Arterial hypertension

Arterial hypertension - an increase in blood pressure at rest systolic (up to 140 mm Hg. Art. And above), diastolic (up to 90 mm Hg. Art. And above), or both.

Arterial hypertension, the cause of which is unknown (primary, essential), occurs most frequently; hypertension with a known cause of occurrence (secondary arterial hypertension) is most often the result kidney disease. Usually the patient does not feel the presence of hypertension until it becomes pronounced or permanent. The diagnosis is established by measuring blood pressure. Other studies are used to determine the cause, assess the risk and identify other cardiovascular risk factors. Treatment of arterial hypertension involves lifestyle changes and medications such as diuretics, b-blockers, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]

Epidemiology

In the US, arterial hypertension is present in about 50 million people. Only 70% of them know that they have arterial hypertension, 59% are treated and only 34% have adequate blood pressure control (BP). Among adults, arterial hypertension is more common in African Americans (32%) than in Caucasians with white skin (23%) or Mexicans (23%). Morbidity and mortality are also higher among African Americans.

Blood pressure rises with age. About two thirds of people over 65 suffer from arterial hypertension. People over 55 years of age with normal blood pressure have a 90% risk of developing hypertension over time. Since an increase in blood pressure is common in the elderly, such “age-related” hypertension may seem natural, but increased blood pressure increases the risk of complications and death. Hypertension can develop during pregnancy.

According to the criteria for the diagnosis of arterial hypertension, adopted by the World Health Organization in conjunction with the International Society of Hypertension (WHO-ISH), and the First Report of Experts of the Scientific Society for the Study of Arterial Hypertension of the All-Russian Scientific Society of Cardiology and the Interagency Council on Cardiovascular Diseases (DAG-1), arterial Hypertension is a condition in which the level of systolic blood pressure is equal to or greater than 140 mm Hg. And / or the level of diastolic blood pressure is equal to or greater than 90 mm Hg. With 3 different blood pressure measurements.

According to the modern classification of arterial hypertension, renal arterial hypertension is understood as arterial hypertension pathogenetically associated with kidney disease. This is the largest group of diseases of secondary arterial hypertension, which is about 5% of the number of all patients suffering from arterial hypertension. Even with normal renal function, renal arterial hypertension is observed 2-4 times more often than in the general population. With a decrease in renal function, the frequency of its development increases, reaching 85-90% in the stage of terminal renal failure. With normal blood pressure, only those patients who suffer from salt-losing kidney diseases remain.

[13], [14], [15], [16], [17], [18], [19]

Causes of hypertension

Arterial hypertension can be primary (85-95% of all cases) or secondary.

[20], [21], [22], [23]

Primary arterial hypertension

Hemodynamic and physiological components (such as plasma volume, plasma plasma renin activity) change, which confirms the assumption that primary arterial hypertension is unlikely to have one cause of development. Even if at the beginning one factor is predominant, then many factors are likely to take part in maintaining high blood pressure all the time (mosaic theory). In systemic arterioles, dysfunction of ion pumps of sarcolemma of smooth muscle cells can lead to a chronic increase in vascular tone. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (for example, the amount of sodium supplied with food, obesity, stress) are probably important only in people with hereditary predisposition.

[24], [25]

Secondary arterial hypertension

Causes of arterial hypertension include renal parenchymal diseases (for example, chronic glomerulonephritis or pyelonephritis, polycystic kidney disease, connective tissue diseases, obstructive uropathy), renovascular diseases, pheochromocytoma, Cushing syndrome, primary hyperdialodenalonism, cardiovascular dysfunction, fever, fever, cholangiosis Excessive alcohol use and the use of oral contraceptives are frequent causes of curable hypertension. Often, the use of sympathomimetics, glucocorticoids, cocaine or licorice contributes to an increase in blood pressure.

