AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Approximately 50 million people in the United States are affected by hypertension (HTN).¹ New data show an increased lifetime risk of developing HTN and an increased risk of cardiovascular complications associated with blood pressures (BPs) previously considered to be normal. Given this information, the Joint National Committee (JNC-7) has introduced a new classification system for HTN.²

• Prehypertension - Systolic blood pressure (SBP) 120-139 mm Hg or diastolic blood pressure (DBP) 80-89 mm Hg
• Stage I HTN - SBP 140-159 mm Hg or DBP 90-99 mm Hg
• Stage II HTN - SBP >160 mm Hg or DBP >100 mm Hg

Hypertensive crises encompass a spectrum of clinical presentations where uncontrolled BPs lead to progressive or impending target organ dysfunction (TOD). The clinical distinction between hypertensive emergencies and hypertensive urgencies depends on the presence of acute TOD and not on the absolute level of the BP.

Hypertensive emergency

Hypertensive emergencies represent severe HTN with acute impairment of an organ system (eg, central nervous system [CNS], cardiovascular, renal). In these conditions, the BP should be lowered aggressively over minutes to hours.

Hypertensive urgency

Hypertensive urgency is defined as a severe elevation of BP, without evidence of progressive TOD. These patients require BP control over several days to weeks.

Emergency department considerations

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 the following:

• Appropriately evaluating patients with an elevated BP
• Correctly classifying the HTN
• Determining the aggressiveness and timing of therapeutic interventions
• Making disposition decisions

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."

Pathophysiology

The pathophysiology of hypertensive emergencies is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typically initial steps in the disease process. This is followed by endovascular injury, with fibrinoid necrosis within the arterioles. If the process is not stopped, a cycle of ischemia, platelet deposition, and further autoregulatory dysfunction ensues. The 4 major organ systems affected by high BP are the CNS, cardiovascular system, renal system, and gravid uterus.

Single-organ involvement is found in approximately 83% of patients presenting with hypertensive emergencies. Two-organ involvement is found in 14% of cases, and multiorgan involvement (>3 organ systems) is found in approximately 3% of patients presenting with a hypertensive emergency.³

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 (12.0%). Less common presentations include intracranial hemorrhage, aortic dissection, and eclampsia.³

Central nervous system

Cerebral autoregulation is the inherent ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) despite changes in blood pressure. As mean arterial pressure (MAP) increases, the cerebral endothelium is disrupted and the blood-brain barrier can become interrupted. Fibrinoid material deposits in the cerebral vasculature and causes narrowing of the vascular lumen. The cerebral vasculature then attempts to vasodilate around the narrowed lumen. This leads to cerebral edema and microhemorrhages. Patients with chronic HTN can tolerate higher MAPs before they have disruption of their autoregulation system. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases.

Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation. Without treatment, hypertensive encephalopathy can lead to cerebral hemorrhage, coma, and death.

Cardiovascular system

HTN affects the structure and function of the coronary vasculature and left ventricle. HTN also activates the renin-angiotensin-aldosterone system, causing systemic vasculature constriction. This results in increasing myocardial oxygen demand by increasing the left ventricular wall tension and leads to left ventricular hypertrophy and coronary compression. During hypertensive emergencies, the left ventricle cannot overcome systemic vascular resistance. This leads to left ventricular failure and pulmonary edema or myocardial ischemia.

Renal system

Chronic HTN causes pathologic changes to the small arteries of the kidney. The arteries develop endothelial dysfunction and impaired vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted, the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during BP fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia.

Frequency

United States

Hypertension affects approximately 25% of the population in the United States.⁴ The prevalence of HTN increases with advancing age. More than half of people aged 60-69 years and approximately three quarters of people aged 70 years or older are affected by this disease.² Hypertensive crises affect about 500,000 Americans or approximately 1% of hypertensive adults.¹

International

Worldwide, approximately 1 billion people have HTN.²

Mortality/Morbidity

Death from both ischemic heart disease and stroke increase progressively as the BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate from both ischemic heart disease and stroke doubles.²

The morbidity and mortality of hypertensive emergencies depend on the extent of TOD on presentation and the degree to which BP is controlled subsequently. With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.¹

• The 1-year mortality rate for an untreated hypertensive emergency is 79%.⁵
• The 5-year survival rate among all patients presenting with a hypertensive crisis is 74%.⁶ 

Race

Hypertension develops at an earlier age, leads to more clinical sequelae, and is more common and severe in African Americans compared with age-matched non-Hispanic whites. Hypertensive crises are also more common in African Americans when compared with other races.

