Hypertensive Crises

Donald G. Vidt

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Hypertensive crises encompass a spectrum of clinical situations that have in common severely elevated blood pressure (BP), usually higher than 180/110 mm Hg, together with progressive or impending target organ damage. Patients with hypertensive crises may present with a range of blood pressures, varied clinical symptoms, and the presence or absence of target organ involvement. Early triage in the emergency department is critical to identify those individuals who may require more aggressive management in the emergency room or admission for parenteral treatment of the true hypertensive emergency. Most hypertensive emergencies and urgencies are preventable and are the result of untreated or inadequately treated stage I or II hypertension, or nonadherence to antihypertensive therapy. 1–3


Hypertensive emergencies are severe elevations in BP, often higher than 220/140 mm Hg, complicated by clinical evidence of progressive target organ dysfunction. These patients require immediate admission and BP reduction (not necessarily to normal ranges) to prevent or limit further target organ damage. Examples include hypertensive encephalopathy, intracranial hemorrhage, acute myocardial infarction, acute left ventricular failure with pulmonary edema, dissecting aneurysm, acute renal failure, and eclampsia of pregnancy. Immediate admission to a monitored unit and parenteral antihypertensive therapy are indicated. It is the clinical state of the patient—in particular, the degree of and/or progression of target organ damage—–that defines a hypertensive emergency and not the absolute level of blood pressure.

Severe hypertension (urgencies) are marked elevations of BP, usually higher than 180/110 mm Hg. Evidence of target organ damage is often present, but nonprogressive and manifesting symptoms may include headache, shortness of breath, and pedal edema. Management in the emergency department (ED) with oral agents is suitable, depending on the individual's presentation, and follow-up within 24 to 72 hours is recommended. In many cases, with blood pressure higher than 180/110 mm Hg, patients present without clinical symptoms and have no clinical evidence of target organ damage. If untreated, they may be initiated on a two-drug regimen or an existing treatment regimen may be modified. Emotional distress or nonadherence with prior treatment are often at fault. These patients do not require BP reduction to normal and, after brief observation in the emergency room, can be discharged, with follow-up scheduled within 3 to 7 days.

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Hypertensive crises affect upward of 500,000 Americans each year. Although the incidence of hypertensive crisis is low, affecting no more than 1% of hypertensive adults, it must be remembered that more than 55 million Americans currently suffer from hypertension, and control rates for BP in our society remain poor. To put these numbers into perspective, it is known that hypertension-related emergency department visits place a significant burden on most busy metropolitan emergency departments. Based on current definitions, one study has found that hypertensive crises account for more than 25% of all patient visits to the medical section of the ED. 4 Hypertensive emergencies accounted for one third of these cases. Although the level of BP is not considered an absolute criterion for the diagnosis of a hypertensive emergency, all patients in that study presented with diastolic BPs exceeding 120 mm Hg.

Early triage of patients presenting with hypertensive crises is critical to help establish the most appropriate initial therapeutic strategies in an effort to limit morbidity and mortality for this patient population.

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Signs, symptoms, and diagnosis

Initial Assessment

A brief but thorough history should address the duration as well as the severity of hypertension, all current medications, including prescription and nonprescription drugs and, of particular importance, the use of recreational drugs. A history of other comorbid conditions and prior cardiovascular or renal disease is essential to the initial evaluation. Direct questioning regarding the level of compliance with current antihypertensive medications may establish inadequacy of treatment or frank noncompliance. 3,5

Frequent or continuous monitoring of BP should be established. Historical information suggestive of neurologic, cardiovascular, and/or renal symptoms should be sought. Specific manifestations such as headache, seizures, chest pain, dyspnea, or edema should be assessed. The clinical characteristics of a hypertensive emergency are listed in Table 1 . The level of BP alone does not determine a hypertensive emergency; rather, it is the degree of target organ involvement that will determine the rapidity with which BP should be reduced to a safer level to prevent or limit target organ damage. Initial therapy will be appropriate for a presumptive diagnosis based on the information available during the initial triage evaluation. The algorithm shown in Table 2 can help the clinician identify those patients who meet the criteria of a hypertensive emergency that requires immediate admission to an intensive care unit (ICU) for continuous monitoring of BP and initiation of parenteral antihypertensive therapy.

