Uncontrolled Blood Pressure

Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled

blood pressures (BPs) lead to progressive or impending end-organ dysfunction (EOD). In these
conditions, the BP should be lowered aggressively over minutes to hours.
Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy,
cerebral vascular accident/cerebral infarction; subarachnoid hemorrhage, and/or intracranial
hemorrhage.[1] Cardiovascular end-organ damage may include myocardial ischemia/infarction,
acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection. Other organ
systems may also be affected by uncontrolled hypertension, which may lead to acute renal
failure/insufficiency, retinopathy, eclampsia, or microangiopathic hemolytic anemia.[1]
With the advent of antihypertensives, the incidence of hypertensive emergencies has declined
from 7% to approximately 1% of patients with hypertension.[2] In addition, the 1-year survival
rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate
of more than 90% with appropriate medical treatment.[3]

History and physical examination

The history and the physical examination determine the nature, severity, and management of the
hypertensive event. The history should focus on the presence of end-organ dysfunction, the
circumstances surrounding the hypertension, and any identifiable etiology.
The most common clinical presentations of hypertensive emergencies are cerebral infarction
(24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart
failure (12%). Other clinical presentations associated with hypertensive emergencies include
intracranial hemorrhage, aortic dissection, and eclampsia,[4] as well as acute myocardial
infarction.
The duration and severity of the patients preexisting hypertension (including the degree of BP
control) should be evaluated, as well as the patient's medication history. Details of
antihypertensive drug therapy and compliance, intake of over-the-counter (OTC) preparations
such as sympathomimetic agents, and use of illicit drugs such as cocaine are important elements
of the medication history. In addition, it is important to elicit information about the presence of
previous end-organ dysfunction, particularly renal and cerebrovascular disease, and any other
medical problems (eg, thyroid disease, Cushing disease, systemic lupus). In female patients,
determine the date of their last menstrual period.
Patients may complain of specific symptoms that suggest end-organ dysfunction may be present.
Chest pain may indicate myocardial ischemia or infarction, back pain may denote aortic
dissection; and dyspnea may suggest pulmonary edema or congestive heart failure. The presence
of neurologic symptoms may include seizures, visual disturbances, and altered level of
consciousness and may be indicative of hypertensive encephalopathy.

The physical examination should assess whether end-organ dysfunction is present. BP should not
only be measured in both the supine position and the standing position (assess volume
depletion), but it should also be measured in both arms (a significant difference may suggest
aortic dissection).
The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive
emergency. Evaluate for the presence of heart failure, which may be indicated jugular venous
distention, crackles on auscultation, and peripheral edema. Central nervous system (CNS)
findings may include changes in the patient's level of consciousness and visual fields, and/or the
presence of focal neurologic signs. Abdominal masses or bruits may be noted.

Evaluation of uncontrolled hypertension

Obtain electrolyte levels, as well as measurements of blood urea nitrogen (BUN) and creatinine
levels to evaluate for renal impairment. A dipstick urinalysis to detect hematuria or proteinuria
and microscopic urinalysis to detect red blood cells (RBCs) or RBC casts should also be
performed
A complete blood cell (CBC) and peripheral blood smear should be obtained to exclude
microangiopathic anemia, and a toxicology screen, pregnancy test, and endocrine testing may be
obtained, as needed.
Imaging should be directed by clinical presentation. If there is clinical evidence of pulmonary
edema or the patient has chest pain, chest radiography and ECG are indicated. Patients with
neurological signs should be evaluated with a head CT scan initially, with more advanced
imaging determined by clinical presentation.

Malignant hypertension
Malignant hypertension and accelerated hypertension are both hypertensive emergencies, with
similar outcomes and therapies. Malignant hypertension may or may not be associated with
clinical conditions present in hypertensive urgency. A patient with malignant hypertension
always has retinal papilledema (as seen in the image below),[5] as well as flame-shaped
hemorrhages and exudates. Other clinical features of malignant hypertension may include
encephalopathy, confusion, left ventricular failure, intravascular coagulation, and impaired renal
function, with hematuria and weight loss.
The pathologic hallmark of malignant hypertension is fibrinoid necrosis of the arterioles, which
occurs systemically, but specifically in the kidneys. These patients develop fatal complications if
untreated, and more than 90% will not survive beyond 1-2 years. See Malignant Hypertension.

