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Hypertensive Urgency
Hypertensive urgency occurs when blood pressure spikes, but there is no damage to the
body's organs as a result and blood pressure can be brought down safely within a few
hours with blood pressure medication.
Hypertensive Emergency
When organ damage occurs as a result of severely elevated high blood pressure, this is
considered a hypertensive emergency. When this occurs, blood pressure must be reduced
immediately to prevent organ damage. This is done in an intensive care unit of a hospital.
• Headache
• Seizure
• Chest pain
• Shortness of breath
• Swelling or edema (fluid buildup in the tissues)
Certain tests will be given to monitor blood pressure and assess organ damage, including:
In a hypertensive emergency, the first goal is to bring down the blood pressure as quickly
as possible with intravenous (IV) blood pressure medications to prevent further organ
damage. Whatever organ damage that has occurred is treated with therapies specific to
the organ that is damaged.
Background
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Table
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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
• Neurological
o Hypertensive encephalopathy
o Cerebral vascular accident/cerebral infarction
o Subarachnoid hemorrhage
o Intracranial hemorrhage
• Cardiovascular
o Myocardial ischemia/infarction
o Acute left ventricular dysfunction
o Acute pulmonary edema
o Aortic dissection
• Other
o Acute renal failure/insufficiency
o Retinopathy
o Eclampsia
o Microangiopathic hemolytic anemia
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
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
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
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
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.
Sex
The lifetime risk for hypertension is 86-90% in females and 81-83% in men.3
Age
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
o Details of antihypertensive drug therapy and compliance
o Intake of over-the-counter preparations such as sympathomimetic agents
o 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.
o Chest pain - Myocardial ischemia or infarction
o Back pain - Aortic dissection
o Dyspnea - Pulmonary edema, congestive heart failure
o Neurologic symptoms - Seizures, visual disturbances, altered level of
consciousness (hypertensive encephalopathy)
Physical
• Vital signs
o BP should be measured in both the supine position and the standing
position (assess volume depletion).
o 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.
o Jugular venous distension
o Crackles
o Peripheral edema
• Abdomen - Abdominal masses or bruits
• CNS
o Level of consciousness
o Visual fields
o Focal neurologic signs
Causes
• Other causes
o Renal parenchymal disease - Chronic pyelonephritis, primary
glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all
secondary causes)
o Systemic disorders with renal involvement - Systemic lupus
erythematosus, systemic sclerosis, vasculitides
o Renovascular disease - Atherosclerotic disease, fibromuscular
dysplasia, polyarteritis nodosa
o Endocrine - Pheochromocytoma, Cushing syndrome, primary
hyperaldosteronism
o Drugs - Cocaine, amphetamines, cyclosporin, clonidine
withdrawal, phencyclidine, diet pills, oral contraceptive pills
o Drug interactions - Monoamine oxidase inhibitors with tricyclic
antidepressants, antihistamines, or tyramine-containing food
o CNS - CNS trauma or spinal cord disorders, such as Guillain-Barré
syndrome
o Coarctation of the aorta
o Preeclampsia/eclampsia
o Postoperative hypertension