The prevalence and incidence of HTN in Mexican Americans are similar to or lower than those in non-Hispanic whites. In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic whites and African Americans.

Sex

Overall, the prevalence and incidence of HTN is slightly higher in men than in women. Hypertensive crises are 2 times more frequent in males than in females.

Age

Hypertensive crises are more common among elderly persons.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

The history should focus on the presence of TOD, the circumstances surrounding the HTN, and any identifiable etiology. The history and physical examination determine the nature, severity, and management of the hypertensive event.

• Medications
• • Details of antihypertensive drug therapy and compliance
  • Intake of over-the-counter preparations such as sympathomimetic agents
  • Use of illicit drugs such as cocaine
• Duration and severity of preexisting HTN
• Degree of BP control
• Presence of previous TOD, particularly renal and cerebrovascular disease
• Date of last menstrual period
• Other medical problems (eg, prior HTN, thyroid disease, Cushing disease, systemic lupus, renal disease)
• Assess whether specific symptoms suggesting TOD are present.
• • Chest pain - Myocardial ischemia or infarction
  • Back pain - Aortic dissection
  • Dyspnea - Pulmonary edema, congestive heart failure
  • Neurologic symptoms - Seizures, visual disturbances, altered level of consciousness (hypertensive encephalopathy)

Physical

The physical examination should assess whether TOD is present.

• Vitals
• • BP should be measured in both the supine position and the standing position (assess volume depletion).
  • BP should also be measured in both arms (a significant difference suggests an aortic dissection).
• ENT: The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency.
• Cardiovascular - Evaluate for the presence of heart failure.
• • Jugular venous distension
  • Crackles
  • Peripheral edema
• Abdomen - Abdominal masses or bruits
• CNS
• • Level of consciousness
  • Visual fields
  • Focal neurologic signs

Causes

The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential HTN. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications.

• Other causes
• • Renal parenchymal disease - Chronic pyelonephritis, primary glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all secondary causes)
  • Systemic disorders with renal involvement - Systemic lupus erythematosus, systemic sclerosis, vasculitides
  • Renovascular disease - Atherosclerotic disease, fibromuscular dysplasia, polyarteritis nodosa
  • Endocrine - Pheochromocytoma, Cushing syndrome, primary hyperaldosteronism
  • Drugs - Cocaine, amphetamines, cyclosporin, clonidine withdrawal, phencyclidine, diet pills, oral contraceptive pills
  • Drug interactions - Monoamine oxidase inhibitors with tricyclic antidepressants, antihistamines, or tyramine-containing food
  • CNS - CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome
  • Coarctation of the aorta
  • Preeclampsia/eclampsia
  • Postoperative hypertension

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Steroid use
Use of over-the-counter or recreational sympathomimetic drugs
Pheochromocytoma
Acute vasculitis
Serotonin syndrome
Other CNS pathology
Coarctation of the aorta

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• Electrolytes, BUN, and creatinine levels to evaluate for renal impairment
• CBC and smear to exclude microangiopathic anemia
• Urinalysis  
• • Dipstick urinalysis (UA) to detect hematuria or proteinuria (renal impairment)
  • Microscopic UA to detect RBCs or RBC casts (renal impairment)
• Optional studies
• • Toxicology screen
  • Pregnancy test
  • Endocrine testing

Imaging Studies

• Chest radiography is indicated in patients with chest pain or shortness of breath.
• • Cardiac enlargement
  • Pulmonary edema
  • Widened mediastinum
• Head CT and/or brain MRI are indicated in patients with abnormal neurologic examinations or clinical concern for the following.
• • Intracranial bleeding
  • Cerebral edema
  • Cerebral infarction
• Chest CT scan, transesophageal echocardiography, or aortic angiography is indicated in cases where aortic dissection is suspected.

