Hypertensive Emergencies

Background

Approximately 50 million people in the United States are affected by hypertension (HTN).^1,2 Substantial improvements have been made with regards to improving awareness and treatment of hypertension. However, approximately 30% of adults are still unaware of their hypertension; up to 40% of people with hypertension are not receiving treatment; and, of those treated, up to 67% do not have their blood pressure (BP) controlled to less than 140/90 mm Hg.³

New data have shown an increased lifetime risk of hypertension and have also highlighted the increased risk of cardiovascular complications with BP levels previously considered to be normal. Given this information, the Joint National Committee (JNC-7) has introduced a new classification system for hypertension.³

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

Hypertensive emergency

Hypertensive emergencies encompass a spectrum of clinical presentations where uncontrolled BPs lead to progressive or impending end-organ dysfunction (EOD). In these conditions, the BP should be lowered aggressively over minutes to hours.

Acute end-organ damage⁴

• Neurological
  • Hypertensive encephalopathy
  • Cerebral vascular accident/cerebral infarction
  • Subarachnoid hemorrhage
  • Intracranial hemorrhage
• Cardiovascular
  • Myocardial ischemia/infarction
  • Acute left ventricular dysfunction
  • Acute pulmonary edema
  • Aortic dissection
• Other
  • Acute renal failure/insufficiency
  • Retinopathy
  • Eclampsia
  • Microangiopathic hemolytic anemia

With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1% of patients with hypertension.⁵ 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.6

Emergency department considerations

Many patients present to the emergency department (ED) with elevated blood pressures; however, only a small proportion of patients will require emergent treatment.

The primary goal of the emergency physician (EP) is to determine which patients with acute hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous parenteral therapy. In contrast, patients presenting with acutely elevated blood pressures (SBP >200 mm Hg or DBP >120 mm Hg) without symptoms require initiation of medical therapy and close follow-up in the outpatient setting.⁷

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 EP must be capable of the following:

• Appropriately evaluating patients with an elevated BP
• Correctly classifying the hypertension
• 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 (SVR) are typically initial steps in the disease process. Increases in SVR are thought to occur from the release of humoral vasoconstrictors from the wall of a stressed vessel. The increased pressure within the vessel then starts a cycle of endothelial damage, local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and the release of more vasoconstrictors. If the process is not stopped, a cycle of further vascular injury, tissue ischemia, and autoregulatory dysfunction ensues.8,9

Single-organ involvement is found in approximately 83% of patients presenting with hypertensive emergencies. Two-organ involvement is found in 14% of patients, and multiorgan involvement (>3 organ systems) is found in approximately 3% of patients presenting with a hypertensive emergency.¹⁰

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%). Less common presentations include intracranial hemorrhage, aortic dissection, and eclampsia.¹⁰

Central nervous system

Cerebral autoregulation is the inherent ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) across a wide range of perfusion pressures.

Patients with chronic hypertension can tolerate higher mean arterial pressures (MAP) 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, especially if blood pressure is decreased into normotensive ranges.

Rapid rises in blood pressure can cause hyperperfusion and increased CBF, which can lead to increased intracranial pressure and cerebral edema.¹¹

Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation and is characterized by hypertension, altered mentation, and papilledema.12

Cardiovascular system

Chronic hypertension causes increased arterial stiffness, increased systolic BP, and widened pulse pressures. These factors act to decrease coronary perfusion pressures, increase myocardial oxygen consumption, and lead to left ventricular hypertrophy.¹² During hypertensive emergencies, the left ventricle is unable to compensate for an acute rise in systemic vascular resistance. This leads to left ventricular failure and pulmonary edema or myocardial ischemia.⁴

Renal system

Chronic hypertension 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.⁴

Frequency

United States

The prevalence of hypertension in the United States from 2003-2004 was approximately 29.3%.¹³ Although significant increases have been made in the control of hypertension, the prevalence of the disease has not decreased.

Factors independently associated with hypertension include age older than 40 years, obesity (body mass index >30 kg/m³), and race (non-Hispanic black race).¹³ Prevalence of the disease increases with advancing age such that approximately half of people aged 60-69 years and three quarters of people aged 70 years or older are affected by hypertension.³

Hypertensive crises affect less than 1% of hypertensive adults in the United States.14

International

Worldwide, approximately 1 billion people have hypertension, contributing to more than 7.1 million deaths per year.¹⁵

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 for both ischemic heart disease and stroke doubles.³

The morbidity and mortality of hypertensive emergencies depend on the extent of EOD 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%.¹⁶

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.¹⁷ Hypertensive crises are also more common in African Americans compared with other races.

The prevalence and incidence of hypertension in Mexican Americans are similar to or lower than those in non-Hispanic whites.¹⁸ In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic whites and African Americans.¹⁹

Sex

The lifetime risk for hypertension is 86-90% in females and 81-83% in men.³

Age

Hypertensive crises are more common among elderly persons.

