Christy Hopkins, MD, MPH,,
Assistant Professor, Department of Surgery,
University of Utah School of Medicine; Clinical Operations
Director, Division of Emergency Medicine, University Health
Care; Medical Director, University Health Care Transfer
Center
Nothing to disclose.
Specialty Editor(s)
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
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Gary Setnik, MD,
Chair, Department of Emergency Medicine,
Mount Auburn Hospital; Assistant Professor, Division of
Emergency Medicine, Harvard Medical School
SironaHealth Salary Management
position; South Middlesex EMS
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position; ProceduresConsult.com Royalty Other
John D Halamka, MD, MS,
Associate Professor of Medicine, Harvard
Medical School, Beth Israel Deaconess Medical Center; Chief
Information Officer, CareGroup Healthcare System and Harvard
Medical School; Attending Physician, Division of Emergency
Medicine, Beth Israel Deaconess Medical
Center
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Robin R Hemphill, MD, MPH,
Associate Professor, Director, Quality and
Safety, Department of Emergency Medicine, Emory
University
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Chief Editor
David FM Brown, MD,
Assistant Professor, Division of Emergency
Medicine, Harvard Medical School; Vice Chair, Department of
Emergency Medicine, Massachusetts General
Hospital
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Background
Approximately 65 million people in the United States are affected by hypertension (HTN).[1] Substantial improvements have been made with regards to improving awareness and treatment of hypertension. However, approximately 22% of adults are still unaware of their hypertension; up to 32% of people with hypertension are not receiving treatment; and, of those treated, up to 36% do not have their blood pressure (BP) controlled to less than 140/90 mm Hg.[2]
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 damage may include the following:[4]
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 that are sustained throughout the ED stay and stay significantly elevated to this level on discharge should have 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."
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]
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, 18] 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.[19] In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic whites and African Americans.[20]
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.
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.
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[18]
Renal parenchymal disease - Chronic pyelonephritis, primary glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all secondary causes)
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.
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.[21]
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.
Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours.[22]
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 mm Hg and DBP < 110 mm Hg. After treatment with fibrinolysis, the SBP should be maintained < 180 mm Hg and DBP < 105 mm Hg for 24 hours.[22]
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 mm Hg) for first 24 hours after onset. Patients without increased ICP, maintain MAP < 110 mm Hg (or SBP < 160 mm Hg) for first 24 hours after symptom onset.[22]
Recent evidence shows that early intensive BP control is well tolerated and can reduce hematoma growth in patients treated within 6 hours after the onset of an ICH. The target systolic BP for these studies was 140 mm Hg and utilized routine intravenous medications. The target SBP was maintained over 7 days.[23, 24]
Treatment guidelines: Maintain SBP < 160 mm Hg until the aneurysm is treated or cerebral vasospasm occurs. Oral nimodipine is used to prevent delayed ischemic neurological deficits, but it is NOT indicated for treating acute hypertension.[22]
Medications to avoid: Avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade.
Treatment guidelines: Maintain SBP < 110 mm Hg, unless signs of end-organ hypoperfusion are present. Preferred treatment includes a combination of narcotic analgesics (morphine sulfate), beta-blockers (labetalol, esmolol), and vasodilators (nicardipine, nitroprusside). Calcium channel blockers (verapamil, diltiazem) are an alternative to beta-blockers.[25]
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.[26]
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.[26]
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.[27] Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Beta-blockers can be added for BP control only after alpha-blockade.
Medications to avoid: Nitroprusside, angiotensin-converting enzyme inhibitors, esmolol
Treatment guidelines: In women with eclampsia or preeclampsia, SBP should be < 160 mm Hg and DBP < 110 mm Hg in the prepartum and intrapartum periods. If the platelet count is < 100,000 cells mm3 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.[28]
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.[25]
Acutely lowering of BP in the ED for clinical situations other than those listed here is controversial and generally should be avoided.
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.[29]
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).
Clinical Context:
Alpha-, beta1-, and beta2-blocker, especially useful with aortic dissection. Lowers BP, reduces incidence of myocardial infarctions and death.
Clinical Context:
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.
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.
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.
Clinical Context:
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.[30]
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.[31]
Clinical Context:
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).
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).
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.
National Heart, Lung, and Blood Institute. Strong Heart Study Data Book: A Report to American Indian Communities. Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; 2001.