Other Tests

• Electrocardiography (ECG) to assess for evidence of myocardial ischemia or left ventricular hypertrophy

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Prehospital Care

• Address the manifestations of a hypertensive emergency, such as chest pain or heart failure. Reduction of BP may not be indicated in the prehospital setting.
• Under most circumstances, attempting to treat HTN directly in the prehospital setting is unwise. In particular, rapid lowering of BP can critically decrease target organ perfusion.

Emergency Department Care

The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of TOD.

• Initial considerations (if the patient is not in distress)
• • Place the patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP higher than 130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment.
  • Consider the context of the elevated BP (eg, severe pain often causes increase in BP).
• Screen for TOD: The patient's history, physical examination, laboratory studies, and diagnostic tests, as outlined in Workup, should be used to determine if TOD exists.
• Patients without evidence of TOD may be discharged with follow-up.
• The misconception remains that a patient never should be discharged from the ED with an elevated BP. As a result of this belief, patients are given oral medicines, such as nifedipine, in an effort to lower BP rapidly before discharge. This is not indicated and may be dangerous.
• Attempts to temporarily lower BP by using these medicines may result in a precipitous and difficult-to-correct drop in BP. Should this occur, target organ hypoperfusion may result. Furthermore, patients who present with high BP may have had this elevation for some time and may need chronic BP control but may not tolerate rapid return of BP to a "normal" level.
• Acute lowering of BP in the narrow window of the ED visit does not improve long-term morbidity and mortality rates. The follow-up recommended for these situations by the Joint National Committee on High Blood Pressure is outlined in Follow-up.
• Patients with TOD usually require admission and rapid lowering of BP using intravenous medications. Suggested medication depends on the affected organ system.
• Even in cases of hypertensive emergencies, the BP should not be lowered to normal levels.
• Rapid reduction in BP below the cerebral, renal, and/or coronary autoregulatory range results in marked reduction in organ blood flow, possibly leading to ischemia and infarction.
• In general, the MAP should be lowered by no more than 20% in the first hour of treatment. If the patient remains stable, the BP should then be lowered to 160/100-110 mm Hg in the next 2-6 hours. Please note the exceptions to this general rule listed below.
• These BP goals are best achieved by a continuous infusion of a short-acting, titratable, parenteral antihypertensive agent along with constant, intensive patient monitoring.
• Rapid BP reduction is indicated in the following circumstances:
• Acute myocardial ischemia
• • Intravenous nitroglycerin  
  • Intravenous beta-blockers
• CHF with pulmonary edema
• • Intravenous nitroglycerin  
  • Intravenous furosemide (Lasix)
  • Intravenous nitroprusside  
  • Intravenous angiotensin-converting enzyme inhibitors
• Acute aortic dissection: In cases of acute aortic dissection, the SBP should be decreased as rapidly as possible to a goal of 100-110 mm Hg or lower.
• • Intravenous labetalol  
  • Alternative – Intravenous nitroprusside with intravenous beta-blocker (eg, esmolol)
• Cerebral vascular accident: Evidence exists that patients who have acute strokes have better outcomes with higher BPs. Antihypertensive therapy is not routinely recommended for patients with acute stroke and HTN.
• • BP control affects the use of thrombolytic agents in ischemic stroke. SBP higher than 185 mm Hg or diastolic pressures higher than 110 mm Hg are contraindications to the use of tissue plasminogen activator (tPA) within the first 3 hours of an ischemic stroke.
  • The current recommendation by the American Stroke Association states that a patient with a recent ischemic stroke and a SBP higher than 220 mm Hg or a DBP higher than 120-140 mm Hg can undergo cautious reduction of BP by about 10-15% (with IV nitroprusside or IV labetalol), if the patient is carefully monitored for neurologic deterioration related to the lower pressure.
• Intracranial hemorrhage (ICH): No evidence exists to suggest that HTN provokes further bleeding in patients with ICH.
• • A precipitous fall in SBP may compromise cerebral perfusion and increase mortality. Do not exceed a 20% reduction in BP.
  • The controlled lowering of BP with intravenous nitroprusside or intravenous labetalol (in the absence of bradycardia) is currently recommended only when the SBP is higher than 200 mm Hg or the DBP is higher than 110.
• Monoamine oxidase (MAO)-tyramine interactions with acute hypertension - Intravenous phentolamine  
• Pheochromocytoma
• • Intravenous phentolamine  
  • Intravenous labetalol
• Hypertensive encephalopathy: Do not exceed a 20% reduction in BP. 
• • Intravenous nitroprusside  
  • Intravenous labetalol  
  • Intravenous fenoldopam
• Acute renal failure
• • Intravenous fenoldopam  
  • Intravenous nicardipine  
  • Intravenous beta-blockers
• Eclampsia
• • Intravenous hydralazine  
  • Intravenous labetalol  
  • Intravenous magnesium
• Sympathomimetic intoxication: Avoid unopposed beta-blockade.
• • Benzodiazepine
  • Intravenous labetalol
  • Intravenous nitroglycerin
• Acutely lowering of BP in the ED for clinical situations other than those listed here is controversial and generally should be avoided.

