Hypertensive Emergencies

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Author

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

eMedicine Salary Employment

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 Consortium Salary Management 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

Nothing to disclose.

Robin R Hemphill, MD, MPH, Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University

Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

Nothing to disclose.

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]

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]

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:

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]

Epidemiology

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, 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.

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.

Physical

The physical examination should assess whether EOD is present.

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.

Laboratory Studies

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

Imaging Studies

Other Tests

Prehospital Care

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).

Rapid BP reduction is indicated in the following circumstances:

Neurological emergencies

Cardiovascular emergencies

Other disorders

Consultations

Medication Summary

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]

Class Summary

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)

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

Esmolol (Brevibloc)

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.

Class Summary

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)

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

Class Summary

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)

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

Sodium nitroprusside (Nitropress)

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

Hydralazine (Apresoline)

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

Fenoldopam (Corlopam)

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]

Class Summary

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]

Clevidipine butyrate (Cleviprex)

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).

Further Inpatient Care

Further Outpatient Care

Transfer

Deterrence/Prevention

Complications

Complications may include the following:

Prognosis

References

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