).
In addition, poor systolic BP control
has been identified as an independent risk factor for the development of hypertensive
10 Despite improvements in the recognition and treatment of hypertension, there
has been an increase in the number of hospitalizations for hypertensive emergencies
in the United States from 2000 to 2007 (101–111 cases per 100,000
hospitalizations). Fortunately, in-hospital mortality associated with these admissions
decreased from 2.8% to 2.6% in this time period.
Hypertensive Emergency versus Urgency
Life-threatening Potentially Not acutely
End-organ damage Acute or progressing Chronic; not progressing
CNS (dizziness, N/V, encephalopathy, confusion,
weakness, intracranial or subarachnoid
Eyes (ocular hemorrhage or funduscopic
changes, blurred vision, loss of sight)
Cardiac (left ventricular failure, pulmonary
edema, MI, angina, aortic dissection)
Renal failure or insufficiency
Treatment strategy Immediate reduction in blood pressure; administer
parenteral therapy (Table 16-2)
Reduction in blood pressure over
several hours to days; administer oral
or end-organ damage. See Chapter 9, Essential Hypertension, for staging of hypertension.
CNS, central nervous system; MI, myocardial infarction; N/V, nausea and vomiting.
CLINICAL PRESENTATION OF HYPERTENSIVE
There are limited data describing the presentation and characteristics of those
patients with a hypertensive urgency. Symptoms may include headache, dizziness,
visual changes, chest discomfort, nausea, epistaxis, fatigue, and psychomotor
It should be noted that not all patients presenting with a hypertensive
CLINICAL PRESENTATION OF HYPERTENSIVE
Similar to hypertensive urgencies, hypertensive emergencies typically occur in those
with a history of hypertension. This suggests that hypertensive emergencies are
13,14 Hypertensive emergencies tend to occur in patients
with catecholamine-producing adrenal tumors (pheochromocytoma) or renal vascular
disease. Additionally, hypertensive emergencies occur more often in African
Americans than in Caucasians, among patients who have no primary care physician,
and those who do not adhere to treatment regimens.
Symptoms associated with hypertensive emergency are highly variable and reflect
the degree of damage to specific organ systems. Rapid, severe BP elevation is not
always the hallmark of a hypertensive emergency. The primary sites of damage are
the central nervous system, heart, kidneys, and eyes. Although hypertensive
emergencies are much less common than hypertensive urgencies, it is often difficult
to know whether end-organ dysfunction is new or has progressed without a thorough
Central nervous system abnormalities are the most commonly reported complications
in hypertensive emergencies. Symptoms may include a severe headache with or
without dizziness, nausea, vomiting, and anorexia. Mental confusion with
apprehension indicates more severe damage, as does nystagmus, localized weakness,
or a positive Babinski sign (i.e., upward extension of the great toe and spreading of
the smaller toes when moderate pressure is applied along a curve from the sole to the
ball of the foot). Central nervous system damage may rapidly progress, resulting in
coma or death. If a cerebrovascular accident has occurred, slurred speech or motor
Cardiac consequences are the second most common complication of hypertensive
emergency reported. Presentations may include heart failure (HF), acute pulmonary
edema, and/or an acute coronary syndrome. Ocular symptoms of hypertensive
emergency usually are related to changes in visual acuity. Complaints of blurred
vision or loss of eyesight are often associated with funduscopic findings of
hemorrhages, exudates (yellow deposits within the retina as a result of leaks from
capillaries and microaneurysms), and occasionally papilledema (edema of the optic
nerve). Acute kidney injury can also develop. Markers of renal dysfunction include
hematuria, proteinuria, and elevated serum blood urea nitrogen and serum creatinine
Oral versus Parenteral Therapy
Hypertensive urgency is not an indication for parenteral treatment; oral
antihypertensive regimens are more appropriate. Practitioners should exercise
caution in the treatment of patients with elevated BP in the absence of target organ
damage. Aggressive dosing to rapidly lower BP is not without risk and can lead to
hypotension and subsequent morbidity. Some have suggested that the term
hypertensive urgency leads to overly aggressive treatment and should be discarded in
favor of a less ominous term such as uncontrolled BP.
emergencies require immediate hospitalization, generally in an intensive care unit,
and the administration of parenteral antihypertensive medications to reduce arterial
16 Effective therapy greatly improves the prognosis, reverses symptoms, and
arrests the progression of end-organ damage.
17–19 Whether treatment can completely
reverse end-organ damage is related to two factors: how soon treatment is initiated
and the extent of damage at the initiation of therapy.
There are two fundamental concepts in the management of hypertensive
emergencies. First, immediate and intensive therapy is required and takes precedence
over time-consuming diagnostic procedures. Second, the choice of drugs will depend
on how their time course of action and hemodynamic and metabolic effects meet the
needs of the emergent situation. If encephalopathy, acute left ventricular failure,
dissecting aortic aneurysm, eclampsia, or other end-organ damage is present, the BP
should be lowered promptly with rapid-acting, parenteral antihypertensive
medications such as clevidipine, esmolol, enalaprilat, fenoldopam, hydralazine,
labetalol, nicardipine, nitroglycerin, or nitroprusside (Table 16-2).
slower BP reduction over the course of several hours or days is acceptable, as in the
case of a hypertensive urgency, rapid-acting oral therapy using captopril, clonidine,
labetalol, or minoxidil may be used (Table 16-3).
3,4,24–26 Figure 16-1 provides an
overview of the management of a hypertensive crisis. A summary of treatment
recommendations for acutely lowering BP for selected indications is listed in Table
Parenteral Medications Commonly Used in the Treatment of Hypertensive
Name)/Class Dose/Route Onset of Action Duration of Action
(Cleviprex)/calciumchannel blocker
Initial: 1–2 mg/hour; titrate dose to desired
2–4 minutes 10–15 minutes after
0.625–1.25 mg IV every 6 hours 15 minutes (max, 1–
250–500 mcg/kg for 1 minute, then 50–300
0.1–0.3 mcg/kg/minute <5 minutes 30 minutes
10–20 mg IV 5–20 minutes 2–6 hours
2 mg/minute IV or 20–80 mg every 10
minutes up to 300 mg total dose
Initiate at 5 mg/hour IV increased by 2.5
mg/hour every 5 minutes to desired BP or a
max of 15 mg/hour every 15 minutes, may
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