Consultations

• Consultations may be indicated for comorbid conditions and their definitive treatment.
• Because HTN is usually a chronic problem, access to a primary care physician and long-term follow-up are essential for all patients.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Once the diagnosis of a true hypertensive emergency is established and TOD is confirmed, BP should be lowered by up to 20% of the MAP or the DBP should be decreased to 100-110 mm Hg over minutes to hours. More rapid reduction in BP should be avoided since it may worsen target organ function.

Drug Category: Beta-adrenergic blockers

These agents are used for hypertensive emergencies, especially with aortic dissection and myocardial infarction. They may be used alone or in combination with sodium nitroprusside. Pure beta-blockers should not be used alone in cases that are the result primarily of alpha stimulation (eg, pheochromocytoma, MAOI-tyramine interaction).

Drug Name	Esmolol (Brevibloc)
Description	Ideal for use in patients at risk for complications from beta-blockers, especially patients with mild to moderately severe LV dysfunction or peripheral vascular disease. Has short half-life of 8 min; thus, easily titratable to desired effect. In addition, therapy may be stopped quickly if necessary.
Adult Dose	Loading dose: 250-500 mcg/kg IV infused over 1-3 min Maintenance infusion: 50 mcg/kg/min IV over 4 min; if adequate effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min IV (for 4 min); this regimen may be repeated up to 4 times if necessary As desired BP approached, skip loading infusion and reduce dose increments in maintenance infusion from 50 mcg/kg/min IV to 25 mcg/kg/min; if necessary, may increase interval between titration steps from 5-10 min
Pediatric Dose	Suggested dose: 100-500 mcg/kg IV over 1 min, then 25-200 mcg/kg/min IV; increase by 25-50 mcg/kg/min IV q5-10min Maximum dose: 50-250 mcg/kg/min IV
Contraindications	Documented hypersensitivity to esmolol or any component of formulation; sinus bradycardia; heart block; cardiogenic shock; bronchial asthma (relative); uncompensated cardiac failure; hypotension; pregnancy (second and third trimesters)
Interactions	Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents Acetylcholinesterase inhibitors may enhance the bradycardic effect of beta-blockers; beta-blockers may enhance the vasopressor effect of alpha/beta-agonists (direct acting); beta-blockers may enhance the orthostatic effect of alpha1-blockers; beta-blockers may enhance the rebound hypertensive effect of alpha2-agonists (effect can occur when alpha2-agonist is abruptly withdrawn) Amiodarone may enhance the bradycardic effect of beta-blockers (possibly to the point of cardiac arrest); beta2-agonists may diminish bradycardic effect of beta-blockers (beta1 selective); calcium channel blockers (nondihydropyridine) may enhance the hypotensive effect of beta-blockers (bradycardia and signs of heart failure have also been reported); beta-blockers may enhance the bradycardic effect of cardiac glycosides; disopyramide may enhance the bradycardic effect of beta-blockers (use caution if coadministering disopyramide and a beta-blocker, especially if both are IV); beta-blockers may enhance hypoglycemic effect of insulin preparations; NSAIDs may diminish antihypertensive effect of beta-blockers; beta-blockers may enhance hypoglycemic effect of sulfonylureas; cardioselective beta-blockers (eg, esmolol) may be safer than nonselective beta-blockers; all beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Hypotension is common; patients need close BP monitoring; administer cautiously in compensated heart failure and monitor for a worsening of the condition; use caution in patients with PVD (can aggravate arterial insufficiency); use caution with concurrent use of beta-blockers and either verapamil or diltiazem; bradycardia or heart block can occur; avoid concurrent IV use of both agents; use beta-blockers cautiously in patients with bronchospastic disease Beta-blockers can mask prominent hypoglycemic symptoms and mask signs of thyrotoxicosis; can cause fetal bradycardia when administered in third trimester of pregnancy or at delivery; use caution in patients with renal dysfunction (active metabolite retained); do not use in treatment of hypertension associated with vasoconstriction related to hypothermia; concentrations >10 mg/mL or infusion into small veins or through a butterfly catheter should be avoided (can cause thrombophlebitis); extravasation can lead to skin necrosis and sloughing