The connection between the kidneys and arterial hypertension has attracted the attention of researchers for more than 150 years. The first among the researchers who made a significant contribution to this problem are the names R. Bright (1831) and F. Volhard (1914), who pointed out the role of primary lesion of the renal vessels in the development of hypertension and presented a link between the kidneys and an increase in blood pressure in in the form of a vicious circle where the kidneys were both the cause of hypertension and the target organ. In the middle of the 20th century, the provision of the primary role of the kidneys in the development of arterial hypertension was confirmed and further developed in the studies of Russian (EM Tareev, GF Lang, AL Myasnikov, etc.) and foreign scientists (N. Goldblatt, AC Guyton et al.). The discovery of renin, produced by the kidney during its ischemia, and the renal prostaglandins: vasodilators and natriuretics - formed the basis for the development of knowledge about the renal endocrine system, which is able to regulate blood pressure. Sodium retention by the kidneys, leading to an increase in circulating blood volume, determined the mechanism for increasing blood pressure in acute nephritis and chronic renal failure.

A great contribution to the study of arterial hypertension was made by A.S. Guyton et al. (1970-1980). In a series of experiments, the authors proved the role of primary renal sodium retention in the genesis of essential arterial hypertension and postulated that the cause of any arterial hypertension is the inability of the kidneys to provide sodium homeostasis at normal blood pressure, including in NaCl elimination. The maintenance of sodium homeostasis is achieved by “switching” the kidney to the mode of operation under conditions of higher blood pressure values, the level of which is then fixed.

Further, in the experiment and in the clinic, direct evidence of the role of the kidneys in the development of arterial hypertension was obtained. They were based on the experience of kidney transplantation. Both in the experiment and in the clinic, transplantation of a kidney from a donor with arterial hypertension caused its development in the recipient, and, conversely, during transplantation of “normotensive” kidneys, previously high arterial pressure became normal.

A significant milestone in the study of the problems of the kidneys and hypertension were the work of V. Brenner et al., Which appeared in the mid-1980s. Keeping the primary retention of sodium by the kidneys as the main mechanism of arterial hypertension pathogenesis, the authors attributed the cause of this disorder to a decrease in the number of renal glomeruli and a corresponding decrease in the filtering surface of the renal capillaries. This leads to a decrease in kidney excretion of sodium (renal hypotrophy at birth, primary kidney disease, the state after nephrectomy, including kidney donors). At the same time, the authors thoroughly developed the mechanism of the damaging effect of arterial hypertension on the kidneys as a target organ. Arterial hypertension affects the kidneys (primary wrinkled kidney as the outcome of arterial hypertension or arterial hypertension accelerates the pace of development of renal failure) due to violations of intrarenal hemodynamics - increasing pressure inside the renal capillaries (intraglacial hypertension) and the development of hyperfiltration. Currently, the latter two factors are considered as leading in non-immune hemodynamic progression of renal failure.

Thus, it was confirmed that the kidneys can be both the cause of hypertension and the target organ.

The main group of diseases that lead to the development of renal arterial hypertension, are renal parenchymal diseases. Separately distinguish renovascular arterial hypertension resulting from renal artery stenosis.

Parenchymal kidney diseases include acute and chronic glomerulonephritis, chronic pyelonephritis, obstructive nephropathy, polycystic kidney disease, diabetic nephropathy, hydronephrosis, congenital renal hypoplasia, kidney injuries, renal-secreting tumors, renopodomy.

The frequency of detection of arterial hypertension in renal parenchymal diseases depends on the nosological form of renal pathology and the state of renal function. In almost 100% of cases, hypertension syndrome accompanies renin-secreting kidney tumor (renin) and lesions of the main renal vessels (renovascular hypertension).

[26], [27], [28], [29], [30], [31], [32],

Pathophysiology of arterial hypertension

Since arterial pressure depends on cardiac output (SV) and total peripheral vascular resistance (OPS), the pathogenetic mechanisms must include an increase in EF, an increase in OSS, or both of these changes.

In most patients, CB is normal or slightly increased, and OPSS is increased. Such changes are characteristic of primary arterial hypertension and hypertension caused by pheochromocytoma, primary aldosteronism, renovascular pathology and renal parenchymal diseases.

