eMedicine Specialties > Emergency Medicine > Cardiovascular

Hypertensive Emergencies

Author: Christy McCowan, 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
Contributor Information and Disclosures

Updated: Jan 26, 2009

Introduction

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.

• 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

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

• Search for CME/CE on This Topic »

• Intravenous Therapy for Hypertensive Emergencies, Part 1
• Alcohol Consumption in Young Adults and Incident Hypertension: 20-year Follow-up from the Coronary Artery Risk Development in Young Adults Study
• Key Articles and Guidelines Relative to Intensive Care Unit Pharmacotherapy: 2009 Update