Drug Category: Alpha-adrenergic blockers

At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in treatment of hypertension. At higher doses, they may cause sodium and fluid retention. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects.

Drug Category: Antihypertensive agents

Sodium nitroprusside is DOC for most hypertensive emergencies. It is potent, rapid in onset, and has a relatively short duration.

Drug Name	Sodium nitroprusside (Nitropress)
Description	Reduces peripheral resistance by acting directly on arteriolar and venous smooth muscle.
Adult Dose	0.3-0.5 mcg/kg/min IV initial infusion, increase in increments of 0.5 mcg/kg/min; titrate to desired effect Average dose: 1-6 mcg/kg/min IV; rates >10 mcg/kg/min may lead to cyanide toxicity
Pediatric Dose	1 mcg/kg/min by continuous IV infusion; increase in increments of 1 mcg/kg/min at intervals of 20-60 min; titrate to desired response; 3 mcg/kg/min usual dose; 5 mcg/kg/min maximum
Contraindications	Documented hypersensitivity to nitroprusside or any component of formulation; treatment of compensatory hypertension (aortic coarctation, arteriovenous shunting); high output failure; congenital optic atrophy or tobacco amblyopia
Interactions	None reported
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Except when used briefly or at low (<2 mcg/kg/min) infusion rates, nitroprusside gives rise to large cyanide quantities; do not use maximum dose for >10 min; use extreme caution in patients with elevated intracranial pressure and patients with hepatic or renal dysfunction (watch for cyanide toxicity in patients with impaired hepatic function); use lowest end of dosage range with renal impairment; thiocyanate toxicity occurs in patients with renal impairment or on prolonged infusions (continuous BP monitoring needed)

Drug Name	Hydralazine (Apresoline)
Description	Principal indication is treatment of eclampsia. Decreases systemic resistance through direct vasodilation of arterioles.
Adult Dose	Initial: 10-20 mg/dose PO q4-6h as needed, may increase to 40 mg/dose; change to oral therapy as soon as possible
Pediatric Dose	0.1-0.2 mg/kg/dose (not to exceed 20 mg) PO q4-6h as needed, up to 1.7-3.5 mg/kg/d in 4-6 divided doses
Contraindications	Documented hypersensitivity to hydralazine or any component of formulation; mitral valve rheumatic heart disease
Interactions	Beta-blockers (metoprolol, propranolol) serum concentrations and pharmacologic effects may be increased (monitor cardiovascular status); propranolol increases hydralazine's serum concentrations; NSAIDs may decrease hemodynamic effects of hydralazine (avoid use if possible or closely monitor cardiovascular status)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	May cause a drug-induced lupuslike syndrome; adjust dose in severe renal dysfunction; use with caution in CAD and pulmonary HTN; monitor BP closely following IV administration; response may be delayed and unpredictable in some patients; titrate cautiously to response; hydralazine-induced fluid and sodium retention may require addition or increased dosage of diuretics

