INTRODUCTION

Hypertension is one of the most common worldwide diseases afflicting humans.

Because of the associated morbidity and mortality and the cost to society,
hypertension is an important public health challenge. Over the past several
decades, extensive research, widespread patient education, and a concerted effort
on the part of health care professionals have led to decreased mortality and
morbidity rates from the multiple organ damage arising from years of untreated
hypertension. Hypertension is the most important modifiable risk factor for coronary
heart disease (the leading cause of death in North America), stroke (the third
leading cause), congestive heart failure, end-stage renal disease, and peripheral
vascular disease. Therefore, health care professionals must not only identify and
treat patients with hypertension but also promote a healthy lifestyle and preventive
strategies to decrease the prevalence of hypertension in the general population.
Pre-hypertension Systolic blood pressure (SBP) 120-139 or diastolic blood
pressure(DBP) 80-89

Stage I HTN SBP 140-159 or DBP 90-99

Stage II HTN SBP >160 or DBP >100

Hypertensive crises encompass a spectrum of clinical presentations where

uncontrolled BPs leads to progressive or impending target organ dysfunction (TOD).
The clinical distinction between hypertensive emergencies and hypertensive
urgencies depends on the presence of acute TOD and not on the absolute level of
the BP.
Hypertensive emergencies represent severe HTN with acute impairment of an organ
system (eg, central nervous system [CNS], cardiovascular, renal). In these
conditions, the BP should be lowered aggressively over minutes to hours.
Hypertensive urgency is defined as a severe elevation of BP, without evidence of
progressive target organ dysfunction. These patients require BP control over several
days to weeks.
Causes
The most common hypertensive urgency is a rapid unexplained rise in BP in a
patient with chronic essential HTN.
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-Barr syndrome
Coarctation of the aorta
Preeclampsia/eclampsia
Postoperative hypertension
Physical
Vitals
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 suggests an aortic
dissection).
ENT: The presence of new retinal hemorrhages, exudates, or papilledema suggests a
hypertensive urgency.
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

Takayasu arteritis is a granulomatous vasculitis of unknown etiology that commonly

affects the thoracic and abdominal aorta. It causes intimal fibroproliferation of the
aorta, great vessels, pulmonary arteries, and renal arteries and results in segmental
stenosis, occlusion, dilatation, and aneurysmal formation in these vessels. Takayasu
arteritis is the only form of aortitis that causes stenosis and occlusion of the aorta.

Takayasu disease has also been referred to as pulseless disease and aortic arch
syndrome. During the acute inflammatory stage, Takayasu disease causes a lowgrade temperature, tachycardia, pain adjacent to the inflamed arteries (eg,
carotodynia), and easy fatigability in 50% of patients. Carotid and clavicular bruits,
asymmetric upper-extremity blood pressures, hypertension, diminished or absent
upper-extremity pulses, and ischemic symptoms can suggest the diagnosis
ANATOMY & PHYSIOLOGY
Central Nervous System
Medulla Oblongata; relays motor and sensory impulses between other parts of the
brain and the spinal cord. Reticular formation (also in pons, midbrain, and
diencephalon) functions in consciousness and arousal. Vital centers regulate
heartbeat, breathing (together with pons) and blood vessel diameter.
Hypothalamus; controls and intergrates activities of the autonomic nervous system
and pituitary gland. Regulates emotional and behavioral patterns and circadian
rhythms. Controls body temperature and regulates eating and drinking behavior.
Helps maintain the waking state and establishes patterns of sleep. Produces the
hormones oxytocin and antidiuretic hormone.
Cardiovascular System
Baroreceptor, pressure-sensitive sensory receptors, are located in the aorta, internal
carotid arteries, and other large arteries in the neck and chest. They send impulses
to the cardiovascular center in the medulla oblongata to help regulate blood
pressure. The two most important baroreceptor reflexes are the carotid sinus reflex
and the aortic reflex.
Chemoreceptors, sensory receptors that monitor the xhemical composition of blood,
are located close to the baroreceptors of the carotid sinus and the arch of the aorta
in small structures called carotid bodies and aortic bodies, respectively. These
chemoreceptors detect changes in blood level of O2, CO2, and H+.
Renal System
Renin-Angiotensin-Aldosterone system. When blood volume falls or blood flow to the
kidneys decreases, juxtaglomerular cells in the kidneys secrete renin into the

bloodstream. In sequence, renin and angiotensin converting enzyme (ACE) act on

their substrates to produce the active hormone angiotensin II, which raises blood
pressure in two ways. First, angiotensin II is a potent vasoconstrictor; it raises blood
pressure by increasing systemic vascular resistance. Second, it stimulates secretion
of aldosterone, which increases reabsorption of sodium ions and water by the
kidneys. The water reabsorption increases total blood volume, which increases
blood pressure.
Antidiuretic hormone. ADH is produced by the hypothalamus and released from the
posterior pituitary in response to dehydration or decreased blood volume. Among
other actions, ADH causes vasoconstriction, which increases blood pressure.
Atrial Natriuretic Peptide. Released by cells in the atria of the heart, ANP lowers
blood pressure by causing vasodilation and by promoting the loss of salt and water
in the urine, which reduces blood volume.