In other patients, the SV is elevated (possibly due to the constriction of the large veins), and OPSS remains relatively normal for the corresponding SV; as the disease progresses, OPSS increases, and the SV returns to normal, probably due to self-regulation. In some diseases that increase SV (thyrotoxicosis, arteriovenous shunts, aortic regurgitation), especially when the stroke volume increases, isolated systolic arterial hypertension is formed. In some elderly patients, isolated systolic hypertension with normal or decreased CB is present, probably due to a decrease in the elasticity of the aorta and its main branches. Patients with persistent high diastolic pressure always have a reduced CB.

With an increase in blood pressure there is a tendency to a decrease in plasma volume; sometimes the plasma volume remains the same or increases. Plasma volume in arterial hypertension increases due to primary hyper aldosteronism or renal parenchymal diseases and can significantly decrease with arterial hypertension associated with pheochromocytoma. With an increase in diastolic blood pressure and the development of sclerosis of arterioles, there is a gradual decrease in renal blood flow. Until the late stages of the development of the disease, OPSS remains normal; as a result, the filtration fraction increases. Coronary, cerebral and muscular blood flow is maintained until such time as the severe atherosclerotic lesion of the vascular bed joins.

[33], [34]

Sodium transport change

In some embodiments of arterial hypertension, sodium transport through the cell wall is impaired due to the anomaly or inhibition of Na, K-ATPase, or due to the increased permeability of the wall to Na. The result is an increased content of intracellular sodium, which makes the cell more sensitive to sympathetic stimulation. Ca ions follow Na ions, therefore the accumulation of intracellular calcium may also be responsible for increased sensitivity. Since Na, K-ATPase can return norepinephrine back to sympathetic neurons (thus inactivating this neurotransmitter), the inhibition of this mechanism may also enhance the effects of norepinephrine, contributing to an increase in blood pressure. Defects in the transport of sodium ions can occur in healthy children if their parents suffer from arterial hypertension.

[35], [36], [37], [38], [39], [40], [41], [42], [43], [44], [45], [46], [47]

Sympathetic nervous system

Sympathetic stimulation leads to an increase in blood pressure, usually to a greater extent in patients with borderline blood pressure (120-139 / 80-89 mm Hg. Art.) Or with arterial hypertension (systolic blood pressure 140 mm Hg., Diastolic 90 mm Hg. Or both changes) than in patients with normal blood pressure. This hyperreactivity occurs in sympathetic nerves or in the myocardium and the muscular sheath of blood vessels - is unknown. High resting heart rate, which may be the result of increased sympathetic activity, is a well-known predictor of arterial hypertension. In some patients with arterial hypertension, the content of catecholamines circulating in plasma alone is above normal.

[48], [49], [50], [51], [52], [53], [54], [55], [56], [57], [58], [59], [60], [61], [62]

Renin-angiotensin-aldosterone system

This system is involved in the regulation of blood volume and, accordingly, blood pressure. Renin, an enzyme synthesized in the juxtaglomerular apparatus, catalyzes the conversion of angiotensinogen to angiotensin I. It is an inactive substance that is converted by ACE, mainly in the lungs, but also in the kidneys and brain, into angiotensin II - a powerful vaso-constrictor that also stimulates autonomous centers in brain, increasing sympathetic activity, and stimulates the release of aldosterone and ADH. Both of these substances contribute to the retention of sodium and water, increasing blood pressure. Aldosterone also contributes to the removal of K ⁺; low potassium content in blood plasma (<3.5 mmol / l) increases vasoconstriction due to the closure of potassium channels. Angiotensin III, circulating in the blood, stimulates the synthesis of aldosterone as intensely as angiotensin II, but has a much lower pressure activity. Since they also convert angiotensin I to angiotensin II, ACE inhibiting drugs do not completely block the formation of angiotensin II.