Drug Name	Fenoldopam (Corlopam)
Description	Short-acting dopamine agonist (DA1) recently approved for management of severe HTN. Increases renal blood flow and sodium excretion. It is 10X more potent than dopamine as renal vasodilator.
Adult Dose	Initial: 0.1-0.3 mcg/kg/min IV (lower initial doses may be associated with less reflex tachycardia); may be increased in increments of 0.05-0.1 mcg/kg/min IV q15 min until target blood pressure reached; maximal infusion rate reported in clinical studies was 1.6 mcg/kg/min
Pediatric Dose	0.2 mcg/kg/min IV initial; may be increased to dosages of 0.3-0.5 mcg/kg/min IV q20-30min (0.8 mcg/kg/min maximum); limited to short-term (4 h) use
Contraindications	Documented hypersensitivity to fenoldopam or any component of formulation
Interactions	Acetaminophen may increase levels (30-70%) when administered concurrently; beta-blockers increase risk of hypotension; avoid concurrent use (if must use concurrently, close monitoring recommended)
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Use caution in patients with glaucoma or intraocular hypertension; dose-related tachycardia can occur, especially at infusion rates >0.1 mcg/kg/min; caution in angina patients; close monitoring of BP necessary (hypotension can occur); monitor for hypokalemia at intervals of 6 h during infusion; continuous infusion only (not for bolus doses); effects of hemodialysis on pharmacokinetics of fenoldopam not evaluated; caution with increased intracranial pressure; contains sulfites (may cause allergic reaction in susceptible individuals)

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Patients with a true hypertensive emergency require the careful titration of intravenous medications for good control and a smooth reduction of their BP.
• Close monitoring is required; therefore, an intensive care unit is the most suitable place for admission.
• Other problems or comorbid conditions need to be addressed appropriately (ie, surgery for aortic dissection).

Further Outpatient Care

• Hypertension is a chronic problem. The most important factor in a patient's overall risks of morbidity and mortality is appropriate long-term care.
• If a patient presents with a high BP but ED evaluation reveals no evidence of TOD, the patient does not need immediate treatment in the ED. The patient does require proper follow-up.
• The Joint National Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no TOD.⁴
• • Prehypertension (SBP 120-139 mm Hg, DBP 80-89 mm Hg: BP should be rechecked within 1 year.
  • Stage I HTN (SBP 140-159 mm Hg, DBP 90-99 mm Hg): BP should be rechecked within 2 months.
  • Stage II HTN: (SBP >160 mm Hg or DBP >100 mm Hg): BP should be confirmed and the patient should begin treatment within 1 month.
  • If BP is >180/110 mm Hg: BP should be confirmed and the patient should begin treatment within 1 week.
  • If SBP is >210 mm Hg or DBP >120 mm Hg: Confirm BP, initiate treatment, and arrange close follow-up.

Transfer

• Transfer requirements are based on the ability of the institution to care for the patient and the patient's associated comorbid conditions.
• • A patient with an uncomplicated hypertensive emergency needs an ICU setting.
  • Patients with comorbid conditions, such as aortic dissection or subarachnoid hemorrhage, may require transfer to a higher level of care.

Deterrence/Prevention

• Good long-term control of HTN is the best method for prevention of acute hypertensive emergencies.
• Patient education and close follow-up in patients who have had a hypertensive crisis are essential to prevent recurrent hypertensive emergencies.
• Proper use of antihypertensive medications by primary care physicians is the major tool in avoiding development of hypertensive emergencies.

Complications

• Congestive heart failure
• Myocardial infarction
• Renal failure
• Retinopathy
• Cerebrovascular accident
• Abrupt lowering of BP may result in inadequate cerebral or cardiac blood flow, leading to stroke or myocardial ischemia.

Prognosis

• The 1-year mortality rate is 79% for patients with untreated hypertensive emergencies.⁵
• Five-year survival rate among all patients who present with hypertensive crisis is 74%.⁶

Patient Education

• Patients need continuing education about antihypertensive medications and complications arising from inadequate BP control.
• Dangers of uncontrolled HTN, including associated serious morbidity and death, must be emphasized.
• Education and maintenance of BP control are important to help prevent further complications.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Administering long-acting oral/sublingual medications to acutely lower nonurgent elevations in BP
• Failure to arrange timely and appropriate follow-up
• Failure to recognize the serious complications of severe HTN

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Nathan Shapiro, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

1. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. Feb 2006;24(1):135-46. [Medline].
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3. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. Jan 1996;27(1):144-7. [Medline].
4. Flanigan JS, Vitberg D. Hypertensive emergency and severe hypertension: what to treat, who to treat, and how to treat. Med Clin North Am. May 2006;90(3):439-51. [Medline].
5. Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. Oct 2003;7(5):374-84. [Medline].
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Article Last Updated: Aug 2, 2007