Hypertension is the continuing increase in systolic blood pressure at rest (?140 mm Hg), diastolic blood pressure (?90 mmHg), or both. Hypertension with no known cause (primary; formerly essential hypertension) is most common. Hypertension with an identified cause (secondary hypertension) occurs generally due to chronic renal disease or primary aldosteronism. Usually, no symptoms develop when the hypertension is not severe or long lasting. The diagnosis is made by a blood pressure measurement. Tests can be performed to determine the cause, determine the extent of damage and to identify other cardiovascular risk factors. Treatment includes lifestyle changes and medications, incl. Diuretics, beta blockers, ACE inhibitors, angiotensin II receptor antagonists and calcium channel blockers.

(See also 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults [JNC 8]).

Hypertension is the continuing increase in systolic blood pressure at rest (?140 mm Hg), diastolic blood pressure (?90 mmHg), or both. Hypertension with no known cause (primary; formerly essential hypertension) is most common. Hypertension with an identified cause (secondary hypertension) occurs generally due to chronic renal disease or primary aldosteronism. Usually, no symptoms develop when the hypertension is not severe or long lasting. The diagnosis is made by a blood pressure measurement. Tests can be performed to determine the cause, determine the extent of damage and to identify other cardiovascular risk factors. Treatment includes lifestyle changes and medications, incl. Diuretics, beta blockers, ACE inhibitors, angiotensin II receptor antagonists and calcium channel blockers. (See also 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults [JNC 8]). In the US, about 75 million people have hypertension (n. D. Talk .: The prevalence in the Western industrialized countries is 25%, aged> 50 years, up to 50%) know about 81% of these people that they have hypertension , only 73% to be treated and only 51% the hypertension is adequately adjusted. In adults, hypertension occurs more often in dark-skinned people (41%) than in light-skinned (28%) or Mexican Americans (28%), and the morbidity and mortality rates are higher in dark-skinned. Blood pressure increases with age. Approximately two-thirds of people> 65 years, hypertension and those with normal blood pressure at the age of 55 years have a 90% lifetime risk of developing hypertension. Because hypertension is so common with increasing age, the age-dependent increase in blood pressure may seem harmless, but the higher blood pressure increases the morbidity and mortality risk. Hypertension can develop (hypertension in pregnancy and pre-eclampsia and eclampsia) during pregnancy. Etiology hypertension may be primary (85 to 95% of cases) Secondary Primary Hypertension The hemodynamic and physiological components (eg., Plasma volume, activity of the renin-angiotensin system) vary and can recognize that the primary hypertension probably has no single cause , Even if is responsible initially a factor that probably several factors involved that increase blood pressure persistently (mosaic theory). In the afferent arterioles systemic malfunction of ion pumps Sarkolemmembranen of smooth muscle cells leads to chronically elevated vascular tone. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (eg., Sodium in the diet, obesity, stress) seem to apply only to genetically susceptible individuals in younger age groups. However, a high sodium intake in patients leads> 65 likely to Hypertonie.Sekundäre hypertension The causes include primary aldosteronism (assumed as the most common cause), renal parenchymal disease (eg. As chronic glomerulonephritis or pyelonephritis, polycystic kidney disease, connective tissue disease, obstructive uropathy) , renovascular disease, pheochromocytoma, Cushing’s syndrome, congenital adrenogenital syndrome, hyperthyroidism, myxedema and coarctation of the aorta. An excessive alcohol consumption and the use of oral contraceptives are common causes of curable hypertension. The intake of sympathomimetic, NSAIDs, corticosteroids, cocaine or licorice usually carries to the deterioration of hypertension control. Since the pathophysiology of the blood pressure cardiac output corresponding output (CO) x the total peripheral resistance (TPR), the pathogenetic mechanism include Increased Cardiac Output Enhanced TPR Both must In most patients, the cardiac output is increased normal or slightly increased, and the TPR. This image is typical of the primary hypertension and hypertension as a result of primary hyperaldosteronism, pheochromocytoma, renovascular disease and renal parenchymal disease. In other patients, the cardiac output is increased (possibly because venoconstriction in large veins) and the TPR is inappropriate normal for the degree of cardiac output. Later in the disease the TPR increases and cardiac output returns to normal level, probably because of autoregulation. Some diseases that increase the cardiac output (thyrotoxicosis, arteriovenous fistula, aortic insufficiency), lead to isolated systolic hypertension, v. a. when the stroke volume is increased. Some older patients have isolated systolic hypertension with normal or low cardiac output, probably due to lack of elasticity of the aorta and its major branches. Patients at high