Renin secretion is controlled by at least four non-specific mechanisms:

• renal vascular receptors that respond to changes in pressure in the affected arteriole wall;
• dense macula receptors {macula densa) that respond to changes in the concentration of NaCI in the distal tubule;
• circulating angiotensin, renin secretion;
• the sympathetic nervous system, like the kidney nerves, stimulates renin secretion indirectly through b-adrenoreceptors.

In general, it is proved that angiotensin is responsible for the development of renovascular hypertension, at least in the early stages, but the role of the renin-angiotensin-aldosterone system in the development of primary hypertension has not been established. It is known that in African Americans and elderly patients with arterial hypertension, renin content tends to decrease. The elderly also have a tendency to reduce the amount of angiotensin II.

Arterial hypertension associated with damage to the renal parenchyma (renal hypertension) is the result of a combination of renin-dependent and volume-dependent mechanisms. In most cases, there is no increase in renin activity in the peripheral blood. Hypertension is often moderate and sensitive to the balance of sodium and water.

[63], [64], [65], [66], [67]

Insufficiency of vazodilatator

Insufficiency of vasodilators (for example, bradykinin, nitric oxide), as well as an excess of vasoconstrictors (such as angiotensin, noradrenaline), can lead to the development of arterial hypertension. If the kidneys do not secrete vasodilators in the required amount (due to damage to the kidney parenchyma or bilateral nephrectomy), blood pressure may increase. Vasodilators and vasoconstrictors (mainly endothelium) are also synthesized in endothelial cells, therefore endothelial dysfunction is a powerful factor in arterial hypertension.

[68], [69], [70], [71]

Pathological changes and complications

There are no pathological changes in the early stages of hypertension. Severe or prolonged arterial hypertension affects target organs (primarily the cardiovascular system, brain and kidneys), increasing the risk of coronary vascular disease (PVA), MI, stroke (mainly hemorrhagic), and renal failure. The mechanism includes the development of generalized atherosclerosis and increased atherogenesis. Atherosclerosis leads to hypertrophy, hyperplasia of the middle choroid and its hyalinization. Mostly these changes develop in small arterioles, which is noticeable in the kidneys and the eyeball. In the kidney, changes lead to a narrowing of the lumen of the arterioles, increasing the round neck. Thus, hypertension leads to a further increase in blood pressure. Since arterioles are narrowed, any slight narrowing against the background of an already hypertrophied muscle layer leads to a reduction in the lumen to a much greater degree than in unaffected arteries. This mechanism explains why the longer there is arterial hypertension, the less likely that specific treatment (for example, surgery on the renal arteries) in secondary hypertension will lead to normalization of blood pressure.

Due to increased afterload, left ventricular hypertrophy gradually occurs, resulting in diastolic dysfunction. As a result, the ventricle expands, leading to dilated cardiomyopathy and heart failure (HF) due to systolic dysfunction. The dissection of the thoracic aorta is a typical complication of hypertension. Almost all patients with abdominal aortic aneurysms exhibit arterial hypertension.

[72], [73], [74], [75], [76], [77], [78], [79], [80], [81], [82]

Symptoms of arterial hypertension

There are no symptoms of arterial hypertension until complications develop in the target organs. Excessive sweating, facial flushing, headache, malaise, nosebleeds and irritability are not signs of uncomplicated hypertension. Severe arterial hypertension can occur with severe cardiovascular, neurological, renal symptoms or lesions of the retina (for example, clinically manifested atherosclerosis of the coronary vessels, heart failure, hypertensive encephalopathy, renal failure).

Early symptom of high blood pressure - IV heart tone. Changes in the retina may include narrowing of the arterioles, hemorrhages, exudation and, in the presence of encephalopathy, swelling of the nipple of the optic nerve. Changes are divided into four groups according to the increased likelihood of a poor prognosis (there are Kiss, Wegener and Barker classifications):

• Stage I - constriction of arterioles;
• Stage II - constriction and sclerosis of arterioles;
• Stage III - hemorrhages and exudation in addition to changes in blood vessels;
• Stage IV - swelling of the nipple of the optic nerve.