Papilledema. Note the swelling of the optic disc, with blurred

margins
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Management of Hypertensive Emergencies

Approximately 3-45% of adult patients have at least one incident of increased BP during their
stay in the emergency department (ED). The fundamental principle in determining the necessary
ED care of the hypertensive patient is the presence or absence of end-organ dysfunction. Many
patients present to the ED with elevated BPs; however, only a small proportion of patients will
require emergency treatment. An important point to remember in the management of the patient
with any degree of BP elevation is to "treat the patient and not the number."
The primary goal of the emergency physician is to determine which patients with acute
hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous
(IV) parenteral therapy. In contrast, patients presenting with acutely elevated BP (systolic BP
[SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) without symptoms and whose BP stays
significantly elevated to this level on discharge should have initiation of medical therapy and
close follow-up in the outpatient setting.[6]
Thus, optimal control of hypertensive situations balances the benefits of immediate decreases in
BP against the risk of a significant decrease in target organ perfusion. The emergency physician
must be capable of appropriately evaluating patients with an elevated BP, correctly classifying
the hypertension, determining the aggressiveness and timing of therapeutic interventions, and
making disposition decisions.
Acutely lowering BP in the ED for clinical situations other than those listed below is
controversial and generally should be avoided.

Pharmacotherapy
Optimal pharmacotherapy is dependent upon the specific organ at risk (see individual sections
below). In patients presenting with hypertensive emergencies, antihypertensive drug therapy has
been shown to be effective in acutely decreasing blood pressure.[7]
Sodium nitroprusside is a commonly used medication. It is a short-acting agent, and the BP
response can be titrated from minute to minute. However, patients must have constant

monitoring in an intensive care unit. The potential exists for thiocyanate and cyanide toxicity
with prolonged use or if the patient has renal or hepatic failure.
Labetalol, an alpha- and beta-blocking agent, has proven to be quite beneficial in the treatment of
patients with hypertensive emergencies. Labetalol is particularly preferred in patients with acute
dissection and patients with end-stage renal disease. Boluses of 10-20 mg may be administered,
or the drug may be infused at 1 mg/min until the desired BP is obtained. Once an adequate BP
level is obtained, oral hypertensive therapy should be initiated, and patients are gradually weaned
from parenteral agents.
Fenoldopam, a peripheral dopamine-1-receptor agonist is given as initial IV dose of 0.1
g/kg/min titrated every 15 minutes.
Clevidipine, a dihydropyridine calcium channel blocker, is administered intravenously for rapid
and precise BP reduction.[8] It is rapidly metabolized in the blood and tissues and does not
accumulate in the body. Initiate IV infusion of clevidipine at 1-2 mg/h; titrate the dose at short
intervals (ie, 90 s) initially by doubling the dose.
As the BP approaches its goal, increase the clevidipine dose by less than double, and lengthen
the time between dose adjustments to every 5-10 minutes. An approximately 1-2 mg/h increase
produces an additional 2-4 mm Hg decrease in SBP. Typically, the therapeutic response is
achieved with 4-6 mg/h, although severe hypertension may require higher doses. Most patients
have received maximum doses of 16 mg/h or less; experience is limited with short-term dosing
as high as 32 mg/h. Because of lipid load restrictions, do not exceed 1000 mL or an average of
21 mg/h within a 24-hour period; experience is limited with use beyond 72 hours.