Table 1: Clinical Characteristics of the Hypertensive Emergency
Blood Pressure (mm Hg) Funduscopic Findings Neurologic Status Cardiac Findings Renal Symptoms Gastrointestinal Symptoms
Usually >220/140 Hemorrhages, exudates, papilledema Headache, confusion, somnolence, stupor, visual loss, seizures, focal neurologic deficits, coma Prominent apical pulsation, cardiac enlargement, congestive heart failure Azotemia, proteinuria, oliguria Nausea, vomiting


Table 2: Algorithm for Triage Evaluation
Severe Hypertension (Urgency)

Parameter Asymptomatic Symptomatic Hypertensive Emergency
Blood pressure (mm Hg) >180/110 >180/110 Usually >220/140
Symptoms Headache, anxiety; often asymptomatic Severe headache, shortness of breath Shortness of breath, chest pain, nocturia, dysarthria, weakness, altered consciousness
Examination No target organ damage, no clinical cardiovascular disease Target organ damage; clinical cardiovascular disease present, stable Encephalopathy, pulmonary edema, renal insufficiency, cerebrovascular accident, cardiac ischemia
Therapy Observe 1-3 hr; initiate, resume medication; increase dosage of inadequate agent Observe 3-6 hr; lower BP with short-acting oral agent; adjust current therapy Baseline laboratory tests; intravenous line; monitor BP; may initiate parenteral therapy in emergency room
Plan Arrange follow-up within 3-7 days; if no prior evaluation, schedule appointment Arrange follow-up evaluation in less than 72 hr Immediate admission to ICU; treat to initial goal BP; additional diagnostic studies

BP, blood pressure; ICU, intensive care unit.

Physical Examination

The physical examination should begin with an assessment of BP using an appropriately sized cuff in both upper extremities and in a lower extremity if peripheral pulses are markedly reduced. Brachial, femoral, and carotid pulses should be assessed. A careful cardiovascular examination, as well as a thorough neurologic examination, including mental status, should be conducted. This assessment will aid in establishing the degree of involvement of affected target organs and should provide clues to the possible existence of a secondary form of hypertension, such as renovascular hypertension. If a secondary cause of hypertension is suspected, appropriate blood and urine samples should be obtained before aggressive therapy is initiated. A careful funduscopic examination should be performed to detect the presence of hemorrhages, exudates, and/or papilledema.

Initial Laboratory Studies

Initial laboratory studies should be limited and rapidly expedited. A urinalysis with microscopic examination of the urinary sediment, an immediate chemistry panel, and an electrocardiogram should be obtained. The urinalysis may reveal significant proteinuria, red blood cells, and/or cellular casts. Cellular casts are suggestive of renal parenchymal disease. Electrolyte abnormalities, particularly hypokalemia or hypomagnesemia, increase the risk of cardiac arrhythmias, and the chemistry panel will also provide evidence of renal or hepatic dysfunction, or both. The electrocardiogram should identify evidence of coronary ischemia, left ventricular hypertrophy, or both, and may reveal pulse deficits, raising the question of aortic dissection. When the clinical examination suggests cerebrovascular ischemia or hemorrhage, or if the patient is comatose, a computed tomography (CT) scan of the head should be immediately obtained.

For the patient with a hypertensive emergency, BP reduction should not be delayed until the results of all diagnostic studies are available for review, but should be initiated as soon as the patient's clinical status is established. Unfortunately, most emergency department patients with severely elevated BP do not receive the evaluation, treatment modifications, or discharge instructions consistent with most current guidelines. Two recent studies evaluating the emergency department management of patients with severe hypertension 6,7 have revealed a number of significant shortcomings. For example, fewer than 10% of patients received all recommended studies, serum chemistries were performed in 70% to 73%, an electrocardiogram in 53% to 70%, a chest x-ray in 24% to 46%, and a urine analysis in only 43% to 44%. Two thirds of patients evaluated did not have a funduscopic examination in the emergency room. It was also distressing to note that although follow-up care was often recommended in both studies, it was infrequently scheduled in writing before patients were discharged from the emergency department.