[83], [84], [85], [86], [87], [88], [89]

Diagnosis of arterial hypertension

Diagnosis of arterial hypertension is based on the results of changes in blood pressure. Anamnesis, physical examination and other methods of research help to identify the cause and clarify the damage to target organs.

Blood pressure should be measured twice (for the first time in the patient's position lying or sitting, again - after the patient stands at least 2 minutes) on 3 different days. The results of these measurements are used for diagnosis. BP is regarded as normal, prehypertension (borderline hypertension), stage I and stage II hypertension. Normal blood pressure is much lower in children.

Ideally, BP should be measured after a patient’s more than 5-minute rest at different times of the day. Tonometer cuff impose on the shoulder. The correct cuff covers two thirds of the biceps muscle of the shoulder; covers more than 80% (but not less than 40%) of the arm. Thus, obese patients need a large cuff. A specialist measuring blood pressure, injects air above the level of systolic pressure and then slowly releases it, producing auscultation of the brachial artery. The pressure at which the first heart sound is heard during the descent of the cuff is systolic blood pressure. The disappearance of the sound indicates diastolic blood pressure. The same principle is used to measure blood pressure on the wrist (radial artery) and thigh (popliteal artery). The most accurate measurement of blood pressure is mercury tonometers. Mechanical tonometers need to be calibrated regularly; Automatic blood pressure monitors often have a large error.

Blood pressure is measured on both hands; if the pressure on one hand is significantly higher than on the other, higher numbers are taken into account. Blood pressure is also measured on the legs (using a larger cuff) to detect aortic coarctation, especially in patients with a reduced or poorly maintained femoral pulse; with coarctation, blood pressure in the legs is significantly lower. If the blood pressure numbers are within the borderline hypertension or vary significantly, it is advisable to perform more blood pressure measurements. Figures of pressure can be raised only from time to time until the moment when arterial hypertension becomes stable; This phenomenon is often referred to as “white coat hypertension,” in which blood pressure rises when measured by a doctor in a medical institution and remains normal when measured at home and monitoring blood pressure daily. At the same time, pronounced sharp increases in blood pressure against the background of normal normal numbers are not usual and may indicate pheochromocytoma or unrecognized use of narcotic substances.

[90], [91], [92], [93], [94], [95], [96]

Anamnesis

When collecting anamnesis, the duration of arterial hypertension and the highest figures of blood pressure, which were previously registered, are specified; any indication of the presence or manifestation of PVA, HF, or other comorbidities (for example, stroke, renal failure, peripheral arterial disease, dyslipidemia, diabetes mellitus, gout), and a family history of these diseases. The history of life includes the level of physical activity, smoking, alcohol and stimulants (prescribed by a doctor and taken independently). Nutrition specifies in terms of the amount of salt consumed and stimulants (for example, tea, coffee).

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Objective examination

An objective examination involves measuring height, body weight and waist circumference; examination of the fundus to detect retinopathy; auscultation of noises in the neck and over the abdominal aorta, as well as a complete cardiological, neurological examination and study of the respiratory system. Abdominal palpation is performed to detect an increase in the kidneys and tumors of the abdominal cavity. Determine the peripheral pulse; a weakened or poorly conducted femoral pulse may indicate aortic coarctation, especially in patients younger than 30 years.

[104], [105], [106], [107], [108], [109], [110], [111]

Instrumental diagnosis of arterial hypertension

With more severe hypertension and in younger patients, instrumental diagnosis is more likely to lead to findings. In general, if arterial hypertension is diagnosed for the first time, routine tests are performed to identify target organ damage and risk factors for cardiovascular disease. Studies include urinalysis, the ratio of urine albumin fraction to creatinine; blood tests (amount of creatinine, potassium, sodium, serum glucose, lipid profile) and ECG. The concentration of thyroid stimulating hormone is often examined. In normal cases, outpatient monitoring of blood pressure, radioisotope renography, chest X-ray, screening for pheochromocytoma and interdependent renin-Na are not needed. The study of plasma renin concentration is not important for the diagnosis or selection of drugs.