Neurologic emergencies
Rapid BP reduction is indicated in neurologic emergencies, such as hypertensive encephalopathy,
acute ischemic stroke, acute intracerebral hemorrhage, and subarachnoid hemorrhage.
In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8
hours.[9] Labetalol, nicardipine, esmolol are the preferred medications; nitroprusside and
hydralazine should be avoided.
For acute ischemic stroke, the preferred medications are labetalol and nicardipine. Withhold
antihypertensive medications unless the SBP is >220 mm Hg or the DBP is >120 mm Hg,
UNLESS the patient is receiving IV or intra-arterial (IA) fibrinolysis; then, the goal BP is an
SBP of < 185 mm Hg and DBP < 110 mm Hg. After treatment with fibrinolysis, the SBP should
be maintained < 180 mm Hg and the DBP at < 105 mm Hg for 24 hours.[9]
For acute intracerebral hemorrhage, the preferred medications are labetalol, nicardipine, and
esmolol; avoid nitroprusside and hydralazine. The treatment is based on clinical/radiographic
evidence of increased intracranial pressure (ICP). If there are signs of increased ICP, maintain the
MAP just below 130 mm Hg (or SBP < 180 mm Hg) for the first 24 hours after onset. In patients

without increased ICP, maintain the MAP < 110 mm Hg (or SBP < 160 mm Hg) for the first 24
hours after symptom onset.[9]
Recent evidence shows that in cases of acute intracerebral hemorrhage, early intensive BP
control is well tolerated and can reduce hematoma growth in patients treated within 6 hours after
the onset of intracerebral hemorrhage.[10, 11] The target systolic pressure for these studies was 140
mm Hg and routine IV medications were used. The target SBP was maintained over 7 days.[10, 11]
In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are also the preferred agents;
again, nitroprusside and hydralazine should be avoided. Maintain the SBP < 160 mm Hg until the
aneurysm is treated or cerebral vasospasm occurs. Although oral nimodipine is used to prevent
delayed ischemic neurologic deficits, it is NOT indicated for treating acute hypertension.[9]

Cardiovascular emergencies
Rapid BP reduction is also indicated in cardiovascular emergencies, such as aortic dissection,
acute coronary syndrome, and acute heart failure.
In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with betablocker), esmolol, and morphine sulfate. However, avoid beta-blockers if there is aortic valvular
regurgitation or suspected cardiac tamponade. Maintain the SBP at < 110 mm Hg, unless signs of
end-organ hypoperfusion are present. The preferred treatment includes a combination of narcotic
analgesics (morphine sulfate), beta blockers (labetalol, esmolol), and vasodilators (nicardipine,
nitroprusside). Calcium channel blockers (verapamil, diltiazem) are an alternative to beta
blockers.[12]
For acute coronary syndrome, beta blockers and nitroglycerin are the preferred drugs. Treatment
is indicated if the SBP is >160 mm Hg and/or the DBP is >100 mm Hg. Reduce the BP by 2030% of baseline. Note that thrombolytics are contraindicated if the BP is >185/100 mm Hg.[13]
In acute heart failure, the preferred medications are IV nitroglycerin or sublingual nitroglycerin
and IV enalaprilat. Treat with vasodilators (in addition to diuretics) for a SBP 140 mm Hg.[13]

Cocaine toxicity/pheochromocytoma
Diazepam, phentolamine, and nitroglycerin/nitroprusside are the preferred drugs. However,
avoid beta-adrenergic antagonists before administering phentolamine.
Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alphaadrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute
coronary syndromes.[14] Pheochromocytoma treatment guidelines are similar to that of cocaine
toxicity. Only after alpha blockade can beta blockers be added for BP control.

Preeclampsia/eclampsia

The preferred medications are hydralazine, labetalol, and nifedipine. Avoid - Nitroprusside,
angiotensin-converting enzyme inhibitors, esmolol. In women with eclampsia or preeclampsia,
the SBP should be < 160 mm Hg and the DBP should be < 110 mm Hg in the antepartum and
intrapartum periods. If the platelet count is less than 100,000 cells mm3, the BP should be
maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia should also be
treated with IV magnesium sulfate to avoid seizures.[15]

Perioperative hypertension
Nitroprusside, nitroglycerin, and esmolol are preferred. Target the perioperative BP to within
20% of the patient's baseline pressure, except if there is the potential for life-threatening arterial
bleeding. Perioperative beta blockers are the first choice in patients undergoing vascular
procedures or in patients with an intermediate or high risk of cardiac complications.[12]
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