  • Most hypertensive crises are preventable.
  • Hypertensive urgencies occur without evidence of progressive target organ damage.
  • Hypertensive emergencies are complicated by evidence of progressive target organ damage.
  • The levels of blood pressure readings alone do not determine action; this is determined by the degree of target organ damage.

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It is well recognized that patients presenting to emergency departments with hypertensive crises, BP higher than 180/110 mm Hg, represent a significant burden for most metropolitan emergency departments. However, these patients must not be allowed to wait their turn for initial evaluation because of the utmost importance of identifying those patients with a true hypertensive emergency; they require prompt transfer to a monitored unit and aggressive parenteral therapy for reduction of BP to a safer level, at which time further evaluation can be safely accomplished. Those patients who do not meet the criteria for a hypertensive emergency can then be managed in a more timely manner. This is best accomplished by using the initial triage evaluation to categorize patients into two groups: (1) those with severe hypertension (symptomatic or asymptomatic) and (2) those with an actual hypertensive emergency.

Emergency Department Treatment of Severe Hypertension—Urgencies

Historically, most patients seen in the ED with severe hypertension do not meet the criteria for a hypertensive emergency. However, they were often classified on the level of BP alone as hypertensive urgencies and were treated aggressively in the ED with many actually being admitted to the hospital for control of BP. An important caveat here is that elevated BP of itself rarely requires emergency therapy. Initial triage should quickly identify those patients who have an elevated BP without any evidence of significant target organ damage or any other impending cardiovascular events. 8 These patients clearly represent most of those seen in the ED. They are usually asymptomatic, although evidence of anxiety, headache, shortness of breath, or pedal edema may be observed.

It is not necessary to reduce BP to normal during the period of observation. A valuable lesson was learned from the adverse ischemic consequences caused by the formerly common ED practice of using oral nifedipine for almost any patient who presented with marked BP elevation. Physicians must also now be aware that aggressive dosing of oral agents may also necessitate a longer period of observation in the ED to minimize the risk of significant hypotension following discharge. Appropriate follow-up within 3 days should be scheduled and written instructions provided to the patient. There are several agents available that can reliably induce an immediate reduction in BP while the patient is under observation in the ED ( Table 3 ).

Table 3: Oral Agents for the Treatment of Hypertensive Agencies
Agent Dosage Onset/Duration of Action (after discontinuation) Precautions
Captopril 25 mg PO; repeat as needed; SL, 25 mg 15-30 min/6-8 hr SL 10-20 min/2-6 hr Hypotension, renal failure, bilateral renal artery stenosis
Clonidine 0.1-0.2 mg PO, repeat hourly as required to total dosage of 0.6 mg 30-60 min/8-16 hr Hypotension, drowsiness, dry mouth
Labetalol 200-400 mg PO; repeat every 2-3 hr 1-2 hr/2-12 hr Bronchoconstriction, heart block, orthostatic hypotension
Amlodipine 2.5-5 mg 1-2 hr/12-18 hr Tachycardia, hypotension

SL, sublingual.