Clinical

History

The history should focus on the presence of end-organ dysfunction (EOD), the circumstances surrounding the hypertension, 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 hypertension
• Degree of BP control
• Presence of previous EOD, particularly renal and cerebrovascular disease
• Date of last menstrual period
• Other medical problems (eg, prior hypertension, thyroid disease, Cushing disease, systemic lupus, renal disease)
• Assess whether specific symptoms suggesting EOD 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 EOD is present.

• Vital signs
  • 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 may suggest aortic dissection).
• Ear, nose, and throat (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 hypertension. 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

Differential Diagnoses

Acute Coronary Syndrome	Hyperthyroidism, Thyroid Storm, and Graves Disease
Aneurysm, Abdominal	Myocardial Infarction
Anxiety	Pregnancy, Eclampsia
Congestive Heart Failure and Pulmonary Edema	Pregnancy, Preeclampsia
Cushing Syndrome	Stroke, Hemorrhagic
Delirium Tremens	Stroke, Ischemic
Dissection, Aortic	Subarachnoid Hemorrhage
Encephalitis	Systemic Lupus Erythematosus
Glomerulonephritis, Acute	Toxicity, Amphetamine
Headache, Cluster	Toxicity, Phencyclidine
Headache, Migraine
Headache, Tension

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

Laboratory Studies

The following laboratory studies are indicated for patients with hypertensive emergencies:

• 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

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 hypertension directly in the prehospital setting is unwise. In particular, rapid lowering of BP can critically decrease end-organ perfusion.

Emergency Department Care

Between 3% and 45% of adult ED patients will have at least one increased BP during their stay in the ED.⁷ The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of end-organ dysfunction (EOD).

• 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. Most evidence suggests that two blood pressure measurements are adequate for screening purposes.²⁰
  • Consider the context of the elevated BP (eg, severe pain often causes an increase in BP).
• Screen for EOD: The patient's history, physical examination, laboratory studies, and diagnostic tests, as outlined in Workup, should be used to determine if EOD exists.
• Patients without evidence of EOD 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, end-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 EOD 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:

Neurological emergencies

• Hypertensive encephalopathy
  • Preferred medications
    • Labetalol
    • Nicardipine
    • Esmolol
  • Medications to avoid
    • Nitroprusside
    • Hydralazine
  • Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours.²¹
• Acute ischemic stroke
  • Preferred medications
    • Labetalol
    • Nicardipine
  • Treatment guidelines: Withhold antihypertensive medications unless the systolic blood pressure (SBP) is >220 mm Hg or the diastolic blood pressure (DBP) is >120 mm Hg UNLESS patient is receiving IV or IA fibrinolysis, then goal BP: SBP <185>21
• Acute intracerebral hemorrhage
  • Preferred medications
    • Labetalol
    • Nicardipine
    • Esmolol
  • Medications to avoid
    • Nitroprusside
    • Hydralazine
  • Treatment guidelines: Treatment based on clinical/radiographic evidence of increased intracranial pressure (ICP). If signs of increased ICP, maintain MAP just below 130 mm Hg (or SBP <180>21
• Subarachnoid hemorrhage
  • Preferred medications
    • Nicardipine
    • Labetalol
    • Esmolol
  • Medications to avoid
    • Nitroprusside
    • Hydralazine
  • Treatment guidelines: Maintain SBP <160>21

Cardiovascular emergencies

• Aortic dissection
  • Preferred medications
    • Labetalol
    • Nicardipine
    • Nitroprusside (with beta-blocker)
    • Esmolol
    • Morphine sulfate
  • Medications to avoid
    • Avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade.
  • Treatment guidelines: Maintain SBP <110>22
• Acute coronary syndrome
  • Preferred medications
    • Beta-blockers
    • Nitroglycerin
  • Treatment guidelines: Treat if SBP >160 mm Hg and/or DBP >100 mm Hg. Reduce BP by 20-30% of baseline. Thrombolytics are contraindicated if BP is >185/100 mm Hg.²³
• Acute heart failure
  • Preferred medications
    • Nitroglycerin
    • Enalaprilat
  • Treatment guidelines: Treatment with vasodilators (in addition to diuretics) for SBP ≥140 mm Hg. IV or sublingual nitroglycerin is the preferred agent.²³

Other disorders

• Cocaine toxicity/pheochromocytoma
  • Preferred medications
    • Diazepam
    • Phentolamine
    • Nitroglycerin/nitroprusside
  • Medications to avoid
    • Beta-adrenergic antagonists prior to phentolamine administration
  • Treatment guidelines: Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes.²⁴ Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Beta-blockers can be added for BP control only after alpha-blockade.
• Preeclampsia/eclampsia
  • Preferred medications
    • Hydralazine
    • Labetalol
    • Nifedipine
  • Medications to avoid
    • Nitroprusside
    • Angiotensin-converting enzyme inhibitors
    • Esmolol
  • Treatment guidelines: In women with eclampsia or preeclampsia, SBP should be <160>3 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.25
• Perioperative hypertension
  • Preferred medications
    • Nitroprusside
    • Nitroglycerin
    • Esmolol
  • Treatment guidelines: Target perioperative BP to within 20% of the patient’s baseline BP, except if there is the potential for life-threatening arterial bleeding. Perioperative beta-blockers are first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk of cardiac complications.²²
• 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 hypertension is usually a chronic problem, access to a primary care provider and long-term follow-up are essential for all patients.

