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: y y y y y y 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

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CNS CNS trauma or spinal cord disorders, such as Guillain-Barr syndrome Coarctation of the aorta Preeclampsia/eclampsia Postoperative hypertension

Physical Vitals y y 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. y y y Jugular venous distension Crackles Peripheral edema

Abdomen Abdominal masses or bruits CNS y y y 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 low-grade 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+. The Cardiovascular System In order to pump blood through the body, the heart is connected to the vascular system of the body. This cardiovascular system is designed to transport oxygen and nutrients to the cells of the body and remove carbon dioxide and metabolic waste products from the body. The cardiovascular system is actually made up of two major circulatory systems, acting together. The right side of the heart pumps blood to the lungs through the pulmonary artery (PA), pulmonary capillaries, and then returns blood to the left atrium through the pulmonary veins (PV). The left side of the heart pumps blood to the rest of the body through the aorta, arteries, arterioles, systemic capillaries, and then returns blood to the right atrium through the venules and great veins.

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.