Treatment for Hypertensive Emergencies

The initial goal for BP reduction is not to obtain a normal BP, but to achieve a progressive controlled reduction to minimize the risk of hypoperfusion to vital organs. Under normal conditions, blood flow to cerebral coronary and renal circulatory beds remains relatively constant, despite wide BP fluctuations. In the presence of severe hypertension, accompanied by intensive systemic vasoconstriction and often significant (but masked) blood volume reduction, the autoregulatory range is shifted upward so that higher levels of BP are tolerated, but organ circulation may be put at risk with sudden reductions in BP. For example, studies on the autoregulation of cerebral blood flow have suggested that the lower limit of autoregulation is approximately 25% below the resting mean arterial pressure in normotensive subjects and in those with uncomplicated hypertension. 3,9 These observations have led to the suggestion that initial reduction in mean arterial pressure should not exceed 20% to 25% below the pretreatment BP. As an alternative, mean arterial pressure can be reduced within the first 30 to 60 minutes to 110 to 115 mm Hg. If this level is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24 hours. With judicious and gradual BP lowering, hypoperfusion is rarely seen and autoregulatory mechanisms reset toward more normal levels. Excessively rapid reductions in BP have been associated with acute deterioration in renal function, ischemic cardiac or cerebral events, and occasional retinal artery occlusion and acute blindness.

Therapy is often initiated before the results of laboratory studies are available. Although aggressive treatment is appropriate, initial therapy should be aimed at a partial reduction in BP in the first 30 to 60 minutes, rather than achievement of normotensive BP levels. Further progressive reduction in BP over the first 24 hours will depend on the clinical state of the patient and adequacy of target organ function. There are significant exceptions to these initial recommendations; these are discussed in more detail later in the section on the treatment of select hypertensive emergencies.

Parenteral Agents

Parenteral therapy may be initiated in the ED if suitable supervision and monitoring of BP can be provided. More appropriately, the patient should be transferred to an intensive care unit (ICU) where continuous nursing supervision and monitoring of BP are available. A number of parenteral agents are effective in the immediate treatment of hypertensive emergencies ( Table 4 ). 8,10,11

Table 4: Treatment of Hypertensive Emergencies
Agent Dosage Onset/Duration of Action (after discontinuation) Precautions
Parenteral Vasodilators
Sodium nitroprusside 0.25-10 μg/kg/min as IV infusion Immediate/2-3 min after infusion Nausea, vomiting; prolonged use may cause thiocyanate intoxication, methemoglobinemia, acidosis, cyanide poisoning; bags, bottles, delivery sets must be light resistant
Nitroglycerin 5-100 μg as IV infusion * 2-5 min/5-10 min Headache, tachycardia, vomiting, flushing, methemoglobinemia; requires special delivery system because of drug binding to PVC tubing
Nicardipine 5-15 mg/hr as IV infusion 1-5 min/15-30 min, but may exceed 12 hr after prolonged infusion Tachycardia, nausea, vomiting, headache, increased intracranial pressure; hypotension may be protracted after prolonged infusions
Fenoldopam mesylate 0.1-0.3 μg/kg/min as IV infusion <5 min/30 min Headache, tachycardia, flushing, local phlebitis, dizziness
Hydralazine 5-20 mg as IV bolus or 10-40 mg IM; repeat every 4-6 hr 10 min IV/>1 hr (IV); 20-30 min IM/4-6 hr (IM) Tachycardia, headache, vomiting, aggravation of angina pectoris, sodium and water retention, increased intracranial pressure
Enalaprilat 0.625-1.25 mg every 6 hr as IV injection Within 30 min/12-24 hr Renal failure in patients with bilateral renal artery stenosis, hypotension
Parenteral Adrenergic Inhibitors
Labetalol 20-40 mg as IV bolus every 10 min; up to 2 mg/min as IV infusion 5-10 min/2-6 hr Bronchoconstriction, heart block, orthostatic hypotension, bradycardia
Esmolol 500-μg/kg bolus injection IV or 50-100 μg/kg/min by infusion; may repeat bolus after 5 min or increase infusion rate to 300 μg/kg/min 1-5 min/15-30 min First-degree heart block, congestive heart failure, asthma
Phentolamine 5-10 mg as IV bolus 1-2 min/10-30 min Tachycardia, orthostatic hypotension

* Requires special delivery system.

PVC, polyvinyl chloride.