Medication

Once the diagnosis of a true hypertensive emergency is established and EOD 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 end-organ function. See specific guidelines under Treatment.

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).

Labetalol (Normodyne)

Alpha-, beta1-, and beta2-blocker, especially useful with aortic dissection. Lowers BP, reduces incidence of myocardial infarctions and death.

Dosing

Adult

20 mg (0.25 mg/kg for an 80-kg patient) IVP over 2 min; may administer 40-80 mg at 10-min intervals, up to 300 mg total dose
Alternatively, IV infusion: Initially, 2 mg/min; titrate to response up to 300 mg total dose, if needed

Pediatric

0.4-1 mg/kg/h IV; maximum dose 3 mg/kg/h

Esmolol (Brevibloc)

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.

Dosing

Adult

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

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

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.

Phentolamine (Regitine)

Alpha1- and alpha2-adrenergic blocking agent, effective for pheochromocytoma and hypercatecholaminergic-induced hypertension.

Dosing

Adult

Load 5-20 mg IV q5min or infuse 0.2-0.5 mg/min

Pediatric

0.05-0.1 mg/kg/dose IV; 5 mg maximum single dose

Antihypertensive agents

Nitroglycerin and nitroprusside cause both arterial and venous dilatation. Nitroglycerin primary affects the venous system and helps to decrease preload. Nitroprusside decreases both preload and afterload, which helps to decrease myocardial oxygen demand.

Nitroglycerin (Nitro-Bid)

Decreases coronary vasospasm, which increases coronary blood flow. Also induces vessel dilatation, decreasing cardiac workload.

Dosing

Adult

Continuous IV infusion: Start 5 mcg/min, increase by 5 mcg/min q3-5min to 20 mcg/min; if no response at 20 mcg/min increase by 10 mcg/min q3-5min, up to 200 mcg/min

Pediatric

Not established; suggested dose start with 0.25-0.5 mcg/kg/min continuous IV infusion and titrate by 1 mcg/kg/min at 20-60 min intervals to desired effect; 1-3 mcg/kg/min usual dose; 5 mcg/kg/min maximum

Sodium nitroprusside (Nitropress)

Reduces peripheral resistance by acting directly on arteriolar and venous smooth muscle.

Dosing

Adult

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

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

Hydralazine (Apresoline)

Principal indication is treatment of eclampsia. Decreases systemic resistance through direct vasodilation of arterioles.

Dosing

Adult

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

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

Fenoldopam (Corlopam)

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.

Dosing

Adult

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

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

Calcium channel blockers

Clevidipine mediates influx of calcium during depolarization in arterial smooth muscle. Reduces mean arterial blood pressure by decreasing systemic vascular resistance, but does not reduce preload.

Clevidipine butyrate (Cleviprex)

Dihydropyridine calcium channel blocker. Rapidly metabolized in blood and tissues and does not accumulate in the body. Administered IV and indicated for rapid and precise blood pressure reduction. Available in a concentration of 0.5 mg/mL as single-use vials (50 mL or 100 mL).

Follow-up

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 end-organ dysfunction (EOD), the patient does not need immediate treatment in the ED. The patient does require proper follow-up. See recommendations below.
• The Joint National Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no EOD.^3,7
  • Prehypertension (SBP 120-139 mm Hg, DBP 80-89 mm Hg: BP should be rechecked within 1 year.
  • Stage I hypertension (SBP 140-159 mm Hg, DBP 90-99 mm Hg): BP should be rechecked within 2 months.
  • Stage II hypertension: (SBP >160 mm Hg or DBP >100 mm Hg): BP should be confirmed and the patient should have follow-up within 1 month.
  • If BP is >180/110 mm Hg: BP should be confirmed and the patient should have follow-up within 1 week. The EP should consider initiating BP treatment upon discharge from the ED.
  • If SBP is >210 mm Hg or DBP >120 mm Hg: Confirm BP, initiate antihypertensive treatment upon discharge from the ED, and arrange close follow-up within 1 week.

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 hypertension is the best method for prevention of acute hypertensive emergencies.
• Patient education and close follow-up care in patients who have had a hypertensive crisis are essential to prevent recurrent hypertensive emergencies.
• Proper use of antihypertensive medications 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.¹⁸
• Five-year survival rate among all patients who present with hypertensive crisis is 74%.²⁶

Patient Education

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

Miscellaneous

Medicolegal 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 hypertension

Source : http://emedicine.medscape.com/article/758544-overview?src=emed_whatnew_nl_0