Depending on the results of the initial examination and examination, additional use of various research methods is possible. If microalbuminuria, albuminuria or proteinuria, cylindruria or microhematuria are detected in the urine analysis, and if the serum creatinine content is elevated (123.6 μmol / l in men, 106.0 μmol / l in women), ultrasound of the kidneys is used to determine their size, which can make a big difference. In patients with hypokalemia, not associated with the appointment of diuretics, should be suspected primary hyperaldosteronism or excessive consumption of salt.

On the electrocardiogram, one of the earliest symptoms of "heart hypertension" is an extended pointed P wave, reflecting atrial hypertrophy (but this is a non-specific sign). The hypertrophy of the left ventricle, accompanied by the appearance of a pronounced apical impulse and a change in the QRS voltage with or without signs of ischemia, may appear later. In the event that any of these symptoms are detected, an echocardiographic examination is often performed. Patients with an altered lipid profile or signs of PVA are prescribed studies to identify other cardiovascular risk factors (for example, determine the content of C-reactive protein).

If aortic coarctation is suspected, chest x-rays, echocardiography, CT or MRI are performed, which allows to confirm the diagnosis.

Patients with labile blood pressure, characterized by significant increases, with clinical symptoms in the form of headache, palpitations, tachycardia, increased breathing, tremor and pallor, should be examined for the possible presence of pheochromocytoma (for example, a study of free plasma metanephrine).

Patients with symptoms suggestive of Cushing's syndrome, connective tissue diseases, eclampsia, acute porphyria, hyperthyroidism, myxedema, acromegaly, or CNS disorders should be examined (see other sections of the manual).

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Treatment of hypertension

Primary arterial hypertension has no cause, but in some variants of secondary arterial hypertension, the cause can be affected. In all cases, blood pressure control can significantly reduce the number of complications. Despite the treatment of hypertension, blood pressure is reduced to the target numbers in only one third of patients with arterial hypertension in the United States.

See also:

• What to do with high pressure?
• High Pressure Tablets

Lifestyle changes In all patients, target values to which blood pressure should be reduced are <140/90 mm Hg. V.; for patients with diabetes mellitus or kidney disease, target numbers are <130/80 mm Hg. Art. Or as close as possible to this level. Even the elderly and elderly patients can normally tolerate the diastolic pressure of 60-65 mm Hg. Art. Without increasing the risk and frequency of cardiovascular events. Ideally, patients or their family members should measure blood pressure at home, what they need to be taught, but they need to be monitored regularly, how they do it, and tonometers should be regularly calibrated.

Recommendations include regular exercise in the open air, at least 30 minutes a day, 3-5 times a week; weight loss to achieve a BMI of 18.5 to 24.9; to give up smoking; diet with an increased pressure ; rich in fruits, vegetables, low-fat foods with a reduced amount of saturated and total fat; sodium intake <2.4 g / day (<6 g table salt) and limiting alcohol intake to 30 ml per day for men and 15 ml per day for women. Stage I (mild hypertension), without signs of target organ damage, lifestyle changes can be effective without prescription. Patients with uncomplicated hypertension do not need to limit activity as long as BP is under control. Changes in dietary patterns can also help control the course of diabetes, obesity, and dyslipidemia. Patients with prehypertension should be convinced of the need to follow these recommendations.

Prognosis for hypertension

The higher the blood pressure and the more pronounced changes in retinal vessels or other manifestations of target organ damage, the worse the prognosis. Systolic blood pressure is the best predictor of fatal and non-fatal complications than diastolic. Without arterial hypertension treatment, the one-year survival of patients with retinosclerosis, cloud-like exudates, narrowing of arterioles and hemorrhages (III stage of retinopathy) is less than 10%, and in patients with the same changes and edema of the optic nerve (IV stage of retinopathy) - below 5%. PVA is becoming the most frequent cause of death in treated patients with arterial hypertension. Ischemic and hemorrhagic strokes are frequent complications of arterial hypertension in patients who have not properly chosen treatment. In general, effective control of blood pressure prevents the development of most complications and increases life expectancy.

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