Preferred Drugs

The type of ongoing acute target organ damage will significantly affect the selection of parenteral agents for BP reduction. It is also important to keep in mind that it is not the absolute level of blood pressure, but rather the clinical status of the patient that determines the hypertensive emergency and influences the choice of antihypertensive agent ( Table 5 ). 3,11

Table 5: Preferred Drugs for Select Hypertensive Emergencies
Emergency Drugs of Choice Target Blood Pressure
Aortic dissection Nitroprusside + esmolol 110-120 SBP as soon as possible
AMI, ischemia Nitroglycerin, nitroprusside, nicardipine Secondary to ischemia relief
Pulmonary edema Nitroprusside, nitroglycerin, labetalol Improve symptoms 10%-15% in 1-2 hr
Renal emergencies Fenoldopam, nitroprusside, labetalol Target BP 20%-25% in 2-3 hr
Catecholamine excess Phentolamine, labetalol Control paroxysms 10%-15% in 1-2 hr
Hypertensive encephalopathy Nitroprusside 20%-25% in 2-3 hr
Subarachnoid hemorrhage Nitroprusside, nimodipine, nicardipine 20%-25% in 2-3 hr
Ischemic stroke Nitroprusside (controversial), nicardipine 0%-20% in 6-12 hr

AMI, acute myocardial infarction; SBP, systolic bood pressure.

Special Considerations in Select Hypertensive Emergencies

Aortic Dissection.

This is a special type of hypertensive emergency because of the exceptionally high short-term risk and the lower recommended target systolic blood pressure. There is general agreement that at the time of diagnosis, and perhaps even when it is suspected, quickly controlling the systolic BP to lower than 120 mm Hg within 10 to 20 minutes supersedes the performance of any time-consuming techniques used to identify the dissection. The location and the extent of the dissection will determine the need for immediate surgery versus long-term medical therapy.

Acute Coronary Syndrome.

This situation includes patients presenting with unstable angina or myocardial infarction. Hypertension is often affected by acute adrenergic stimulation caused by ischemic chest pain or severe anxiety, but relief of chest pain is a priority, together with opening the coronary artery responsible in the case of a myocardial infarction for improved myocardial oxygen supply. The level of BP will determine the use of nitroglycerin or nitroprusside in this situation. Nicardipine can also be a useful alternative. Control of BP is an important adjuvant to therapy. A reduction of 10% to 20% over the first 1 to 3 hours will often be sufficient to alleviate chest pain. It is also an important step before consideration of thrombolytic therapy.

Congestive Heart Failure.

Congestive heart failure along with severe hypertension often results in pulmonary edema and a sharp reduction in effective circulating blood volume. In this setting, the agents of choice are those that reduce preload and afterload. The most effective is sodium nitroprusside or fenoldopam, although nitroglycerin can also be valuable, particularly if BP is not markedly elevated. Appropriate and timely use of a parenteral loop diuretic is also usually necessary.

Acute or Chronic Renal Failure.

This can be associated with severe hypertension. In particular, new or acutely worsening azotemia or the presence of dysmorphic red cells or red cell casts in the urine should prompt early and aggressive therapy. A gradual reduction in BP of 20% to 25% during the first 1 to 3 hours is particularly helpful. Nitroprusside, labetalol, and nicardipine are all effective; however, strong consideration should be given to fenoldopam as the agent of choice because of its favorable effects on renal function. 12

Adrenergic Crises.

The typical background for a hypertensive emergency caused by catecholamine excess includes the presence of a pheochromocytoma, cocaine or amphetamine intoxication, and dietary noncompliance in patients taking monoamine oxidase inhibitors. In all these situations, care must be taken to select antihypertensive therapies that will not result in unopposed α-adrenergic stimulation, which could worsen the hypertension. Phentolamine may be useful as an initial agent to control paroxysms but is difficult to titrate for ongoing therapy. Beta blockers are generally avoided but labetalol has proved a useful agent with its alpha and beta blocking characteristics. When an occasional hypertensive crisis is observed secondary to clonidine withdrawal, immediate reinstitution of clonidine is appropriate. BP will often respond to one or two doses of clonidine, 0.1 to 0.2 mg.

Hypertensive Encephalopathy.