fixed diastolic blood pressure often have a decreased cardiac output. The plasma volume tends to decrease when the blood pressure rises; rare plasma volume remains normal or increases. In a hypertension as a result of a primary aldosteronism or renal Parenchymkrankheit plasma volume tends to be rather high, with a pheochromocytoma it can be quite low. The renal blood flow decreases gradually as the diastolic blood pressure rises and atherosclerosis begins. The GFR remains normal until late stages of the disease; as a result, the filtration fraction is increased. The coronary, cerebral and muscular blood flow is maintained in these regions until a severe atherosclerosis also occurs in these vascular beds. Morbid sodium transport in many cases of hypertension of sodium transport across the cell membrane is pathologically altered, as the sodium-potassium pump (Na +, K + -ATPase), defective or inhibited or because the permeability for sodium ions is increased. The result is an increased intracellular sodium content, which makes the cell more sensitive for a sympathetic stimulation. Calcium follows sodium, can be so that an accumulation of intracellular calcium responsible for the increased sensitivity. Since the Na +, K + -ATPase may noradrenaline pumped back into the sympathetic neurons (and is inactivated in this way the neurotransmitters), inhibition could lead this mechanism and enhances the activity of norepinephrine and increase blood pressure. Defects in sodium transport can in normotensive children of hypertensive parents auftreten.Sympathisches nervous system A sympathetic stimulation increases blood pressure, usually greater in patients with prehypertension (systolic blood pressure 120-139 mmHg, diastolic Bludruck 80-89 mmHg) or (hypertensive systolic blood pressure ?140 mmHg, diastolic blood pressure ?90 mm Hg or both increased) than in normotensive patients. (N. D. Talk .: In the US, a blood pressure of 120 to 139 mmHg systolic and diastolic 80-89 mmHg is called prähypertensiv. This division is in the definition of the German Hypertension in force). Whether this excessive response is due to the sympathetic nervous system or the myocardium and vascular smooth muscle cells is not known. A high resting pulse rate, which may be caused by an increased sympathetic activity, is a well known predictor of hypertension. Some hypertensive patients, circulating Plasmacatecholaminspiegel are higher than normal.Renin-angiotensin-aldosterone system This system helps to regulate blood volume at rest and hence blood pressure. Renin, an enzyme that is formed in the juxtaglomerular apparatus, catalyzes the conversion of angiotensinogen to angiotensin I. This inactive product is made of angiotensin-converting enzyme (ACE) mainly in the lungs, but also in the kidneys and the brain to angiotensin II , a potent vasoconstrictor, split, of this also stimulates the autonomic centers in the brain to increase sympathetic discharge and aldosterone and Vasopresin release. Aldosterone and vasopressin cause sodium and water retention and increase blood pressure. Aldosterone also increases the excretion of potassium. Low plasma potassium levels (<3.5 mEq / l) increase the vasoconstriction by closing the potassium channels. Angiotensin III, which is present in the circulation, which promotes aldosterone as effective as angiotensin II, but has far less effect on blood pressure. Since Chymaseenzyme also convert angiotensin I to angiotensin II, drugs that inhibit ACE not suppress angiotensin II production completely. Renin secretion is controlled by at least four mechanisms that are not mutually exclusive: A renal vascular receptor responsive to changes in the tension in the afferent arteriolar wall A macula densa receptor recognizes changes in the flow rate or the concentration of sodium chloride in the distal tubule Circulating angiotensin has a negative feedback effect on renin secretion the sympathetic nervous system stimulates the renin secretion mediated by beta-receptors (via the renal nerve) It is generally accepted that angiotensin is responsible for renovascular hypertension, at least in the early stage. However, the role of the renin-angiotensin-aldosterone system in primary hypertension has not been established. In dark-skinned and elderly patients with hypertension but renin levels tend to be low. Elderly patients also tend to have low angiotensin II levels. Hypertension due to chronic renal parenchymal disease (renoprivale hypertension) arises from the combination of renin-dependent and volume-dependent mechanisms. In most cases, the increased renin activity is not detected in the peripheral blood. Hypertension is typically moderate and sensitive to a balanced sodium and lack Wasserhaushalt.Vasodilatatorische The lack of a vasodilator (z. B. bradykinin, nitric oxide) may be more than the excessive increase of a vasoconstrictor (z. B. Angiotensin, norepinephrine) cause hypertension , When the kidneys do not produce adequate amounts of vasodilators (due to renal parenchymal disease or with bilateral nephrectomy), the blood pressure may rise. Vasodilators and vasoconstrictors (mainly endothelin) are also produced in endothelial cells. Therefore, the endothelial dysfunction influenced to a large degree the Blutdruck.Pathologie and complications In the early phase of hypertension no