Arterial Hypertension

Front 1

Hypertension

Back 1

is sustained elevation of resting systolic BP (≥ 140 mm Hg), diastolic BP (≥ 90 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential hypertension) is most common; hypertension with an identified cause (secondary hypertension) is usually due to a renal disorder. Usually, no symptoms develop unless hypertension is severe or long-standing. Diagnosis is by sphygmomanometry. Tests may be done to determine cause, assess damage, and identify other cardiovascular risk factors. Treatment involves lifestyle changes and drugs, including diuretics, β-blockers, ACE inhibitors, angiotensin II receptor blockers, and Ca channel blockers.

Front 2

BP increases with age

Back 2

About 2⁄3 of people > 65 have hypertension, and people with a normal BP at age 55 have a 90% lifetime risk of developing hypertension. Because hypertension becomes so common with age, the age-related increase in BP may seem innocuous, but higher BP increases morbidity and mortality risk. Hypertension may develop during pregnancy

Front 3

Primary hypertension

Back 3

Hemodynamics and physiologic components (eg, plasma volume, plasma renin activity) vary, indicating that primary hypertension is unlikely to have a single cause. Even if one factor is initially responsible, multiple factors are probably involved in sustaining elevated BP (the mosaic theory). In afferent systemic arterioles, malfunction of ion pumps on sarcolemmal membranes of smooth muscle cells may lead to chronically increased vascular tone. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (eg, dietary Na, obesity, stress) seem to affect only genetically susceptible people.

Front 4

Secondary hypertension

Back 4

Secondary hypertension: Causes include renal parenchymal disease (eg, chronic glomerulonephritis or pyelonephritis, polycystic renal disease, connective tissue disorders, obstructive uropathy), renovascular disease (see below), pheochromocytoma, Cushing's syndrome, primary aldosteronism, hyperthyroidism, myxedema, and coarctation of the aorta. Excessive alcohol intake and use of oral contraceptives are common causes of curable hypertension. Use of sympathomimetics, corticosteroids, cocaine, or licorice commonly contributes to hypertension.

Front 5

Abnormal Na transport

Back 5

In some cases of hypertension, Na transport across the cell wall is abnormal, because the Na-K pump (Na+, K+-ATPase) is defective or inhibited or because permeability to Na+ is increased. The result is increased intracellular Na, which makes the cell more sensitive to sympathetic stimulation. Ca follows Na, so accumulation of intracellular Ca may be responsible for the increased sensitivity. Because Na+, K+-ATPase may pump norepinephrineSome Trade Names
LEVOPHED
Drug Information
back into sympathetic neurons (thus inactivating this neurotransmitter), inhibition of this mechanism could also enhance the effect of norepinephrineSome Trade Names
LEVOPHED
Drug Information
, increasing BP. Defects in Na transport may occur in normotensive children of hypertensive parents.

Front 6

Renin-angiotensin-aldosterone system

Back 6

This system helps regulate blood volume and therefore BP. Renin, an enzyme formed in the juxtaglomerular apparatus, catalyzes conversion of angiotensinogen to angiotensin I. This inactive product is cleaved by ACE, mainly in the lungs but also in the kidneys and brain, to angiotensin II, a potent vasoconstrictor that also stimulates autonomic centers in the brain to increase sympathetic discharge and stimulates release of aldosterone and ADH. Aldosterone and ADH cause Na and water retention, elevating BP. Aldosterone also enhances K excretion; low plasma K (< 3.5 mEq/L) increases vasoconstriction through closure of K channels. Angiotensin III, present in the circulation, stimulates aldosterone release as actively as angiotensin II but has much less pressor activity. Because chymase enzymes also convert angiotensin I to angiotensin II, drugs that inhibit ACE do not fully suppress angiotensin II production.

Front 7

Hypertensive Emergencies

Back 7

A hypertensive emergency is severe hypertension with signs of damage to target organs (primarily the brain, cardiovascular system, and kidneys). Diagnosis is by BP measurement, ECG, urinalysis, and serum BUN and creatinine measurements. Treatment is immediate BP reduction with IV drugs (eg, nitroprusside, β-blockers, hydralazine).

Front 8

Target-organ damage in hypertensive emergencies

Back 8

includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure. Damage is rapidly progressive and often fatal.

Front 9

Hypertensive encephalopathy

Back 9

may involve a failure of cerebral autoregulation of blood flow. Normally, as BP increases, cerebral vessels constrict to maintain constant cerebral perfusion. Above a mean arterial pressure (MAP) of about 160 mm Hg (lower for normotensive people whose BP suddenly increases), the cerebral vessels begin to dilate rather than remain constricted. As a result, the very high BP is transmitted directly to the capillary bed with transudation and exudation of plasma into the brain, causing cerebral edema, including papilledema.

Front 10

Renovascular Hypertension

Back 10

is BP elevation due to partial or complete occlusion of one or more renal arteries or their branches. It is usually asymptomatic unless long-standing. A bruit can be heard over one or both renal arteries in < 50% of patients. Diagnosis is by physical examination and renal imaging with duplex ultrasonography, radionuclide imaging, or magnetic resonance angiography. Angiography is done before definitive treatment with surgery or angioplasty.

Front 11

Atherosclerosis

Back 11

is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. Risk factors include dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension. Symptoms develop when growth or rupture of the plaque reduces or obstructs blood flow; symptoms vary by artery affected. Diagnosis is clinical and confirmed by angiography, ultrasonography, or other imaging tests. Treatment includes risk factor and dietary modification, physical activity, and antiplatelet drugs.

Front 12

Aspirin

Back 12

antiplatelet drug,indicated for secondary prevention and recommended for primary prevention of coronary atherosclerosis in patients at high risk (eg, diabetics with or without atherosclerosis, patients with ≥ 20% risk of cardiac events within 10 yr ). Optimal dose and duration are unknown, but 70 to 160 mg po once/day indefinitely is commonly used for primary prevention because it is effective while minimizing risk of bleeding. For secondary prevention and for patients with poorly controlled risk factors, 325 mg is a proven option. In about 10 to 20% of patients taking aspirin for secondary prevention, ischemic events recur. The reason may be aspirin resistance; assays to detect lack of thromboxane suppression (indicated by elevated urinary 11-dehydro thromboxane B2) are being studied for clinical use. Some evidence suggests that ibuprofenSome Trade Names
ADVIL
MOTRIN
NUPRIN
Drug Information
can interfere with aspirin's antithrombotic effect, so other NSAIDs are recommended for patients taking aspirin for prevention.

Front 13

Nonatheromatous arteriosclerosis

Back 13

is age-related fibrosis in the aorta and its major branches.
causes intimal thickening and weakens and disrupts the elastic lamellae. The smooth muscle (media) layer atrophies, and the lumen of the affected artery widens (becomes ectatic), predisposing to aneurysm or dissection. Hypertension is a major factor in development of aortic arteriosclerosis and aneurysm. Intimal injury, ectasia, and ulceration may lead to thrombosis, embolism, or complete arterial occlusion.

Front 14

Mönckeberg's arteriosclerosis

Back 14

(medial calcific sclerosis) affects patients > 50; age-related medial degeneration occurs with focal calcification and even bone formation within the arterial wall. Segments of the artery may become a rigid calcified tube without luminal narrowing. The diagnosis is usually obvious by plain x-ray. This disorder is clinically important only because it can greatly reduce arterial compressibility, causing extremely but falsely elevated BP readings.