This is a potentially lethal complication of severe hypertension and may be seen in association with a number of hypertensive emergencies. When markedly elevated BP exceeds the autoregulatory ability of the brain to maintain constant cerebral perfusion, the resultant diffuse cerebral edema can lead to progressive neurologic dysfunction. The finding of exudates, hemorrhages, and/or papilledema on funduscopic examination, together with new focal neurologic findings, altered level of consciousness, new-onset seizures, or sensory deficits, supports this diagnosis. Although hypertensive encephalopathy typically follows a more subacute time course, it is nevertheless a diagnosis of exclusion and requires that stroke, intracranial hemorrhage, seizure disorders, or mass lesions be ruled out. Distinguishing among these potential mechanisms of injury can be clinically difficult, and has a significant impact on subsequent therapy. The best approach is to use an available imaging procedure to clarify the diagnosis.

When hypertensive encephalopathy is suspected, BP should be promptly lowered with nitroprusside or labetalol, with careful monitoring and frequent neurologic assessments. BP reduction can be associated with dramatic improvement in cerebral function. However, deterioration in neurologic function will require re-evaluation and consideration of other possible diagnoses.

Subarachnoid Hemorrhage.

Acute BP reduction is warranted in subarachnoid hemorrhage and the agent of choice again would be sodium nitroprusside. Nicardipine has also proved effective. Another dihydropyridine calcium antagonist, nimodipine, has demonstrated antihypertensive and anti-ischemic effects that may improve long-term outcomes of subarachnoid hemorrhage but not necessarily ischemic stroke.

Ischemic Stroke.

There is considerable controversy regarding the optimal management of patients suffering from an ischemic stroke in the setting of hypertension. Stroke may result from hypertension or the hypertension may be a consequence of the event itself. In the latter situation, BP elevations will often remit during the first several days of hospitalization. The stroke may result in the creation of watershed areas of tissue that are not ischemic and remain viable as long as perfusion is maintained; they may depend on the higher perfusion pressure conferred by the systemic hypertension. Thus, acute reductions in BP may result in extension of the ischemic damage to these areas.

Several smaller studies have failed to demonstrate risk reduction by early aggressive treatment of severe hypertension. I prefer not to pursue BP reduction aggressively unless the BP following admission persists at higher than 220 mm Hg/120 mm Hg, there is evidence of neurologic deterioration, or both. First-line agents include nitroprusside, nicardipine, fenoldopam, and labetalol. I recommend avoiding reductions in mean arterial pressure higher than 10% in the first 1 to 3 hours or higher than 20% in the first 6 to 12 hours, with careful and frequent monitoring of neurologic status. The use of parenteral agents with short half-lives is most appropriate in this situation.


  • Hypertensive emergencies warrant prompt ICU admission for rapid treatment and continuous blood pressure monitoring.
  • Most hypertensive urgencies can be managed on an ambulatory basis.
  • Excessive blood pressure reduction has been associated with acute deterioration of renal function, ischemic cardiac and cerebral events, and acute blindness.
  • A decrease of 20% to 25% in mean arterial pressure from pretreatment blood pressure has been recommended.

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Regardless of the type of hypertensive emergency or the antihypertensive agent used to control BP, a primary objective should be to start an oral regimen as soon as the patient can tolerate it. This approach facilitates earlier tapering and discontinuation of parenteral agents and may facilitate earlier hospital discharge. Switching abruptly from intravenous to oral therapy may result in a precipitous rise in BP if appropriate agents are not chosen. Consequently, careful monitoring of BP during this period is critical. If appropriate follow-up care can be arranged, even those patients who needed emergent or urgent treatment can safely be discharged on oral medications, with a follow-up visit within 24 to 72 hours in the outpatient setting. A patient who is discharged from the ER or outpatient setting without a confirmed follow-up appointment represents a missed opportunity to get that patient back into treatment. Optimal control of BP and persistent follow-up should be a management priority.