pathological changes will occur. A severe or long-term hypertension damage target organs (primarily the cardiovascular system, the brain and kidneys), increases the risk of coronary heart disease (CHD) and myocardial infarction heart failure stroke (particularly haemorrhagic) kidney failure die The pathogenesis involves the development of generalized atherosclerosis and a accelerated atherogenesis. Atherosclerosis is characterized by a medial hypertrophy, hyperplasia and characterized -hyalinisierung; it is v. a. noticeable in the small arterioles, particularly in the eyes and kidneys. In the kidneys, the changes result in a narrowing of the arteriolar vessel lumen and increase the TPR lead; Thus hypertension leads to a further increase in hypertension. In addition, each small further reduction in the already hypertrophied muscle cells leads to a greater reduction than lumens in arteries with normal vessel diameter. These effects may explain why it is the longer the hypertension is present, is less likely that a specific treatment (eg. As a renovascular surgery) results in secondary causes to normalizing blood pressure. Due to the increased afterload of the left ventricle hypertrophy gradually, leading to diastolic dysfunction. Under certain circumstances, the ventricles dilated well and this leads to dilated cardiomyopathy and heart failure due to systolic dysfunction, which is often reinforced by atherosclerotic coronary heart disease. A thoracic aortic dissection is a typical consequence of hypertension. Almost all patients with abdominal aortic aneurysms have hypertension. Symptoms and complaints Hypertension is usually asymptomatic until complications develop in the target organs. Dizziness, a flushed face, headache, fatigue, nosebleeds and nervousness are not caused by an uncomplicated hypertension. Severe hypertension (hypertensive emergencies) can cause serious cardiovascular, neurological, renal and retinal symptoms (eg. As symptomatic coronary artery disease, heart failure, hypertensive encephalopathy, renal failure). A fourth heart sound is one of the earliest signs of hypertensive heart disease. Changes in the retina include narrowing of the arterioles, hemorrhages, exudates and in patients with encephalopathy also papilledema ([/ B] (hypertensive retinopathy). The changes are divided into 4 groups (after the Keith-Wagener-Barker classification) with progressively poorer Prognosis: step 1: stricture ( "constriction") only of arterioles grade 2: constriction and sclerosis of arterioles grade 3: bleeding and exudates in addition to vascular changes grade 4: papilledema diagnosis Several measurements of blood pressure to confirm urinalysis and albumin creatinine ratio urine, if abnormal, renal ultrasonography is contemplated blood tests: Fast lipids, creatinine, potassium renal ultrasonography, when creatinine is increased evaluation of aldosteronism, if potassium is reduced ECG If left ventricular hypertrophy is present, echocardiography contemplated Sometimes measurement of thyroid stimulating hormone evaluation of pheochromocytoma or a sleep disorder when blood pressure increase is sudden and alternating or severely Hypertension is diagnosed by blood pressure measurements and classified. A medical history, helping the physical examination and other tests to identify the etiology and to determine whether these organs are damaged. Blood pressure should be measured two times - first in supine or sitting, then after the patient is ?2 minutes. The measurements must be made on each of 3 different days. The average of these measurements is used for diagnosis. Blood pressure is considered normal, prähypertensiv or in the stage 1 (mild) or stage 2 hypertension classified (Editor's note .: To recommendation of the German Hypertension takes place the division into optimal, normal, high normal and hypertension; see table..: JNC-7 classification of blood pressure in adults). In infants and children, the normal blood pressure Much is lower. Ideally, the blood pressure of> 5 min is measured calm and at different times of the day. A blood pressure cuff is applied to the upper arm. A suitable blood pressure cuff covers two thirds of the biceps. The inflatable cuff is long enough to encompass> 80% of the arm. The width of the cuff is at least 40% of the upper arm circumference. Therefore obese patients need larger cuffs. The blood pressure cuff is inflated over the expected systolic blood pressure and then gradually released, while auscultating over the brachial artery. The pressure at which the first beat is heard when the pressure drops, the systolic blood pressure. The complete disappearance of sounds determines the diastolic blood pressure. The same principle is applied to the blood pressure in the forearm (radial artery) or thigh (popliteal artery) to measure. Blood pressure measuring devices that contain mercury, are the most accurate (n. D. Ed .: Sphygnomanometer to Riva-Rocci). Mechanical devices should be calibrated regularly. Automatic devices are often not accurate. Blood pressure is measured in both arms. A blood pressure in one arm> 15 mmHg higher than the others, is associated with higher mortality and requires an evaluation of the upper vascular system when measuring pattern is found. Blood pressure is also measured at the thigh (with a much larger sleeve) in order