The vast majority of patients presenting to the hospital with severe hypertension have been previously diagnosed with hypertension. The most common history obtained from patients presenting with a hypertensive crisis is that of a patient diagnosed with chronic hypertension who has been noncompliant with treatment or has been undertreated by his or her health care provider. Patients who have regular follow-ups and are compliant with their antihypertensive medications are clearly at lower risk for the development of a hypertensive crisis. Focusing on the initial identification and aggressive treatment to goal BP, together with routinely scheduled follow-up for the uncomplicated hypertensive patient, are critical for preventing accelerated hypertension and eventual presentation with a hypertensive crisis.

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  1. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and the Treatment of High Blood Pressure. Hypertension. 42: 2003; 1206-1252.
  2. Management of hypertensive emergencies and urgencies.. Oparil S, Weber MA. Hypertension—A Companion to Brenner and Rector's The Kidney. 2nd ed. 2005; ;Philadelphia. 826-837.
  3. Hypertensive emergencies and urgencies: Uncontrolled severe hypertension.. Battegay EJ, Lip GYH , Bakris GL. Hypertension—Principles and Practice. 2005; ;Boca Raton, Fla. 651-669.
  4. Hypertensive urgencies and emergencies: Prevalence and clinical presentation. Hypertension. 27: 1996; 144-147.
  5. Hypertensive crises: Emergencies and urgencies. J Clin Hypertens. 6: 2004; 520-525.
  6. Characteristics and management of patients presenting to the emergency department with hypertensive urgency. J Clin Hypertens. 8: 2006; 12-18.
  7. Evaluation and treatment of patients with severely elevated BP in academic emergency deparments: A multicenter study. Ann Emerg Med. 47: 2006; 230-236.
  8. Hypertensive emergencies and urgencies.. Black HR, Elliott WJ. Hypertension—A Companion to Braunwald's Heart Disease. 2007; ;Philadelphia. 517-524.
  9. Regulation of cerebral blood flow in health and disease. J Cardiovasc Pharmacol. 9: 1992; S89-S93.
  10. Drug treatment of hypertensive urgencies and emergencies. Semin Nephrol. 25: 2005; 272-280.
  11. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 48: 2006; 316-325.
  12. Fenoldopam versus nitroprusside for the treatment of hypertensive emergency. Ann Pharmacother. 38: 2004; 755-759.

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Suggested Readings

  • Characteristics and management of patients presenting to the emergency department with hypertensive urgency. J Clin Hypertens. 8: 2006; 12-18.
  • Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee: Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and the Treatment of High Blood Pressure. Hypertension. 42: 2003; 1206-1252.
  • Fenoldopam versus nitroprusside for the treatment of hypertensive emergency. Ann Pharmacother. 38: 2004; 755-759.
  • Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 48: 2006; 316-325.
  • Drug treatment of hypertensive urgencies and emergencies. Semin Nephrol. 25: 2005; 272-280.
  • Hypertensive emergencies and urgencies: Uncontrolled severe hypertension. Battegay EJ, Lip GYH , Bakris GL. Hypertension—Principles and Practice. 2005; ;Boca Raton, Fla. 651-669.
  • Evaluation and treatment of patients with severely elevated BP in academic emergency deparments: A multicenter study. Ann Emerg Med. 47: 2006; 230-236.
  • Hypertensive emergencies and urgencies. Black HR, Elliott WJ. Hypertension—A Companion to Braunwald's Heart Disease. 2007; ;Philadelphia. 517-524.
  • Regulation of cerebral blood flow in health and disease. J Cardiovasc Pharmacol. 9: 1992; S89-S93.
  • Hypertensive crises: Emergencies and urgencies. J Clin Hypertens. 6: 2004; 520-525.
  • Management of hypertensive emergencies and urgencies. Oparil S, Weber MA. Hypertension—A Companion to Brenner and Rector's The Kidney. 2nd ed 2005; ;Philadelphia. 826-837.
  • Hypertensive urgencies and emergencies: Prevalence and clinical presentation. Hypertension. 27: 1996; 144-147.