to exclude a coarctation of the aorta, v. a. in patients with reduced or delayed pulses in the femoral artery. In a coarctation of the blood pressure in the legs is significantly lower. If the blood pressure in hypertensive low range or striking labile, more blood pressure measurements are desirable. Blood pressure values ??can be sporadic increases before the hypertension is persistent. This phenomenon is probably the so-called. “White coat hypertension” responsible, in which the blood pressure is elevated when it is measured in the doctor’s room, but normally, when measured at home or ambulatory monitors. Extreme increases in blood pressure, which alternate with normal values, but are uncommon and may talk for a pheochromocytoma, a sleep disorder such as sleep apnea or not added drug use. History The history includes information about the known duration of hypertension and previously measured values. Any history of or all of the symptoms of coronary heart disease, congestive heart failure or other relevant concomitant diseases (e.g.., Stroke, renal insufficiency, peripheral vascular disease, dyslipidemia, diabetes and gout) are detected, as well as a family history of these diseases. The social history includes the training status and the consumption of tobacco, alcohol and stimulant drugs (prescribed or illegally). A diet history focuses on the salt and stimulants intake (eg. As coffee, tea, caffeinated soft drinks, energy drinks) .Körperliche examination The physical examination includes the measurement of body size, body weight, waist circumference, the fundoscopic examination of the fundus in view to retinopathy, auscultation wind noise on the neck and abdomen and a complete cardiac, respiratory and neurological examination. The abdomen is examined for an enlargement of the kidney and the presence of abdominal masses. The peripheral arterial pulses are sampled. Decreased or absent pulses of the femoral speak for aortic coarctation, especially in patients <30 years. A unilateral renal artery noise can in thin patients with renovascular hypertension werden.Tests heard more severe the hypertension and the younger the patient is, the more detailed the investigation. Basically, if the hypertension is diagnosed, are routine tests performed to detect organ damage identification of cardiovascular risk factors These tests include urinalysis and albumin: creatinine ratio in urine, blood samples (creatinine, potassium, sodium, plasma glucose in the fasting state, lipid profile and often thyrotropin) ECG ambulatory blood pressure monitoring, a renal scintigraphy, an X-ray chest film screening tests for pheochromocytoma and renin-sodium profiles are not routinely performed. The peripheral plasma renin activity is not helpful in the diagnosis or medication choice. Depending on the results of the first tests, further tests may be necessary. When the urinalysis discovered a albuminuria (proteinuria), cylinders in the urine or hematuria, or if the serum creatinine is increased (? 1.4 mg / dl [124 .mu.mol / l] in men; ? 1.2 mg / dl [106 .mu.mol / l] in women), renal ultrasonography for determination of renal size can be useful. Patients with hypokalemia, which is not associated with an intake diuretics are examined for the presence of a primary aldosteronism and a high salt intake down. The ECG is characterized by a broad, knotted P-wave, which speaks for a Vorhofhypertrophie which, although may be non-specific, one of the earliest signs of hypertensive heart disease. Left ventricular hypertrophy, characterized by a sustained apical impulse and increased QRS rashes with or without ischemia may occur later. If one of these two characters is present, often an echocardiogram is performed. In patients with a pathological lipid profile or symptoms of coronary heart disease, further tests may for cardiovascular risk factors (eg., C-reactive protein) may be useful. When a coarctation of the aorta is believed to help a chest x-ray absorption, echocardiography, CT or an MRI to confirm the diagnosis. Patients with unstable significantly elevated blood pressure and symptoms such as headache, palpitations, tachycardia, excessive sweating, tremor and pallor be on the presence of a pheochromocytoma toward investigated (for. Example, by measuring the free Plasmacatecholaminmetaboliten). A sleep study should also be seriously considered. Patients with symptoms that speak for Cushing's syndrome, a connective tissue disease, eclampsia, acute porphyria, hyperthyroidism, a myxedema, acromegaly or CNS disease are investigated further (see elsewhere in the MSD Manual). LinksventrikulärerHypertrophie ECG © Springer Science + Business Media var model = {thumbnailUrl: '/-/media/manual/professional/images/515-left-ventricular-hypertrophy-on-ekg-s108-springer-high_de.jpg?la=de&thn = 0 & mw = 350 ', imageUrl' /-/media/manual/professional/images/515-left-ventricular-hypertrophy-on-ekg-s108-springer-high_de.jpg?la=de&thn=0 ', title:' LinksventrikulärerHypertrophie ECG ", description: ' u003Ca id = " v38395843 ""class = "" anchor "" u003e u003c / a u003e u003cdiv class = "" para "" u003e u003cp u003eDieses ECG showing voltage criteria for left ventricular hypertrophy (LVH) u003c / p u003e u003c / div u003e 'credits'. © Springer Science + Business Media'

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